Cardiovascular And Ischemic Hd 1

Front 1

Pericardium

Back 1

encloses the heart and root of the great vessels

Front 2

2 layers of pericardium

Back 2

-fibrous pericardium (outer tough fibrous tissue)
-serous pericardium (inner smooth layer)

Front 3

serous pericardium composed of a parietal and visceral layer, space between two layers contains what?

Back 3

A thin layer of lubricating fluid called pericardial fluid

-about 30cc

Front 4

True or False: the Apex is formed by the tip of the left ventricle of the heart.

Back 4

True

Front 5

Four boarders of the Heart

Back 5

~Right border: right atrium and in line with the superior and inferior vena cavae
~Inferior border is almost horizontal and formed by the Rt Ventricle, small part of Lt Ventricle at Apex.
~Lt border , Lt Ventricle and part Lt Atrium
~Superior border made of both Atria.

Front 6

Three layers of heart

Back 6

Endocardium, Myocardium, Epicardium

Front 7

Flow of Blood through heart

Back 7

Front 8

Two main arteries that supply the heart

Back 8

~Left Main Coronary Artery- LCA
~Right Coronary Artery- RCA

Front 9

LCA gives rise to...

Back 9

Left Anterior Descending- LAD and Left Circumflex-LCX

Front 10

RCA gives rise to...

Back 10

Posterior Descending Artery PDA

Front 11

Variances in coronary artery anatomy

Back 11

85% are RCA dominant
8% Circumflex is dominant
7% both RCA and Circumflex give rise to posterior descending branches.

Front 12

what makes skeletal muscle cells different then cardiac muscle cells

Back 12

Cardiac cells only have one or two nuclei, skeletal cells have many nuclei.

Front 13

what does the myocardial cell membrane contain that establishes electrical continuity within the myocardium

Back 13

Intercalated disk

Front 14

The Basic unit of electrical stimulation

Back 14

Action Potential, ion fluxes through specific ion channels create depolarization, the trigger for muscular contraction.

Front 15

Myocardium contains 3 types of electrophysiologic types:

Back 15

pacemaker cells: SA and AV nodal cells
Specialized rapidly conducting tissues: Purkinje fibers
Cardiac muscle cells themselves

Front 16

The Heart is innervated (the distribution or supply of nerve fibers or nerve impulses to a body part) by both...

Back 16

Sympathetic and Parasympathetic nervous system

Front 17

Systole is...

Back 17

Ventricular contraction, when the ventricles push blood out into the pulmonary and systemic circulation

Front 18

Diastole is...

Back 18

Ventricular relaxation, when the ventricles are filling up with blood again.

Front 19

First heart sound, S1, caused by...

Back 19

nearly simultaneous closure of the tricuspid and mitral valves, preventing backflow of blood into the atria.

Front 20

second Heart sound S2.

Back 20

After blood has ejected, the aortic and pulmonic valves close.

Front 21

Period from S1-S2

Period from S2 to the next S1

Back 21

Systole

Diastole

Front 22

Cardiac Auscultation

Back 22

Listening to the sounds of the heart

Front 23

Electrocardiogram-ECG

Back 23

Diagnostic method to record the heart's electrical activity. Surface representation of myocardial depolarization and re-polarization.

12 lead ECG is standard, placed at different angles

Front 24

disorders ECG can identify

Back 24

-conduction abnormalities
-cardiac dysrhythmias
-cardiac hypertrophy
-pericarditis
-electrolyte imbalances
-myocardial ischemia
-myocardial infarction (MI) and extent of recovery from MI

Front 25

Most Common Heart Disease

Back 25

Ischemic Heart Disease

Front 26

Insufficient myocardial perfusion (blood flow) that causes 600,000 deaths per year.

Back 26

Ischemic Heart Disease!

Front 27

Patients with Ischemic Heart Disease present with...

Back 27

Angina ( cardiac chest pain)
Myocardial infarction
Congestive heart failure
Sudden death

Front 28

Decreased blood flow to tissue resulting in decreased tissue oxygen and increased build-up of tissue metabolites that are harmful

Back 28

Ischemia

Front 29

Infarction

Back 29

decreased blood flow to a tissue to such and extent that tissue death occurs

Front 30

Slowly progressive disease that affects the arteries, in which fatty deposits and fibrous tissue occlude the lumen, and cause of angina pectoris.

