Cardiovascular

Front 1

What is the absolute refractory period of cardiac muscle?

Back 1

250ms

Front 2

What is the approximate delay in the AV node?

Back 2

0.1s

Front 3

Cardiac output (CO) is...

Back 3

The amount of blood pumped per minute.

HRxSV

Front 4

Cardiac reserve is...

Back 4

The difference between resting and maximal CO.

Front 5

How do we calculate stroke volume?

Back 5

EDV-ESV

EDV = amount of blood collected in a ventricle during diastole.

ESV = amount of blood remaining in a ventricle after contraction.

Front 6

What three factors affect stroke volume?

Back 6

Preload
Contractility
Afterload

Front 7

How do exercise and slow heart rate increase stroke volume?

Back 7

Increased venous return and improved ventricular filling.
(Frank-Starling)

Front 8

What is contractility?

Back 8

Contractile strength, independent of stretch and EDV.

Front 9

What increases contractility?

Back 9

Increased sympathetic stimuli
Certain hormones (eg. epi)
Ca2+ and some drugs

Front 10

What decreases contractility?

Back 10

Acidosis
Increased extracellular K+
Calcium channel blockers/Beta bockers

Front 11

How is striated muscle (skeletal and cardiac) organized?

Back 11

Front 12

Why do muscle cells have a striated appearance?

Back 12

Myofilaments, the critical contractile elements are in register with each other.

Front 13

What are the three troponins invovled in muscle contraction?

Back 13

Troponin-T: binds to tropomyosin, anchoring the troponin complex

Troponin-C: binds Ca2+, an essential step in initiating contraction

Troponin-I: binds to actin, inhibiting actin-myosin interaction.

Front 14

What does tropomyosin do?

Back 14

Tropmyosin holds F-actin (a polymer of G-actin) together.

The entire structure is called a thin filament.

Front 15

What is the preferred enzyme test for myocardial injury?

Back 15

Cardiac isoforms of troponin T and I (cTnT and cTnI)

Rise 2 - 6 hours after injury.
Peak 12 - 16 hours
cTnI elevated for 5-10 days.
cTnT elevated for 5-14 days

Front 16

Thick filaments are made of Myosin II. What is Myosin II made out of?

Back 16

Each myosin II molecule contains two polypeptide heavy chains and four light chains (two each of two types).

Each myosin heavy chain (MHC) has globular head with one binding site for ATP and another for actin; also demonstrates ATPase and motor activity.

Myosin light chains (MLC) play structural and regulatory roles.

Front 17

What do the filaments bind to in the structure of a sarcomere?

Back 17

Thick filaments bind to M lines.
Thin filaments bind to Z lines.

Front 18

What are the stages of the muscle contraction cycle on the level of actin and myosin?

Back 18

Attachment (rigor formation)
Release
Bending
Force generation
Attachment: The Sequel

Front 19

What actually causes shortening of the muscle cell?

Back 19

Rapid contraction cycles that move the thin filaments along the thick filaments.

Front 20

What role does ATP play in muscle contraction?

Back 20

When ATP is absent the myosin head is tightly bound to actin.
(called “rigor configuration” because it causes rigor mortis in the complete absence of ATP).

Binding of ATP to the myosin head causes conformational changes in the actin binding site and reduces the affinity of the myosin head for the actin molecule.

The head then uncouples from the thin filament.

The Myosin head then undergoes further conformational changes, initiated by the breakdown of ATP, which cause it to bend. (Mg++ is a critical cofactor for this ATPase).

The Myosin head then binds weakly to new binding site on a neighboring actin molecule if Ca2+ is present.

Phosphate is released and the binding affinity between myosin and actin then increases.

The force is generated by the myosin head as it returns to its unbent position because it forces movement of the thin filament along the thick filament.During this “power stroke” ADP is lost from the myosin head.

With loss of ADP the myosin head is again left attached to the thin filament (rigor configuration) but to a different actin molecule, one closer to the Z line.

If ATP still available the cycle can repeat.

Front 21

What do we see when we look at contraction at the level of the sarcomere? (sliding filament model)

Back 21

I band and H band narrow but the A band maintains its width.

Front 22

What are the key regulators of muscle contraction?

Back 22

ATP
Calcium
Mg
Na
beta adrenergic receptors.

Front 23

What is the role of the sarcolemma and the transverse tubules?

Back 23

The sarcolemma conducts AP quickly over the surface of the muscle fiber.

T tubules are continuous with the sarcolemma and transduce the action potential into the sarcoplasmic reticulum which has stores of calcium to initiate contraction.

Front 24

How is excitation/contraction coupling different in cardiac muscle than in skeletal muscle?

Back 24

In skeletal muscle release of Ca++ from the sarcoplasmic reticulum is directly voltage dependent.

In cardiac muscle release of Ca++ from SR is Ca++ activated (calcium-dependent calcium release).

Front 25

How is an action potential propagated in cardiac muscle different from one propagated in a neuron?

Back 25

Both are about 100 mV
But
DURATION of cardiac muscle AP is two orders of magnitude longer than in nerve cell or skeletal muscle.
(cardiac AP ~ 300 ms; Nerve cell AP ~3ms)

Front 26

Why happens to skeletal muscle as it ages?

Back 26

It starts to increasingly resemble cardiac muscle.

Front 27

Compared to skeletal muscle how is cardiac muscle structurally different?

Back 27

Contains more and larger mitochondria.

Contains more glycogen granules.

Contains larger and more numerous T tubules (in ventricular muscle).

Contains multicellular “fibers” that are electrically and mechanically coupled via intercalated disks.

Intercalated discs cross the muscle cells transversely (parallel to the striations).

Front 28

Activity initiated in a cardiac muscle cell propagates in which direction?

Back 28

Any direction.

Except at the boundary between the atria and the ventricles because of the presence of non conducting fibrous tissue.

Front 29

What does each intercalated disc contain?

Back 29

Transverse components visible with light microscopy and
lateral components which are not evident with light microscopy.

Fascia adherens-
Anchor for thin filaments of terminal sarcomere.
Major transverse component.

Maculae adherens (desmosomes)-
Prevent cells from pulling apart under tension.
Transverse and lateral.

Gap junctions (communicating junctions)-
Major lateral component. Create ionic continutity and permit cardiac muscle cells to behave as a syncytium.

Front 30

How much faster than regular cardiac muscle fibers does the conduction system conduct impulses?

Back 30

4x

Front 31

What are the cellular characteristics of the SA node?

Back 31

Smaller than other cardiac cells.

Fewer and more poorly organized myofilaments.

Lack intercalated disks but have some intercellular junctions.

!!Slow SPONTANEOUS depolarization in the late stage of each action potential!!

Isolated nodal cells depolarize 80-100 /minute. (faster than normal HR because of denervation).

Fastest cell will control the rest in SA node.

Front 32

What does the SA node look like histologically?

Back 32

Embedded within fibrocollagenous supporting tissue.

Fibers fuse with surrounding atrial muscle fibers.

Connected to internodal fiber bundles which run to the AV node.

Front 33

At what rate does conduction occur in the atria?

Back 33

0.3 m/s

Front 34

At what rate does conduction occur in the internodal fibers?

Back 34

1 m/s

Front 35

Roughly how long is the AV node delay?

Back 35

0.1 s

Front 36

What is the intrinsic rate of the AV node?

Back 36

40-60

Should not autodepolarize unless SA node or internodal fibers are dysfunctional.

Front 37

What is the conduction rate in purkinje fibers?

Back 37

~0.3-0.5 m/s

Front 38

What are the histological characteristics of purkinje fibers?

Back 38

Large size

Abundant glycogen

Do not contain large amounts of contractile fibers so not as eosinophilic as cardiac muscle cells.

Frequent gap junctions/infrequent intercalated discs.

Insulation by sheath of connective tissue.

Front 39

How does the duration of the action impulse compare between the epicardium and endocardium?

Back 39

Duration is much shorter near the epicardium so the termination of activity appears as if it were propagating from the epicardium toward the endocardium.

Front 40

What is the total time from SA node firing to distribution of the impulse along the entire heart?

Back 40

~225 ms

Front 41

How long does the entire cardiac cycle take?

Back 41

~0.8s

Front 42

What is the average stroke volume?

Back 42

~70cc

Front 43

What percentage of patients with MI die before they reach the hospital?

Back 43

~1/3

Front 44

What ions cause depolarization to occur?

Back 44

Calcium induced sodium driven depolarization.

Calcium.

Potassium repolarization.

Front 45

What direction does contraction occur in ?

Back 45

A clockwise ringing type motion from the apex to the base of the heart.

Front 46

What proportion of the cells in the heart are fibrous (non muscle)?

Back 46

~ 2/3

Front 47

How does a propagating sodium channel impulse induce contraction?

Back 47

The propagating sodium current hits an L-type calcium channel at the bottom of the invagination into the myocyte.

This open a gate that allows a small amount of calcium to enter the cell and bind the ryanodine receptor channel on the sarcoplasmic reticulum.

The SR then releases a large amount of calcium into the cytoplasm.

The calcium causes contraction.

Front 48

In general, electrical conduction always preceeds...

Back 48

Mechanical contraction.

Front 49

How long is atrial systole?

Back 49

0.1 s

Front 50

How long is ventricular systole?

Back 50

0.4 s

Front 51

How long is ventricular diastole?

Back 51

0.4s

Front 52

What is a normal end diastolic volume?

Back 52

~135 cc

Front 53

What is a normal end systolic volume?

Back 53

~ 65cc

Front 54

How do we calculate EF?

Back 54

EF=SV/EDV

Front 55

Cardiac output is a function of stroke volume and HR, what influences each?

Back 55

HR by automaticity.

SV by contractility, afterload and preload.

Front 56

By what means does the central nervous system influence the heart?

Back 56

Front 57

How does autonomic tone influence heart rate?

Back 57

Front 58

End diastolic volume can be though of as a measure of...

Back 58

Preload

Front 59

What increases preload?

Back 59

Inspiration
Exercise
Aortic Regurg
Systemic Shunt

Front 60

What decreases preload?

Back 60

Valsalva
Dehydration
Atrial Fibrillation
Medications (diuretics etc.)

Front 61

When we refer to afterload we are generally referring to....

Back 61

Mean arterial pressure or Aortic Valve/ outflow tract resistance.

Front 62

Increased afterload causes...

Back 62

Longer isovolumetric contraction and slower rate of muscle fiber shortening.

Front 63

How does contractility influence SV?

Back 63

Increased contractility results in a greater stroke volume at any given preload or afterload.

Front 64

One of the best ways we can measure contractility is the...

Back 64

End systolic pressure volume ratio.

Front 65

How do Epi and NE influence the myocardium?

Back 65

Inotropic
Chronotropic

Front 66

Under normal physiological conditions, excercise causes...

Back 66

Rapid Relaxation
Heart fills under low pressure
Stroke volume increases

In contrast, when a person with CHF excercises there is:

Slow Relaxation
Heart fills under high pressure
Stroke volume only has a small increase.

Front 67

People with CHF can generate more work with their myocardium but they do it at the expense of...

Back 67

Higher end diastolic pressure.

Front 68

CHF is characterized by increased...

Back 68

Pressure in the left ventricle.

Front 69

Why is a CHF a situation where the worse it gets, the worse it gets?

Back 69

Front 70

CHF pathophysiology can be thought of as an imbalance of...

Back 70

Front 71

What are the three fates of chronic heart failure cells?

Back 71

They can be signalled to...
Grow
Become fibrotic
Designate themselves for death.

Front 72

What are the thrre hemodynamic defense mechanisms that lead to worsening heart failure?

Back 72

Sympathetic-Myocyte death
Renin angiotensin-Myocyte hypertrophy
Aldosterone-Cardiac fibrosis

Front 73

According to the ACC/AHA, what are the four stages of CHF?

Back 73

A. High Risk no structural changes

B. Structural changes without syndrome

C. Syndrome controlled with therapy

D. Syndrome uncontrolled despite therapy

Front 74

What are the NYHA classes of CHF symptoms?

Back 74

I.
No limitation of activity
II.
Mild limitation activity improves by slowing down.
III.
Marked limitation improves with rest.
IV.
Severe limitation or symptoms at rest.

Front 75

What type of hypertrophy do we find in systolic heart failure?

Back 75

Eccentric hypertrophy.

Front 76

What type of hypertrophy do we find in diastolic heart failure?

Back 76

Concentric hypertrophy.

Front 77

Near normal SV
Normal EDV
Steep diastolic PV relationship
is....

Back 77

Diastolic heart failure

Front 78

Low SV
High EDV
Steep diastolic PV relationship
is...

Back 78

Systolic heart failure.

Front 79

What are the epidemiological differences between systolic and diastolic heart failure?

Back 79

Younger males usually systolic HF.

Older females usually diastolic HF.

Front 80

How does the sarcoplasmic reticulum content of cardiac muscle compare to skeletal and smooth muscle?

Back 80

SR is less abundant than in skeletal muscle, but greater in density than smooth muscle

!Sarcolemma has specialized ion channels that skeletal muscle does not – voltage-gated Ca2+ channels!

Front 81

A junctional rythm from the AV node would be at a rate of about...

Back 81

55 bpm

Front 82

What are five causes of heart failure?

Back 82

Pump failure.
Obstruction to flow.
Regurgitant flow.
Disorders of Conduction.
Disruption of the continuity of the circulatory system.

Front 83

What is the ideal sarcomere length?

Back 83

2 - 2.4 micrometers

Front 84

How do ventricular pressure curves work?

Back 84

A hypodynamic heart has lower dP/dt, higher diastolic pressure, and reduced ejection time (C).

A hyperdynamic heart has lower diastolic pressure, higher dP/dt, brief ejection phase (B).

Front 85

How do pressure/volume loops work?

Back 85

Starting at the Southeast corner and working Counterclockwise:


Mitral valve closure.(point)=EDV

Isovolumic contraction.(line)

Aortic valve opening.(point)

Ejection.(line)

Aortic valve closure.(point)

Isovolumic relaxation.(line)

Mitral valve opening. (point)=ESV

Diastolic filling (line).

Repeat.

Rate of change (dP/dV) at aortic valve closure (NW corner) is a measure of contractility.

Front 86

What is LV ESPVR?

Back 86

The slope of the line represents left ventricular end-systolic pressure volume relationship and is an indicator of inotropy.

Contractility is improved with
inotropic drugs and the slope
is moved up and to the
left.

Ischemia reduces blood flow,
decreasing myocardial
contractility. The slope therefore moves down and right.

Front 87

What changes in ion concentrations occur in a cardiac muscle fiber following depolarization?

Back 87

Phase 0: Na+ channels open

Phase 1: Na+ channels close

Phase 2: Ca++ channels open; fast K+ channels close

Phase 3:Ca++ channels close; Slow K+ channels open.

Phase 4: Resting potential

Front 88

What is Poiseuille’s Law ?

Back 88

For a steady state, laminar flow newtonian fluid through a cylindrical tube, the flow (Q)
varies directly as the pressure difference (P1 - P0) and
the fourth power of the radius, (r) for the tube, and it varies
inversely with the length (l) of the tube and the viscosity (n) of the fluid.

Q= p(P1 - P0) r^4/8nl

In humans the principal resistance to flow is lumen caliber.

Front 89

SVR = BP/CO which means that...

Back 89

BP=CO*SVR=(MAP-CVP)/(CO x 80 dynes x sec x cm-5)

Front 90

During pregnancy BP...

Back 90

Decreases.
The fetal circulation is a low resistance circuit.

Front 91

Small boxes on ECG strips are...

Back 91

0.04s

Large boxes are 0.2s

(300,150,100,75,60,50)

Front 92

Purkinje cells are found on the border between the...

Back 92

Endocardium and myocardium

(larger cells with pale staining centers because of glycogen stores)

Front 93

What are the valves made of ?

Back 93

They are extensions of the endocardium.

Leaflets of collagenous tissue covered by endothelium are built around a CENTRAL FIBROUS SHEET(lamina fibrosa).

Spongiosa is on the atrial or blood vessel side of each valve. Ventricularis is on ventricular side.

!!!NO MUSCLE!!!

Front 94

What is the histological difference between endocardium and epicardium?

Back 94

Both endocardium and epicardium have simple squamous epithelium on the surface.
Only the epicardium though contains nerve bundles, larger blood vessels and large fat deposits.

Front 95

Why is it that when we destroy cardiac muscle cells we cannot regenerate them?

Back 95

Unlike skeletal muscle which has sattelite cells, the myocardium does not have progenitor cells.

Front 96

What is contained in the endocrine granules of atrial cardiac muscle cells?

Back 96

Atrial natiuretic hormone.

Released when atrial fibers are excessively stretched.

Increases excretion of water, Na and K by the kidney.

Also inhibits renin and aldosterone to lower BP.

More of these endocrine granules are found in the RA than LA.

Front 97

What are the three layers of a blood vessel?

Back 97

Tunica intima – closest to lumen; endothelial cells oriented along direction of blood flow.

Tunica media – middle layer with elements oriented circumferentially

Tunica adventitia – outermost layer with elements ordered longitudinally.

Front 98

What is the tunica intima made of ?

Back 98

Endothelium with basal lamina.
Subendothelial connective tissue (particularly in elastic vessels near the heart.)

Front 99

What is the tunica media made of?

Back 99

Smooth muscle.

Variable amount of elastin and collagen.

Dominant layer in arteries.

Front 100

What is the tunica adventitia made of?

Back 100

Collagenous fibers and a few elastic fibers.

Major component in veins, with significant smooth muscle.

Contains vaso vasorum and nervi vascularis in larger vessels

Front 101

What factors are secreted by endothelium?

Back 101

Prostacyclin
Nitric oxide
tPA
Thrombomodulin
Thromboplastin
PAF
vWF

Front 102

What do atherosclerotic plaques do to the relationship between endothelium and the intima?

Back 102

Foam cells and friends create a spatial seperation which prevents endothelial cells from regulating smooth muscle.

Front 103

What are arterioles?

Back 103

Smallest branches of the arterial tree.

Start of the microvascular system.

30 to 400 micrometers in diameter.

Intima of endothelial cells with basement membrane.

Media with 1-2 layers of smooth muscle cells; as the arterioles become smaller the smooth muscle cells become increasingly discontinuous.

Adventitia is insignificant.

Regulate vascular resistance and flow into and through capillary beds.

Front 104

Why are postcapillary venules important?

Back 104

Primary site of migration of leukocytes out of blood stream.

Regulated by factors produced by endothelial cells (e.g., selectins, integrins) and factors produced by cells outside of blood vessels (e.g., interleukins).

Front 105

What are the differences between medium arteries and veins?

Back 105

Front 106

At any given time, how much blood is in the venous system?

Back 106

about 65-70%

This is sometimes called capacitance.

Front 107

What are pericytes?

Back 107

Cells which are unique to capillaries and found adjacent to endothelium.
Contractile proteins within the pericytes provide some regulation of capillary diameter.

Front 108

How does transport occur in capillaries?

Back 108

The endothelial cells for tight junctions so most transport is done through the endothelium by pinocytotic vesicles.
(continuous capillaries found in muscle nerve and connective tissue)

Front 109

What is a fenestrated capillary?

Back 109

Contain fenestrae, bridged by diaphragms of extracellular material.

Found in the pancreas, intestines, endocrine glands, and renal glomeruli (where they lack diaphragms).

The basal lamina remains continuous but inner surface looks bumpy.

Front 110

Skeletal muscle is characterized by...

Back 110

peripherally located nuclei.

Front 111

What is a sinusoid?

Back 111

Have large fenestrae without diaphragms, gaps between endothelial cells, and a scanty, discontinuous or absent basal lamina.

Bigger than capillaries and found in regions that require a lot of transport like the bone marrow, liver, spleen, and lymphoid organs.

They have irregular shapes.

