Ischemic Heart Disease Flashcards
what is the first branch off the aorta
coronary arteries
what are the branches (in order) off the left coronary artery, and what do they supply?
- left anterior descending (LAD): anterior 2/3 of septum, anterior LV, anterolateral papillary muscle
- 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
what are the branches off the right coronary artery, and what do they supply?
- AV nodal artery
- SA nodal artery (60%)
- posterior descending artery (80% R dominant): posterior 1/3 of septum, posterior/inferior LV, posteromedial papillary muscle
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
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)
which part of the conduction system would be blocked if the blood supply in the posterior descending artery were cut off (for most individuals)?
PDA (of right coronary artery) supplies AV node and bundle of His —> 1st/2nd degree heart block if artery is blocked
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)?
LAD supplies L/R bundle branches —> bundle branch block will occur if artery is blocked
in which coronary arteries is atherosclerosis most likely to occur?
50% occur in proximal LAD (left anterior descending)
25% in right coronary artery (RCA)
coronary blood flow is determined by _____
systemic arterial pressure (during diastole)
coronary artery blood flow increases when oxygen demand of the heart increase
why can’t myocardium increase oxygen extraction when oxygen demand increases?
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
where is the lowest oxygen saturation in the cardiovascular system?
coronary sinus blood (veins draining the heart)
what maintains constant coronary blood flow over a range of perfusion pressures?
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)
how does metabolic control play a role in autoregulation of the coronary arteries?
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
how does increased HR affect coronary blood flow?
coronary blood flow increases primarily during diastole
as heart rate increases, time for diastole shortens —> coronary artery (esp. left coronary artery) flow is diminished
which layer of the heart is most vulnerable when coronary blood flow is limited?
subendothelium - farthest away from coronary arteries
especially during systole when coronary arteries are compressed
increased SNS activity results in [vasodilation/vasoconstriction] of coronary arteries?
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]
how is ischemic heart disease divided?
chronic stable angina
or
acute coronary syndrome (ACS) - includes unstable angina, non-ST elevation MI, and ST elevation MI
what are the #1 and #2 causes of narrowing of blood vessel lumen, which can lead to ischemia?
- atherosclerosis
- vasospasm
what is the CV consequence of Kawasaki disease?
Kawasaki disease: vasculitis syndrome particularly affecting children, can lead to coronary artery aneurism
describe how ischemia alters cardiac biochemical function, mechanical function, and electrical function
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!
describe hibernating myocardium
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)
what is the risk of transient ischemia vs prolonged ischemia?
transient ischemia —> stable angina
prolonged ischemia —> myocardial infarction
what is angina pectoris
paroxysmal, recurrent attacks of substernal chest discomfort caused by transient myocardial ischemia
what causes the sensation of angina associated with myocardial ischemia?
ischemic myocardium releases adenosine, lactate, bradykinin, and histamine (vasodilators)
cardiac sympathetic afferent impulses converge with impulses from somatic structures, causing referred cardiac pain
how do patients typically describe their pain from stable angina pectoris?
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
how does a patient with stable angina pectoris usually present?
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)
what are the 3 P’s that have strong negative predictive value of cardiac ischemia?
- Pleuritic: if it’s worse with inspiration, it’s more likely due to a lung issue
- Position: if it’s worse lying down, it’s more likely pericarditis
- Palpation: if pressing makes it worse, probably not ischemia
explain why stable angina might wake a patient from sleep?
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
what does ST segment depression vs elevation indicate?
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
what does the ST segment of an ECG correspond with in a myocyte action potential?
ST segment corresponds with phase 2 (plateau phase) - should be an isoelectric (silent) phase in healthy myocytes
which 2 drugs classes are typically prescribed for pectoral angina and what are they used for?
- 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 - anti-platelet drugs:
a. aspirin: thromboxane inhibitor
b. clopidogrel: ADP receptor antagonist
what is the clinical effect of vasospastic/variant/Prinzmetal angina?
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
what are the distinguishing features of Prinzmetal “vasospastic” angina?
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
which patients are most at risk for asymptomatic “silent” ischemia?
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
