Unit 6 Cardiovascular

Front 1

What are contraindications for PA line?

Back 1

• Vascular access issues.
o The pulmonary arterial catheter goes in through the central venous (IJ, subclavian, or femoral veins). Therefore, any contraindication to venous access (e.g., active bacteremia, coagulopathy, etc.) will be a contraindication for PA line insertion
• LBBB
o Inserting a PA line can cause RBBB, inducing complete heart block
• Acute pulmonary embolism right atrial thrombus, or RV thrombus or mass

Front 2

What is the differential for tall A waves in a PA line pressure tracing?

Back 2

• Tricuspid stenosis
• Pulmonic stenosis
• Pulmonary HTN
• Cor pulmonale

Front 3

What is the differential for blunting of the Y descent in a PA line pressure tracing?

Back 3

Cardiac tamponade

Front 4

What is the differential for a prominent X and Y descent in a PA line pressure tracing?

Back 4

• Constrictive pericarditis
• Restrictive cardiomyopathy

Front 5

What is the differential for a prominent C wave in a PA line pressure tracing?

Back 5

1st degree AV block

Front 6

What is the differential for a prominent C-V wave in a PA line pressure tracing?

Back 6

Tricuspid regurgitation

Front 7

What is the differential for cannon A waves in a PA line pressure tracing?

Back 7

AV dissociation (can be due to a PVC, complete heart block, AVNRT)

Front 8

Where in the vascular system is the resistance the greatest?

Back 8

The resistance is greatest in the arterioles. Furthermore, resistance increases with viscosity, length, and radius.

Front 9

What factors determine preload? Afterload?

Back 9

Preload = EDV, end-diastolic pressure
Afterload = MAP, systemic vascular resistance

Front 10

What are the equations for: 1) MAP 2) Pulse pressure 3) BP 4) CO 5) SV 6) EF 7) Resistance

Back 10

• MAP = (SBP + (2 x DBP))/3
• Pulse pressure = SBP – DBP
• BP = CO x TPR
• CO = HR x SV
• SV = EDV – ESV
• EF = SV/EDV
• Resistance = pressure / flow

Front 11

What are the primary determinants of SV?

Back 11

• Preload
• Afterload
• Contractility
• Ventricular mass (greater mass, greater SV)

Front 12

What drugs affect preload?

Back 12

• Venodilators decrease preload
• IV fluids increase preload

Front 13

What drugs affect afterload?

Back 13

• Vasodilators decrease afterload
o Hydralazine, nitroprusside, minoxidil
• Vasopressors increase afterload
o phenylephrine, vasopressin

Front 14

Can you describe how ventricular compliance is influenced by the following factors: filling volume, wall thickness, ventricular size?

Back 14

• Increased filling volume decreases compliance
• Increased wall thickness decreases compliance
• Increased ventricular size increases compliance

Front 15

What are normal values for the pressure in the following areas of the cardiovascular system: RA, RV, PA, PCWP?

Back 15

See image

Front 16

What are normal values for: SV, SI, CO, CI, SVR, PVR?

Back 16

See image

Front 17

What does the V wave in the PA line pressure wave form represent on an ECG?

Back 17

T wave – ventricular repolarization

Front 18

What does the C wave in the PA line pressure wave form represent on an ECG?

Back 18

QRS (ventricular depolarization)

Front 19

What are causes of decreased ventricular compliance?

Back 19

• Increased intrathoracic pressure
• Increased pericardial pressure
• Increased pressure or volume of opposite ventricle
• Myocardial ischemia
• Myocardial disease

Front 20

What are the common hemodynamic profiles in shock for: cardiogenic shock, septic shock, and hypovolemic shock, in terms of RA pressure (CVP), cardiac output, and SVR?

Back 20

(see table)

Front 21

What is the “double product?”

Back 21

The double product is (HR x peak systolic BP) and is often used clinically, e.g., in treadmill exercise testing

Front 22

What is the primary cause of heart attack?

Back 22

The primary cause of heart attack is the rupture of unstable plaques into vessels that are <70% stenosed and clinically silent.

Front 23

Can you describe the generation and progression of atherosclerosis?

Back 23

1. Endothelial injury (e.g., oxidized LDL)
2. Monocyte migration, cytokine formation foam cell formation, smooth muscle proliferation, plaque and cap formation
3. Rupture of cap, thrombus formation

Front 24

What are the most important risk factors for stroke (modifiable and nonmodifiable)?

Back 24

• Nonmodifiable
o Age
o Sex
o heredity
• Modifiable
o HTN
o Cigarette smoking
o Hyperlipidemia
o Diabetes
o Physical inactivity
o Obesity

Front 25

What is the definition of angina?

Back 25

Angina is pain or discomfort in the chest or adjacent areas caused by insufficient blood flow to the heart.

Front 26

How do fibrinolytic agents work?

Back 26

Fibrinolytic agents are a class of drugs known as plasminogen activators, which convert plasminogen into plasmin. Plasmin enzymatically cleaves the fibrin strands, which bind the platelets and red blood cells together within the thrombus, leading to clot dissolution. A naturally occurring serine protease, t-PA is endogenously secreted by the vascular endothelium and helps maintain, along with other hematologic components, a balance between hemostasis and fibrinolysis.

Front 27

How do statins affect risk of diabetes?

Back 27

• Statins increase risk of diabetes.
• Effect size about 1 in 500 to 1 in 1000
• More likely in older heavier patients.

Front 28

Which statin is not metabolized by the CYP P450 system?

Back 28

• Pravastatin
• CYP 3A4 = LAS – lovastatin, atorvastatin, simvastatin
• 2C9 = fluvastatin, less so rosuvastatin, weakly pitavastatin

Front 29

Which statin is the most potent?

Back 29

• Pitavastatin is most potent. After that is…
• Rosuvastatin; has low lipophilicity and high hepatocyte selectivity due to its large polar side chain. Half life of 19 hours, which allows for twice weekly dosing.
• Fluvastatin is least potent.

Front 30

What is the mechanism of action for colesevelam?

Back 30

Colesevalam is a bile acid binding gel that binds bile acids in the gut and causes depletion of hepatic cholesterol pools, increasing production of more LDL receptors and thus reducing cholesterol levels in the blood. Bile acid binding sequestrants (older preparations – cholestyramine and colestipol) are among the safest lipid lowering drugs.

Front 31

Why is Cholestyramine used in digitalis toxicity?

Back 31

Cholestyramine can decrease availability of digoxin tablets by 17-30%.