Front 112

What is the purpose of AV shunts in the skin?

Back 112

Opening the AV sphincters (under CNS control) diverts blood to the deeper shunts thus conserving heat.

Closing the shunts diverts blood to the capillary bed thus dissipating heat.

Front 113

What are the characteristics of lymphatic capillaries?

Back 113

Single layer of endothelial cells with no fenstrae or tight junctions and an incomplete basal lamina.

Endothelial cells overlap but have intercellular spaces that facilitate vessel permeability.

Bundles of lymphatic anchoring filaments terminate on the abluminal plasma membrane and maintain patency of the flimsy vessels.

Front 114

Large lymphatic vessls can be recognized by the fact that...

Back 114

Their tissues are not as well organized into layers as veins and arteries.

Front 115

How do we define atherosclerosis?

Back 115

A variable combination of changes in the intima
of arteries, consisting of focal accumulation of lipids,
cells, fibrous tissue, complex carbohydrates, blood,
blood products and calcium, and associated medial
changes with progression of disease.

Front 116

What is arterioscleorsis?

Back 116

A more general term than atherosclerosis which refers to any proliferative or degenerative stiffening of arteries.

Front 117

Where are the sites with a higher predilection for atherosclerosis?

Back 117

Proximal main coronary arteries.

Carotid arteries and circle of willis.
(~ 10 years after coronaries)

AA and iliac arteries
(more prevalent in smokers)

Femoral and popliteal arteries.
(more common in smokers)

Front 118

The first abnormal macroscopic (usually forensic) finding in athersclerosis is...

Back 118

Fatty streaks.

Macrophage foam cells that have ingested cholesterol ester droplets.

Fatty streaks progress more rapidly in men than women.

Front 119

What is the approximate size of molecule that can get through endothelial lining?

Back 119

<40,000 MW

Proteins and lipoproteins should not get in but they are sometimes taken up by the non receptor mediated process transcytosis.
(strictly concentration dependant).

Front 120

What cell types are involved in formation of an atherosclerotic plaque?

Back 120

Endothelial cells:
Endothelial dysfunction occurs early but actual desquamation (loss) does not occur until later.

Macrophages:
Early and Late

T-cells:
Early and late, but in smaller numbers than macrophages.

Smooth muscle cells: Accumulate in intima at a later stage than macrophages.

Mast cells:
Later
(minor component)

Neutrophils:
Not usually found in atherosclerotic plaques, except following plaque rupture.

Front 121

Where do we see an increase in cholestrol ester in atherosclerotic plaques?

Back 121

Intracellular first.
Extracellular lipid deposition is later.

Front 122

What role does connective tissue (fibrous tissue) play in the formation of plaques?

Back 122

Collagen:
Tensile strength
Synthesis is stimulated by SMCs of Athero. Plaques

Elastin:
Provides elasticity to the arterial wall.

Proteoglycans:
Binds LDL/VLDL in sub-endothelial space, which increases retention and facilitates oxidation, etc.

Front 123

Besides lipids and fibrous tissue, what other components are involved in plaque formation?

Back 123

Calcium and some magnesium

Bone formation

Blood products (old fibrin or new thrombi)

Front 124

So how does the pathogenesis of athersclerosis actually begin?

Back 124

Concentration dependant transcytosis of lipoproteins into the sub-endothelial space of the arterial wall, retention of LDL/VLDL by matrix.

Proteoglycans, expression of monocyte adhesion molecules on the endothelial cells.

Recruitment of monocytes into the artery wall and their differentiation into macrophages.

These macrophages then begin to express scavenger receptor A and CD36 that recognize abnormal lipoprotein made as a result of oxidation or other mechanisms.

The macrophages then engulf these abnormal lipoproteins and become foam cells.

Front 125

How do Foam Cells form once macrophages begin to accumulate in the sub-endothelium of the arterial wall?

Back 125

The cholesterol that cannot be converted to free cholestrol and transported out by HDL remains as esterified cholestrol droplets in the cytoplasm.

Front 126

What is the only risk factor that by itself will cause atherosclerosis?

Back 126

Hypercholesterolemia

Front 127

What is the benefit of lowering Plasma Lipoprotein concentrations?

Back 127

Lipid lowering not only reduces the transcytosis of plasma lipoproteins into the arterial wall, which reduces the development of foam cells, it also acts as an anti-inflammatory intervention, by decreasing the number of macrophage foam cells and T-cells, and increasing connective tissue synthesis. This is known as plaque remodeling. The result is a more stable plaque, less susceptible to rupture.

Front 128

How does plaque rupture occur and how does it lead to thrombosis and the Acute Coronary Syndrome?

Back 128

Macrophage foam concentrate at the unstable shoulders of the plaque and secrete matrix metalloproteinases (MMPs).

MMP's break down collagen.

Rupture of the plaque interrupts the endothelial surface which exposes blood platelets to underlying collagen and to macrophages that also secrete tissue Factor.

This causes platelet aggregation which initiates thrombosis.

Front 129

What determines whether or not a plaque is unstable?

Back 129

The amount of collagen on the edges.

Lots of collagen, less likely to rupture.

Front 130

HRT in women who have not had a hysterectomy MUST include...

Back 130

Progesterone along with the Estrogen.

Front 131

What is the advantage of conjugated equine estrogen at time of menopause?

Back 131

CEE reduces CHD in women who have hada hysterectomy if given AT THE TIME of menopause (~51).

If given later it increases the risk of stroke and CVD.

Front 132

What proportion of circulating cholestrol comes from biosynthesis?

Back 132

~80%

Front 133

What is the relationship between risk of CHD and LDL?

Back 133

log linear.

For every 30 mg/dL change in LDL-C, the relative risk for CHD is changed by ~30%.

This extends down to about 40mg/dL.

Front 134

How is HDL Anti-atherogenic ?

Back 134

Mediates cholesterol efflux (via binding to macrophage foam cell ABCA1 and ABCG1 transporters) from atherosclerotic plaques and other tissues which is the first step in reverse cholesterol transport.

Anti-inflammatory by reducing expression of adhesion molecules (p-selectin, VCAM-1, etc.) on endothelial cells.

Stimulates nitric oxide production (eNOS) in endothelial cells which stimulates vasodilation.

Anti-oxidant properties.

Front 135

How does smoking increase the risk of CHD?

Back 135

Increased atherosclerosis.

Increased chance of sudden death (acute thrombotic event). This is the major effect.

Cessation of smoking reduces the risk of CHD to nearly that of a nonsmoker in < 3 years.

Front 136

The primary risk factors for CHD include....

Back 136

Elevated Plasma Chol. (LDL)
Low HDL
Hypertension
Cigarette Smoking
Diabetes Mellitus

Front 137

The secondary risk factors for CHD include...

Back 137

Obesity
Sedentary life style
Type A personality
etc.

Front 138

Flow in a vessel is given by...

Back 138

Delta P / resistance

Front 139

Resistance is approximately given by..

Back 139

(Vessel length*Blood viscosity) /r^4

ή * L/r^4


The radius is therefore by far the biggest factor influencing vascular resistance.

Front 140

Poiseuille’s equation for a single vessel is derived from flow in a vessel and resistance in a vessel. What is it?

Back 140

Flow ~ (ΔP * r^4)/ (ή * L)

Front 141

The vessels that have the largest impact on peripheral resistance in a series arrangement are...

Back 141

The arterioles.

Front 142

For vessels in a parallel arrangement, we calculate resisatnce using...

Back 142

An ohms law relationship.

Front 143

The sum of all the peripheral resistance in the body excluding the pulmonary resistance is called...

Back 143

Systemic vascular resistance or total peripheral resistance.

SVR and therefore BP is primarily regulated by changing the diameter of the precapillary arterioles.

Front 144

How do we calculate SVR?

Back 144

SVR= (MAP-CVP) / CO

SVR is CALCULATED this way but not determined by these parameters.

Front 145

Precapillary arterioles by default have a certain amount of tone to them generated by vascular smooth muscle. How is this tone and thus their diameter regulated?

Back 145

Extrinsically (Innervation and hormones-neurohumoral control)

Intrinsically (local factors like tissue metabolites, local hormones, myogenic tone and endothelial factors)

Front 146

What Autonomic CNS elements regulate the cardiovascular system?

Back 146

Medulla:
contains cell bodies for parasympathetic (vagal) and sympathetic efferent nerves

Hypothalamus:
modulates medulla activity during exercise or temp regulation.

Higher centers (cortex):
modulate cardiovascular function at times of emotional stress (fear, anxiety)

Front 147

What are the charcteristics of the parasympathetic nervous system?

Back 147

Preganglionic fibers are long:
Preganglionics synapse in or near organ.
Neurotransmitter is ACh.
Receptor is nicotinic.

Postganglionic fibers are short:
Neurotransmitter is ACh.
Receptors are muscarinic.

Front 148

What are the characteristics of the sympathetic nervous system?

Back 148

Sympathetic ganglia are near spinal cord.

Preganglionic fibers are short:
Neurotransmitter is Ach
Receptors on postganglionic fiber are nicotinic.
Postganglionic fibers are long.
Neurotransmitter is NE.
Receptors on tissues are alpha and beta adrenergics.

Front 149

The left vagus stimulates..

Back 149

the AV node

Causes AV block.

Front 150

The right vagus stimulates...

Back 150

The SA node.

Causes decreased firing rate.

Front 151

What happens during concurrent stimulation of the sympathetic and parasympathetic nervous systems?

Back 151

The parasympathetic predominates.

Front 152

What happens with concurrent sympathetic & parasympathetic blockade as in coadministration of atropine and propranolol?

Back 152

Intrinsic heart rate.

Front 153

What are the characteristics of the neural control of the cardiovascular system?

Back 153

Rapid response.
Relatively constant blood pressure via feedback systems (reflex control).

Global as well as discrete control of various regional circulations.

Coordination of circulatory control with movement and emotional states.

Front 154

What are the important reflex pathways associated with the cardiovascular system?

Back 154

Arterial Baroreflex
Cardiopulmonary Baroreflex
Chemoreceptor Reflex

Front 155

Where are the arterial baroreceptors located?

Back 155

Carotid sinus
Aortic arch

Front 156

Where do the afferent fibers from the carotid sinus and aortic arch baroreceptors (stretch receptors) project to?

Back 156

The nucleus solitarius.

Front 157

What are the baroreceptors in the carotid sinus and aortic arch sensitive to?

Back 157

Mean pressure.

Pulse pressure (i.e. SP-DP).

Rate of change of pressure (dP/dt).

Front 158

What is the relation between arterial BP (baroreceptor input) & sympathetic nerve activity?

Back 158

Sigmoid.

Mid-point of curve near prevailing BP (set point)

Maximum sensitivity at mid-point of curve.

Small deviations from the setpoint result in large changes in nerve firing rates.

Front 159

What are the two centers in the medulla that govern the sympathetic nerve activity?

Back 159

Depressor center = caudal ventrolateral medulla (CVLM)
(Activation decreases SNA and BP)

Pressor center = rostral ventrolateral medulla (RVLM)
(Activation of this center increases SNA and BP.)

The CVLM inhibits the RVLM.

Front 160

Increased baroreceptor input results in...

Back 160

decreased SNA
increased PSNA

Front 161

Increased baroreceptor input results in...

Back 161

decreased SNA
increased PSNA

Front 162

What are the cardiopulmonary baroreceptor reflexes?

Back 162

Stretch receptors located in the heart respond to atrial filling (stretch); increased volume leads to sympathetic activation.

Increased blood volume and venous pressure activate other receptors that inhibit vasopressin release (causing diuresis).

Front 163

What is the purpose of chemoreceptors?

Back 163

The primary purpose is to regulate respiratory activity to maintain normal pH, pO2 and pCO2.

Secondary purpose is to affect CV function via medullary centers.

Front 164

Where are the chemoreceptors located?

Back 164

Aortic bodies
Carotid bodies

Front 165

What stimulates the carotid and aortic bodies?

Back 165

Increased CO2
Acidosis
Decreased O2

Also stimulated by hypoperfusion. Ordinarily these structures have more blood flow/g tissue than any other.

Front 166

Where are catecholamines made?

Back 166

Released by adrenal medulla in a ratio of 80% Epi and 20 % NE in response to stress.

NE is also released by sympathetic nerve activation at the blood vessel.

Noerpinephrine stimulates renin release and subsequently AngII and aldosterone.

Front 167

How does the renin angiotensin system work?

Back 167

Front 168

What is vasopressin and what stimulates it's release?

Back 168

Released by the posterior pituitary.

Acts on the kidneys to increase blood volume and constricts blood vessels.

Important for long term blood pressure control.

Stimulated by:
Angiotensin II.
Hyperosmolarity
Decreased atrial receptor firing.
Sympathetic stimulation.

Front 169

What is atrial natiuretic peptide?

Back 169

Peptide synthesized, stored and released by atrial myocytes in response to distention, Ang II, endothelin and sympathetic stimulation.

Responsible for long-term sodium and water balance, blood volume and arterial pressure.

Counter-balances the RAAS.

Used clinically as a marker of wall stress (eg. heart failure)

Front 170

What is vasodilator reserve?

Back 170

The difference between basal and maximum flow.

Front 171

What does A-V02 difference measure?

Back 171

A-V O2 difference is a measure of oxygen extraction.

Small A-V O2 Diff. suggests additional oxygen can be extracted without greatly increasing flow.

Front 172

Which organ has the highest variability in blood flow? Which has the least?

Back 172

Skeletal muscle ~2400%
Kidney ~ 16%

Front 173

Autoregulation of blood flow in organs occurs over a wide range of perfusion pressures, but has limits. What are those limits?

Back 173

60-70 mmHg for maximal dilation and ~170 mmHg for maximal constriction.

Front 174

What is the difference between active and reactive hyperemia?

Back 174

Active hyperemia results from increased use.

Reactive hyperemia results from ischemia.

Front 175

Low oxygen concentration is generally a vasodilator, what is the exception?

Back 175

The lung where low O2 is a vasoconstrictor.

Front 176

What are some examples of endothelial factors that affect blood flow?

Back 176

Nitric oxide and prostacyclin (dilators);

Endothelin, leukotrienes, thromboxanes (constrictors)

Front 177

What are the tissue vasodilator factors?

Back 177

Phosphate
lactate
CO2
K+
H+
Decreased PO2

Front 178

What does shear stress do to the lumen of a vessel?

Back 178

Causes the endothelium to produce NO and increases it.

Front 179

What is the myogenic response of renal and GI blood vessels?

Back 179

Originates from the smooth muscle (no neural input) in response to sudden pressure changes.

With increase in pressure, the smooth muscle contracts to preserve vascular resistance and vessel diameter.

With decrease in pressure, the smooth muscle relaxes and the vessel dilates.

Front 180

What physical factors affect vascular resistance?

Back 180

Temp.
Tissue compression.

Front 181

What is the difference between receptor dependant and receptor independant vasodilators?

Back 181

Receptor dependant vasodilators affect the nitric oxide synthase process of converting L-arginine to L-citrulline.

Receptor independant vasodilators like nitroprusside are direct NO donors which can activate cGMP driven vasorelaxation in smooth muscle even if the endothelial cells are damaged
(ie. angioplasty).

Front 182

What are the receptor dependant vasodilators?

Back 182

Substance P
Histamine
5-HT
BK
AcH

Front 183

How do alpha 1 receptor agonists cause vasoconstriction?

Back 183

They increase intracellular calcium in smooth muscle.

(Neuropeptide Y co-released with NE augments vasoconstriction action of NE)

Front 184

What endogenous vasoconstrictors act on vascular smooth muscle?

Back 184

Angiotensin II
Arginine vasopressin
NE and Epi.
Endothelin
Increased PO2

Front 185

Where are the compressive forces on the coronaries highest during systole?

Back 185

At the subendocardial level.

This makes it more vulnerable to ischemia because the subendocardium is fed EXCLUSIVELY during diastole.

Front 186

What sort of vasodilator reserve does the coronary circulation have?

Back 186

Very high.
(80 ml/min/100g vs >400 ml/min/100g)

Highly regulated by tissue metabolism especially adenosine which is a very strong vasodilator in the heart.

Front 187

In general, how do local factors interplay with autonomic innervation in the heart?

Back 187

Local factors like metabolites tend to predominate.

Front 188

What sort of oxygen extraction reserve does the heart have?

Back 188

Very little.
Changes in oxygen demand must be met with changes in oxygen delivery.

Front 189

What constitutes the blood brain barrier?

Back 189

Majority of capillary endothelium in the brain has tight junctions. It is surrounded by a basement membrane that is contiguous with astrocytes.

Front 190

How is cerebral perfusion predominantly regulated?

Back 190

!!! CO2!!!

Heavily relies on autoregulation.

Adequate cerebral perfusion is also determined by systemic arterial pressure.

Front 191

What is the main autoregulatory metabolite of the coronary circulation?

Back 191

Adenosine

Front 192

What local factors are most important in regulating skeletal muscle perfusion?

Back 192

Adenosine
K+
Hypoxia
Innervation

Local factors can overcome sympathetic innervation during a fight or flight response.

Front 193

Regulation of cutaneous circulation is predominantly...

Back 193

Neural.

Front 194

What happens to cutaneous circulation when we are hot?

Back 194

Deep A-V anastomoses constrict and shunt blood towards the superficial "radiator" plexi.

Increased Core T means decreased cutaneous vascular resistance.

Front 195

What percentage of CO normally goes to the splanchnic circulation?

Back 195

About 20%

contains ~15% of the circulating blood volume (BV).

Front 196

How is the splanchnic circulation controlled?

Back 196

Mostly neural control of arterioles and veins.


Neurally released NE acts at a1 adrenergic receptors on VSM.

High resting sympathetic VC tone; denervation or a1 adrenergic blockade increases splanchnic BF by ~1.5 times.

Front 197

What percentage of CO do the kidneys receive?

Back 197

~20%

Front 198

What is the difference between pulmonary and bronchial circulation?

Back 198

Bronchial feeds the respiratory tissues whereas pulmonary is the systemic gas exchange circulation.

The bronchial circulation is derived from the aorta (left side).

Front 199

At what percentage of blood volume loss more or less do we start decompensating?

Back 199

~40%

Front 200

What are the compensation mechanisms for volume loss? (Hemorrhage)

Back 200

Short-term (seconds to minutes):
baroreflex, chemoreflex, ischemic response

Intermediate (minutes to hours):
renin angiotensin system, fluid shifts

Long term (hours to days): renal salt and water conservation, new red cells, fluid replacement.

Front 201

What is claudication?

Back 201

Leg pain with ambulation.

Front 202

What are the hallmark signs of acute leg ischemia?

Back 202

Pulselessness
Pain
Pallor
Poikilothermia (cold)
Paresthesias
Paresis/Paralysis

(Always an emergency)

Front 203

A normal pulse on doppler is...

Back 203

Triphasic

Biphasic or Monophasic (blunted, lacking flow reversal)

Front 204

Which skin changes are associated with arterial pathology?

Back 204

Decreased temp
Pallor, mottling
Hair loss
Ulceration
Gangrene

Front 205

Which skin changes are associated with venous pathology?

Back 205

Edema
Varicosities
Dermatitis (lipodermatosclerosis)
Thickened skin
Bronze discoloration
Ulceration
Gaiter distribution

Front 206

What is an antibrachial index?

Back 206

Opening pressures measured by Doppler, supine, at rest.

Highest of dorsalis pedis or posterior tibial in each leg divided by highest brachial artery pressure.

Report a left and right leg but can use same arm pressure.

Front 207

What are normal values for ABI?

Back 207

>1.0 Normal or possibly non-compressible from heavy calcification (e.g. diabetes)

<0.9 Abnormal, likely claudication (mean 0.6), marker of increased risk for heart disease.

<0.6 Rest pain (mean 0.3)

<0.3 Non-healing ulcers or gangrene.