Back 30

Atherosclerosis

Front 31

Thrombosis

Back 31

Clotted blood and involves platelets, and fibrin produced from the blood coagulation system.

Front 32

Embolus

Back 32

Any substance that circulates in the bloodstream and becomes lodged with in a vessel lumen resulting in occlusion

Front 33

Two most common lesions of atherosclerosis

Back 33

Fatty streak and fibrous plaque

Front 34

Fatty lesions

Back 34

-most have them by age 20
-yellow discoloration on the inner surface of the artery
-precursor lesion that develops into fibrous plaque

Front 35

Fibrous Lesion

Back 35

Fibrous Plaques are the pathologic lesions that caus the morbidity and mortality of atherosclerosis.

-most common in the aorta, then coronary arteries, popliteal, descending thoracic aorta, internal carotid, and cerebral vascular arteries

Front 36

Risks for developing atherosclerosis

Back 36

modifiable risk:
Hyperlipidemia, hypertension, cigarettes, and diabetes

non-modifiable risk:
Men, age, and family history of coronary disease

minor risk:
obesity, sedentary lifestyle, and stressful behavior

Front 37

Angina Pectoris (cardiac chest pain) results from...

Back 37

Imbalance between myocardial oxygen supply and demand

Front 38

most common cause of angina pectoris

Back 38

inability of atherosclerotic coronary arteries to supply heart with oxygen-rich blood, in conditions of demand.

can also occur with valvular disease, hypertension, and coronary artery vasospam.

Front 39

Pain of angina described as...

Back 39

Pressure, heaviness, or squeezing sensation

Front 40

Pain location in substernal area, percorium, or epigastrium with pain radiating to what areas?

Back 40

Left arm, jaw, and neck.

usually only lasting a few minutes

Front 41

Angina may be provoked by

Back 41

Exterion, emotion, cold weather, and eating or smoking.

Front 42

Relive angina by

Back 42

resting, remove provoking factors, or the drug nitroglycerin.

Front 43

Acute Myocardial Infarction (AMI)

Back 43

result of prolonged ischemia that has led to irreversible necrosis of the myocardial tissue.

Front 44

85% of AMI cases is associated with

Back 44

occluded coronary artery, mainly atherosclerosis

Front 45

how many people in US suffer from MI each year, and what is the hospital mortality rate?

Back 45

over 1.5 million people and around 15%

Front 46

which area of the heart is most commonly affected by MI?

Back 46

the left ventricle

Front 47

Clinical presentation for MI

Back 47

-Pale
-Diaphoretic(sweaty)
-Anxious

maybe increased heart rate, respiration, and blood pressure.

Front 48

what are the 2 main diagnostic test used for diagnosing MI

Back 48

ECG: serial ECG tracings to show evolution of myocardial damage. "Q-waves" develop with infarction and necrosis. can locate area of damage

Cardiac serum protein markers: proteins presented in blood for a defined period of time after injury and during injury.

Front 49

a protein and enzyme that show up in blood after a few hours of injury

Back 49

Myoglobin: muscle protein, dissipates within a day

Creatine Kinase: enzyme last for 3 days in blood

Front 50

Troponin

Back 50

Early and late marker: Cardiac muscle enzyme released 6 hours after injury, stays elevated for about a week

Front 51

Stable Angina

Back 51

occurs with exertion, rest can help heal

Front 52

Unstable Angina

Back 52

Pain at rest and/or at night, more dangerous, bad prognosis, and usually 3 months.

Front 53

If blood flow to heart does not get better in 6 hours...

Back 53

Necrosis of heart tissue that can not be reversed

Front 54

complications of AMI

Back 54

-Arrhythmias
-Rupture of the Lt Ventricle wall
-Aneurysm

Front 55

Arrthyhmia

Back 55

-occur due to interruption of the blood supply to the pacemaker cells
-extremely common and major cause of mortality.

Front 56

Rupture of Lt Ventricular wall

Back 56

-result from the necrotic heart tissue tearing
-hemorrhage occurs in the pericardial space
-deadly and often occurs within the first 2 weeks after a MI.