Front 32

What is the mechanism of action of niacin?

Back 32

• Niacin is a potent inhibitor of adipose tissue lipolysis (GPCR). It suppresses lipolysis in adipocytes by niacin activating its receptor GPR109A which inhibits lipase, blockingrelease of FFAs.
• Decreases flux of FFA used by liver for VLDL production.
• Inhibits VLDL synthesis; see decrease in large TG rich VLDL
• Decrease in assemply of apo B containing lipoproteins
• See decreased small dense LDL
• See increased HDL Apo A-1
o Inhibits hepatic removal
o Best drug for raising HDL-c
• Reduces Lp(a) – only lipid drug to do this

Front 33

What drug would you use to lower TGs> 500 mg/dL? What are potential side effects of the chosen drug?

Back 33

• Fibrates have major effect on lowering TG levels. Fenofibrate is more potent than gemfibrozil. Also increases HDL if baseline levels are low (5-20%). Used to help prevent pancreatitis.
• Cholelithiasis is a worry with all fibrates; can also cause mild GI symptoms, myositis when combined with statins, must reduce fenofibrate dose with renal impairment
• Omega 3 fatty acids are also useful for those with eleated triglycerides in preventing pancreatitis

Front 34

What is the mechanism of action of Omega 3 fatty acids in lipid metabolism?

Back 34

• Omega 3 fatty acids inhibit both hepatic production and utilization of TG rich particles.
• Lower TG in a dose-related fashion
• Slightly increase HDL
• Don’t use it to lower LDL-c

Front 35

What is ezetimibe, and what is its mechanism of action?

Back 35

Ezetimibe is a cholesterol absorption inhibitor that works by decreasing cholesterol absorption in the intestine; it decreases biliary and dietary cholesterol.

Front 36

What are major side effects of niacin (nicotinic acid)?

Back 36

• flushing,
• hyperglycemia,
• hyperuricemia, can lead to gouty arthritis
• upper GI distress, exacerbates peptic ulcer disease
• hepatotoxicity

Front 37

What are these cells, and what are they pathognomonic for?

Back 37

These are Anitschkow cells--activated macrophages--found in Aschoff nodules. They are pathognomonic for rheumatic heart disease. The microscopic lesion of acute rheumatic carditis is the Aschoff nodule, a collection of lymphocytes and histiocytes which is most easily found in the fibrous interstitial septa of the myocardium.

Front 38

What valves are most commonly affected in rheumatic heart disease?

Back 38

Most of the time it’s mitral that gets affected in rheumatic heart disease, and sometimes also aortic. You probably won’t have aortic valve affected without the mitral valve affected as well.

Front 39

What’s the most common cause of mitral stenosis?

Back 39

Postinflammatory scarring (likely due to rheumatic heart disease)

Front 40

Briefly, what’s the pathogenesis of Marfan’s syndrome? What about Ehlers-Danlos syndrome?

Back 40

Marfan’s is an inherited connective tissue disorder with a defect in fibrillin. 98% have cardiovascular defects.
Ehlers-Danlos is a congenital defect in type III procollagen.

Front 41

What’s the main cause of sudden death in Wolf-Parkinson-White syndrome?

Back 41

Afib that conducts rapidly over the accessory pathway, degenerating to ventricular fibrillation.

Front 42

What is the underlying substrate for polymorphic ventricular tachycardia, and what is its mechanism in patients with Long QT syndrome?

Back 42

• Mechanisms for VT may be diverse but are often due to reentry in areas of fibrosis, similar to patients with prior myocardial infarction
• In long QT syndrome, polymorphic VT is likely initiated by triggered activity from early after depolarizations which leads to functional reentry due to dispersion of repolarization.

Front 43

Conceptually, what are 3 strategies for treating rentry?

Back 43

1) Increase the refractory period of the slow conducting tissue that is part of the reentrant circuit
2) Further slow the conduction
3) Suppress the premature beats that often set up the physiology

Front 44

What are examples of drugs that would be used to treat bradycardia?

Back 44

• Atropine
• Epinephrine
• Isoproterenol

Front 45

What are the 5 classes of drugs, and what is a representative/prototype drug from each class (include sub-classes)?

Back 45

• Class I – Na+ channel blockers
o Ia – procainamide
o Ib – Lidocaine
o Ic – Flecainide
• Class II – Beta blockers
o Metoprolol
• Class III – K+-channel blockers
o Amiodarone
• Class IV – Ca++- channel blockers
o Verapamil
• Non-classified
o Digoxin
o Adenosine
o Mg++

Front 46

Can you describe the Na+ channel blocking and K+ channel blocking abilities of the class I drug subclasses?

Back 46

• Na+ Channel blocking
o IB-low
o IA-medium
o IC-high
• K+ channel blocking
o IB- none
o IC-very low
o IA-moderate

Front 47

What are important side effects of procainamide?

Back 47

Procainamide is a class Ia Na+ channel blocker
• Procainamide can cause Lupus in long term therapy, characterized by arthralgia, pleuritis, and pericarditis. Not a real clinical concern since it only occurs with long term administration, and the drug isn’t available PO in the US any longer. However, it may still show up on the boards.
• It can cause Torsades de Pointes due to its significant K+ channel blocking activity, prolonging the QT-interval.

Front 48

What are important side effects of quinidine?

Back 48

• Quinidine is a class Ia Na+ channel blocker that can cause cinchonism, CNS toxicity including tinnitus, hearing loss delirium, and psychosis.
• It can cause Torsades de Pointes due to its significant K+ channel blocking activity, prolonging the QT-interval.
• It can also cause heart block and faster ventricular response in afib due to vagolytic effects

Front 49

What are important side effects of disopyrimide?

Back 49

• Disopyrimide is a class Ia Na+ channel blocker
• It can cause anti-muscarinic side effects from binding to M2 receptors, including urinary retention, constipation, blurred vision, dry mouth, close-angled glaucoma
• It can cause Torsades de Pointes due to its significant K+ channel blocking activity, prolonging the QT-interval.
• It can also cause heart block and faster ventricular response in afib due to vagolytic effects

Front 50

What are important side effects of lidocaine?

Back 50

• Lidocaine is a class Ib antiarrhythmic
• It can cause CNS toxicity: confusion, delirium, parasthesias, grand mal seizures

Front 51

What are the major clinical uses of flecainide?

Back 51

• Flecainide is a class Ic antiarrhythmic
• Acute conversison of afib to sinus rhythm
• Miantenance of sinus rhythm in afib

Front 52

What are typical side effects of beta blockers?