Front 208

What is duplex ultrasonography?

Back 208

Combines B-mode ultrasound & color Doppler with spectral analysis. Increased velocities and spectral broadening correlate with degree of stenosis.

Gold standard in screening for carotid occlusive disease and DVT.

Used in renal, mesenteric, extremity arteries and bypass grafts to define stenoses.

Front 209

What does a DVT look like on duplex utrasonography?

Back 209

Noncompressible enlarged vein , abnormal flow, visible thrombus.

Front 210

What does a normal Pulse-Volume Recordings and Segmental Pressures study look like?

Back 210

Front 211

What does an abnormal (left sided occlusion) Pulse-Volume Recordings and Segmental Pressures study look like?

Back 211

Front 212

What is the advantage of digital subtraction angiography (DSA) for PVD?

Back 212

Detailed lumen structure.

Invasive procedure though which involves radiation.

Relatively contraindicated in kidney problems because of the dye.

Can also cause drug reactions with metformin.

Front 213

What is the advantage of CT angiography for PVD?

Back 213

Non-Invasive (radiation)

Contraindications
Iodinated contrast
renal insufficiency
allergic reactions
drug reactions
Metformin

Front 214

Is MR angiography currently better or worse imaging than CT angiography?

Back 214

Resolution of MR is worse.

Front 215

What is the timeline of atherosclerosis?

Back 215

Front 216

What are the major conclusions of the PDAY study about AAA?

Back 216

The percentage of arterial surface with atherosclerotic lesions was the greatest in distal abdominal aorta (AA).

Total lesion area for the AA was greater in women than in men.

Smoking selectively affects atherosclerotic changes in AA at a younger age than in the coronary arteries.

Front 217

How do we discern intermittent claudication from arthritis pain?

Back 217

Occurs in muscle groups, not in joints.

Reproducible from one day to the next, and initially may become more noticeable while walking on incline.

Goes away with relaxation.

Front 218

How do we tell pseudoclaudication from intermittent claudication?

Back 218

Pseudoclaudication occurs with standing and variable walking distance.

Intermittent claudication does not occur with standing and usually within a fixed walking distance.

Front 219

What causes pseudoclaudication?

Back 219

Spinal compression.

Front 220

Regardless of patient age the most common cause of peripheral arterial disease over 40 is...

Back 220

Atherosclerotic disease.

Front 221

What is Buergers disease?

Back 221

Thromboangiitis obliterans (Buerger's disease) is a cigarette smoking related vasculitis.

Front 222

How do we differentiate between patients with Buergers disease and peripheral atherosclerosis?

Back 222

Front 223

How do we differentiate thrombosis from embolism?

Back 223

Acuity is the main factor as evidenced by onset and presence of collateral flow.

Front 224

What are the independant risk factors for PAD in descending order?

Back 224

Diabetes
Current smoking
Age
Hypertension
Homocysteine
Total cholestrol

Front 225

Which ORGAN is most likely to get atheromatous emboli?

Back 225

kidney

Front 226

What skin changes are associated with atheromatous embolization?

Back 226

Blue toes
Livedo reticularis (net)

Front 227

What are the major collateral pathways in the lower extremities?

Back 227

Lumbar aortic branches (Aortic disease)

Internal iliac system and pelvic circulation
(CIA disease)

Circumflex femoral arteries (CFA disease)

Profunda femoris
(SFA disease)

Geniculate arteries
(PA disease)

Front 228

Arterial occlusions generally occur at the ...

Back 228

Bifurcations of arteries.

Front 229

Typically the supply of oxygen to the tissues should occur at a ratio of...

Back 229

2:1

Front 230

Why does excercise cause a decrease in area pressure in chronic PAD?

Back 230

Increased demand causes vasodilation of collateral vessls that are developed because of the occlusion.

Front 231

PAD puts patients at greatly increased risk of subsequent...

Back 231

MI
Stroke
More PAD

Front 232

What is Leriche’s Syndrome?

Back 232

Focal occlusive disease of the distal aorta and proximal iliac arteries.

Front 233

What are the MOA's of the antiplatelet Rx?

Front 234

The best risk reducing drug for PAD patients is...

Back 234

Plavix.

Better than aspirin in CAPRIE study.

Front 235

What is Cilostazol?

Back 235

Approved for claudication. (symptoms. Plavix for risk reduction)

Platelet aggregation inhibitor.

!Vasodilator!

phosphodiesterase III inhibitor which raises cGMP.

!contraindicated in patients with heart failure!

Best with smoking cessation and excercise.

Front 236

Flow times resistance (Q*R) is equal to...

Back 236

Delta P

(BP = CO x SVR)

Or

BP = [LVEDV-LVESV] x HR x SVR

Front 237

Where are alpha 1 receptors predominantly found?

Back 237

Vascular smooth muscle.

Stimulation causes vascular constriction (Pressor effect).

Front 238

Alpha 2 receptors are found in vascular smooth muscle at lesser density than Alpha 1 receptors but the main clinical use of Alpha 2 receptors is...

Back 238

Stimulation causes negative feedback on presynaptic neurons.

The more we stimulate alpha 2 the less response we will have to other stimuli.

Alpha 2 receptors in the brain also have roles in pain and sedation.

Front 239

What are the main effects of beta 1 stimulation?

Back 239

Inotropic effect (cAMP)

Chronotropic effect – all tissues

Lusitropic (relaxation) effect

They also have a positive feedback effect on presynaptic receptors and increase the response to epi and NE.

Front 240

What is the normal Beta1:Beta2 ratio in the heart?

Back 240

4-6:1

1-1.5:1 in CHF

Front 241

What is the main clinical use of Beta 2 receptors?

Back 241

Bronchodilation (relaxation of bronchial smooth muscle).

They also produce a small amount of vasodilation.

Front 242

What is the main clinical use of dopamine (DA) receptors?

Back 242

There are many dopamine receptors on the splanchnic vasculature and stimulation of these vasodilates and improves flow to gut, kidneys, liver etc..

There are relatively few in the heart so inotropy and chronotropy are minimal.

Front 243

What is the main clinical use of vasopressin (V) receptors?

Back 243

Causes very intense vasoconstriction.

Front 244

What is the primary mediator of beta agonists?

Back 244

To generate cyclic AMP which causes enhanced calcium influx and enhanced calcium release from the sarcoplasmic reticulum.

Inhibiting phosphodiesterase with drugs helps because it slows degradation of C-AMP.

Front 245

How do we increase preload?

Back 245

Fluids
α-agonists in low doses

Front 246

How do we decrease afterload?

Back 246

ACE inhibitors
Nitroprusside
PDE inhibitors

Front 247

How do we increase contractility?

Back 247

β-adrenergic agents
PDE inhibitors

Front 248

How do we increase vascular resistance?

Back 248

α-adrenergic agents

Front 249

What are the dosing ranges of epinephrine?

Back 249

β-effects (Inotropy and chronotropy) predominate up to 0.1 μg/kg/min ~(5-7 μg/min)

α-effects at ~0.1 μg/kg/min

Very non-specific beta agonist.

Myocardial O2 demand is a real problem.

Front 250

What is Dobutamine (Dobutrex)?

Back 250

Inotrope with Vasodilating effects.

+chronotrope

Myocardial O2 demand may be less of problem than Epi.

Typically used in acute MI and mild cardiogenic shock.

Front 251

What is the main effect of norepinephrine (Levophed)?

Back 251

Mostly an alpha pressor

Some beta effects.

Mostly used in Sepsis.
(ie. Distributive shock with good CO)

Front 252

Phenylephrine (Neosynephrine)?

Back 252

“Pure” weak α-agonist

Essentially no β-effects

Vasoconstriction & increased SVR with no support of cardiac function.

Mild Sepsis, Hypotension with good CO.

Front 253

What is the unique characteristic of dopamine (intropin)?

Back 253

Dose-Dependent Pharmacology.

DA stimulation 0.5-3 μg/kg/min
(renal dose dopamine)

β-effects 2-10 μg/kg/min

α-effects 7-20 μg/kg/min

Front 254

What is vasopressin (Pitressin)?

Back 254

Causes Intense vasoconstriction through V-receptors with no α- or β- stimulation.

Predilection for splanchnic vessels can cause gut ischemia.

Used in ACLS, Severe shock, CABG (on ACEi).

Front 255

What are the phosphodiesterase inhibitors milrinone and amrinone?

Back 255

Vasodilators & Inotropes

Augments β-adrenergic stimulation.

Used in CABG (Vasoconstricted with low CO)

Front 256

The most common cause of occlusive renal artery disease is...

Back 256

Atherosclerosis.

Front 257

How does renal artery stenosis cause problems?

Back 257

Once renal blood flow is less than 80%, the parenchyma receives less blood flow and causes it to release renin.

All problems stem from Renin causing increased conversion of angiotensin to angiotensin 1.

Front 258

What is the effect of unilateral renal stenosis?

Back 258

One kidney compensates but there is:

Reduced arterial pressure.
Elevated plasma renin activity.
Enhanced lateralization of diagnostic tests.
GFR in stenotic kidney may fall.

Front 259

What is the effect of bilateral renal stenosis?

Back 259

Reduced arterial pressure only after volume depletion.

May lower GFR.

Plasma renin activity is normal or low.

Front 260

What are the clinical implications of renovascular hypertension?

Back 260

Paroxysmal hypertension.
Treatment-resistant hypertension.
Hypertensive nephropathy.
Renal failure.
Flash pulmonary edema.
Accelerated cardiovascular disease.

Front 261

Among hypertensives: patients that are older, have higher diastolic pressure, and higher serum creatinine are more likely to have ...

Back 261

Renovascular hypertension

Front 262

What are the lesions responsible for adult renovascular hypertension?

Back 262

Atherosclerosis (75%)

Fibromuscular Dysplasia (20%)

Miscellaneous Lesions (5%)

Front 263

What are the causes of fibromuscular dysplasia of the renal arteries?

Back 263

Medial Fibroplasia (85%)
String of Beads - Women
(renal arteries, carotids,iliac)

Intimal Fibroplasia (5%)
Focal - Children

Perimedial (Subadventitial) Dysplasia (10%)
Progressive

Front 264

How does Isotopic captopril renography work?
(not the most important test to order but conceptually important)

Back 264

Measures filtered radioactive tracer before and after ACE inhibitor.

Angiotensin II maintains GFR in kidney with renal artery stenosis via increased vasoconstriction in the efferent arteriole.

ACE inhibitor> reduced synthesis of Angiotensin II, diminished efferent arteriole vasoconstriction and thus decreased GFR.

Therefore less uptake of filtered radioactive tracer after ACE inhibitor.

If they have renal stenosis uptake will be markedly reduced.

Front 265

Statistically where do embolic phenomena from the heart go in the gut?

Back 265

Superior mesenteric artery
(Feeds the majority of the small bowel)

Front 266

What are the collateral systems in the gut?

Back 266

Celiac and SMA: Gastroduodenal collaterals

SMA and IMA:
Mesenteric collaterals.

IMA also connects with hypogastric (internal iliac artery)

Front 267

What is the relative incidence of the various visceral ischemic syndromes?

Back 267

Mesenteric Artery Occlusion 75%
(Embolus 35%, Thrombus 65%)

Mesenteric Vein Occlusion 15%

Non-Obstructive Mesenteric Ischemia 10%

Front 268

What are the risk factors for visceral ischemic syndromes?

Back 268

Any unexplained, severe abdominal pain

Age greater than 60 years

Arrhythmia – atrial fibrillation.

Congestive heart failure.

Digitalis therapy (uncompensated CHF)

Recent myocardial infarction

Previous arterial emboli

Hypercoagulable state

Hypovolemia

Front 269

What should lead me towards the diagnosis of an embolic visceral ischemic syndrome?

Back 269

Sudden onset severe abdominal pain (periumbilical)

Paucity of physical findings

Bowel evacuation.

Cardiac embolic risk such as atrial fibrillation.

Front 270

What should lead me towards the diagnosis of a thrombotic visceral ischemic syndrome?

Back 270

Insidious abdominal pain

Systemic toxicity

Physical findings

Underlying chronic visceral ischemia

Front 271

What should lead me towards the diagnosis of a mesenteric vein occlusion visceral ischemic syndrome?

Back 271

Insidious, diffuse abdominal pain.

Vague prodromal period.

Nausea, vomiting, distention.

Hypovolemic, cardiovascular collapse.

Front 272

What are the key symptoms of CHRONIC visceral ischemia?

Back 272

Post-prandial abdominal pain

Food avoidance

Weight loss

Front 273

How do people typically die of visceral ischemic syndromes?

Back 273

Remote Organ Dysfunction - SIRS

Causes pulmonary endothelial cell Injury, Hepatocellular dysfunction and Renal insufficiency.

Front 274

How does the superficial system of veins drain into the deep system of veins in the leg?

Back 274

Direct connections at the saphenofemoral junction, saphenopopliteal junction and by perforators.

Front 275

What affects the hydrostatic pressure in veins?

Back 275

Static pressure of fluid column.
Transmitted right atrial pressure.
Overall volume status.
Thoracoabdominal pressure.

Front 276

What are varicose veins?

Back 276

Genetic component – thought autosomal dominant with variable penetrance.

Valve Incompetence at:
Saphenofemoral junction
Saphenopopliteal junction
Perforators

Pain, aching sensation, worse as day proceeds, better in the morning.

Compression stockings
Elevation
Intervention focuses on eliminating source of reflux. May need to remove varicosities.

Front 277

What are telangectasias? (spider veins)

Back 277

Same process as varicose veins on a smaller scale.

Symptoms– cosmetic, sometimes pain at the site.

Treatment – exclude larger vein reflux, injection sclerotherapy, laser.

Front 278

What skin changes are associated with venous stasis?

Back 278

Lipodermatosclerosis

Pigmentation – hemosiderin deposition

Eczema

Ulceration – often at site of perforating vein.

Front 279

How do we manage venous stasis ulcerations?

Back 279

Aggressive Compression.

Elevation.

Antibiotics and debridement when infected or necrotic.

Skin grafts.

Front 280

What is the CEAP classification of venous stasis disorders?

Back 280

Clinical Signs, Etiology, Anatomy, Pathophysiologic dysfunction.

Allows standardized communication of venous disorders.

Front 281

What is virchows triad?

Back 281

Stasis
Vessel wall injury Hypercoagulability

Front 282

What are the hypercoagulability risk factors for DVT?

Back 282

Inherited thrombophilia
Malignancy
Pregnancy
Surgery
Trauma

Front 283

What are some stasis risks for DVT?

Back 283

Immobility.

Valvular dysfunction or venous obstruction.

Pregnancy- pelvic vein compression.

Front 284

What sort of DVT risk does surgery pose?

Back 284

Risk varies with type and length of operation.

Highest with hip/knee/pelvic procedures (~50-60%).

Intermediate for neurosurgical and oncologic procedures.

May be due in part to increased procoagulant activity

Over 50% develop !!in the OR!!

Front 285

What is Homans sign?

Back 285

Poor sensitivity and specificity indication of DVT.

Calf pain with dorsiflexion of the foot.

Front 286

What lab diagnostic test is useful for DVT?

Back 286

D-dimers.

Venous Duplex in the vascular lab has very high sensitivity and specificity too.

Front 287

What is postphlebitic syndrome?

Back 287

Symptomatic chronic venous insufficiency after deep venous thrombosis which occurs in ~28% of post-DVT patients.

Front 288

Morbidity from DVT occurs due to...

Back 288

Venous insufficiency.

Mortality is primarily due to pulmonary embolisms.

Front 289

Where do pulmonary embolisms come from?

Back 289

>90% from legs.

Risk thought lower for calf vein DVT than more proximal DVT.

Front 290

What is a paradoxical embolism?

Back 290

DVT that travels through a PFO (ASD) to the systemic circulation.

Front 291

What means do we have of trying to prevent DVT?

Back 291

Mechanical – compression stockings, intermittent compression devices, mobilization

Pharmacologic – low dose anticoagulants.

Front 292

Why is trauma a high risk for DVT?

Back 292

Possibly due to depletion of coagulation inhibitors or upregulation of fibrinopeptides.

Increased even more with LE or pelvic fractures, spinal cord injuries, and major venous injuries.

Frequently bilateral/ multifocal

Front 293

What is the usual treatment for DVT?

Back 293

Anticoagulation.

Graduated compression stockings.

Thrombolysis of clot in rare cases.

Front 294

What is Phlegmasia Cerulea Dolens?

Back 294

Limb threatening extensive venous thrombosis.

Often associated with cancer (20-40% of cases)

Surgical/interventional emergency

Front 295

Some lymphatics have smooth muscle contractions but for the most part flow is driven by....

Back 295

Variations in intrathoracic and intra-abdominal pressures.

Front 296

What is the difference between lymphedema and edema?

Back 296

Lymphedema = protein-rich interstitial volume overload, secondary to lymph drainage failure in the face of normal capillary filtration.

Edema = increased interstitial fluid volume that is enough to produce clinical, palpable swelling (more generic term)

Front 297

Primary lymphedema...

Back 297

A congenital problem.

Secondary lymphedema is acquired.

Front 298

What is the most common worldwide cause of lymphedema?

Back 298

Wuscheria bancrofti (filariasis)

In the U.S, the most common cause is malignancy and associated treatments.

Front 299

What are some primary lymphedemas?

Back 299

Congenital (<1 year)
Familial type = Milroy’s Disease
(VEGFR-3 mutation)

Lymphedema praecox
(age 1-35)
Most common
Usually unilateral, adolescent women.
Hypoplastic lymphatics

Lymphedema tarda (age >35)
Congenitally “weakened” lymphatics, event triggers onset.

Front 300

What are the common signs and symptoms of lymphedema?

Back 300

Painless swelling initially dorsum of foot.

Eventual proximal involvement.

Subcutaneous fibrosis.

Skin becomes hyperkeratotic, papillomatous or verucous

Recurrent infections.

Front 301

How do we treat lymphedema?

Back 301

No cure.
Elevation has little effect.
Exercise.
Compression garments/devices.
Manual lymph drainage.
Skin care practices.
Surgery in rare cases.

!Diuretics will not help!

Front 302

What is the principal modifiable risk factor for stroke?

Back 302

Hypertension

Atrial fib and carotid stenosis are also risk factors.

Front 303

What percentage of strokes are ischemic?

Back 303

80%

20% are hemorragic.

Front 304

Anterior strokes typically originate from...

Back 304

The carotids.

The vast majority of arterial related strokes occur secondary to embolization.

Front 305

Speech issues are usually related to...

Back 305

left sided strokes.

Front 306

What is the most common cardiac source of embolisms?

Back 306

Left atrium during A-fib.

Front 307

The risk for embolic liberation of a carotid bifurcation plaque is related to....

Back 307

The bulk of the plaque which is in turn related to the degree of occlusion (stenosis).

The stability of its luminal surface which is related to intraplaque hemorrhage and plaque composition.

Front 308

What are the greatest risks for atherosclerotic carotid plaques?

Back 308

Advanced age
Cigarette smoking

Not Hypertension.

Front 309

What is most common mode of presentation of carotid occlusion?

Back 309

Asymptomatic

Front 310

What are neurological symptoms of carotid derived stroke?

Back 310

TIA
Amaurosis fugax
Completed Stroke
Vertebrobasilar symptoms*

Front 311

What is a TIA?

Back 311

Unilateral symptoms with or without aphasia (left hemisphere) lasting less than 24 hours.

Front 312

What is Amaurosis fugax?

Back 312

Temporary ipsilateral monocular visual loss due to embolization of the temporal artery or its branches.

Front 313

What is the gold standard for assessing carotid stenosis?

Back 313

Carotid duplex

Front 314

The best available natural history data on carotid disease comes from ....

