Foley

Question 1

What are the 5 determinants of myocardial oxygen consumption rate?

Answer 1

afterload

preload

HR

contractility

external cardiac work: amy of work that a ventricle must do to eject blood under pressure

Question 2

Which layers of the heart are compressed more in systole? What can this lead to?

Answer 2

endocardial layers are compressed more than the epicardial layers of the left ventricle

these layers are also under perfused, compared to epicardial layers

this leads to the endocardial layers being more at risk for infarct

Question 3

Which blood flow (diastolic vs systolic, epicardium vs endocardium) is most restricted in CAD?

Answer 3

endocardial diastolic flow

Question 4

What can cause a net underperfusion of the endocardium? (4)

Answer 4

Partial or complete coronary artery obstruction.–> decrease inflow–> O2 debt in endocardium, not made up in diastole

Low aortic pressure relative to left ventricular pressure, esp during diastole (severe systemic hypotension, aortic stenosis)

Increased cardiac work in the presence of partial coronary obstruction.

Severely elevated ventricular end diastolic pressure (in severe CHF)–> increase squeezing of vessels–> decrease blood to endocardium more

Question 5

What has the greatest effects on coronary blood flow?

Answer 5

LOCAL vascular control mechanisms

even though there are plenty of SNS alpha 1 innervations to the heart, the increased metabolism causes vasodilation of the vessels instead of constriction (alpha1)

Question 6

Which autonomic innervations are there to the coronary arterioles?

Answer 6

SNS innervation of alpha 1 receptors –> vasoconstriction(not as much as the metabolic dilation in normal hearts)

beta 2 receptors=> NOT innervated by SNS but can respond to beta-2 agonists causing vasodilation

Question 7

What happens with sympathetic innervation in an abnormal heart?

Answer 7

vasoconstriction that is not overridden by the metabolic effects causing vasodilation==>

Question 8

What is coronary reserve capacity?

How is this affected by CAD? Why is this bad?

Answer 8

the coronary blood flow during maximum coronary vasodilation minus resting coronary blood flow.

CAD decreases the maximum coronary blood flow which decreases the coronary reserve capacity –> increases the chances that the hearts O2 demand will exceed its O2 supply

Question 9

What happens in coronary artery disease?

Answer 9

stenosis of epicardial arteries can increase resistance to blood flow through the affected vessels ->

increases in coronary blood flow during increased metabolic activity may be severely limited in these pts.

will eventually cause ischemia even in resting conditions

Question 10

What is myocardial ischemia?

Answer 10

Occurs any time that the the oxygen demand of the myocardium is not met by the oxygen supply delivered by the coronary circulation.

result in abnormal ventricular performance and abnormal cardiac mm function (may be reversible if coronary flow is restored before permanent damage is done)

Question 11

What are some aspects of abnormal ventricular performance?

Answer 11

found during symptoms of angina

1. increased LVEDV
2. decreased CO, SV, EF
3. ventricular fxn curve shifted down and to the right

Question 12

What are some aspects of abnormal cardiac muscle function?

Answer 12

1. decreased mm fiber shortening and velocity of shortening
2. diminished myocardial force development
3. reduced cardiac mm and ventricular compliance
4. asynergy of contraction (areas do not contract simultaneously or with the same force and velocity)
   * reversible if coronary flow is improved.

Question 13

What is myocardial stunning?

Answer 13

an acute ischemic episode causes mechanical dysfunction of the heart, followed by repercussion

if re-perfuse before permanent damage, may be able to achieve full recovery

Question 14

What is myocardial hibernation?

Answer 14

a gradual, progressive reduction in mechanical performance and metabolic rate which develops as coronary blood flow is gradually decreased (i.e. in CAD)

reduced metabolic rate allows for full function to be restored long after the injury took place

IS capable of some positive inotropic stimuli

Question 15

What is the distinguishing feature of systolic dysfunction heart failure? What are some causes?

Answer 15

reduction in contractility –> decrease ejection fraction ( decreased Ca2+ stored/released from SR

• reduced densities of T-tubules
• decreased affinity of Troponin C for Ca2+

Question 16

What does heart failure do to they frank-starling curve?

Answer 16

shift it down and to the right and flatten it

Question 17

What initially compensatory factors can promote the development of hypertrophy and remodeling in heart failure?

Answer 17

angiotensin II

aldosterone

endothelin-1

Question 18

What can result from the increase in sympathetic stimulation as a result of compensating for heart failure?

Answer 18

increases SNS firing in early compensation can lead to eventual depletion of Norepinephrine from cardiac nn terminals

–> will get limited SNS effects on the heart

• plasma catecholamine levels increase
• severe heart failure: myocardial beta-1 receptor down regulation

Question 19

What can cause abnormal diastole?

Answer 19

• extracellular changes –> reduction in cardiac compliance
• abnormalities in titin (a protein within sarcomeres which contributes to the elasticity)
• inhibition of relaxation
• impaired release of cross-bridges due to low ATP
• leak of Ca2+ ions from SR—> less relaxation