Back 52

• Bronchospasm
• Depression
• Cognitive impairment
• Hypotension
• Bradycardia
• Heart block
• Sexual dysfunction in males

Front 53

If a patient were on amiodarone, which lab tests would you be interested in monitoring?

Back 53

• PFTs – can cause pulmonary fibrosis
• LFTs
• TFTs – amiodarone is a heavily iodinated compound that also blocks the conversion of T4 to T3. It can cause hypothyroidism and hyperthyroidism
• EKG
o Can cause sinus bradycardia
o Can cause AV block
o RARELY causes Torsades de Pointes despite QT prolongation

Front 54

What are the most common side effects of calcium channel blockers?

Back 54

• Constipation and peripheral edema are the most commonly encountered side effects of CCBs.
• Can also get hypotension and some pro-arrhythmic effects (sinus bradycardia, heart block).

Front 55

What is the mechanism of action and therapeutic use for adenosine?

Back 55

• Adenosine interacts directly with A1 adenosine receptors in the heart, activating K+ channels, indirectly leading to decreases in L-type calcium channel activity and If (the funny current). The net effect is marked hyperpolarization and transient elective heart block.
• It’s used for diagnosis and termination of supraventricular tachycardias (gets rid of QRS complexes so you can see underlying AF or Aflutter) by producing a transient heart block. It’s very effective at terminating reentrant rhythms (e.g., AVNRT, AVRT).

Front 56

What are clinical uses and side effects of digoxin?

Back 56

• Digoxin is used to control ventricular response in atrial fibrillation and atrial flutter, usually in conjunction with a beta-blocker or a CCB
• It can improve contractility in patients with LV systolic dysfunction
• Major side effects: disorientation, hallucination, “yellow vision”
• Can also cause anorexia, nausea, vomiting
• Treatment of digoxin toxicity would include administration of Digibind, anti-digoxin antibody fragments

Front 57

What drugs would be used for rate control in afib and atrial flutter?

Back 57

• Class II – beta blockers – slows conduction through AV node
• Class IV – CCBs – slows conduction through AV node
• Digoxin – slows conduction through the AV node

Front 58

What drugs would be used for acute conversion of afib and atrial flutter or maintenance of sinus rhythm in afib or atrial flutter?

Back 58

Class Ic – Na+ Channel blockers – slows conduction through Na+ channel block, interfering with reentry
Class III – K+ channel blockers – lengthens AP duration through K+ channel block, interfering with reentry

Front 59

What drugs would be used to suppress symptomatic PVCs, VT in the setting of MI?

Back 59

• Class II – beta blockers can slow conduction in sick (ischemic) tissue
• Class III agents – amiodarone only, interferes with reentry by prolonging repolarization
• Class Ib – Na+ channel blockers – lidocaine, mexelitine – interferes with reentry by slowing conduction

Front 60

How would you treat Torsades de Pointes?

Back 60

• Stabilize the electrical membrane with Mg++
• Shorten the prolonged QT interval with isoproterenol and overdrive pacing (pacing the heart rate faster than its native rate).
• Electrical cardiovert with phenytoin

Front 61

Where does aortic coarctation occur?

Back 61

It occurs at the level of the ligamentum arteriosum.

Front 62

What are the 4 components of Tetralogy of Fallot?

Back 62

• Infundibular (funnel-shaped) Pulmonary Stenosis
o The outflow tract of the RV, beneath the pulmonary valve, is abnormally formed/developed resulting in stenosis. You get pressure hypertrophy of the RV.
• RVH
• VSD
• Overriding Aorta

Front 63

What are the top 3 main risk factors for vascular disease?

Back 63

• Cigarette smoking
• Diabetes
• HTN

Front 64

What are the 3 main PAD symptoms?

Back 64

• Claudication (pain with walking)
• Rest pain (pain at rest)
• Tissue loss/ulceration

Front 65

What is the only drug approved for claudication?

Back 65

Cilostazol

Front 66

What are 3 main symptoms in the clinical presentation of chronic mesenteric ischemia?

Back 66

• Post prandial pain
• Weight loss
• Food fear

Front 67

What test is most helpful in diagnosing mesenteric ischemia?

Back 67

CTA; it’s rapid, noninvasive, and you can see the bowel

Front 68

What are the most common presentations for carotid stenosis?

Back 68

• Asymptomatic
• Transient Ischemic Attack (TIA)
• Stroke

Front 69

What’s the difference in the inflammation between atherosclerotic occlusive disease and aneurysmal disease?

Back 69

For anureysms, the inflammation is out in the adventitia, while for occlusive disease, the inflammation is in the lumen/intima.

Front 70

Which MMPs are important for aneurysms?

Back 70

• MMP-2 – elevated in small, stable aneurysms
• MMP-9 – elevated in large, rapidly expanding aneurysms

Front 71

What is the most common etiology for the generation of abdominal aortic aneurysm?

Back 71

Atherosclerotic degenerative disease

Front 72

What 3 main symptoms are diagnostic for a typical presentation of a ruptured abdominal aortic aneurysm?

Back 72

• Pain
• Hypotension
• Pulsatile mass

Front 73

At what diameter of the AAA do you recommend surgical repair?

Back 73

When the aneurysm gets to 5.5 cm diameter—and the risk of rupture exceeds the risk of mortality from surgery—is when you recommend surgical repair.

Front 74

What are the 2 mainstays of therapy for patients with DVTs?

Back 74

1) Anticoagulation
2) Compression stockings

Front 75

What’s the most common cause of left axis deviation?

Back 75

Left anterior divisional block.
Left posterior divisional block causes right axis deviation.

Front 76

What are the 2 main pathophysiologic mechanisms underlying heart failure symptoms?

Back 76

• Reduced CO
• Elevated filling pressures

Front 77

What do forward failure and backward failure mean?

Back 77

• Forward failure = decreased cardiac output
• Backward failure = increased LV filling pressures

Front 78

What are characteristics of Stage B heart failure?

Back 78

Stage B is asymptomatic HF with some sort of structural defect (e.g., MI, LVH).

Front 79

What are characteristics of systolic dysfunction?

Back 79

• Implies contractile dysfunction
• Clinically usually manifests as decreased EF
• May or may not have signs/symptoms of HF
• Does not equal systolic HF

Front 80

What are characteristics of diastolic dysfunction?

Back 80

• Implies slowed relaxation, non-compliant ventricle, or both
• Clinically manifests as increased filling pressures
• May or may not have signs/symptoms of HF
• Does not equal diastolic HF

Front 81

In which type heart failure do you get concentric hypertrophy? Eccentric hypertrophy?