Back 314

Asymptomatic Carotid Atherosclerosis Study (or ACAS) demonstrated a five year risk of ipsilateral hemispheric stroke of 11% for lesions in excess of 60%. This equates to about a 2% per year risk.

The NASCET study which assesed symptomatic patients suggested 2 year stroke risk ~15-30% (50% or greater stenosis).

The risk of strokes in either group parallelled lesion severity.

Front 315

How do we decide whether to treat patients with carotid disease medically or surgically?

Back 315

Symptomatic patients < 50% diameter reducing stenosis and asymptomatic patients <60% stenosis are usually treated medically.

We recommend carotid endarterectomy plus optimal medical therapy for symptomatic patients with 50-99% carotid stenosis or asymptomatic patients with 60-99% stenosis and low perioperative risk.

Front 316

What are considered vetebrobasilar symptoms?

Back 316

Dizziness
Vertigo
Diplopia
Blurred vision
Ataxia
Drop attacks
Bilateral sensory disturbances

These are typically due to low flow states rather than embolisms.

Front 317

What sort of flow limiting lesions cause vetebrobasilar symptoms?

Back 317

almost always multiple vessels
(3 or more)

Innominate artery
Subclavian arteries
Vertebral arteries (Retrograde flow)
Carotid arteries

-Systemic hypotension
Bradyarrhythmias
Tachyarrhythmias
Autonomic dysfunction
Anatomic compression

Front 318

What test is important if we suspect vertebrobasilar disease?

Back 318

Transcranial doppler to assess intracranial flow.

In contrast to carotid disease, this often requires advancing to angio to fully asess.

Front 319

Known vertebrobasilar ischemia must...

Back 319

Must be treated through bypass, endarterectomy, angioplasty and stenting depending on the lesion type and patient fitness.

Front 320

What is Giant Cell Arteritis (temporal arteritis)?

Back 320

Most common in older Caucasian women.

Temporal headaches
Jaw claudication
Polymyalgia rheumatica
Amaurosis fugax
Constitutional symptoms
!Elevated sedimentation rate!

Dx- temporal artery biopsy
Tx-- corticosteroids

Front 321

What are the causes of carotid dissection?

Back 321

Spontaneous:
Cocaine/methamphetamine use
Associated Horner’s syndrome common.
Treatment- anticoagulation

Traumatic:
Compression-extension injury
Occurs high in the neck (C2)
Treatment- anticoagulation if possible.
Can lead to pseudoaneurysms.

Front 322

How do we define an aneurysm?

Back 322

Focal dilatation of an artery involving an increase in diameter of at least 50% as compared the expected normal diameter.

True aneurysms- Have all the vessel wall layers.

False aneurysms- Have none of the vessel wall layers.

Front 323

What are the most common aneurysms?

Back 323

White males
Atherosclerotic
Infrarenal
Enlarge and rupture

Greater than 60% of ruptured aneurysm patients never make it to the hospital.

Front 324

How does the matrix of collagen and elastin vary down the aorta?

Back 324

Decreasing matrix concentrations from proximal to distal aorta.

58% decrease in elastin between supra and infrarenal aorta. (absent vaso-vasorum)

Front 325

What are some of the more exotic explanantions for the epidemiology of AAA?

Back 325

Elastin is not synthesized in adult aorta (T-1/2 40 to 70 years) which explains age bias.

Genetics probably has to do with up-regulation of matrix metalloproteinases (MMPs). Susceptibility alleles for AAA involving the DRB1 major histocompatibility locus.

Possible chlamydial pneumoniae infection cause.(some suggest give doxycycline).

Aortic aneurysm antigenic protein (AAAP-40) shares AA sequence with treponema and CMV. Possible autoimmune reaction through molecular mimicry.

Front 326

What are the hazards with AAA?

Back 326

Emboli
Thrombosis
Infection
Coagulopathy
Fistulae
!!Rupture!!

Front 327

How do we diagnose AAA?

Back 327

Most are asymptomatic.

Occasionally patients describe abdominal pulsation or even palpate pulsatile mass.

Abdominal or back pain (left flank). Can radiate to groin.

Most asymptomatic aneurysms are picked up on Ultrasound or CT done for other reasons.

Front 328

Is angiography an adequate screening tool for AAA?

Back 328

No.

Front 329

What is the Law of Laplace?

Back 329

Tension = radius x pressure.

Front 330

What is the best screening tool for AAA?

Back 330

Ultrasound.

Generally, 6 month interval ultrasound warranted for AAA > 4 cm.

Front 331

How can we slow the rate of expansion of an aortic aneurysm?

Back 331

Beta blockers

Front 332

What is the accepted cutoff for surgical repair of AAA?

Back 332

5.5 CM

SOME USE A SMALLER CUTOFF FOR WOMEN AND COPD PATIENTS.

Front 333

What are the important comorbidities of AAA?

Back 333

Coronary Artery Disease
Pulmonary Disease
Renal Failure

Front 334

Several studies regarding smaller AAA (< 5 cm) have demonstrated...

Back 334

Trend toward more rapid expansion above 5 cm

Trend toward rupture above 5 cm

Recommendation for repair at 5 cm for younger, lower risk patients.

Recommendation for repair at 6 cm for higher risk patients.

Lower intervention rates at later age of detection.

Front 335

Fever of unknown origin or GI bleed with previous aortic grafting is...

Back 335

Aortoenteric fistula or infected aortic graft until proven otherwise.

Front 336

Who is a good candidate for aortic endograft?

Back 336

Patients with an AAA warranting surgical repair that can tolerate a surgical procedure, can await/tolerate extensive imaging studies, are generally poor candidates for open repair and are committed to long-term follow-up.

Front 337

What is the mortality of rupturing a AAA?

Back 337

>90%

Front 338

What is aortic dissection?

Back 338

Separation of the aortic wall layers by extra luminal blood that usually enters the aortic wall through an intimal tear.

Relatively rare.

BP must be controlled.

Without treatment most will die within 2 weeks.

Front 339

What diseases predispose to aortic dissection?

Back 339

Marfan, Coarctation, Ehlers-Danlos.

Cocaine use.

Rebound from abrupt discontinuation of B-Blockers.

Pregnancy. (More than 50% of dissection in women <40)

Front 340

Marfan syndrome is an autosomal dominant trait with variable penetrance. It is a defect in...

Back 340

fibrillin-1

pectus excavatum, arachnodactyly, eye problems etc.

Front 341

What is the debakey classification of aortic dissection?

Back 341

Type 1: whole arch
Type 2: ascending aorta
Type 3: descending aorta

Ascending aortic dissection is a true surgical emergency. 1%-3% for every untreated hour. May require replacement of ascending aorta, aortic valve, and CABG.

Type 3 is the one that can sometimes be treated medically.

Front 342

How does an aortic dissection present?

Back 342

Sharp, ripping, tearing pain (95%)
Abruptness is most specific characteristic.
Usually does not radiate to neck, shoulder, or arm as in acute coronary syndrome.
Location may reflect distribution of dissection.

Typically hypertensive.

Widened mediastinum.

Acute aortic regurgitation (diastolic murmur)

Shock:
Pericardial tamponade
Coronary compression MI
Rupture

Obstruction of branch arteries:
Stroke / Spinal cord ischemia.
Renal failure.
Pulse Deficit.

Front 343

What else is on the differential with aortic dissection?

Back 343

Acute MI
Thoracoabdominal Aneurysm
Pericarditis
Pulmonary Embolus
Mediastinal Tumors
Plueritis
Acute Cholecystitis

Front 344

What imaging techniques can be used to diagnose aortic dissection?

Back 344

CT, MRI, TEE, Angiography.

CT scan most common but center dependent.

Front 345

How do we treat dissection medically?

Back 345

Aggressive blood pressure control with B-Blockers and nitroprusside.

A-line, ICU, CV access.

Monitor for signs of progression or end-organ ischemia.

Long-term aggressive blood pressure control and risk factor modification.

Front 346

What are the surgical indications for chronic descending aortic dissection?

Back 346

Aneurysmal degeneration > 60 mm.

Chronic ischemia secondary to stenosis.

Front 347

What is a unique epidemiological charcteristic of lower extremity aneurysms?

Back 347

Profound male predominance (30:1)

Largely Atherosclerotic/degenerative

Popliteal most common followed by femoral. (femoral most common if include false aneurysms)

!!Strongly Associated with Atherosclerotic aneurysms elsewhere!!
(70% of patients with this will have aortic aneurysm)

Front 348

The danger with peripheral aneurysms is that...

Back 348

More likely to embolize or thrombose than to rupture.

Front 349

What are visceral aneurysms?

Back 349

Splenic artery most common.

Biggest concern is rupture.

Risk of rupture is increased with pregnancy.

Tx if > 2.5-3.0 cm. especially if pt. pregnant.

Front 350

What is the most common site of mycotic aneurysms?

Back 350

Femoral artery.

Front 351

In most of the population, acute valve dysfunction and electrical conduction problems are due to an occlusion in the ...

Back 351

Right coronary circulation.

Front 352

What is MVO2?

Back 352

myocardial oxygen consumption .

Front 353

Coronary venous outflow is increased and peaks ....

Back 353

During systole.

Coronary perfusion happens during diastole though which favors subendocardial vessels during diastole.

Front 354

What factors influence MVO2?

Back 354

Heart Rate

Systolic pressure (or myocardial wall stress)

Left ventricular contractility

Front 355

Are there collateral vessels in the normal human heart?

Back 355

No.

Preexisting small vessels undergo proliferative changes of endothelium & smooth muscle in response to ischemia.

May happen in as little as 3wks – 6 months.

Vascular Endothelial Growth Factor (VEGF) is under investigation because of genetic link.

Front 356

Coronary flow is inversely proportional to...

Back 356

Coronary vascular resistance.

Front 357

What percentage of O2 does the myocardium extract from coronary blood flow?

Back 357

75%

This is compared to the 25% extraction of most tissues.

Front 358

Why is the left coronary more affected by shortening of the diastolic phase than the right?

Back 358

The mechanical compression of the right ventricle muscle is not as profound as that of the left ventricle during systole.

Front 359

Myocardial pressure is greater at the endocardium than the epicardium so an excessively shortened diastole means change in the endocardium/epicardium perfusion ratio. Why is this not a problem under normal conditions?

Back 359

Greater blood flow to the Endocardium in diastole compensates for greater blood flow to the Epicardium in systole.
Net result is about equal flow to epicardium & endocardium over the entire cardiac cycle.

Ischemia & cell death usually start in the Endocardium & progress towards the Epicardium particularly in tachycardic states.

Front 360

What does increased sympathetic tone do to coronary blood flow?

Back 360

Overall increased coronary blood flow.
BUT
So does increased parasympathetic tone.

Front 361

What endothelial factors control coronary blood flow?

Back 361

Prostacyclin (PGI-2) –relaxation via cAMP

Nitric oxide (EDRF-NO) – relaxation by ACh released NO, (cAMP mediated mechanism)

Endothelin – potent vasoconstrictor assoc w/ injured endothelium

Disease states alter the actions and release of NO, PGI2, and Endothelin.

Front 362

Basal MVO2 is about...

Back 362

8-10 ml/min/100g tissue

Front 363

How do we calculate arterial O2 content?

Back 363

CaO2 =
1.38* Hgb * Sat+.003(PaO2)

Front 364

How is most of the myocardial oxygen used?

Back 364

Pressure work 64% of total
Basal requirements 20%
Volume work 15% of total
Electrical activity 1% of total

This means pressure overload has a bigger effect than a volume overload on ischemia.

Front 365

!! If we double HR, we increase MVO2 by...

Back 365

Double.
1:1

Front 366

!! If we double contractility, we increase MVO2 by...

Back 366

90%

Front 367

!! If we double the aortic pressure we increase the MVO2 by....

Back 367

Double
1:1

Front 368

If we double wall stress, we increase MVO2 by...

Back 368

50%
2:1

Front 369

If we double volume work, we increase MVO2 by...

Back 369

8%

Front 370

For one cardiac cycle, work is equal to...

Back 370

W= Mean aortic pressure*SV

Front 371

Coronary blood flow is distributed to chambers based on workload. Who gets the most in descending order?

Back 371

LV>RV>LA>RA

Front 372

Adenosine is formed by the myocardium when demand for O2 is greater than the supply immediately available. What does it do?

Back 372

It binds adenosine receptors and causes vasodilation ie. increased coronary flow.

Front 373

Coronary autoregulation refers to the ability of the heart to maintain constant coronary flow over a wide range of perfusion pressures. What are the bottom limits of this ability to autoregulate?

Back 373

Mean pressure 40 mmHg
Diastolic pressure 30 mmHg

Front 374

What metabolic factors adversely affect coronary blood flow?

Back 374

Decreased PO2
Acidosis

Front 375

What do hyperkalemic states adversely affect?

Back 375

Myocardial contractility.

Front 376

Under normal circumstances what substrates does the myocardium use for energy?

Back 376

40% of MVO2 is due to oxidation of carbohydrates
60% is from fatty acids

However, the heart uses whatever substrate is in highest concentration in the blood.Glucose and lactate are utilized at a similar rate.
Ketone bodies can also be used.
Pyruvate uptake is very low though.

The hypoxic heart produces lactate & can utilize lactate as a substrate.

Front 377

In a normal heart, coronary flow can increase by about...

Back 377

500-600%

Front 378

What are the underlying goals of the treatment of ischemic heart disease?

Back 378

Reduce CAD risk factors
Improve Supply & CBF
Decrease Demand

Front 379

What are the typical ECG changes of an anterior MI?

Back 379

Front 380

How do we improve oxygen supply to the myocardium?

Back 380

Decrease HR:
Beta blockers (BBs)
Calcium Channel Blockers (CCBs)

Restore DBP:
Intra-aortic balloon pump.

Lower LVEDP:
Nitrates
CCB’s
ACE inhibitors
Angiotensin receptor blockers (ARB’s)

Lower CVR:
Revascularize
Prevent thrombosis
Antiplatelet agents
Limit/reverse atherosclerosis
Lipid lowering agents
Dilate/relax coronary arteries with Nitrates (NTG, nitroprusside) and CCB’s


Increase oxygen content:
1.38 x Hgb x O2Sat + 0.003 x PaO2

Front 381

What do dihydropyridine CCB's like verapamil and diltiazem do?

Back 381

Decrease heart rate.

Non-dihydropridine CCB's lower LVEDP and are a little more vasodilatory in the coronary circulation.

Front 382

What is a typical coronary venous oxygen saturation?

Back 382

About 30%

Front 383

If CBF, Substrate, or oxygen (MVO2) demand exceeds supply, ischemia may be either...

Back 383

Regional or global

Front 384

What is the standard paper speed for an EKG?

Back 384

25mm/s

Front 385

The gold standard for visualizing coronary arteries is...

Back 385

Coronary angiography

Front 386

What are the three acute coronary syndromes?

Back 386

Unstable Angina

Non ST-Elevation Myocardial Infarction (NSTEMI); (Non Q Wave Myocardial Infarction)

ST-Elevation Myocardial Infarction (STEMI); (Q Wave Myocardial Infarction)

Front 387

In a small subset of AMI there is no plaque rupture but erosion of the endothelium exposes plaque contents to thrombogenic forces in the blood. Who is this most common in?

Back 387

Women

Front 388

A small subset of MIs (less than 10%) occur in the absence of atherosclerotic plaque thrombosis stimulated by disruption or erosion. What are potential mechanisms of this?

Back 388

Vasospasm
(cocaine users)

Emboli
(left sided cardiac thrombus, vegetation, paradoxical embolus)

Unexplained secondary event.

Front 389

What are the charcteristics of an unstable plaque?

Back 389

High lipid content and a thin fibrous cap.

Front 390

What are Bivalirudin and Argatroban?

Back 390

Direct thrombin inhibitors.

Front 391

What is the main biochemical consequence of ischemia?

Back 391

Anaerobic glycolysis within seconds.

Inadequate ATP and creatine phosphate as well as accumulation of noxious breakdown products like lactic acid.

Without reperfusion - hypoxia and decreased removal of noxious metabolites (potassium, calcium, amphiphilic lipids, and oxygen-centered free radicals) leads to impaired ventricular function and predisposition to lethal arrhythmias.

Front 392

Where does ischemia usually start in the heart?

Back 392

Subendocardium.

Progresses towards the epicardium.

Front 393

What is the effect of transient hypoxia and accumulation of metabolites on myocardial function?

Back 393

Diminished diastolic relaxation.

Abnormal systolic contraction, (abnormal wall motion, and diminished stroke volume)

Front 394

What determines the size of a myocardial infarction?

Back 394

Size of the vascular bed supplied by the obstructed vessel.

Duration of coronary occlusion.

Metabolic/oxygen needs of myocardium at risk.

Extent of collateral vessels.

Alterations in blood pressure, heart rate, and rhythm.

Front 395

What is the diagnostic definition of an MI?

Back 395

Detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least one value above the 99th percentile of the upper reference limit (URL) together with evidence of myocardial ischemia with at least one of the following:

• Symptoms of ischemia

• ECG changes indicative of new ischemia (new ST-T changes or new left bundle branch block [LBBB])

• Development of pathological Q waves in the ECG

• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.

Front 396

What are the diagnostic criteria for prior MI?

Back 396

Development of new pathological Q waves with or without symptoms

Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract, in the absence of a non-ischemic cause

Pathological findings of a healed or healing myocardial infarction

Front 397

What are the commonly used enzyme markers for MI?

Back 397

Creatine Kinase-MB- isoenzyme (CK-MB)

Troponin I and Troponin T (more specific)

Aspartate serum transaminase(AST), Lactate Dehydrogenase(LDH1/LDH2 ratio) and myoglobin will also rise with acute myocardial infarction.

Front 398

What is the expected pattern for Creatine Kinase(CK) and MB isoenzyme in the setting of acute MI?

Back 398

MB/total CK > 4%;

Initial rise within 4-6 hours, peaks within 16-24 hours, and returns to baseline within 3-4 days.

Front 399

What is the expected pattern for cardiac-specific troponins in the setting of acute MI?

Back 399

T or I; rise within 4-6 hours; peak within 24 hours, remain elevated up to 7-14 days.

Front 400

What pattern do we expect to see with lactate dehydrogenase in the setting of acute MI?

Back 400

LDH1/LDH2 > 0.50;
Peak late and are elevated for several days.

Front 401

What trend do we expect for Aspartate Serum Transaminase (AST) in the setting of acute MI?

Back 401

Intermediate time elevation.
(12-24 hours)

Front 402

The problem with myoglobin as an enzyme marker for MI is that it...

Back 402

Is not specific for MI.

Front 403

Tropnin levels correlate with ....

Back 403

MI mortality.

Front 404

What are the ECG findings of acute MI?

Back 404

ST depression or deep T wave inversions in a consistent anatomical distribution suggest ischemia.

Hyperacute(Peaked) T waves (earliest signs of injury)

ST elevation in a consistent anatomical distribution suggests ongoing myocardial injury.

Diagnostic Q waves in a consistent anatomical distribution suggest prior myocardial infarct.

Front 405

What is the significance of ST Elevation in acute MI?

Back 405

ST elevation in a consistent anatomical distribution suggests ongoing myocardial injury.

ST-Elevation MI (Q Wave MI) occurs when occlusive thrombi persist resulting in myocardial necrosis.

Non ST-Elevation MI (Non Q Wave MI) results from incomplete or spontaneously recanalized thrombotic occlusions after ischemia that is persistent enough to elicit necrosis.

In general patients with ST-elevation need fibrinolytic therapy while those with ST-depression or T-wave inversion with or without positive cardiac enzymes need potent antiplatelet therapy.
(GP IIb-IIIa inhibitors )

Front 406

What does non-ST elevation MI (a cousin of unstable angina but with elevated enzymes) tell us?