-survival rate low

Front 57

Aneurysm

Back 57

-Late complication of Mi, 2 weeks to months after MI
-develops as the ventricular wall is weakend from clean up of tissue by phagocytic cells
- localized outward bulge

Front 58

Treatments

Back 58

-aspirin, to decrease clot formation
-beta-blockers, to reduce the work the heart has to do, decreasing demand for oxygen
-nitroglycerin, to improve oxygen
-morphine, calm the patient

Front 59

Thrombolytic therapy

Back 59

reoxygenate the heart, break down throbus lodged in the artery by intravenous enzymes, TPA and Streptokinase. Given within the first 6 hours

Front 60

Primary coronary angioplasty

Back 60

-improves coronary blood flow by enlarging the disease artery's lumen
-pressurized balloon is inflated in the vessel to open obstruction

Front 61

Define Stenosis

Back 61

narrowing of the valvular opening, usually due to valvular tissue thickening that prevents it from opening properly

Front 62

insufficiency and regurgitation mean the same thing.
T or F?

Back 62

True: valvular incompetence that prevents complete valve closure, allowing blood to flow back up into previous chamber

Front 63

Valvular Heart Disease affects how many valves?

Back 63

one or all the valves

Front 64

consequences of valvular heart disease are

Back 64

- arrhythmias
- heart failure
- pulmonary congestion
- dyspnea (trouble breathing)
- synocpe (fanting)

Front 65

Heart Failure

Back 65

When heart is unable to pump blood forward at a rate to meet the body's metabolic demands or when the heart can only meet the demands if the filling pressure are abnormally high, or both.

Front 66

Cardiac auscultation can reveal...

Back 66

abnormal murmurs and or particular sounds indicative of valvular disease.

Front 67

Mitral valve prolapse

Back 67

when the leaflet is floppy and enlarged and protrudes into the left atrium.

Front 68

what is the major diagnostic tool for valvular heart disease

Back 68

Echocardiography

Front 69

Chest radiograph

Back 69

in which cardiac enlargement, valvular calcification and interstitial edema in the lungs can appear

Front 70

treatment for valvular heart disease is

Back 70

usually valve replacement

Front 71

Acute Rheumatic Fever - ARF

Back 71

-Inflammatory condition that involves the skin, heart, and connective tissues.

-significant cause of valvular lesions, in mostly developing countries, due to lack of antibiotics.

-usually in childhood

Front 72

what is the bacteria that causes ARF?

Back 72

Group A Streptococci, causing streptococcus pharyngitis (strep throat)

Front 73

why is it important to get on antibiotics if you have strep throat?

Back 73

Because 3% of people with strep will develop ARF 2-3 weeks after

Front 74

what parts of the heart does ARF affect?

Back 74

can affect all 3 layers of heart

valves become inflamed, and one or more valve can be permanently distorted and thickened.

Front 75

when do symptoms of valvular dysfunction from ARF occur?

Back 75

may not be until 10-30 years after ARF

-40% develop mitral stenosis
-25% develop aortic regurgitation or stenosis

Front 76

Mitral valve stenosis- MVS

Back 76

Fibrous thickening of the valve leaflets, fusion of the commissures and leaflets calcification due to inflamation.

Photograph of a short-axis section from the base of the heart of a 44-year-old woman with rheumatic mitral stenosis shows diffuse fibrous leaflet thickening (arrow) and commissural fusion (arrowhead) that cause the valve to resemble a fish mouth. A large anteroseptal myocardial infarction with associated mural attenuation also is depicted. (Courtesy of William D. Edwards, MD, Department of Pathology, Mayo Clinic, Rochester, Minn.)

Front 77

What is MVS almost always caused by?

Back 77

Acute Rheumatic Fever

Front 78

when mitral valve becomes stiff and hard to push through Lt atrium and the pressure decreases. T or F ?

Back 78

False: Increases pressure to push through the stenotic valve.

Front 79

The increase pressure from MVS is transferred back to the lungs causing what?

Back 79

Pulmonary congestion, and after time Pulmonary Arteriolar Hypertension

Front 80

Which side of the heart becomes hypertrophied (enlarged) due to MVS and pulmonary congestion?

Back 80

Right side, because of lungs congestion, there is greater pressure to push against and right side then has to work harder.

Front 81

MVS leads then to right- heart failure T or F ?

Back 81

True, eventually right side gives up

Front 82

Due to Right heart failure, what other conditions with the patient have?

Back 82

-Liver congested and enlarged
-Ascites and edema in lower extremities
-trouble breathing
-reduced exercise capacity

Front 83

Mitral Regurgitation

Back 83

Leaflets of mitral valve do not close properly, back flow of blood into the left atrium.