Back 81

• Concentric hypertrophy – diastolic HF
• Eccentric hypertrophy – systolic HF

With systolic heart failure you have lengthening of the myocyte (lower diameter); with diastolic HF, you get thickening of the myocyte

Front 82

Which of the following is not an indication of poor perfusion in HF?
A) Decreased exercise tolerance
B) Decreased urine output
C) Moderately elevated total bilirubin, alkaline phosphatase
D) Cool extremities
E) Altered mental status, confusion

Back 82

Answer: C) Moderately elevated total bilirubin, alkaline phosphatase

Front 83

What factors can precipitate acute decompensation in patients with HF?

Back 83

• Increased metabolic demands
o Fever, infection, anemia, tachycardiac, hyperthyroidism, pregnancy
• Increased circulating volume (increased preload)
o Increased dietary Na+, increased fluid intake, renal failure
• Increased afterload
o Uncontrolled systemic HTN, pulmonary embolism (increased RV afterload)
• Reduced cardiac output
o Reduced contractility: myocardial ischemia/infarction, negative inotropes, EtOH
o Reduced stroke volume/abnormal heart rate: tachy- and bradyarrhythmias
• Medication non-compliance
o Most common cause of HF exacerbation/hospitalization

Front 84

Acute pulmonary edema can be a life-threatening situation. How do you treat acute pulmonary edema?

Back 84

• Loop diuretics
• Morphine
• Nitrates
• Oxygen
• Positive pressure ventilation

Front 85

What are the 3 ANCA-associated (pauci immune-associated) vasculitides?

Back 85

1. Wegener Granulomatosis
2. Microscopic Polyangitis
3. Churg-Strauss Syndrome

Front 86

Which vasculitides involve both the lungs and kidneys (alveolar hemorrhage + glomerulonephritis)?

Back 86

• Microscopic polyangiitis (p-ANCA)
• Granulomatosis with polyangiitis (c-ANCA) aka. Wegener’s
• Churg-Strauss syndrome (p-ANCA)
Others that we aren’t responsible for on the unit 6 exam:
• SLE (anti-SM)
• Goodpasture’s syndrome (anti-GBM Ab)

Front 87

What two vasculitides that we discussed are associated with mononeuritis multiplex (peripheral neuropathy due to involvement of arteries associated with nerves)?

Back 87

1. Polyarteritis Nodosa
2. Churg-Strauss Syndrome (70%)

Front 88

What vasculitis is associated with young children, fever, conjunctivitis, and desquamative rash?

Back 88

• Kawasaki disease; occurs in children 2-5
• T-cell delayed hypersensitivity
• Endothelial Antibodies
• Classic Pentad
o Fever
o Conjunctivitis
o Strawberry tongue
o Cervical lymphadenitis
o Desquamative rash
• Untreated: risk of coronary artery ectasia and aneurysms
• Treatment = Aspirin 100 mg/kg/day, IVIG **IMPORTANT**

Front 89

What disease is associated with young, heavily smoking males?

Back 89

• Thromboangiitis Obliterans (Buerger’s disease)
• Medium-small arteries
• Can involve nerve and vein
• Very segmental
• Tibial and radial arteries most involved
• Symptoms
o Rest Pain
o Instep claudication
o Raynaud’s phenomenon
o Limb ischemia
• Treatment = STOP SMOKING

Front 90

What disease is associated with children less than 10 and palpable lesions on the lower extremities?

Back 90

• Henoch-Schonlein Purpura
• Small vessels
• Children less than 10
• IgA deposition in capillaries and venules
• Necrotising lesions
• Paplable purpura – buttocks, lower extremites
• Other symptoms
o Polyarthralgia w/o arthritis
o Abdominal pain
o Renal involvement
o Often antecedent URI-type illness
• Prognosis usually good; usually self-resolving; steroids can help sx

Front 91

Which vasculitides involve the lungs? Kidneys?

Back 91

• Lungs
o Granulomatosis with polyangiitis (Wegner’s granulomatosis)
o Microscopicpolyangitis
• Kidneys
o Microscopic polyangiitis (nephritic syndrome, often RPGN clinically)

Front 92

What epidemiologic populations are affected by Kaposi’s sarcoma?

Back 92

• Classic– elderly Mediterranean men
• Endemic – children in Africa
• Transplant-associated – after transplant and immunosuppression
• Epidemic – associated with AIDS

Front 93

What vasculitis is associated with patients> 50 years, jaw claudication, and polymyalgia rheumatic (pain or stiffness, usually in the neck, shoulders and hips)? What is the appropriate treatment?

Back 93

Giant cell arteritis; treat with steroids, which are the mainstay of treatment for temporal arteritis.

Front 94

What large vessel vasculitis involves the ascending aorta and immediate branches, has constitutional symptoms, and has been described as a “pulseless disease?”

Back 94

• Takayasu’s Arteritis; associated with Asian women < 50
• Constitutional symptoms
• Involves ascending aorta and immediate branches
• “Pulseless disease”

Front 95

What disease is associated with PVC manufacturing?

Back 95

Angiosarcoma (exposure to chemicals such as arsenic or vinyl chloride)

Front 96

What is microRNA-33’s role in cardiovascular disease?

Back 96

MicroRNA-33 is intronic to the SREBP gene, which codes for a transcription factor critical in the regulation of cholesterol and lipid metabolism. Research suggests that microRNA-33 targeting of ABCA1 diminishes the efflux of cholesterol to HDL. Thus, knockdown of microRNA-33 increases HDL levels (in mice and monkeys).

Front 97

What artery is most resistant to atherosclerosis (in the context of coronary artery bypass grafts)?

Back 97

The internal mammary artery

Front 98

How does K+ infusion arrest the heart?

Back 98

K+ reduces repolarization and stops the inactivation gate of the fast acting Na+ channel, impairing it and resulting in cardiac arrest.

Front 99

What is distal runoff, and what vessel has the best distal runoff?

Back 99

• Distal runoff is the blood flow in the post stenotic region of a blood vessel
o Distal runoff is an important factor in the success of vaascular grafts
o Poor distal runoff promotes thrombosis formation within the graft
• Order from best to worst distal runoff’
o 1) LAD
o 2)LCX
o 3)RCA

Front 100

When would you use a tissue valve versus a mechanical valve in surgical repair of valvular disease?