Back 406

Total occlusion of culprit vessel much less likely vs. ST elevation MI.

More likely to have multivessel CAD.

More likely to have prior MI's

More likely to have history of diabetes, hypertension, heart failure, and peripheral vascular disease.

Less likely to be smokers or have dyslipidemia.

Elderly patients more likely to have non-ST elevation MI's.

Front 407

Changes in which ECG leads correlate with which vessels?

Back 407

II, III and aVF:
inferior MI RCA

V1-V4:
Anterior MI LAD

I and AVL:
Lateral MI L.circumflex
or
Anterolateral MI LAD
(With V4-V6)

V1-V3:
Septum and anteroseptum MI LAD
(with ST elevation)
or
Posterior MI L.Circumflex
(With ST depression)

Front 408

How do we know the dominance of a coronary circulation?

Back 408

Artery of origin of PDA determines “dominance”.

Front 409

What determines the prognosis of MI?

Back 409

Early prognosis is determined by presence of arrhythmias, sudden cardiac death, and development of complications.

Late prognosis is determined by left ventricular function.

Front 410

What are clear indications of high risk MI patients on admission?

Back 410

Heart rate > 100 bpm

BP < 100 mm Hg

Pulmonary edema(rales greater than one half way up)

Shock

Front 411

What are the complications associated with acute MI?

Back 411

Arrhythmias: heart block, bradycardia, or ventricular arrhythmias.

Congestive heart failure and pulmonary edema.

Cardiogenic shock

Pericarditis: early or late(Dressler’s Syndrome)

Mechanical Complications: ventricular septal defect; papillary muscle rupture with development of severe mitral regurgitation; or rupture of the left ventricular free wall.

Development of scar or ventricular aneurysm.

Front 412

What should we look out for with inferior wall MI?

Back 412

RV ischemia occurs in up to half of all inferior infarcts
(only 10-15% show classic hemodynamic abnormalities)

RV infarction accompanying inferior infarct=significantly higher mortality(25-30%)

High priority candidate for reperfusion.

Front 413

What is a secondary AMI?

Back 413

infarcts may occur secondary to insufficient perfusion relative to myocardial demand during certain pathologic conditions.

Anemia
Hypoxia
Acidemia
Infection
High catecholamine state.

Front 414

What is the algorithm for managing non ST elevation MI?

Back 414

Front 415

What is the algorithm for managing ST elevation MI?

Back 415

Front 416

What factors favor an invasive strategy in non ST elevation acute coronary syndromes?

Back 416

Recurrent angina or ischemia at rest or with low-level activities despite intensive medical therapy.

Elevated cardiac biomarkers.

New or presumably new ST segment depression.

Signs or symptoms of heart failure or new or worsening mitral regurgitation.

Hemodynamic instability.

Sustained ventricular tachycardia.

PCI within 6 months.

Prior CABG.

High risk score.

Reduced left ventricular function(EF < 40%).

Front 417

Which cardiac ion channels are passive?

Back 417

Sodium
Calcium
Potassium

Front 418

What do we mean when we say ion exchangers?

Back 418

Ion exchangers are selective (for at least two ions) and passive.

Unlike ion channels they can reverse directions.

Na/Ca exchanger in cardiac muscle.

Front 419

Ion pumps are selective, and actively transport ions across membranes against concentration or voltage gradients. Which ones exist in cardiac muscle?

Back 419

Na+/K+ pump
Ca2+ exporter

Front 420

What is the resting potential membrane potential of a cardiac cell?

Back 420

-90mV

Based on Nernst equation.

Front 421

What is the intracellular ion content of a cardiac cell in the resting state?

Back 421

High K+
Low Na+
Low Ca2+

Resting potential is primarily due to Na+/K+ pump.

K+ wants to rush out.
Na+ wants to rush in.

Front 422

What is happening electrophysiologically when a cardiac myocyte is at rest?

Back 422

Na+ channels are closed

Ca++ channels are closed

Some K+ channels are closed
Some K+ channels are open

Cell is actively pumping out Na+ and Ca++

K+ is leaking out passively, leaving behind a negative intracellular charge (– 90 mV)

Front 423

What is the threshold potential of cardiac myocytes?

Back 423

-70mV

Front 424

What causes the ion channels to open in a cardiac myocyte?

Back 424

Voltage.
They are said to be voltage gated channels.

Front 425

How is the depolarization of a cardiac myocyte different from a neuron?

Back 425

It is much longer

Front 426

What are the primary channels responsible for myocyte depolarization?

Back 426

Voltage gated Na+ channels.

Activate rapidly, and inactivate rapidly.

Inactivation happens so rapidly that it occurs before any of the other channels have even responded.

Can be closed, open or inactivated.

Front 427

What is phase zero of the cardiac action potential?

Back 427

Rapid depolarization due to fast sodium channel opening.

Front 428

What is phase 1 of the cardiac action potential?

Back 428

Transient outward current – mostly K+ efflux.

Small repolarization immediately following phase 0 (rapid depolarization).

Front 429

What is phase 2 of the cardiac action potential?

Back 429

Plateau phase

All about calcium.

Depolarization of the cell triggers Ca++ channels to open.
Slower and sustained Ca++ influx prolongs depolarization, and triggers release of Ca++ from the Sarcoplasmic Reticulum which precipitates contraction through calcium activated calcium release.
(excitation-contraction coupling)

Front 430

What is phase 3 of the cardiac action potential?

Back 430

Rapid repolarization.

Ca++ channels close.

Voltage-gated K+ channels remain open, repolarize cell.

Na+ channels begin to revert to resting (closed) state.

Front 431

What is phase 4 of the cardiac action potential?

Back 431

Resting state.

All Na+ channels closed etc.

Front 432

When does phase 4 of the cardiac action potential happen?

Back 432

Diastole
(end of T wave to beginning of P wave)

All other phases happen during systole.

Front 433

How do Na+ channel blocking drugs affect the cardiac action potential?

Back 433

Slows upstroke of phase 0 so its not a line straight up anymore.

!!Widens the QRS complex on ECG!!

Front 434

How do K+ channel blocking drugs affect the cardiac action potential?

Back 434

They prolong phase 3 rapid repolarizaton and therefore prolong the QT interval on ECG.

Front 435

What is the absolute refractory period?

Back 435

Beginning of phase 0 to end of phase 2.

All Na+ channels are inactivated – cannot reopen in any circumstance; must first get to resting (closed) state.

All Ca++ channels are open

Cell is completely inexcitable

No stimulus of any strength is able to generate a new action potential.

Effective refractory period is absolute refractory period plus a small portion of phase 3.

Front 436

What is the relative refractory period?

Back 436

Phase 3.

Cell is beginning to repolarize.

Cell has not yet returned to resting state.

Most Na+ channels are still inactivated but some are moving towards resting (closed).

Ca++ channels are mostly closed which means they can reopen.

A strong stimulus can induce an action potential that will be lower amplitude and slower velocity than “normal” but the action potential will be strong enough to propagate normally to adjacent cells.

Front 437

What happens if a premature beat or pacing stimulus arrives during the effective refractory period?

Back 437

No response

Front 438

What hapens if a premature beat or pacing stimulus arrives after the Relative Refractory Period?

Back 438

Normal action potential

Front 439

What happens if a sufficiently strong premature beat or pacing stimulus arrives after the Effective Refractory Period but during the Relative Refractory Period?

Back 439

Slower-onset action potential within the cells directly activated, but normal propagation to adjacent cells.

Front 440

What is a pacemaker current?

Back 440

Slow influx of positive ions into cells with automaticity (during the normally flat phase 4) that eventually reaches threshold and causes spontaneos depolarization.

This happens in cells of the conduction sytem
or
in myocytes that have been ischemically or metabolically injured.

Front 441

“What is the "resting” potential for Sinus and AV nodal cells and how is their pattern of depolarization different?

Back 441

-60mv

Na+ channels are not active in Sinus or AV nodal cells so depolarization happens through calcium channels.

Ca++ channels are slower than Na+ channels so:

Phase 0 has a slower, more gradual rise.

Phase 1 does not occur because it is a response to rapid Na+ “overshoot” in other cells.

Phase 2 also doesn’t occur since the calcium channels are used up driving phase 1.

Phase 3 still occurs normally because voltage-gated K+ channels are the same as in other cells.

The pattern of depolarization in these cells is therefore almost sinusoidal.

Front 442

From an electrophysiological standpoint, why can the atria go faster than the ventricles?

Back 442

They have a shorter effective refractory period.

Atrial Fibrillation (>350 bpm)
Atrial Flutter (300 bpm)

Front 443

What makes the sinus node the dominant rhythm?

Back 443

Under normal conditions, sinus node automatic rhythm is faster than any other location.

Front 444

What makes AV nodal conduction slower than atrial, ventricular and His-Purkinje cells?

Back 444

Phase 0 in the AV node is driven by slow Ca++ channels instead of fast Na+ channels.

Intrinsic rythm is 40-60bpm but can produce accelerated junctional rhythm (>60bpm)

Front 445

What is the refractory period of the His-purkinje system relative to atrial cells?

Back 445

Much longer.

Front 446

Why is impulse conducted fast in the His-purkinje system?

Back 446

Greater density of Na+ channels than other cells.

Greater density of gap junctions than other cells.

Front 447

Which cells have a longer refractory period, atrial or ventricular myocytes?

Back 447

Ventricular myocytes.

Front 448

How does the autonomic nervous system influence AV nodal conduction?

Back 448

Sympathetic stimulation increases conduction velocity and automaticity.(+chronotropy and dromotropy)

Parasympathetic stimulation decreases conduction velocity and automaticity.
(-Chronotropy and dromotropy)

Probably mediated mainly by indirect effects on Ca++ channel function.

Front 449

How do chronotropic drugs affect the conduction system in the heart?

Back 449

Alter automaticity
(Usually SA node)

Front 450

How do dromotropic drugs affect the conduction system in the heart?

Back 450

Alters the speed of propagation of an impulse.
(usually AV conduction)

Front 451

What is a physiologic AV block?

Back 451

Long refractory periods in the presence of abnormally fast atrial rhythms protect the ventricles.

Front 452

What are the normal automaticity rates of the conduction system?

Back 452

Sinus Node:
60- 100 bpm (at rest)

AV Node and His bundle:
40- 60 bpm

Bundle Branches, Purkinje system:
30- 40 bpm

Front 453

Junctional escape rhythms originate from...

Back 453

The AV junction

Front 454

Ventricular escape rhythms originate from...

Back 454

The Purkinje network.

Front 455

What can we say about the reliability of the different escape or ectopic rhythms?

Back 455

Ectopic atrial rhythm:
Usually pretty reliable

AV Node +/- His bundle:
Good, but a little less reliable.
More easily suppressed than sinus or atrial rhythms.

Purkinje network:
Not reliable.
Easily suppressed.

Front 456

What are the three primary mechanisms for tachyarrythmias?

Back 456

Abnormal Automaticity. (ischemia or metabolic)

Triggered Activity.
(afterdepolarizations)

Reentry phenomena.

Front 457

What is an afterdepolarization?

Back 457

Spontaneous depolarization occurs during or just after the previous action potential.

If the afterdepolarization reaches threshold it generates another action potential.

Early afterdepolarizations interrupt phase 3 of the first AP and are usually caused by reactivation of Ca++ channels. They prolong the QT interval, they can be self-perpetuating and they can preciptate dangerous rhythms like torsades depointes.

Delayed afterdepolarizations occur during phase 4. These mostly happen in the setting of intracellular Ca++ overload.
Associated with Dig. Toxicity but other arrhythmias also have this mechanism.

Front 458

What is the most common mechanism of tachyarrythmias?

Back 458

Re-entry phenomena

Front 459

What conditions need to be met for a re-entry phenomenon to occur?

Back 459

There need to be at least two pathways for electrical current.

Unidirectional block needs to be possible in at least one pathway.

There needs to be sufficient difference in the speed of the pathways to get re-entry going.

Front 460

What is typical AV node re-entry?

Back 460

Impulse goes down the slow pathway and back up the fast pathway.

Almost always due to a premature beat

Premature beat comes in very soon after the preceding beat
and the fast pathway is still refractory from the previous beat.

The fast pathway therefore cannot be activated by the premature beat.

The ERP of the cells (!!not the “speed” of the pathway!!) determines whether the unidirectional block will occur.

Front 461

What is “atypical” AV node reentry?

Back 461

Prototype example Wolf-parkinson-white syndrome.

In WPW, the accesory pathway is the fast pathway and the AV node is the slow pathway.

The reentrant loop uses the slow pathway (AV node) as the retrograde limb.

Causes atrioventricular re-entrant tachycardia.

Front 462

What is the primary mode of V-Tach after an MI? (possibly after reperfusion)

Back 462

Differences between damaged and healthy tissue cause a difference in conduction (slow and fast pathway) which allows for re-entry phenomena.

Front 463

What is though to be the cause of Idiopathic Ventricular Tachycardia?

Back 463

Re-entry in the ventricles.

Front 464

What are the classes of antiarrhythmic drugs?

Back 464

Class 1 –
Na+ channel blockers
Further divided into subgroups 1A, 1B, 1C

Class 2 –
Beta blockers

Class 3 –
K+ channel blockers

Class 4 –
Ca++ channel blockers (CCB)

Others –
adenosine, digoxin

Front 465

Where are beta receptors found?

Back 465

β-1 receptors in heart.

β-2 receptors in vascular smooth muscle and bronchial smooth muscle.

Front 466

What are beta blockers? (Class 2 antiarrythmics)

Back 466

Only "antiarrrythmics that improve survival".

Don't actually affect the heart directly but reduce sympathetic stimulation.

Slow automaticity in sinus node AND AV node by slowing phase 4 depolarization.

-Chronotrope, -dromotrope,-inotrope

Can induce bradycardia.

Cardioselective examples:
Atenolol
Metoprolol
Esmolol

Non-selective beta blockers:
Propranolol
Labetalol – also α-block
Carvedilol – also α-block

Non-selectives can exacerbate asthma and Raynaud's.

IV Labetalol useful in hypertensive emergencies because of alpha blockade.

Front 467

What two subclasses of CCB's (class 4 antiarrythmics) exist?

Back 467

Dihydropyridine (DHP):
Nifedipine, Amlodipine, Felodipine, etc., etc.

Nondihydropyridine (non-DHP):
Diltiazem
Verapamil

Front 468

Why do only diltiazem and verapamil (Non-DHP CCB's) have clinically relevant effects on cardiac action potential amongst the CCB's?

Back 468

DHP-CCBs are such potent vasodilators that no one can take a high enough dose to actually affect the cardiac Ca++ channels.

Front 469

How do diltiazem and verapamil work?

Back 469

Block the L-type calcium channels in the Sinus and AV nodal cells. (!!AV node most!!)

Similar clinical effect to beta blockers.
Negative chronotropy
Negative dromotropy
Negative inotropy
(major problem unlike in beta blockers, relatively contraindicated in sytolic heart failure)

Usually do not cause significant sinus bradycardia unless patient already has sinus node dysfunction.
If patient does have sinus node dysfunction, the effect can be profound.

Can “shut down” a junctional escape rhythm.

Especially useful to slow ventricular response rate during atrial tachyarrhythmias.

Can interrupt any reentrant loop that uses the AV node as part of the circuit ( eg. AV Node Reentry, AV Reentrant Tachycardia)

Can cause peripheral edema.

Various drug interactions often guide use.

Front 470

By what mechanism is Digoxin a positive inotrope?

Back 470

Digoxin poisons the Na+-K+ pump.

Increases Na+ concentration inside cell.

Na+-Ca++ exchanger keeps more Ca++ in cell to balance this.

More Ca++ enters SR and therefore more Ca++ is available for contraction.

Front 471

How is digoxin an antiarrythmic?

Back 471

Primary effect on cardiac rhythm is through augmentation of vagal tone.

Primarily affects Sinus and AV nodes.

Like verapamil and diltiazem the AV node is the primary target. The sinus node is not usually affected, but can be profoundly supressed in patients with pre-existing sinus node dysfunction.

Much less effective in slowing AV nodal conduction than verapamil and diltiazem but does not cause hypotension.

Narrow therapeutic index.

Front 472

What are the charcteristics of Dig toxicity?

Back 472

Nausea / vomiting, visual disturbances (seeing yellow-green halos around things).

High-grade AV block along with atrial tachycardias.

Ventricular tachyarrhythmias due to delayed afterdepolarizations.

Digoxin is cleared by the kidney, so must keep track of renal function.

Severe toxicity may need digibind and dialysis.

Front 473

What are the half life and side effects of adenosine?

Back 473

about 10 seconds

Can precipitate bronchospasm in asthmatics which may persist after adeonsine is cleared.

Rarely can precipitate atrial fibrillation but typically not with usual doses (6mg-12mg).

Front 474

What is adenosine used for?

Back 474

First line drug for terminating AV node involving re-entry.

Slows the sinus.

No noticeable effect on ventricular cardiac cells.

Front 475

Which drugs are specifically targeted toward the cardiac action potential?

Back 475

Class 1 and 3 antiarrythmics.

Have direct effects on atrial and ventricular cells.

Front 476

What do class 1 antiarrythmics do?

Back 476

Na+ channel blockers.

Make fewer Na+ channels available for conduction. Cumulative effect is to slow conduction through the affected tissue.


Raise the threshold somewhat for initiation of action potential.

Slow the upstroke of phase 0.

May also decrease slope of phase 4 in cells with abnormal automaticity.

Slows or terminates automaticity but sinus node not usually affected unless already have sinus node dysfunction.

Can resolve rentry issue but can also exacerbate them. This is the primary danger of – incessant VT.
Patients with prior myocardial infarction should not take type 1 drugs unless they already have an ICD.

Front 477

What are the drugs classified as class 1 antiarrythmics?

Back 477

Class 1A:
Quinidine
Procainamide
Disopyramide

Prolong QRS and QT (Torsades).
Also block K+ channels.
Lots of side effects.

Class 1B:
Lidocaine
Mexiletine

Only work in ventricle.
Preferentially target ischemic cells.
Shorten QT.

Class 1C:
Flecainide
Propafenone

Most potent.
Prolong QRS the most.
No direct effect on QT.
Negative inotropes (bad in heart failure).

Front 478

What are the main side effects of quinidine?

Back 478

Major GI side effects (N/V/D)

“cinchonism” = tinnitus, confusion, visual disturbance, etc.

Autoimmune thrombocytopenia

Major interaction with digoxin
(Raises digoxin level)

Front 479

What is unique about procainamide?

Back 479

Only 1A drug used intravenously.

Breakdown product = NAPA (N-acetyl procainamide) active metabolite.

Patients can be slow or fast acetylators but we check both Procainamide + NAPA for blood levels.

Lupus-like syndrome in up to ⅓ of patients with Fever, rash, arthralgias, etc.
Requires stopping the drug.

Front 480

What is unique about the class 1A antiarrythmic Disopyramide?

Back 480

Strong anticholinergic effect:
Dry mouth, urinary retention, constipation, exacerbation of glaucoma etc,

-inotrope unlike procainamide and quinidine.

Front 481

What is the major concern with class 1A antiarrythmic?

Back 481

Class 1A drugs also block K+ channels to some extent.
They can prolong the QT interval.
This can cause Torsades de pointes (aka polymorphic ventricular tachycardia).

Front 482

Lidocaine was once recommended prophylactically during AMI why?

Back 482

Preferentially affects ischemic tissue and could be useful for ventricular arrythmias during AMI.

HOWEVER, Trial data proved this false – it increased mortality in AMI.

Front 483

Why is it important to remeber that lidocaine is cleared by the liver?

Back 483

Liver disease (obviously).

Heart failure means less hepatic perfusion.

Lidocaine also has serious CNS side effects at high levels, confusion and seizures.

Levels should be monitored carefully for prolonged continuous infusion.