Front 84

Proper closure of mitral valve depends on what 3 structures?

Back 84

chordae tendineae, papillary muscles, and a tight mitral annulus (ring)

Front 85

what causes the components of mitral valve to malfunction?

Back 85

Acute myocardial infarct could damage papillary mucsle or ARF could calcify the annulus

Front 86

because of blood regurgitation into the left atrium and the pressure due to extra volume, what happens to the left side of the heart?

Back 86

Both the atrium and ventricle can become dilated to compensate for the greater stroke volume... eventually resulting to left ventricular failure.

Front 87

Mitral Valve Prolapse - MVP

Back 87

mitral valves flop into the left atrium during left ventricular systole (contraction)

mid-systolic click can be heard during auscultation

Flippy floppy

Front 88

MVP affects what % of normal population?

Back 88

About 7% and slightly more common in women

common and usually asymptomatic

Front 89

definitive diagnosis of MVP made with?

Back 89

Echocardiography :)

Front 90

MVP puts patients at more risk for?

Back 90

infective endocarditis(one reason why people take prophylactic antibiotics), arrhythmias, and mitaral insufficiency

Front 91

Aortic Stenosis

Back 91

Calcified and harden aortic valve

Front 92

What are the 3 pathways to aortic stenosis?

Back 92

1.Rheumatic heart disease

2.Congenitally deformed valve (bicuspid): leads to abnormal blood flow, calcium deposits, and hardens valve.

3. Senile: wear and tear with old age

Front 93

most common cause of aortic stenosis?

Back 93

Senile

Front 94

what happens to the Lt ventricle when it struggles against the stiff AO valve?

Back 94

Hypertrophy of Lt ventricle, which leads to Lt ventricle becoming stiff as well

Front 95

with AO valve stenosis the Lt ventricle works harder and then doesn't fill as easy because it is becoming stiff, what happens to the Lt Atrium?

Back 95

Also becomes hypertrophied

Front 96

Aortic Insufficiency (AI)

Back 96

Occurs from abnormalities of the valve leaflets or dilation of the aortic root which stretches leaflets and prevents form closing tightly, creating backflow to Lt ventricle during diastole

Front 97

Acute AI

Back 97

left ventricle can't handle increasing volume and high pressure goes to left artrium and pulmonary tree.

Front 98

Acute AI results in...

Back 98

Severe Dyspnea (difficultly breathing) , and usually is a surgical emergency

Front 99

Chronic AI

Back 99

Left ventricle compensates by dilation and hypertrophy

can last many years with out problems, but eventually will need intervention to prevent heart failure.

Front 100

Infectious Ednocarditis (IE)

Back 100

-One of the most serious infections
-acute and chronic types
-colonization and invasion of heart valves by bacteria

Front 101

what does IE look like?

Back 101

Vegetation of bacteria on heart valves

Front 102

What is the best way to diagnose IE

Back 102

Ultrasound and Blood work

Front 103

IE is life threatening and results in death up to 60%. T or F?

Back 103

True

Front 104

Why is IE so deadly?

Back 104

The bacteria grow and erode valve surface, exposing underlying collagen. Platelets bind to the damage and envelop the organisms into a vegetation. Which then protects the organisms from antibodies and antibiotics.

Front 105

Acute IE

Back 105

-organisms with high virulence ( high ability to cause disease) enter the blood stream and circulate the heart valves.(such as Staphylococcus aureus)
-Causing scaring, valve proforation, perivalvular abcesses
-life threatening and aggressive medical treatment needed.

Front 106

major risk factor for Acute IE?

Back 106

IV drug abusers

Front 107

Acute IE vegetations occur mostly where?

Back 107

Tricuspid and pulmonic valves

Front 108

Chronic IE

Back 108

-Low virulence organisms get into blood stream
-require previously damaged valve to attach
-rheumatic heart disease
-MVP
-prosthetic heart valves

Front 109

what should patients with increase of IE take ?

Back 109

Prophylactic Antibiotics

Front 110

Chronic IE is a slower progressing disease and more likely to kill the patient. T or F ?

Back 110

False: least likely to kill them

Front 111

Both chronic and acute IE are dangerous because?

Back 111

vegetation can break off and embolize to other organs, causeing ishecmic damage.

Front 112

most common organs affect by vegetation embolus

Back 112

Lungs, Brain, Spleen, Kidneys

Front 113

IE treatment of choice?

Back 113

Valve replacement