Back 100

Tissue valves are less durable than mechanical valves. For mechanical valves, they need to be on anti-coagulation. If you have an old patient who needs valve replacement, you prefer to give them a tissue valve, because they won’t live long enough to worry about the valve wearing out. A young patient needs a mechanical valve, but they’ll have to live with Coumadin for the rest of their life.
Infective endocarditis is usually treated with an aortic pulmograft from a cadaver. (Cadaveric aortic valve, because there’s no foreign tissue – it’s all human tissue.)

Front 101

What is the most common cause of acute MI?

Back 101

Plaque disruption with thrombus formation is the most common cause of acute MI!

Front 102

Which of the following is NOT a direct sequelae of an acute myocardial infarction? A) Aneurysm B) Heart Failure C) Arrhythmia D) Aortic Dissection

Back 102

D) Aortic Dissection

Front 103

What are the 3 criteria for LV enlargement on an ECG?

Back 103

1. S in V1 + R in V5 or V6 > 35 mm
2. R in I + S in III >= 25 mm
3. R in aVL >= 12 mm

Front 104

What are the 4 criteria for RV enlargement on an EKG?

Back 104

1. V1: R wave is larger than S wave
2. V6: S wave is larger than R wave
3. Limb leads: Right axis deviation (axis between 90 degrees and 180 degrees)
4. Usually, right atrial p-wave abnormality is present

Front 105

What is the mechanism of action of nitrates in the treatment of cardiovascular disease?

Back 105

• Mechanism of action—reduce preload, afterload, coronary vasodilation
• Increase in cyclic GMP leads to relaxation of vascular smooth muscle
• Preparations
o Sublingual—onset in 1 minute; lasts 5-15 minutes
o Oral—isosorbide dinitrate short acting (several hours)
o Oral—isosorbide mononitrate (short acting and once daily preparations)
o Transdermal—patch worn for 12-24 hours; ointment lasts 6 hours
• Headaches are a significant side effect

Front 106

What is the mechanism of action of calcium channel blockers in the treatment of cardiovascular disease?

Back 106

• Block calcium channels in vascular smooth muscle, leading to coronary vasodilation, peripheral vasodilation, decreased myocardial contractility, and decreased heart rate.
• Useful for angina, hypertension, and supraventricular tachycardias
• Types of CCBs:
o Dihydropyridines—amlodipine, nifedipine, nicardipine, felodipine, isradipine
o Diltiazem
o Verapamil
• CCBs can be negatively inotropic, and constipation is a big problem, because they relax vascular smooth muscle in the colon

Front 107

What is the mechanism of action of ranolazine?

Back 107

• Ranolazine helps shut the Na+ inward gate of the late Na+ current, reducing intracellular Na+, providing less substrate for the Na+/Ca++ exchanger
• By inhibiting Na+ and Ca++ overload ranolazine may reduce consumption of ATP, improve contractile function and reduce electrical instability
• Ranolazine can increase the QT interval on ECG

Front 108

What are the pathophysiologic sequelae of mitral stenosis?

Back 108

• Pulmonary venous congestion
• Pulmonary arterial hypertension
• Right Ventricular Dysfunction
• Systemic venous congestion
• Low Cardiac Output
• Atrial Fibrillation
• Systemic embolization

Front 109

What is the classic triad of symptoms of aortic stenosis?

Back 109

1. Dyspnea
2. Angina
3. Presyncope and syncope

Front 110

What are the most common causes of aortic stenosis?

Back 110

1. Congenital (especially bicuspid valves)
2. Degenerative (calcific)
3. Rheumatic

Front 111

What is a normal aortic valve area, and what is the definition of severe aortic stenosis?

Back 111

Normal aortic valve area is > 3.0 sq cm, and severe AS is defined as a valve area < 1.0 sq cm.

Front 112

Can you explain the paradoxical splitting of the second heart sound?

Back 112

• Paradoxic splitting can occur with aortic stenosis, and P2 occurs before A2 due to delayed emptying of the LV.
• The pulmonic valve is working normally and moves to the right temporally as it should, but since A2 is on the wrong side, you get narrowing of the split upon expiration.

Front 113

When would surgery be recommended for an aortic stenosis patient?

Back 113

Only if there are symptoms; there’s no evidence that aortic valve replacement improves outcome in asymptomatic patients.

Front 114

What are the sequelae of aortic regurgitation?

Back 114

Aortic regurgitation represents a combination of both increased LV preload and increased LV afterload that leads to:
1. LV hypertrophy and LV dilatation, which compensate for increased afterload but ultimately may lead to LV systolic dysfunction, elevated LV diastolic pressures and pulmonary congestion
2. Widened pulse pressure with elevated systolic BP and reduced diastolic BP

Front 115

How do you treat aortic regurgitation?

Back 115

There’s no established medical therapy for AR other than treating HTN in patients, which could increase severity of AR. Ultimately, patients with severe AR may require surgical aortic valve replacement.

Front 116

What are the sequelae of mitral regurgitation?

Back 116

Mitral regurgitation represents volume overload of both the LV and LA, leading to:
1. Elevated LA pressure, which may lead to
a. Pulmonary venous congestion, which may lead to
b. Pulmonary arterial HTN, which may lead to
c. RV dysfunction, which may lead to
d. Systemic venous congestion
2. LV dilatation, which compensates for increased preload but ultimately may lead to LV systolic dysfunction, which contributes further to elevated LA pressure
3. LA dilatation, which may lead to
a. AF, which can lead to
b. systemic arterial embolization

Front 117

Does aortic regurgitation cause increased preload or increased afterload?

Back 117

Trick question; aortic regurgitation represents a combination of both increased LV preload and increased LV afterload.

Front 118

What are the indications for surgery for mitral regurgitation?

Back 118

1. Development of symptoms
2. LV systolic dysfunction
3. Pulmonary HTN
4. Atrial fibrillation
In valvular stenosis, it is safe to wait until symptoms to develop before recommending surgery.
In valvular regurgitation, in addition to symptoms, one should consider surgery when there is LV systolic dysfunction or severe LV dilatation.

Front 119

What is the leading cause of mitral regurgitation in the USA?

Back 119

Mitral valve prolapse is a common congenital lesion (up to 5% of the population) and the leading cause of MR in the USA.

Front 120

Which of the following does NOT create left ventricular hypertrophy:
A) HTN
B) Aortic regurgitation
C) Mitral regurgitation

Back 120

C) Mitral regurgitation does not cause LVH, because it does not increase afterload. Afterload is what causes the muscle to hypertrophy. As soon as the ventricle wants to shorten during MR, it sees an out (a way to relieve its pressure, and thus there’s no increased afterload.