Front 484

What is mexilitene?

Back 484

Oral only

Practically speaking, probably okay to consider this an oral form of lidocaine.

Not very effective, but mixes well with certain other antiarrhythmics when needed.

Front 485

What class of drug is Phenytoin (dilantin) ?

Back 485

technically a class 1B antiarrythmic but is almost never used for this purpose.

Front 486

What are the class 1C antiarrythmics Flecainide and Propafenone?

Back 486

The most potent Na+ channel blockers.

Markedly decrease upstroke of phase 0

“Clean” drugs – no effect on K+ channels.
No direct effect on QT interval.

Can cause bad arrhythmias, but not Torsades.

Negative inotropes
(contraindicated in systolic heart failure)

Primarily used for atrial arrhythmias (AFib)

Also can be used to “shut down” accessory pathways (i.e. Wolff-Parkinson-White syndrome.

Flecianide side effects like fatigue and visual disturbance are common, but not usually severe enough to stop the drug if it’s working.

Propafenone has beta blocking properties and can produce dizziness. How much depends on individual patient’s metabolism.

Front 487

What do we mean by the use dependance of Na+ channel blockers?

Back 487

Na+ channel blocking drugs bind preferentially to open channels. The more the channels are open (being used), the greater the blockade

This means that Na+ channel blockers are even more effective at faster heart rates like a-fib (300-400bpm) and may even convert it back to sinus.

Front 488

What do mean when we say that K+ channel blockers (Class 3 antiarrythmics) have reverse use dependance?

Back 488

K+ channel blockers have greater effect during slower heart rates.
This makes them less useful in terminating atrial fibrillation (when atrial rates are very fast) than sodium channel blockers.

It also means that bad arrhythmias such as Torsades are more likely during slower heart rates if the QT is prolonged.

“pause-dependent Torsades” = Polymorphic VT occurring after a sinus pause.

Front 489

Which drugs are the potassium channel blockers (Class 3 antiarrhythmics)?

Back 489

Sotalol
Dofetilide and Ibutilide
Amiodarone
Dronedarone

Front 490

How does hypokalemia influnce the use of potassium channel blockers?

Back 490

Effect of the drug is magnified.

Front 491

What are some caveats to keep in mind when we use potassium channel blockers?

Back 491

They all prolong the QT interval.

Torsades (polymorphic VT) is a risk with most
(exception = amiodarone)

Torsades is more likely when:
Too much drug on board
Renal or hepatic failure, depending on drug.
Hypokalemia
Bradycardia and especially sinus pauses.

Despite all this, K+ channel blockers can be used in patients with prior AMI.

Front 492

What are some caveats specific to the Class 3 antiarrhythmic Sotalol?

Back 492

Also has beta blocker activity.
Can be good or bad depending on patient.

Cleared by the kidney.
Can accumulate in renal failure and cause Torsades.

QT must be monitored periodically.

Front 493

What are the class 3 antiarhythmics Dofetilide and Ibutilide?

Back 493

Ibutilide = intravenous; Dofetilide = oral
Otherwise, basically same characteristics.

Ibutilide is given IV to convert Afib.
Torsades in up to 10%
Can partially prevent by giving IV magnesium first.

Dofetilide is cleared by liver and kidney.
Renal clearance seems especially important.

Dofetilide is relatively safe in heart failure.
Not a negative inotrope

QT must be monitored periodically

Front 494

What is amiodarone?

Back 494

Class 3 antiarrhythmic.

Has properties of all four antiarrhythmic classes:
Some Na+ channel blocking.
Some β-blocking.
A lot of K+ blocking.
Some Ca++ channel blocking.

Probably why it works for almost every arrhythmia.

“safest antiarrhythmic" drug for your heart, and most dangerous one for every other part of your body.

Has a LOT of iodine which contributes to noncardiac toxicities.

Prolongs QT but very rarely causes Torsades
(QT monitoring not necessary)

Almost never causes ventricular arrhythmias
but can’t be counted on to prevent them.
Only ICDs have been shown to improve mortality in patients at risk for fatal arrhythmias.

Irreversible pulmonary toxicity is most serious but can take up to ten years to develop. Not a drug for young people.
Thyroid issues, liver injury photosensitivity and bluish skin with high doses also a problem.
(Blue, blind and coughing up your liver and thyroid)

Front 495

What is Dronedarone?

Back 495

New drug similar to amiodarone.

No iodine
Less toxicities
May not be as protected from Torsades.

QT must be monitored but
Torsades risk probably low.

Interferes with creatinine secretion – raises serum creatinine level but GFR is actually not affected.

Front 496

Which antiarrhythmics are okay to give in the setting of systolic heart failure?

Back 496

Front 497

Which antiarrhythmics are okay to give in the setting of prior MI with myocardial scar but without systolic heart failure?

Back 497

Front 498

Which antiarhythmics are best for a healthy ventricle?

Back 498

Everything is okay (hooray!)

Type 1 antiarrhythmics (especially 1C – flecainide and propafenone) may actually be safer than type 3 drugs in patients with a structurally normal ventricle (no scar, normal systolic function etc.)

Front 499

Leading cause of mortality in adult women?

Back 499

CV disease

Front 500

True or False:
Men have first MI ~10 years before women have their first MI.

Back 500

True

Front 501

True or False:
Women are just as likely to have ST segment elevation MI as men, but clinicians are less likely to recognize it.

Back 501

False
Women are less likely to have ST segment elevation, and have higher prevalence of “silent MI”.

Front 502

Women often have "atypical" pattern for angina. What is this pattern?

Back 502

neck/jaw pain, dyspnea, or fatigue

Front 503

What is a goal LDL for those with CHD or high risk?

Back 503

<70

Front 504

What is a goal LDL for those with 2 or more risk factors for CHD?

Back 504

<100

Front 505

What is a goal LDL for those with 0-1 risk factors for CHD?

Back 505

<160

Front 506

What are some of the gender differences in risk factors for CHD?

Back 506

Diabetes is a much stronger predictor of CHD risk in women than in men.

High Triglycerides carry greater risk in women.

Physical inactivity more prevalent among women.

Smoking may be stronger risk factor in middle-aged women.

CRP levels are higher in women. (iffy)

Front 507

What key processes in the development of CHD does estrogen affect?

Back 507

Lipid levels
Arterial vasodilation
Clot formation/breakdown

Some evidence to suggest that progesterone attenuates estrogen’s favorable effects.

Front 508

What effects does estrogen have on endothelium?

Back 508

Stimulates NO synthesis
(Vasodilation
Increases Plasma renin activity
Inhibits ACE activity
Protects LDL from oxidation
Increases endothelial regrowth

Front 509

How does estrogen affect coagulation?

Back 509

!!procoagulant!!

Increases Prothrombin
Decreases antithrombin III

Contributes to increased venous thromboembolic events.

Front 510

What is the result of injury to various blood vessel layers?

Back 510

Endothelium:
Thrombi, thickening, & spasm leading to pain of ischemia & loss of function of organ.

Media:
Aneurysm; rupture leading to pulsatile mass, hypotension and pain.

Adventitia:
Weakening, false aneurysm with resulting lump(hematoma), pain.

Front 511

How do various size arteries respond to injury?

Back 511

Large vessels:
Aneurysm , rupture.

Medium arteries:
Thicken and narrow (stenosis) or thrombose which may lead to tissue ischemia.

Small arteries & arterioles:
Arteriolar narrowing can cause hypertension.

Capillaries:
Petechial hemorrhage, microthrombi (DIC), narrowing in diabetes.

Front 512

In broad terms, what are the three types of athersclerotic lesions in vessels?

Back 512

Fatty streak
(small, intracellular fat , "innocuous")

Atheroma
(raised, lipid center "dangerous")

Fibrous plaque
(intimal scar, "innocuous")

Front 513

What are the three major elements of an atheroma?

Back 513

Necrotic center of extracellular lipid

Fibrous cap

Proliferating cells (myofibroblasts)

Front 514

What are the possible complications of an atheroma?

Back 514

Ulceration (of the plaque)

Thrombosis
(often caused by ulceration)

Medial damage, causing aneurysms.

Hemorrhage into plaque.

Calcification.

Front 515

What are the implications of arterial inflammation (arteritis)?

Back 515

It can:

Weaken vessel walls causing aneurysm or rupture.

Narrow the lumen causing ischemia.

Damage the endothelium, resulting in thrombosis.

Become complicated by arteriosclerosis (e.g., syphilitic aortitis with secondary atherosclerosis)

Front 516

What is Kawasaki disease?

Back 516

AKA muco-cutaneous lymph node syndrome

Idiopathic Necrotizing Arteritis.
in children (typically under 5) with skin and lymph node involvement as well as rash.
Sometimes (~10%) includes autoimmune coronary arteritis and aneurysmal dilation of the coronaries.
Can also cause unexpected late stage death due to cornary aneurysm.

Presumably virally related but we dont know which virus.

Front 517

What is Takayasu arteritis?

Back 517

An Idiopathic Necrotizing Giant CellArteritis.

Causes thickening of aortic arch.
Blindness/CNS deficits(carotids)
↓pulses in upper extremities, ‘pulseless disease’.

Women, 15- 45 years most commonly affected

Front 518

What is thromboangiitis obliterans (Buerger disease)?

Back 518

An Idiopathic Necrotizing Arteritis involving pain and ischemia, legs and arms.

Relatively young men.

Leads to gangrene of extremities.

Genetic predisposition possible.

Almost exclusively in smokers
May improve with smoking cessation.

Front 519

What is phlebitis?

Back 519

Acute inflammation of veins, usually with thrombosis.

Caused by bacterial, parasitic, physical, chemical, allergic injury.

Examples:
Pylephlebitis (portal vein) from abdominal infection (e.g., appendicitis)

Dural sinuses in infections of ear and face.

Pulmonary veins in pneumonia.

Iliofemoral veins in puerperal sepsis.

Hepato-veno-occlusive disease from chemotherapy.

Migratory thrombophlebitis- "Trousseau syndrome"-
Transient attacks, variable sites Associated with internal cancers (e.g., pancreatic CA).

Idiopathic Thrombophlebitis (phlebothrombosis)

Front 520

What disease is associated with migratory thrombophlebitis?

Back 520

Pancreatic cancer.

Front 521

What is phlebothrombosis?

Back 521

Venous thrombosis without inflammation. (no -itis)

Usually in deep veins of legs (DVT) or pelvic veins.

Exact incidence uncertain, but high (autopsy patients, as high as 60%)

Pain, tenderness, swelling, or may be asymptomatic.

Up to ~50% can develop pulmonary embolisms.

Clots usually form in relation to valve cusps (sites of maximum stasis) and propagate upward.

Front 522

What are varicose veins?

Back 522

Abnormally dilated, tortuous veins.

Produced by prolonged increase in intraluminal pressure.

Often in relation to injury or defect of the vein proximally.

Different names at different sites.
(Varciocele-testes, Hemmorhoids-perianal etc.)

Do NOT cause pulmonary embolism. Too superficial to get into the deep veins.

Front 523

What is the mechanism of atherosclerotic aneurysms?

Back 523

Atheromas cause medial destruction through ulcerated plaques.

Front 524

What are the complications of athersclerotic aneurysms?

Back 524

Rupture (retroperitoneal hemorrhage),

Stenosis of ureter by pressure or fibrosis,

Occlusion of aortic branch (renal, mesenteric),

Embolism (thrombo- or atheromatous)

Front 525

What is the mechanism of syphillitic aneurysm?

Back 525

Tertiary syphilis involves vasa vasorum.
Causes vasculitis, and medial damage.

Presentation varies but usually includes dyspnea, stridor, dysphagia, cough, pain
congestive heart failure due to aortic insufficiency (AI).

Tree barking on intima commonly seen post-mortem.

Front 526

What causes mycotic aneurysms?

Back 526

"Mycotic" refers to any infection, not necessarily fungal.

Infection causes destruction of media.

Can complicate to distal or bland infarcts.

Typically one of the Sequelae of infective endocarditis or endarteritis.

Front 527

What is a dissecting hematoma of the aorta?(pseudoaneurysm)

Back 527

AKA Aortic dissection

Age 40-60, males 6:1

95% have intimal tear in ascending aorta.
5% have no intimal tear (probably just small)

If hemorrhage extends to aortic branches, can cause differences in pressure and pulse in arms or legs.

Type A:
Most common - involves ASCENDING AORTA & may extend distally

Type B:
Begins distal to subclavian artery, extends distally (3x better prognosis than Type A, because does not involve vessels to head)

Type A can cause Hemopericardium from proximal rupture and aortic valve damage.

Associated with hypertension, trauma and Marfan's syndrome.

Front 528

How do we calculate QTC?
(corrected QT interval)

Back 528

QT interval/(square root of R-R interval)

QTC is more important for following drug effects and is usually calculated by the machine.

Front 529

What is the primary etiology of valvular heart disease?

Back 529

Rheumatic heart disease has been displaced by degenerative disorders as the primary etiology.

Front 530

Coarctation has an association with...

Back 530

A bicuspid aortic valve.

Front 531

What valve disease are dialysis patients at high risk for?

Back 531

Aortic stenosis.
Mitral valve calcification.

Front 532

What is the problem with having a bicuspid aortic valve?

Back 532

Can develop AS or AR with time.

Congenital in 1-2% of the population.

Frequent cause of symptomatic aortic stenosis in young patients.

Associated with other congenital abnormalities (especially coarctation) in 20% of cases.

80% of coarctation patients have BAV.

Front 533

What does aortic stenosis sound like?

Back 533

Mid to late peaking systolic ejection murmur.

Crescendo-decrescendo.

The later in systole the peak is heard the worse the lesion is.When the stenosis is severe enough, you can no longer hear the second heart sound.

Front 534

What is the pressure relationship between the LV and aorta in the systole of an aortic stenosis patient?

Back 534

There is a bigger difference than in a normal heart.

Front 535

What is the etiology of aortic stenosis?

Back 535

In a young patient think
congenital:

Bicuspid (2% of population)
3:1 male:female distribution
Co-existing coarctation (6% of patients)
Rarer causes include unicuspid valve, Sub-aortic stenosis (Discrete or
Diffuse aka Tunnel)

In a middle aged patient (4th and 5th decade) think bicuspid or rheumatic disease.

In an old patient (6th, 7th, 8th decade) think degenerative —MOST COMMON aortic stenosis.

Front 536

Rheumatic aortic stenosis is usually associated with...

Back 536

Concurrent mitral valve disease.

Front 537

How fast does aortic stenosis progress?

Back 537

1 cm^2/year

Front 538

What triad of symptoms is classically associated with aortic stenosis?

Back 538

angina, syncope, heart failure
(Also GI bleeding from AVMs)

Symptom development is correlated with survival.

Angina (if untreated):
5 year survival

Syncope:
3 year survival

Heart failure:
2 year survival

Front 539

What physical signs are associated with aortic stenosis?

Back 539

“Diamond” shaped, harsh, systolic crescendo-decrescendo ejection murmur.

Usually heard best at RUSB and radiates to carotids.
Can also radiate to the apex and mimic mitral regurgitation (the Gallavardin phenomenon)

Paradoxical S2 (delayed left ventricular emptying)

S4 (with left ventricular hypertrophy)

S3 (with left ventricular failure)

Intensity of murmur DOES NOT predict severity.

Presence of thrill DOES NOT predict severity.

Decreased, delay & prolongation of pulse amplitude.

Carotid pulsations characterized by delayed and weakened upstroke (the pulsus parvus et tardus)

Front 540

How do we discern the carotid sounds of aortic stenosis from carotid stenosis?

Back 540

Listen all the way up to the mandible.
Aortic stenosis should gradually disipate.

Front 541

How do we classify the severity of aortic stenosis?

Back 541

Normal aortic valve area:
2-3 cm^2

Mild AS >1.5 cm^2
Moderate AS 1.0-1.5 cm^2
Severe AS <1.0 cm^2; (mean gradients >50 mmHg)

Front 542

How do we treat aortic stenosis?

Back 542

Asymptomatic patients—follow expectantly

Endocarditis prophalaxis

Annual echo with severe AS or when symptoms change.

Patient education regarding symptoms

Surgery in patients with severe, symptomatic aortic stenosis or who need open heart for other reasons.

Front 543

What are the causes of aortic insufficiency?

Back 543

Bicuspid aortic valves, especially when associated with aortic root dilitation.

Infective endocarditis.

Rheumatic heart disease.(usually stenosis but can cause incompetence)

Radiation.

Subvalvular (subpulmonary aka suprachristal VSD)

Myxomatous disease.

Marfan’s or other connective tissue disorders.

Chronic aortitis (syphilitic).

Acute causes:
Aortic dissection
Infective endocarditis
Traumatic

Front 544

What is the effect of aortic regurgitation on the LV?

Back 544

Dilation.
Eccentric Hypertrophy.

When the LV starts to dilate, the valve needs to be fixed even if the patient is asymptomatic.

Front 545

How does chronic aortic regurgitation present?

Back 545

May remain asymptomatic or nearly so for a long time. Symptoms occur after considerable cardiomegaly and myocardial dysfunction.

exertional dyspnea, orthopnea, PND.

Uncomfortable awareness of the heart beat especially on lying down.

Syncope is rare and angina is less common than in patients with AS

Diffuse apical impulse.

Laterally and inferiorly displaced hyperdynamic heart.

Variable thrill over the base, suprasternal notch or carotids.

Carotid shudder.

S1 is soft, A2 is soft or absent, S3 and S4.

Early diastolic decrescendo murmur (high frequency) begins immediately after A2 best heard by the diaphragm, radiates to the apex.
Severity of AR correlates with duration of the murmur

In severe AR Mid to late diastolic apical decresecendo rumble heard best at right sternal border(Austin Flint murmur). This is a result of leakage from the aortic valve shutting the anterior leaflet of the mitral valve.





.

Front 546

What are some physical exam signs of aortic regurgitation?

Back 546

Bobbing of the head (de Mossert’s sign), with every heart beat, waterhammer or collapsing type pulses.

Traube’s sign refers to booming systolic and diastolic sounds over the femoral artery.

Durozierz’s sign consists of systolic and diastolic murmur over the femoral artery.

Quinke’s sign: capillary pulsations seen in fingertips.

Hill’s signs: popliteal systolic pressure exceeding brachial artery systolic pressure by 50-60 mmHg, etc.

Front 547

What are the X-ray findings of aortic regurgitation?

Back 547

LV enlargement which can be massive (cor bovinum).

Dilation of ascending aorta, egg-shell calcification of ascending aorta seen in luetic AR.

Valve calcification is uncommon.

Front 548

What is the ideal study for following a patient with aortic regurgitation serially?

Back 548

Echo

Front 549

Which aortic regurgitation patients do we NOT want to operate on?

Back 549

Asymptomatic patients with preserved LVEF and normal LV size.

We think about operating as soon as ventricle starts getting dilated.

Front 550

Fixed splitting is pathgnemonic for...

Back 550

ASD

Front 551

What is the etiology of mitral stenosis?

Back 551

Primarily rheumatic fever
(Scarring and fusion of valve)

Pure or predominant MS in~40% of rheumatic patients.

Rarely congenital.

2/3 female.

Front 552

What causes the symptoms of mitral stenosis?

Back 552

Increase in LA pressure causes pulmonary congestion and edema.

Diastolic murmur because of turbulence across the stenotic valve.

Front 553

What are the valve areas with various mitral stenoses?

Back 553

Normal valve area: 4-6 cm2

Mild mitral stenosis:
MVA 1.5-2.5 cm2
Minimal symptoms

Mod mitral stenosis
MVA 1.0-1.5 cm2
Usually no symptoms at rest.

Severe mitral stenosis
MVA < 1.0 cm2

Front 554

What is a common response of the LA to mitral stenosis?

Back 554

Valvular atrial fibrillation.

