Ischemic Heart Disease

Question 1

what is the first branch off the aorta

Answer 1

coronary arteries

Question 2

what are the branches (in order) off the left coronary artery, and what do they supply?

Answer 2

1. left anterior descending (LAD): anterior 2/3 of septum, anterior LV, anterolateral papillary muscle
2. left circumflex: lateral/posterior LV, left atrium, anterolateral papillary muscle, SA node branch (40%), PDA in L dominant (10%)

*note anterolateral papillary muscle has dual blood supply - protected from ischemia

Question 3

what are the branches off the right coronary artery, and what do they supply?

Answer 3

1. AV nodal artery
2. SA nodal artery (60%)
3. posterior descending artery (80% R dominant): posterior 1/3 of septum, posterior/inferior LV, posteromedial papillary muscle

Question 4

where do the following conduction system parts receive their blood supply from in most individuals?
a. SA node
b. AV node
c. bundle of His
d. L/R bundle branches

Answer 4

a. SA node: SA nodal artery, branch of right coronary artery (40% from left circumflex)

b. AV node: posterior descending artery (RCA)

c. bundle of His: posterior descending artery (RCA)

d. L/R bundle branches: left anterior descending (LCA)

Question 5

which part of the conduction system would be blocked if the blood supply in the posterior descending artery were cut off (for most individuals)?

Answer 5

PDA (of right coronary artery) supplies AV node and bundle of His —> 1st/2nd degree heart block if artery is blocked

Question 6

which part of the conduction system would be blocked if the blood supply in the left anterior descending artery were cut off (for most individuals)?

Answer 6

LAD supplies L/R bundle branches —> bundle branch block will occur if artery is blocked

Question 7

in which coronary arteries is atherosclerosis most likely to occur?

Answer 7

50% occur in proximal LAD (left anterior descending)

25% in right coronary artery (RCA)

Question 8

coronary blood flow is determined by _____

Answer 8

systemic arterial pressure (during diastole)

coronary artery blood flow increases when oxygen demand of the heart increase

Question 9

why can’t myocardium increase oxygen extraction when oxygen demand increases?

Answer 9

coronary artery blood flow increases when oxygen demands of the heart increase

70% of O2 in the coronary arterial blood is removed as blood flows through the heart - it can’t extract any more because it already takes so much

other muscles (outside the heart) are able to extract more when needed, but not the heart

Question 10

where is the lowest oxygen saturation in the cardiovascular system?

Answer 10

coronary sinus blood (veins draining the heart)

Question 11

what maintains constant coronary blood flow over a range of perfusion pressures?

Answer 11

autoregulation: as coronary perfusion pressure increases, the muscular tone of the arterials in the heart increases

Q (flow) = pressure/resistance

via stretch-induced increase in smooth muscle tone (constrict flow to keep it constant)

Question 12

how does metabolic control play a role in autoregulation of the coronary arteries?

Answer 12

autoregulation keeps a constant flow in coronary arteries over a range of perfusion pressures

metabolites are produced from using energy that in turn help regulate smooth muscle tone: adenosine, lactate, CO2, K+ which induce vasodilation

therefore metabolism generates products that increase flow into myocardial tissue - when metabolic needs increase, coronary blood flow increases

Question 13

how does increased HR affect coronary blood flow?

Answer 13

coronary blood flow increases primarily during diastole

as heart rate increases, time for diastole shortens —> coronary artery (esp. left coronary artery) flow is diminished

Question 14

which layer of the heart is most vulnerable when coronary blood flow is limited?

Answer 14

subendothelium - farthest away from coronary arteries

especially during systole when coronary arteries are compressed

Question 15

increased SNS activity results in [vasodilation/vasoconstriction] of coronary arteries?

Answer 15

SNS action on coronary arteries is vasoconstriction via alpha adrenergic receptors

BUTTT

coronary resistance is predominantly under local METABOLIC control (adenosine, CO2, K+ produced by energy expenditure induce vasodilation)

SNS activity increases metabolic activity and myocardial oxygen consumption, so actually net effect is that increased SNS activity results in vasodilation

[this is considering a normal, healthy heart - cocaine is an example when SNS-induced vasoconstriction out weighs metabolic-induced vasodilation]

Question 16

how is ischemic heart disease divided?

Answer 16

chronic stable angina
or
acute coronary syndrome (ACS) - includes unstable angina, non-ST elevation MI, and ST elevation MI

Question 17

what are the #1 and #2 causes of narrowing of blood vessel lumen, which can lead to ischemia?

Answer 17

1. atherosclerosis
2. vasospasm

Question 18

what is the CV consequence of Kawasaki disease?