Front 121

Can you describe the ventricular remodeling that occurs in the following conditions: a) aortic stenosis b) mitral regurgitation c) aortic regurgitation

Back 121

a) In aortic stenosis, there’s concentric hypetrophy due to the increased afterload
b) In mitral regurgitation, there’s dilatation/increased volume but no increase in the wall mass (i.e., no hypertrophy), because there’s no increased afterload
c) With aortic regurgitation, there’s eccentric hypertrophy due to an increased dilatation/increased volume as well as an increase in the wall mass due to an increased preload and afterload
For aortic valve disease, think Afterload->LVH
For Mitral valve disease: think pulmonary congestion and atrial fibrillation

Front 122

What structural change in the aorta can cause aortic regurgitation?

Back 122

Anything that can make the aorta enlarge can pull apart the valve leaflets and cause aortic regurgitation.

Front 123

Why do you get an S3 in aortic regurgitation?

Back 123

S3s are very common, because you’re dealing with a dilated chamber. (S3 is just a marker of a dilated ventricle.) Another marker of aortic regurgitation is a wide pulse pressure (note the systolic is 140 and diastolic is like 60). You get a decrescendo murmur that starts louder and gets softer.

Front 124

Generally, what has a poorer outcome, valvular stenosis or regurgitation?

Back 124

In general, stenosis, or narrowing of the valve leading to restriction of outflow leads to a poorer outcome than regurgitation or insufficiency.

Front 125

What pathogens are the most common cause of infective endocarditis?

Back 125

Most common organisms are Strep. Viridans and staph aureus.
Vegetations are most commonly on valves of the left ventricle.

Front 126

Which layer of the heart is most commonly involved in rheumatic carditis?

Back 126

Rheumatic carditis is a pancarditis, meaning all the layers of the heart are involved – endocardium, myocardium, and pericardium.

Front 127

What are the Jones criteria for acute rheumatic fever?

Back 127

J – joints (polyarthritis)
O – other (carditis)
N – nodules (subcutaneous nodules)
E – Erythema Marginatum
S – Syndenham chorea

Front 128

Which valve is most commonly involved in nonbacterial thrombotic endocarditis?

Back 128

• The aortic valve is most common, and the mitral valve next most frequently involved.
• Malignancies are found in 50% of cases.
• Morphologically, there will be small nodules on lines of valve closure, and the nodules may be bulky and friable.
• The valve leaflets are otherwise normal.

Front 129

What is this pathognomonic for?

Back 129

• The image shows an Aschoff nodule, which is pathognomonic for Rheumatic Heart disease.
• Aschoff bodies
o Fibrinoid necrosis (necrotic collagen)
o Mononuclear inflammatory infiltrate (usually T lymphocytes)
o Anitschkow cells
 Histiocytes with vesicular nuclei and abundant cytoplasm
Histiocytes are cells that are part of the mononuclear phagocyte system (e.g., macrophage, dendritic cell).

Front 130

Can you describe the murmurs for: a) mild aortic stenosis b) severe aortic stenosis c) mitral regurgitation d) mitral valve prolapse?

Back 130

See image

Front 131

Can you describe the murmurs for: a) mitral stenosis b) mild aortic regurgitation c) severe aortic regurgitation?

Back 131

(see image)

Front 132

What is the most frequent valvular abnormality?

Back 132

• Aortic stenosis
• Acquired>>congenital
• Senile calcification, degenerative, “wear and tear”, >10 % due to rheumatic fever
• 1-2% congenitally bicuspid
• Heaped-up calcified masses in sinuses of valsalva

Front 133

Can you describe the pathophysiology of dilated cardiomyopathy?

Back 133

• In DCM, the left ventricle is dilated and systolic pump function is depressed.
o Results in elevated LV end diastolic pressure, LA pressure, and pulmonary venous pressure
 Causes dyspnea
o Reduced cardiac output
 Causes fatigue and compensatory mechanisms
• Activates sympathetic, adrenal , and RAAS systems, which increase systemic vascular resistance
o Leads to hypertrophy, apoptosis and fibrosis
• Majority of patients who die, die suddenly, presumably from arrhythmic causes

Front 134

Can you describe the pathophysiology of restrictive cardiomyopathy?

Back 134

• Conditions that cause infiltrative processes in myocardium are the most common causes
o Amyloidosis
o Hemochromatosis
o Sarcoidosis
o Etc
• Thickening and stiffening of ventricular myocardium
o Results in restriction of ventricular filling
o Reduces forward output
o elevates LV and RV filling pressures
o results in systolic dysfunction (late manifestation of the disease)

Front 135

Can you describe the pathophysiology of hypertrophic cardiomyopathy?

Back 135

• There’s marked LV hypertrophy, which increases the LV ventricle
o Impairs ventricular filling in disastole and results in small end-diastolic volumes and elevated filling pressures
• Myocardial ischemia develops commonly in HCM due to marked myocardial hypertrophy which outstrips the vasodilator capacity of the coronary circulation

Front 136

What type of murmur can you get with dilated cardiomyopathy, and why?

Back 136

You can get a systolic murmur of mitral regurgitation, because the normal heart has the papillary muscles in a unique alignment. In DCM, the papillary muscles have abnormal alignment, causing mitral regurgitation.

Front 137

What are physical findings for pericarditis?

Back 137

• Kussmaul’s sign
o Increase in venous pressures in the neck on inspiration as opposed to expiration
• Jugular venous distention
• Pericardial knock

Front 138

What is pulsus paradoxus, and what could it be indicative of?

Back 138

Pulsus paradoxus occurs in cardiac tamponade and reflects exaggerated decreased systolic and diastolic pressures during inspiration.

Front 139

What is cardiac tamponade?

Back 139

Cardiac tamponade results if more than 250 mL of fluid accumulates in the pericardial space, especially if it accumulates quickly.

Key findings on physical exam include:
1) Jugular venous distension
2) Systemic hypotension
3) A “small, quiet heart” on physical exam
4) Pulsus paradoxus
a. Decrease of systolic blood pressure (more than 10 mm Hg) during normal inspirations

Front 140

What is an important parasitic cause of myocarditis?

Back 140

An important parasitic cause of myocarditis is by Trypanosoma cruzi, transmitted by the reduviid bug (which harbors the parasite in its feces). About 20M people in South America are affected with T. cruzi.

Front 141

What’s the most common primary tumor of the heart?

