Cad/mi

Front 1

1. chronic pathological condition in which coronary blood flow is inadeqaute to meet myocardial needs
2. #1 cause of 1?
3. Arterial injury caused by accumulation of hyperproliferative cells and lipids in vessel intima

Back 1

1. CAD
2. coronary atherosclerosis
3. Atherosclerosis

Lifetime risk is 1/2 for men 1/3 for women

Front 2

1. Type of cholesterol that accumulated in macrophages (foam) cells in vessel wall?
2. What cholesterol is chemotactic and mitogenic for macrophages?

Back 2

1. Foam cells
2. LDL

VSM cells transformed from contractile to a secretory, hyperproliferative phenotype; endothelial injury causes platelet adherence & release of PDGF; fibrin accumulates

Front 3

1. Flow in coronary a. is controlled by metabolic or nervous?
2. Resistance vessel that controls flow?
3. Hrt phase in which vessels are impeded? why?

Back 3

1. Metabolic - so autoregulated
2. Arterioles
3. Systole, due to contraction. Subendocardial layers are most effected

Front 4

1. Scoronary arterioles dilated or constricted if there is a CA. stenosis?
2. What does the stenosis do to coronary reserve?
3. How big of a reduction in coronary a. diameter can be tolerated at rest w/ no reduction in flow?

Back 4

1. They dilate to compensate for the increased resistance
2. Decreases it -> so better chance of becoming SOB w/ exertion
3. 75%

Q = (Pi - Ps) + (Ps-Po) / Rs + Rarterioles

Front 5

1. % occlusion that will decrease maximal coronary flow?
2. If there is no coronary reserve, will metabolic flow regulation occur?
3. why is the ventricular endocardium more sensitive to ischemia than epicardium?

Back 5

1. 50%
2. no - already maximally dilated
3. Systolic compressive forces limits blood flow more significantly in this area so less reserve

Front 6

1. What occurs when vessels nearest the ventricles are maximally vasodilated; and vessels more superficial dilate due to metabolic stimuli... Leads to a drop in pressure?
2. Imbalance between O2 supply & consumption causes?

Back 6

1. Pressure drops; more flow stays superficial and the ischemia worsens -> Ka coronary steal phenomenon
2. Myocardial ischemia

Front 7

1. 3 factors that determine O2 demand
2. 2 factors that determine O2 supply
3. Arrange SV, HR and ventricular systolic pressure in terms of O2 consumption

Back 7

1. Contractile state, HR, Wall tension
2. AV O2 difference, Regional myocardial distribution
3. VSP = HR > Stroke vlume

Pressure work is more costly than volume work

Front 8

Determinants of Myocardial Oxygen Consumption (MVO2)
1. Ventricular systolic pressure - Very important! A 50% increase in LVSP will result in about 50% increase in oxygen consumption
2. Stroke volume - relatively less important. 50%increase in LVSV will result in about 5% increase in oxygen consumption.
3. Heart rate - Very important! 50% increase in HR produces about 50% increase in oxygen consumption.

Back 8

4. LV chamber radius - quantitative effect unclear, but likely important, especially in pathology, via effects on LV wall tension.
T (wall tension) = P (LVP) X R (LV radius)

5. Contractility - increased contractile state results in increased oxygen consumption. Effects unclear, likely related to EC-coupling.

Front 9

1. What is the pressure rate product?
2. ST elevation is an indication of?
3. ST depression/downsloping or T wave inversion is indicative of?

Back 9

1. determination of myocardial oxygen consumption
2. Transmural ischemia
3. Subendocardial ischemia

Front 10

1. Drop in MAP after MI is offset by what responses?
2. What do the responses AE?

Back 10

1. Baroreceptor (^ sympathetic stimulation - other areas become hyperfxl) & RAAs
2. increases the O2 and energy demand of the compromised heart --> if CO stays below normal can proceed to hrt failure & circulatory shock

Front 11

MI:
1. Sympathetic stimulation of viable myocardium and blood vessels to reestablish normal MAP. Contractility of entire heart partially recovers due to sympathetic activation of remaining working myocardium.
2. Area surrounding ischemia/infarct becomes hyperfunctional due to increased preload and sympathetic stimulation of cardiac myocytes
3. Expansion of extracellular and blood volumes due to autotransfusion and reduced urinary output (longer-term effects).

Back 11

4. Sympathetic stimulation elicits positive inotropy, elevated preload due to venous contraction, and expansion of blood volume; these compensations serve to return cardiac output back toward normal, but at the cost of increased energy demand in a compromised heart!
5. If these compensations return CO to normal, patient recovers. However, if CO remains below normal for extended period of time, heart failure and circulatory shock (cardiogenic shock) ensue.

Front 12

MI consequences:
a. Severely reduced CO, heart failure, hypotension, and possibly shock and death (>40% infarct of LV)!
b. Arrhythmias: extremely common and often the
cause of death from MI! Often ventricular fibrillation causes early sudden death.
c. Cardiac “blowout”: infarcted area loses mechanical strength as cells die and the supporting matrix is remodeled by the scarring process. A fissure (rupture) may occur in the wall, leading to ejection of blood into the pericardium!

Back 12

d. Edema: especially pulmonary edema with left sided failure; reduced contractility of LV myocardium leads to rise in left atrial volume and pressure; consequently, pulmonary capillary
hydrostatic pressure rises leading to increased filtration, interstitial fluid volume and lymph flow
Peripheral edema w/ rt sided failure
e. Papillary m. infarction common (40% of posterior wall) gives valve dysfxn

Front 13

1. Type of a. that will lower odds of MI and make them less severe

CAD interventions: pharm, balloon angioplasty, coronary atherectomy, CABG, Coronary stent

Back 13

1. Collateral circulation - usu limited development; and inadequate

Women are still not receiving standard medical Rx in MI

Front 14

1. What can decrease mortality in pts w/ ischemic hrt disease?
2. What will NO do to coronary flow (ischemia) [angiogenesis]
3. Collateral growht

Back 14

1. Exercise by coronary collateral growth, coronary blood flow increase, and increase coronary endothelial fxn
2. improve (decrease) [enhance]
3. promote