Answer 18

Kawasaki disease: vasculitis syndrome particularly affecting children, can lead to coronary artery aneurism

Question 19

describe how ischemia alters cardiac biochemical function, mechanical function, and electrical function

Answer 19

biochemical: increase in anaerobic metabolism (glucose to lactate) produces acidosis, ATP depletion causes ATP pump to stop working (—> K+ leakage)

mechanical: ATP depletion impairs relaxation* and contractibility, papillary muscle dysfunction causes mitral regurgitation

electrical: ventricular arrhythmias can lead to sudden cardiac death

*recall muscle relaxation also requires ATP!

Question 20

describe hibernating myocardium

Answer 20

heart has reduced its level of activity due to chronic inadequate blood supply

chronic ischemia without acute injury, revascularization can lead to gradual return to normal (reversible)

Question 21

what is the risk of transient ischemia vs prolonged ischemia?

Answer 21

transient ischemia —> stable angina

prolonged ischemia —> myocardial infarction

Question 22

what is angina pectoris

Answer 22

paroxysmal, recurrent attacks of substernal chest discomfort caused by transient myocardial ischemia

Question 23

what causes the sensation of angina associated with myocardial ischemia?

Answer 23

ischemic myocardium releases adenosine, lactate, bradykinin, and histamine (vasodilators)

cardiac sympathetic afferent impulses converge with impulses from somatic structures, causing referred cardiac pain

Question 24

how do patients typically describe their pain from stable angina pectoris?

Answer 24

visceral pain is felt differently than somatic pain

usually described as pressure/tightness/discomfort in retrosternal area (not well localized) that lasts 2-10 minutes (crescendo-decrescendo)

radiates to ulnar aspect of left arm, neck, jaw

Question 25

how does a patient with stable angina pectoris usually present?

Answer 25

episodic clinical symptoms from transient myocardial ischemia

usually has fixed epicardial coronary artery stenosis

usually asymptomatic with normal activity - symptoms occur with increased myocardial oxygen demand because blood flow does not increase with exercise as it should (>70% occlusion)

slowly developing lesions can allow collateral circulation to develop (more common in R side of heart because wall is thinner than L side)

Question 26

what are the 3 P’s that have strong negative predictive value of cardiac ischemia?

Answer 26

1. Pleuritic: if it’s worse with inspiration, it’s more likely due to a lung issue
2. Position: if it’s worse lying down, it’s more likely pericarditis
3. Palpation: if pressing makes it worse, probably not ischemia

Question 27

explain why stable angina might wake a patient from sleep?

Answer 27

changes in breathing during sleep can decrease O2 tension

increased blood volume in the heart while supine can increase wall stress

changes in coronary vasomotor tone at night can cause vasospastic angina

Question 28

what does ST segment depression vs elevation indicate?

Answer 28

ST depression: subendocardial ischemia (incomplete occlusion)

ST elevation: transmural ischemia (MI), pericarditis

*this is why MI ECG progresses from ST depression to ST elevation, because ischemia gets worse and becomes transmural

Question 29

what does the ST segment of an ECG correspond with in a myocyte action potential?

Answer 29

ST segment corresponds with phase 2 (plateau phase) - should be an isoelectric (silent) phase in healthy myocytes

Question 30

which 2 drugs classes are typically prescribed for pectoral angina and what are they used for?

Answer 30

1. anti-angina drugs:
   a. nitrates to address symptoms as needed - systemic venodilation decreases LVEDV
   b. beta blockers to prevent angina symptoms from developing - reduce myocardial O2 demand
2. anti-platelet drugs:
   a. aspirin: thromboxane inhibitor
   b. clopidogrel: ADP receptor antagonist

Question 31

what is the clinical effect of vasospastic/variant/Prinzmetal angina?

Answer 31

transient and reversible constriction of coronary vasculature leading to ischemia

impaired vascular smooth muscle tone in coronary arteries, linked to vascular smooth muscle hyper-reactivity, low NO (endothelial dysfunction), and autonomic imbalances

Question 32

what are the distinguishing features of Prinzmetal “vasospastic” angina?

Answer 32

transient and reversible constriction of coronary vasculature leading to ischemia

diagnosis of exclusion - usually younger patients lacking typical risk factors, angina attacks unrelated to physical activity/HR/BP, attacks occur at rest and at night for 5-15minutes

PE is unremarkable but may see transient ST elevation or depression

Question 33

which patients are most at risk for asymptomatic “silent” ischemia?

Answer 33

silent ischemia: objective evidence of myocardial ischemia in absence of chest discomfort or “anginal equivalent” (atypical signs of angina)

higher risk in elderly and patients with diabetes mellitus