Back 141

The most common primary tumor of the heart is cardiac myxoma, which commonly (75%) involves the LA or mitral valve, leading to impairment of ventricular filling. Famously, the clinical findings include a diastolic murmur that varies with the patient position since myxomas are ball-like and mobile.

Front 142

What is the pattern of inheritance for familial hypertrophic cardiomyopathy?

Back 142

Autosomal dominant

Front 143

What is the equation for transpulmonary gradient, MAP, PVR, SVR, Wall stress?

Back 143

• Transpulmonary gradient = mPAP – PCWP

• MAP = (SBP + (2*DBP))/3

• PVR = [(mPAP - PCWP)/CO]*80

• SVR = [(MAP - CVP)/CO]*80

• Wall stress = (P x r)/2h

Front 144

Can you describe the effect of the Class I, Na+ channel blockers on the action potential duration?

Back 144

See image

Front 145

What drug can be useful for treating Hypertrophic Obstructive Cardiomyopathy, and what are its main side effects?

Back 145

You can use disopyramide (class Ia Na+ channel blocker) for treating HOCM, and side effects include antimuscarinic effects (e.g., urinary retention, constipation, blurred vision, dry mouth, closed-angle glaucoma).

Front 146

Which B-blockers have solely B1 effects?

Back 146

Atenolol and metoprolol

Front 147

Which B-blockers have alpha and beta blocking capability?

Back 147

Labetolol and Carvedilol

Front 148

What are the effects of B1-blockade on renin release?

Back 148

B1 blockade also lowers blood pressure by decreasing renin release.

Front 149

What is the use of alpha 2 agonists like Clonidine in the treatment of cardiovascular disease?

Back 149

Alpha2 agonists like clonidine stimulate the alpha 2 receptor and inhibit NE release from the CNS, causing a decrease in cardiac output and decrease in vascular resistance.

Front 150

What’s the difference between dihydropyridines and non-dihydropyridine agents (CCBs)?

Back 150

The dihydropyridines (e.g., Nifedipine, Amlodipine, Felodipine) have a more peripheral effect, while the non-dihydropyridine agents (e.g., Verapamil, Diltiazem) also affect the smooth muscle, but have a varying effect on the heart.

In other words, dihydropyridines are selective for vascular smooth muscle and do not affect the heart.

Front 151

What is the mechanism of action of calcium channel blockers (CCBs)?

Back 151

CCBs block the transmembrane Ca++ current, resulting in relaxation of the muscle cell, particularly vascular smooth muscle cells.

Front 152

What is the mechanism of action of minoxidil?

Back 152

Minoxidil, a peripheral vasodilator that lowers blood pressure by relaxing peripheral vasculature, works by opening K+ channels in smooth muscle cell membranes. That stabilizes the membrane and makes contraction less likely. It dilates arterioles not veins.
Side effects include hypotension, flushing, tachycardia, dizziness, palpitations occur with all peripheral vasodilators.

Front 153

What is the definition of a hypertensive emergency, and what agents are used to lower blood pressure in a hypertensive emergency?

Back 153

A hypertensive emergency is defined as “an acute decompensation of vital organ function secondary to the elevated blood pressure.”
Agents that are used to lower blood pressure in a hypertensive emergency are:
• Na+ Nitroprusside
• Labetolol
• Hydralazine
• Enalaprilat
• Fenoldapam

Front 154

What is Qp:Qs, and what cutoff is considered an indication for the repair of a shunt lesion?

Back 154

• Qp:Qs is the ratio of flow through the pulmonary circuit (lungs) compared with the flow through the systemic circuit (cardiac output to the body).
• A Qp:Qs of >2 is accepted as an indication for repair of the shunt lesion, because it indicates such excessive pulmonary blood flow that complications will be seen if the shunt lesion is not repaired.
• Qp:Qs is measured by cardiac catheterization

Front 155

What is Eisenmenger’s syndrome?

Back 155

Eisenmenger’s syndrome is when there’s an intracardiac L-R shunt, and pulmonary vascular resistance increases to the point that it exceeds the systemic vascular resistance, and the shunt reverses to become a R-L shunt.

Front 156

Should you close the shunt in a patient with Eisenmenger’s syndrome? Why or why not?

Back 156

You should NOT close the shunt, because that would require all the blood to go through the pulmonary system at high pressure, and the RV isn’t optimized to have high pressure go through there. It’s better to preserve CO and not have perfect O2 saturations.

Front 157

What is an example of pressure hypertrophy? Volume hypertrophy?

Back 157

• An example of pressure hypertrophy would be aortic stenosis.
• An example of volume hypertrophy would be an atrial-septal defect where blood flows from the LA to the RA.
• When myocardium fails, they use the term dilatation

Front 158

What is a normal range for the ankle to brachial index?

Back 158

The ankle to brachial index is a measure of the ratio of the blood pressure in the lower legs to the blood pressure in the arms. Lower blood pressure in the leg is an indication of blocked arteries (peripheral artery disease).
• 0.9-1.2 is normal
• Above 1.2 is abnormal vessel hardening from PAD
• Less than 0.9 represents PAD

Front 159

Why do emboli lodge in the SMA more than the celiac artery?

Back 159

The SMA has more of an oblique angle, as compared to the acute angle of the celiac.

Front 160

Of the following types of mesenteric ischemia, which has the greatest mortality?
A) Embolic
B) Thrombotic
C) Nonocclusive
D) Venous Thrombosis

Back 160

Thrombotic and Nonocclusive have the greatest mortality, although embolic is the most common.

Front 161

What are the main symptoms for acute mesenteric ischemia?

Back 161

• Sudden pain out of proportion to exam (they’ll be screaming, like the worst pain they’ve ever had)
• Gut emptying
• Nausea
• Vomiting
• Diarrhea

Front 162

What are types A and B of aortic dissection, and what age groups do they commonly affect?

Back 162

Type A involves the ascending aortic arch, and type B doesn’t.
• 50-60 years of age – Type A
• 60-70 years of age – Type B

Front 163

How are aneurysms defined (i.e., what is the criterion for an aneurysm)?

Back 163

• An aneurysm is a localized, blood-filled balloon-like bulge in the wall of a blood vessel.
• An aneurysm is defined as at least a 50% increase in diameter compared with the expected normal diameter.

Front 164

What are protective factors against abdominal aortic aneurysms and what are important risk factors?

Back 164

• Protective
o Female sex
o Black race
o Diabetes mellitus
• Risk factors
o Current smoker
o Ever smoked
o Old age
o Family history
o Symptomatic atherosclerosis
o Hypercholesterolemia

Front 165

What are the main symptoms for DVT? PE?