!!Very high risk for stroke!!

Front 555

What happens to the shape of the LV in mitral stenosis?

Back 555

It becomes rounded.

Front 556

What are the anatomical and functional features of mitral stenosis?
(picture)

Back 556

Front 557

Syncope is associated with...

Back 557

Stenotic valve lesions.

Front 558

What are the chronic causes of mitral regurgitation?

Back 558

Myxomatous disease (prolapse)

Rheumatic heart disease

Annulo-aortic ectasia

Other connective tissue disorders

Dilated cardiomyopathy (annular dilation)

Ischemia (papillary muscle dysfunction)

Front 559

What are the acute causes of mitral regurgitation?

Back 559

Infective endocarditis

Myxomatous disease (choral rupture, flail mitral valve)

Ischemic heart disease (post-infarction papillary muscle rupture)

Front 560

The murmur associated with mitral regurgitation is a..

Back 560

Holosystolic murmur heard best at the apex which radiates to the axilla.

Front 561

The increased load in chronic mitral regurgitation causes what type of compensation?

Back 561

Left Ventricle Dilates AND Hypertrophies

Increased Stroke volume
(in a sense)

Left Atrium also dilates

Front 562

What is the natural course of chronic mitral regurgitation?

Back 562

Tolerated well

Long A-Symtomatic (or minimal Sx)–10 years or More

Mild MR may have Normal life span.

BUT
If Irreversible LV Dysfunction then MVR is no help.

Front 563

What are the physical findings of mitral regurgitation?

Back 563

Apical impulse, laterally displaced and hyperdynamic.

!Pan – systolic murmur in apex, axilla right precordium or back!

S-1: Normal or decreased

S-2: May be wide split
(A2 early)

S-3: Palpable

S-4: Rare in severe chronic MR (dilated LA, AF)

Normal until very late:
JVD

Front 564

What is mitral valve proplapse?

Back 564

Systolic displacement of the mitral leaflet into the left atrium of at least 3 mm beyond the mitral annulus in the parasternal or apical long-axis view.

Mitral regurgitation.

Thickened or myxomatous mitral leaflets.

Typically have symptomatic PAC's and unexplained chest pain.

Midsystolic click.

Front 565

What are the characteristics of Normal, Physiologic Valvular Regurgitation?

Back 565

Always trivial or at most mild

Usually central

Valve anatomically normal appearing.

Front 566

What is the risk of being anticoagulated for a prosthetic valve?

Back 566

About 1%/ patient year hemorrhage.

Front 567

NOT on test!

What are the current prosthetic mechanical valves?

Back 567

Front 568

NOT on test.

What are the current tissue prosthetic valves?

Back 568

Front 569

What normal changes occur in the CV system as we age?

Back 569

Increased stiffness of the left ventricle and arteries.

Decreased maximal heart rate and cardiac output during exercise.

Effectively this means substantial reduction in CV reserve.

Front 570

What CV diseases are nearly unique to the elderly population?

Back 570

Diastolic heart failure and calcific aortic stenosis.

Front 571

What happens to blood pressure as we age?

Back 571

Systolic pressure goes up but diastolic pressure remains pretty constant.

Front 572

What is the first-line antihypertensive in the elderly?

Back 572

Thiazide diuretic
(with lifestyle changes)

Start low, titrate slowly.

Monitor closely for adverse effects, especially orthostatic hypotension.

Caution regarding pseudohypertension (mismeasuring with cuff and scope) from stiff arteries.

Goal BP: same as in younger patients

Front 573

How do we calculate attributable risk?

Back 573

Prevalence*risk ratio

Front 574

What are the "typical" atypical symptoms in elderly patients with MI?

Back 574

Confusion
Dyspnea
Lassitude
New onset CHF
New arrhythmia
Syncope
Stroke
Sudden death

Front 575

At what age does the CVD risk for men equal that of women?

Back 575

Cardiovascular risk for women rises after menopause and becomes similar to men by age by 70.

Front 576

What kind of relationship exists between the risk of CVD and BP?

Back 576

Continuous, consistent, and independent of other risk factors.

Each increment of 20/10 mmHg doubles the risk of CVD across the entire BP range starting from 115/75 mmHg.

Also sometimes synergistic with other risk factors.

Front 577

How do we stage hypertension?

Back 577

Normal:
<120 AND <80

Prehypertension:
120–139 or 80-89

Stage 1 hypertension:
140–159 or 90-99

Stage 2 hypertension:
>=160 or >=100

Front 578

Using too small a cuff produces a BP reading that is...

Back 578

Artificially high
and vice versa.

Front 579

For people over age 50, which blood pressure measurment is a bigger risk factor?

Back 579

Systolic

Front 580

Persons who are normotensive at age 55 have a life time risk of developing hypertension of...

Back 580

90%

Front 581

When do we use two or more antihypertensives?

Back 581

If BP is >20/10 mmHg above goal.

Front 582

What does BP typically do at night?

Back 582

BP drops by 10 to 20% during the night; if not, signals possible increased risk for cardiovascular events.

Front 583

What is the recommended goal of antihypertensive therapy?

Back 583

BP <140/90 mmHg
or
BP <130/80 mmHg in patients with diabetes or chronic kidney disease.

Front 584

People with a tendency to alcohol excess will often have an elevated...

Back 584

Diastolic BP

Front 585

What are the guidelines for treating HTN?
(picture)

Back 585

Front 586

Why are serum potassium and creatinine monitored 1–2 times per year in patients on antihypertensives?

Back 586

To monitor potassium wasting in diuretics and watch for hyperkalemia on an ACE inhibitor.

Front 587

What are good antihypertensive drug options for patients with heart failure?
(compelling indication)

Back 587

THIAZ, BB, ACEI, ARB, ALDO ANT (Spironolactone)

Front 588

What are good antihypertensive drug options for patients post MI?
(compelling indication)

Back 588

BB, ACEI, ALDO ANT (Spironolactone)

Front 589

What are good antihypertensive drug options for patients with high risk of CAD?
(compelling indication)

Back 589

THIAZ, BB, ACE, CCB

Front 590

What are good antihypertensive drug options for patients with diabetes?
(compelling indication)

Back 590

THIAZ, BB, ACE, ARB, CCB

Front 591

What are good antihypertensive drug options for patients with chronic kidney disease?
(compelling indication)

Back 591

ACEI, ARB

Front 592

What are good antihypertensive drug options for patients that require recurrent stroke prevention?
(compelling indication)

Back 592

THIAZ, ACEI

Front 593

What minority population has the highest prevalence of HTN?

Back 593

African americans.

They are generally less renin sensitive and do better with diuretics and CCB's.

Front 594

When treating hypertension in patients with PAD, we typically also give...

Back 594

Aspirin

Front 595

When someone has postural hypotension, we need to be especially careful with the antihypertensives...

Back 595

ACE inhibitors.

Afterload reduction can exacerbate the problem.

Front 596

Which antihypertensives are contraindicated in women who are pregnant or have intentions of becoming pregnant?

Back 596

ACEI and ARBs contraindicated in pregnancy.

Pregnant women with HTN should be followed carefully. Methyldopa, BBs, and vasodilators, preferred for the safety of the fetus.

Oral contraceptives may increase BP in contrast to HRT which does not.

Front 597

Which antihypertensive is associated with angioedema?

Back 597

ACE inhibitors

Front 598

Where do the various diuretics act in the nephron?

Back 598

Loop diuretics:
Ascending limb of the loop of Henle (Still in the medulla).
Block the exchange of Na+, K+ and Cl- . Very powerful diuretics.

Thiazides:
Block ion exchange in the distal convoluted tubule.
(In the cortex)
Less potent than loop diuretics.

K+ sparing diuretics (aldosterone anatagonists):
End of the nephron. Right before it re-enters the medulla and becomes the collecting duct. Less potent than thiazides.

Front 599

What are the most commonly prescribed thiazide diuretics in the US?

Back 599

HCTZ
(12.5-25mg)

Chlorthalidone
(12.5-50mg) >25mg ill advised

Metolazone
(most potent, 2.5-10mg)

All PO drugs, chlorthiazide is IV equivalent but rarely used.

HCTZ has slightly shorter T1/2 than others (12-18hours vs 24)

Can cause hypovolemia, hypokalemia, hypomagnesemia, hyponatremia, HYPERglycemia, gout and rash (contain sulfur).

May cause vasodilation after several weeks (double whammy)

Front 600

What loop diuretics are available in the U.S?

Back 600

Furosemide (shortest acting)
Bumetanide
Torsemide
Ethacrynic acid (does not contain sulfur)

Can cause hypovolemia, hypokalemia, hypomagnesemia, hyponatremia, HYPERglycemia, gout and rash (most contain sulfur).

Not good antihypertensives because of short half life. Also do not vasodilate like thiazides.

Better than thiazides for creatinine clearance <30.

Front 601

What K+ sparing diuretics are available in the U.S?

Back 601

Aldosterone antagonists:

Spironolactone 12.5-50mg
(Hyperkalemia, Gynecomastia)

Eplerenone 25-50mg
(Hyperkalemia)

Non-aldosterone-antagonists:

Triamterene
Amiloride
(both can cause hyperkalemia and rash)

Very weak diuretics.

Sometimes given with amphotericin B antifungal to preserve potassium.

Front 602

The suffix -sartan means..

Back 602

Angiotensin receptor blocker (ARB)

Front 603

The suffix -pril means...

Back 603

ACE inhibitor.

Front 604

What does the relatively new antihypertensive drug Aliskiren do?

Back 604

Directly inhibits Renin.

Front 605

The peak/trough ratio of a once a day ACE inhibitor tells us...

Back 605

What percentage of blood pressure reduction is found after 24 hours.

Front 606

What is the shortest acting ACE inhibitor?

Back 606

Captopril
TID or QID.

Great in critical care setting but bad for outpatient.

Front 607

Enalapril is used once a day for hypertension control but twice a day for...

Back 607

Heart failure or prevention of vascular complications.

Only ACE inhibitor available IV.

Front 608

What are the contraindications for ACE inhibitors and company (ARB's and aliskerin)?

Back 608

Bilateral Renal Artery Stenosis
Pregnancy
Angioedema to other ACEIs
Hyperkalemia (K+>5meq/L)

Can cause an increase in serum creatinine and nephrotoxicity. Paradoxically thouhg, they can be used to halt progression of kidney disease.

ACE inhibitors can cause a dry non-productive cough. ARB's do not do this.

Front 609

What are the major side effects of beta blockers?

Back 609

Drowsiness, lethargy, confusion, bronchoreactive events, AV nodal blockade.

Front 610

What is the often forgotten effect of beta blockers?

Back 610

They block renin receptors by binding beta receptors in the kidneys.

Front 611

Which beta blocker has a high lipid solubility and why is this important?

Back 611

Propranolol.
Makes it across the blood brain barrier quite welland has more CNS effects.

Front 612

The ideal beta blocker for cardiac use only is...

Back 612

Highly beta 1 selective.
Low lipid solubility.

Front 613

Labetalol and carvedilol are useful drugs because...

Back 613

They also have alpha effects which vasodilate and reduce blood pressure.

Front 614

Most commonly prescribed beta blockers are...

Back 614

Metoprolol.
(25-100mg bid, B1 selective, moderate lipid solubility)

Labetalol
(100-300mg bid, non-selective, moderate lipid solubility)

Carvedilol
(3.125-25mg bid, non-selective, moderate lipid solubility)

Front 615

What are common adverse reactions of beta blockers?

Back 615

Drowsiness, Lethargy

Bradycardia/ Heart Block

Bronchoreactive Events

May mask signs of hypoglycemia

Front 616

What are the contraindications for beta blocker use?

Back 616

Symptomatic Bradycardia/Hypotension

Decompensated HF

Use with caution: asthma, diabetes
(only sign of hypoglycemia not masked by beta blockers is diaphoresis)

Front 617

What is the effect of diltiazem and verapamil on the heart?

Back 617

Decrease AV nodal conduction.
Decrease HR.
Decrease contractility.

Minimal effect on vascular resistance.

Verapmail reduces HR and contractility more.

Not typically use for HTN unless there are Arrhythmias too.

Front 618

What is the effect of dihydropyridine CCB's on the vasculature?

Back 618

Vasodilation

All end in -pine.

Front 619

What are terazosin, doxazosin and prazosin?

Back 619

Pure alpha 1 blockers.

Reserved for unique cases: males with benign prostatic hypertrophy.

1st dose syncope, dizziness, lethargy.

↑ in CV events when used as monotherapy.

Front 620

What are clonidine and methyldopa?

Back 620

Alpha2-receptor Agonists
(reduce sympathetic outflow)

Add-on therapy with diuretics.

Available as transdermal preparation.

Nasty (not dangerous) side effects.

Front 621

What are Hydralazine and Minoxidil?

Back 621

Vasodilators.

Use with diuretic and beta-blocker to counteract compensatory changes.

Minoxidil causes sodium retention and hair growth.

Front 622

Maximum heart rate is about...

Back 622

220-age

Front 623

Where is the accessory pathway in WPW?

Back 623

Bundle of kent.

Front 624

Bicuspid aortic valve have an association with....

Back 624

Coarctation.

Front 625

How much fluid should there normally be between the viseceral and parietal (fibrous) pericardium?

Back 625

10-50cc

Front 626

Congenital absence of pericardium is usually an incidental diagnosis on CT, MR or CXR. It is associated with...

Back 626

Atypical chest pain or sudden death.
This is unlikely a causal relationship though.

Front 627

Percardial cysts are quite common and usually don't require unless...

Back 627

They impinge on the heart or an adjacent structure.

Front 628

The most common etiology for infectious pericarditis is...

Back 628

Viral
(coxsackie A & B, echovirus, mumps, adenovirus, HIV)

Bacterial causes are very bad and include:
!Mycobacterium tuberculosis!, Pneumococcus, Streptococcus, Staphylococcus, Legionella

Fungal:
histoplasmosis, coccidioidomycocis, candidiasis,
blastomycosis

Front 629

The mechanism of uremic pericarditis in dialysis patients...

Back 629

Is not currently understood.

Front 630

What diseases are associated with hypersensitivity pericarditis?

Back 630

Systemic lupus erythematosus
Rheumatoid arthritis Scleroderma
Acute rheumatic fever

Front 631

What drugs can cause hypersensitivity pericarditis?

Back 631

procainamide
hydralazine
isoniazid
others

Front 632

What is Dressler's syndrome?

Back 632

Late presenting (days to weeks) hypersensitivity pericarditis after an MI.

Front 633

How does acute pericarditis typically present?

Back 633

SUDDEN severe retrosternal or left precordial pain:
May refer to back or trapezius.
May be preceded by low-grade fever.
May be pleuritic or positional (worse supine).

With viral pericarditis, usually 1-2 weeks after “viral illness”.

Resting tachycardia
Low-grade fever
(if infectious etiology)
Pericardial friction rub.
(Classically triphasic but can be any)

ECG:
Diffuse ST elevation early
Depression of PR segment
T inversion late
Low voltage in QRS (if large)
Electrical alternans (if large)
A-Fib

Elevated Sed rate and WBC.

Echo can sometimes show pericardial effusion but not always.

Front 634

Some of the features that help us discern early pericarditis from STMI on ECG are...

Back 634

Pericarditis elevations don't typically conform to an anatomical distribution like MI and generally appear in the epicardial leads (I, II, aVL, aVF, V3-V6). They are thus said to be are more diffuse.

Endocardial leads aVR, V1 and V2 will also show ST depression in percarditis

Camel hump type shape in the ST segments is also suggestive of pericarditis.

PR depression is commonly seen in pericarditis.

Front 635

What ST changes are charcteristic of stage II of pericarditis?

Back 635

Normalization

In stage 3 we start seeing ST depressions and T inversions.

Front 636

How do we treat acute pericarditis?

Back 636

If a significant pericardial effusion is not present, treatment is targeted to symptoms - usually NSAID's.

If peri-infarct pericarditis, may prefer high dose aspirin.

Steroids and Colchicine for resistant pericarditis.

Front 637

What type of fluid is found in a pericardial effusion?

Back 637

Serosanguinous effusions - neoplasm, Tb, uremia, idiopathic, non-infectious cause.

Hemopericardium - trauma, myocardial rupture, aortic dissection, coronary artery rupture.

Purulent effusion - secondary to direct invasion of the pericardial space by infectious organisms.

Front 638

What imaging findings do we expect with a pericardial effusion?

Back 638

Cardiomegaly or “water-bottle” shape on CXR.

ECG - low voltage

Echocardiography - imaging procedure of choice.

Front 639

How does cardiac tamponade present?

Back 639

Presentation may mimic heart failure: Dyspnea on exertion and orthopnea

Tachycardia and tachypnea

Jugular venous distention

Hypotension and poor peripheral perfusion

Shock and profound hemodynamic collapse

Pulsus Paradoxus (>10mmHg)

Can range from very mild to cardiogenic shock.

Beck's triad:
Hypotension, JVD, Muffled heart sounds.

Tx: Fluids, pressors, percardiocentesis and/or pericardectomy.

Front 640

What is constrictive pericarditis?

Back 640

Results from dense fibrosis, adhesion of the parietal/ visceral layers and eventually calcification from any cause of pericarditis including radiation, prior infectious pericarditis and cardiac surgery.

Much more chronic than tamponade.

RHF symptoms.

Prominent Y descent with JVP.

“Kussmaul’s sign” - exagerated jugular venous filling with inspiration.

“pericardial knock”- characteristic abnormal sound in diastole.

Front 641

What do we look for on CXR to in restrictive pericarditis?

Back 641

White calcification line around the heart. Can see on CT and MRI too along with pericardial thickening.

Echocardiography:
signs of ventricular interdependence; respiratory variation in left and right ventricular filling.

Prognosis is poor but we try stripping the pericardium surgically.

Front 642

The main hemodynamic difference between tamponade and constrictive pericarditis is that...

Back 642

In tamponade, the heart is affected throughout diastole.

In restrictive pericarditis it is only affected towards the end of diastole.

Front 643

The most common manifestation of blunt trauma to the heart is...

Back 643

Cardiac contusion.

New arrhythmias or ECG changes.

LV wall motion abnormality on echo.

Front 644

What is an aortic transsection?

Back 644

Shear forces in decceleration injuries can cause damage to the descending aorta.

Clinical manifestations can be delayed (~1month) and resemble an aneurysm.

Front 645

What is the effect of hyperthyroidism on the heart?

Back 645

Hyperkinetic cardiovascular state with fall in systemic vascular resistance, increase in cardiac output, and enhanced left ventricular emptying; may develop atrial fibrillation.

Front 646

What is the effect of hypothyroidism on the heart?

Back 646

Hypertension, bradycardia, and pericardial effusions.

Front 647

What is the effect of pheochromocytoma on the heart?

Back 647

Catecholamine induced myocardial necrosis.

Front 648

What part of the heart do metastatic carcinoid processes usually affect?

Back 648

Right heart.

Front 649

What are the three major classes of cardiomyopathies?

Back 649

Dilated Cardiomyopathy:
Systolic dysfunction
Reduced ejection fraction

Restrictive Cardiomyopathy:
Diastolic dysfunction
Ejection fraction may be normal

Hypertrophic Cardiomyopathy:
A genetic condition, not really a class but a single disease.

Front 650

What is the most common non-ischemic cardiomyopathy etiology?

Back 650

Idiopathic dilated cardiomyopathy.

May be the result of viral myocarditis or toxic myocarditis but etiology no longer apparent at time of presentation.

3 times more common in african american males.

Genetic predisposition, sometimes familial.

Heart biopsy is not diagnostic.

No specific treatment - general CHF treatment.

Front 651

What causes viral myocarditis?

Back 651

Multiple viruses but most commonly enterovirusses (Coxsackie B - 50% of all cases).