Back 165

See image

Front 166

What vein is the most common to thrombose?

Back 166

Superior mesenteric vein is the most common site of venous thrombosis.

Front 167

Why does the ventricular wall thicken in systemic hypertension?

Back 167

One of the adaptive mechanisms by which the heart combats the ill-efects of systemic HTN is to increase its wall thickness, which decreases wall stress.

Front 168

What factors determine ejection fraction?

Back 168

• Preload
• Afterload
• Contractility

Front 169

Why do patients with heart failure almost universally have atrial enlargement?

Back 169

It’s due to chronic pressure overload of the atria due to the HF state. Atrial fibrosis accompanies atrial enlargement, which causes atrial arrhythmias such as AF and atrial flutter.

Front 170

What are important differences between systolic heart failure and diastolic heart failure (besides ejection fraction and filling pressure)?

Back 170

• In DHF, wall thickness is increased while SHF has decreased wall thickness
• In DHF, LV EDV is normal, while it’s increased in SHF

Front 171

Can you describe the different classes of the NYHA functional classification system?

Back 171

(see image)

Front 172

What are typical signs/symptoms of CHF?

Back 172

• Symptoms
o Dyspnea on exertion
o Orthopnea
o Paroxysmal nocturnal dyspnea (PND)
o Fatigue
o Leg swelling
o Abdominal pain/bloating
• Signs
o Tachycardia
o Tachypnea
o Elevated JVP
o Pulmonary rales
o S3 gallop
o Increased P2 (in patients with pulmonary HTN)
o Hepatomegaly
o Peripheral edema

Front 173

How do you treat someone who’s warm and wet? Cold and wet? Cold and dry?

Back 173

• Warm and wet (67% of patients): congested with good perfusion; diuresis is most important. Uptitrate and ensure treatment with other life-saving heart failure medications (e.g., beta-blocker, ACE-inhibitor/ARB, and spironolactone)
• Cold and wet (28%) – congested with poor perfusion; these patients cannot undergo successful diuresis until their perfusion improves. Vasodilators are the mainstain of therapy in this situation. Inotropes can also help, but these agents increase mortality, so use with caution (can be used as a bridge to ventricular assist device or cardiac transplantation).
• Cold and dry (5%) – no congestion but poor perfusion; these patients are typically end-stage HF patients and require increased vasodilator and/or inotropic therapy. Consider ventricular assist device and/or cardiac transplantation in these patients.

Front 174

Of the IV vasodilators, nitroglycerin and nesiritide, which can be used in hypotensive patients?

Back 174

Nesiritide (recombinant BNP) is a natriuretic peptide and promotes natriuresis, but also acts as a potent vasodilator. It should NOT be used in hypotensive patients. Nitroglycerin and nesiritide can generally be used in patients who are “warm and wet,” but should be used with caution in patients who are “cold,” because they can acutely worsen hypotension.
I think it’s okay to use nitroglycerin, but nitroprusside is the vasodilator of choice if the patient is cold, because it won’t decrease preload as much as other agents.

Front 175

What is the optimal range for digoxin, and why can hypokalemia increase digoxin levels?

Back 175

• The optimal range for digoxin is 0.5 – 0.8 ng/mL, which is below the usual therapeutic range. Above this dose, digoxin increases mortality.
• Hypokalemia can increase digoxin levels since digoxin normally competes with K+ ions for the same binding site on the Na+/K+ ATPase pump.

Front 176

Can you use beta-blockers for CHF patients?

Back 176

Beta-blockers improve survival and outcomes in systolic HF by combating the maladaptive neurohormonal response that occurs n HF.

Front 177

What are the determinants of stroke volume?

Back 177

Contractility (increased) - anything that increases intracellular calcium
Preload (increased)
Afterload (decreased)

Front 178

What’s the most common type of congenital cyanotic disease?

Back 178

Tetralogy of Fallot

Front 179

At what level of narrowing in obstruction do you start to see problems?

Back 179

65%

Front 180

What class of drugs are the treatment of choice for Prinzmetal's angina (angina caused by vasospasm)?

Back 180

CCBs are the treatment of choice for Prinzmetal's angina. They cause vasodilation of the coronary arteries and peripheral resistance arteries.

Front 181

What are the 3 major determinants of myocardial O2 demand?

Back 181

The 3 major determinants of myocardial O2 demand are:
1) Ventricular wall stress
a. Related to ventricular pressure and the radius of the ventricle and inversely proportional to the wall thickness, wall stress is the tangential force acting on the myocardial fibers, tending to pull them apart, and energy is expended in opposing that force
2) Heart rate
a. The amount of ATP consumed per minute increases with heart rate and so do the O2 requirements. Conversely, slowing the HR with a beta blocker decreases ATP utilization and O2 consumption
3) Contractility

Front 182

What is the equation for the Fick principle version of cardiac output?

Back 182

CO = rate of O2 consumption/(arterial O2 content - venous O2 content)

Front 183

What is the definition of syncope?

Back 183

Syncope is defined as transient loss of consciousness with loss of postural tone. Some include that it is also due to decreased cerebral blood flow. It’s important to distinguish syncope from:
• Vertigo
• Seizures
• Falls
Syncope can be associated with a prodrome of dizziness but not with a sensation of motion.

Front 184

Can you give a broad pathophysiological diagnosis of syncope?

Back 184

• Neurally-mediated Syncope (25%)
o Bradycardiac (cardio-inhibitory)
o Hypotensive (vaso-depressor)
o Vasovagal (mediated by emotional distress, fear, pain, etc.)
o Situational (cough, sneeze, GI stimulation, micturition, post-prandial, etc.)
o Carotid sinus syncope (hypersensitivity of carotid body to pressure)
• Cardiac Arrythmias (14%)
o Brady and tachy-arrhythmias are the most common serious cause of syncope
• Neurologic Disease (10%)
o Seizure disorders
o Syncopal migraines
o TIAs or strokes
• Postural Hypotension (8%)
o Primary etiology is volume depletion or autonomic failure
• Cardiovascular mechanical disorders (4%)
o Could be due to PE
o Aortic stenosis can reduce ability to increase CO during exercise
• Metabolic and Toxic causes (3%)
o Narcotics, phenothiazines, and recreational drugs are most commonly associated drugs
• Psychiatric disrorders (2%)
• Unknown (34%)

Front 185

What is the equation for BP that relates HR, SV, and SVR?

Back 185

see image