Immunologic mechanism - develops weeks after the original infection.

More aggressive and fulminant in infants and pregnant women.

Front 652

Lyme disease spirochete myocarditis is associated with...

Back 652

Heart block.

Front 653

What is an important protozoal cause of cardiomyopathy in South America?

Back 653

Trypanosomiasis
(Chaga’s Disease-T. cruzi)

Front 654

How does peripartum cardiomyopathy differ from idiopathic cardiomyopathy.

Back 654

Clear relationship to recent pregnancy with a high risk of relapse on subsequent pregnancies.

Embolic phenomena are more common.

Better Prognosis (1/3 recover completely, 1/3 stabilize, 1/3 progress)

Evidence of inflammation on heart biopsy is actually a good prognostic sign.

Front 655

What are the clinical risk factors for peripartum cardiomyopathy?

Back 655

Multiparity
Advanced maternal age
Twin pregnancies
Pre - eclampsia

Front 656

How do we treat peripartum cardiomyopathy?

Back 656

Onset is typically from third trimester up to several months post partum.

No Specific therapy (conventional heart failure therapy ) except anticoagulation is important.

Surgical sterilization is highly recommended because of the risk of relapse on subsequent pregnancies.

Front 657

What is hypertrophic cardiomyopathy?

Back 657

Cardiac muscle disease characterized by abnormal hypertrophy, mainly involving the ventricular septum.

Histology : Myofibrillar disarray

Functional abnormalities:
Outflow tract obstruction
Diastolic dysfunction
Atrial and Ventricular arrhythmias.

50% autosomal dominant.

Front 658

What clinical findings are consistent with hypertrophic cardiomyopathy?

Back 658

Loud fourth heart sound.

Brisk bifid carotid pulse.

Harsh systolic ejection murmur like aortic stenosis but doesn’t usually radiate to the neck and it is labile. (varies with maneuvers) Increases on standing, diminishes with raising of the legs.

Sometimes also pansystolic murmur (mitral regurg)

Echo findings:

Assymetric septal hypertrophy.

Systolic anterior motion of the mitral valve.

Gradient across ventricular outflow tract and likely mitral regurgitation.

Front 659

Whta diseases are considered predisposing to infective endocarditis?

Back 659

Rheumatic heart disease.

Congenital heart disease
(PDA, Fallot’s tetralogy,
coarct, VSD, ASH)

Degenerative heart disease
(calcific AS, mitral annular
calcification)

Mitral valve prolapse
(very high risk)

Front 660

What can we say about the epidemiology of native valve infective endocarditis?

Back 660

Native valve endocarditis in now a disease of middle-aged adults, most of whom will have an underlying valvular lesion (e.g., degenerative heart disease) that predisposes to infection.

Rheumatic heart disease and congenital heart disease are increasingly uncommon predisposing lesions in developed countries.

IV drug use is a major risk factor for acquisition of infection.

Front 661

How does native valve endocarditis actually occur?

Back 661

The development of native valve IE usually requires 2 concurrent or sequential events→The formation of a nonbacterial thrombus on an endothelial surface AND a transient bacteremia with an organism capable of adhering to a platelet-fibrin matrix.

Front 662

What are the pathophysiological consequences of endocarditis?

Back 662

Local tissue injury/Valve damage

Local extension of infection
Valve ring abscess
Myocardial abscesses
Pericarditis

Distant emboli (bland & septic)
Immune complex phenomena

Front 663

Recent data suggest that strep has been replaced as the most common etiological agent of native valve endocarditis by..

Back 663

S.Aureus

80-90+% of cases of native valve IE are caused by gram positive cocci (Staph, Strep, Enterococci)

GNRs frequently cause bacteremia but rarely cause IE

Strep, enterococci, & CNS cause subacute disease; S. aureus causes acute disease

IVDU-associated IE usually due to S. aureus & most often involves tricuspid valve

IE is “culture negative” in 5-10% of cases.

Front 664

If I am postulating a diagnosis of native valve infective endocarditis and blood cultures are growing an organism other than a Gram positive coccus, what should I do? .

Back 664

Alternative diagnoses should be strongly entertained

Front 665

The most important clinical manifestations of infective endocarditis we are looking out for...

Back 665

Fever
Heart murmurs
Embolic phenomena
Skin manifestations

Front 666

What are Osler's nodes?

Back 666

Tender erythematous nodules in the pulps of the fingertips or toes that are related to endocarditis.

Front 667

What are some of the major complications of infective endocarditis?

Back 667

Congestive heart failure
Systemic emboli
Mycotic aneurysms
Renal disease

Front 668

What is the leading cause of death in infective endocarditis?

Back 668

CHF

Front 669

How do we diagnose infective endocarditis?

Back 669

Diagnosis predicated on compatible clinical syndrome with demonstration of !continuous! bacteremia.

Documentation of presence of valvular vegetations (echo, surgery) desirable but not essential.

Front 670

As defined by the Duke criteria, a definitive diagnosis of infective endocarditis is most convincingly established when ...

Back 670

Appropriate microbiology→2 or more blood cultures obtained at different times that are positive for a Gram positive coccus.

Evidence of endocardial involvement→Demonstration of a valvular vegetation or a new regurgitant murmur via echo.

Front 671

How do we manage infective endocarditis?

Back 671

Prolonged IV course (4-6 weeks) of bactericidal agent.
Careful monitoring of therapy warranted. !document clearance of bacteremia!

Surgery:
Indicated in face of defined complications.
Prior duration of ATB Rx not a determining variable.
Less than 5% of prosthetic valves inserted during active IE become infected.

Front 672

What are the complications that warrant surgical intervention in infective endocarditis?

Back 672

Uncontrolled heart failure.

Multiple embolic episodes.

Persistent bacteremia despite appropriate antibiotics.

Fungal (i.e., Candida) endocarditis

Infection due to a MDR organism (ie, VRE)

Development of heart block, bundle branch block, or purulent pericarditis

Prosthetic valve dehiscence or obstruction

Relapse following “adequate” trial of antibiotic therapy

Front 673

What is early prosthetic valve endocarditis?

Back 673

< 2 mos of surgery

Secondary to intraop or periop contamination.

Valvular dysfunction with perivalvular leak common

Staph, GNRs, fungi

Surgery!

Front 674

What is late prosthetic valve endocarditis?

Back 674

> 2 mos post-surgery

Secondary to seeding of valve during bacteremia from non-cardiac site

S. aureus, coag neg staph, Strep sp.

Medical cure possible though surgery freq’ly necessary

Front 675

As compared to native valve IE, PVE is associated with a more...

Back 675

Varied microbiology.

Frequent metastatic complications.

Greater need for surgical intervention, and a poorer outcome.

Front 676

What is the current stance on prophylaxing patients for procedure with a potential to cause infective endocarditis?

Back 676

The focus on prevention of IE has shifted from antibiotic prophylaxis before “risk procedures” to optimizing dental hygiene and health in recognition of the fact that only an extremely small number of cases of IE might be prevented by antibiotic prophylaxis even if prophylaxis is 100% effective.

Still done though.

Front 677

The majority of prosthetic valve endocarditis cases are...

Back 677

Late PVE (~67-85% of cases)

> 2 mos post-surgery.

Seeding of valve during bacteremia from non-cardiac site.

Front 678

What percentage of coronary artery stenosis does there need to be to produce ischemic symptoms?

Back 678

75%

Front 679

What is found in an infarct at various post infarction stages?

Back 679

<24 hours Early acute
Thin wavy fibers and contraction bands histologically.

1-6 days Acute:
PMN's

1-3 weeks Organizing:
Granulation tissue.
Acute and chronic inflammation; Macrophages and Fibroblasts.

>3 months remote:
Collagen

Front 680

What is the time interval from myocardial ischemia to irreversible damage?

Back 680

20-40 minutes

Front 681

When does postMI rupture (free wall, septal or papillary) typically happen?

Back 681

First week after MI.The acute phase.

Usually latter part of the week.

This is when there is maximal necrosis.

Front 682

When is post-MI aneurysm most likely to happen?

Back 682

Can happen any time from the acute phase onwards (24 hours and up) but most likely in the organizing stage. (1-3 weeks)

Front 683

When does post-MI CHF usually happen?

Back 683

Any time after the MI.

Front 684

Whe are post MI arrythmias most likely to happen?

Back 684

Early acute stage. <24hours

Front 685

When are post MI mural thrombus and pericarditis most likely?

Back 685

Acute and organizing stages
(24 hours to 3 weeks)

Pericarditis is more common in organizing stage than acute stage.

Front 686

What can cause pure right sided failure?

Back 686

intrinsic lung disease.
(cor pulmonale)

Usually not heart disease.

Front 687

What disease are Aschoff bodies & Anitschkov myocytes associated with?

Back 687

Acute rheumatic fever

Verrucae is the name of the "vegetations" seen on the valve,

Front 688

What valves does rheumatic heart disease usually affect?

Back 688

Mitral > Aortic > Tricuspid > Pulmonic

Mitral alone 48%, Mitral + aortic 42%

R. sided valves only rarely; TR usually due to CHF

Front 689

How does chronic rheumatic heart disease affect mitral valve morphology?

Back 689

Thickening of valve leaflet, especially along lines of closure

Fusion of commissures

Thickening, shortening and fusion of chordae tendinae

Result is mitral stenosis

Front 690

Fish mouth deformity of the aortic valve is associated with...

Back 690

Rheumatic heart disease.

Front 691

Acquired aortic stenosis in middle age is almost always..

Back 691

Rheumatic heart disease.

Front 692

What are the major etiologies of aortic insufficiency?

Back 692

Rigidity - rheumatic, degenerative

Destruction – microbial endocarditis

Collapse - prolapse through VSD, or due to myxomatous degeneration

Disease of AoV ring:
Cystic medial degeneration
Marfan Syndrome
Dissecting aneurysm (medial degeneration or hypertension)
Syphilitic aortitis
Ankylosing spondylitis

Front 693

What is the epidemiology of infective endocarditis in IV drug users?

Back 693

Right sided valve endocarditis more common in addicts than in non-addicts
(but still the majority of cases in addicts are left sided)

Front 694

What is marantic endocarditis?

Back 694

Nonbacterial thrombotic endocarditis.

Small (1-5 mm), sterile fibrin & Plt thrombi loosely adherent to valves (lines of closure), mainly MV

Due to systemic hypercoagulability

May embolize systemically

Front 695

What is Libman-Sacks endocarditis?

Back 695

A non-infective endocarditis (valvulitis) occurring in SLE & anti-phospholipid syndrome patients.

MV & TV most commonly affected

Microscopic: fibrinoid necrosis

Fibrinous vegetations on either side of valve

Valve deformations may occur

Front 696

Carcinoid heart disease causes...

Back 696

Mainly right-sided valvular lesions.

Elaboration by

Argentaffinomas of bioactive products including serotonin, bradykinin, histamine, PG, etc.

Front 697

What are the epidemiological features of mitral valve proplapse?

Back 697

Sex: F:M:: 6:4
Age: 20 - 40

Front 698

What are the clinical features of mitral valve proplapse?

Back 698

May be asymptomatic.

Mid-systolic click
Atypical chest pain
Dyspnea
Fatigue
Pysch. manifestations

Can secondary infective endocarditis and sudden cardiac death.

Morphology of MVP includes stretched, redundant valves, usually mitral but sometimes also tricuspid and semilunar valves.

Front 699

What is the normal thickness of the LV wal?

Back 699

<1.5cm

Healthy heart weight typically 300-350g.

Front 700

Atheroscelrosis does not ever occur in the pulmonary artery unless...

Back 700

There is pulmonary hypertension.

Front 701

What are the clinical features of hypertrophic cardiomyopathy? (HOCM)

Back 701

Impaired ventricular compliance
Pump failure
Systolic murmur Dysrhythmias
Sudden death

Key histological feature is myofiber disarray.

Familial in 50% (AD, variable penetrance)

Front 702

How does amyloidosis affect the heart?

Back 702

Infiltrates myocardium and cause a restrictive cardiomyopathy.

Characteristic Congo Red staining.

Can mimic ischemic heart disease in symptoms (failure, EKG changes)

Can have amyloid limited to heart and vessels .

Front 703

Major risk factors for CVD include hypertension, dyslipidemia, diabetes, smoking, and family history. Ideal prevention and/or control of the first four factors can reduce CVD rates by approximately what proportion in the United States?

Back 703

75%

Front 704

What population has the highest YPLL (years of potential life lost) form CV disease?

Back 704

African americans

Front 705

What is the single most important predictive risk factor of CHF?

Back 705

Age

!!Hypertension is the most important "biological predictor"!!

Front 706

Prevalence is equal to...

Back 706

Incidence*duration.

Front 707

How does ethnicity affect CVD risk?

Back 707

Black race associated with increased mortality from IHD

Hispanic and Asians less IHD mortality than Whites.

Front 708

What is the “Stroke Belt”?

Back 708

Southern states have more Stroke than others regions.

Front 709

AHA Guidelines for Primary and Secondary Prevention include...

Back 709

Cessation of smoking

Lipid assessment & treatment

Blood pressure control

Diabetes management

Aspirin for appropriate candidates

Front 710

What factors affect myocardial oxygen demand?

Back 710

Heart rate
Contractility
LV filling pressure
Afterload

Front 711

Angina precipitated with exertion is...

Back 711

Stable angina

Front 712

How does percent diameter reduction in the coronaries correlate with ischemic symptoms?

Back 712

<50% should not cause significant mechanical obstruction of coronary blood flow

50-75% may cause a relative obstruction if myocardial oxygen demand is severely increased

>75% is considered a severe obstruction that will mechanically impede coronary flow even at low levels of activity

>90% is a critical stenosis !

Front 713

What is unstable angina?

Back 713

New onset angina less than two months

Angina at low levels of activity

Angina at rest

Increase in frequency or severity of previously stable angina

All anginal type rest pain without evidence of myocardial infarction

Front 714

What drugs reduce myocardial oxygen demand?

Back 714

beta blockers
nitrates
ACE inhibitors

Front 715

What drugs reduce coronary artery spasm?

Back 715

CCB's
Nitrates

Front 716

By current clinical definitions, unstable angina turns into acute MI when...

Back 716

It occurs and persists at rest in spite of optimal medical therapy.

Pain duration greater than 20 minutes - may come and go but is persistent.

Accompanying EKG changes show transmural infarction.

Front 717

On what time scale does coronary revascularization need to take place?

Back 717

30 minutes - reversible ischemia

1-3 hours - window of opportunity

>6 hours - high chance of irreversible necrosis

Front 718

What are the three main goals of treating ischemic heart disease?

Back 718

Relieve angina
Prevent myocardial infarction
Promote longevity

Front 719

What vessels can be used for CABG?

Back 719

Saphenous vein graft (SVG)

Internal mammary artery (LIMA or RIMA)

Free radial artery

Gastroepiploic artery

Front 720

At what rate do saphenous vein grafts close?

Back 720

~5%/year

Front 721

What are sirolimus and paclotaxil?

Back 721

Antiproliferative agents that are used on stents to prevent intimal hyperplasia.

Sirolimus is in the "Cypher" stent.
Paclitaxil is in the "Taxus" stent.

Front 722

How does late restenosis with drug eluting stents compare to bare metal stents?

Back 722

Significantly better <10%
Compared to the 20+% of bare metal stents.

Front 723

What is late stent thrombosis?

Back 723

potentially life threatening complication of PCI/stenting.

!!0.6%/year!!

Suspected causes are discontinuation of antiplatelet therapy, late incomplete apposition, polymer hypersensitivity/inflammation and delayed endothelialization.

Front 724

CABG is genrally better for...

Back 724

Severe obstruction multivessel disease.

Front 725

So how do we decide what to do with ischemic patients?

Back 725

Stenoses of 50-75%:
1,2,3 vessel - try medical therapy
If angina persists consider PCI-DES or CABG

Stenoses of >75%:
1,2,3 vessel - individualize based on lesion morphology, LV function – PCI-DES vs CABG

3 vessel - diffuse, poor LV, diabetic - CABG
left main - CABG

Front 726

Embryologically valve tissues are derived from...

Back 726

Muscle tissue.

Front 727

What is the overall incidence of congenital heart defects?

Back 727

1:100 live births

Front 728

How long does it take for the pulmonary bed of a newborn to become fully "relaxed"?

Back 728

4-8 weeks.

Most shunt lesions do not have any physical findings or sx until pulm resistance drops “enough”

Front 729

What is the most common reason for CHF in pediatrics?

Back 729

Pressure &/or volume load .

Intrinsic muscle problems are possible but not likely.

Front 730

What signs and symptoms of CHF are not commonly seen in kids?

Back 730

Peripheral edema
Ascites

Front 731

What is the single most common congenital heart disease?

Back 731

VSD

Front 732

What determines the presentation and physical exam findings in VSD?

Back 732

The size of the hole

Front 733

What are the indications for surgically correcting a VSD?

Back 733

Huge hole with uncontrollable CHF

Hole large enough to cause pulm HTN

Large heart later, other complications.

Front 734

What are the exam findings of a small VSD?

Back 734

Child thriving

Heart not large

Murmur begins at onset of systole (with S1) and continues as long as a pressure gradient exists between left & right ventricles = holosystolic

Loudness & pitch vary with size & location. Louder sound means smaller hole.

Front 735

What is the second most common congenital heart defect?

Back 735

ASD

Front 736

What are the findings of ASD?

Back 736

Palpably enlarged right ventricle

Murmurs from normal valves with too much blood flow (relative stenosis)
Pulmonary flow
Tricuspid flow

Widely (“fixed”) split second sound.

Almost never causes symptoms.

If hole large, closure recommended by pre-school age to prevent mortality and morbidity in early adulthood.

Front 737

What are the physical findings of PDA?

Back 737

Size of defect determines symptoms and physical findings

Flow occurs as long as Ao pressure > PA pressure (ie continuously)

Typically - large heart with continuous “machinery” type murmur best heard under left clavicle; bounding pulses

Front 738

What are the physical findings of congenital pulmonary stenosis?

Back 738

Usually no symptoms unless severe PS in a newborn
RV may feel enlarged if very thick

May have palpable thrill if severe

Murmur occurs as blood ejected across valve orifice = systolic ejection murmur

Heard best over pulm art = LUSB

Usually radiates into lung fields

Front 739

What are the cyanotic heart defects?

Back 739

Hey
Harry,
This
Turkey
Tastes
Terrible !

Hypoplastic right heart syndrome:
Tricuspid atresia; pulm atresia

Hypoplastic left heart syndrome.

Transposition of the great arteries

Total anomalous pulm venous return (TAPVR): (Transposition of the pulmonary veins)

Tetralogy of Fallot

Truncus arteriosus

Front 740

What is the most common cyanotic heart defect?

Back 740

Tetralogy of Fallot.

Combination of 4 abnormalities due to conal septum malalignment:

Large VSD
(non-restictive to pressure)
Pulmonary stenosis
Aorta over-rides the VSD
Right ventricular hypertrophy

Cyanosis varies by the amount of obstruction of blood flow to lungs:

May be minimally cyanotic (pink tet) if PS very mild

May be critically cyanotic (blue tet) if PS severe (ductal dependant).

Front 741

What are the exam findings in tetralogy of fallot?

Back 741

Palpably enlarged right ventricle.

May have thrill.

Murmur is produced by the PS, not by the VSD.
Systolic ejection murmur radiates into lung fields
Usually can’t hear pulmonary closure (single S2) due to stenosis.

Front 742

What are the charcteristics of transposition of the great arteries?

Back 742

Male dominance (60-70%)

Usually large well-grown infants.

Cyanotic from the “get-go”

Must have mixing of the circulations in order to survive
ASD or non-restrictive PFO
PDA
Some have a VSD

Keep PDA open with prostaglandin E1 or balloon atrial septostomy sometimes required emergently.