Week 2: ischemic heart disease Flashcards

1
Q

Give clinical definition of ischemic heart disease

A

Condition in which imbalance between myocardial oxygen supply and demand results in myocardial hypoxia and accumulation of waste metabolites, most often caused by atherosclerotic disease of the coronary arteries (often termed coronary artery disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe determinants of myocardial oxygen supply

A

-depends on oxygen content of blood (remains fairly constant) and rate of coronary blood flow
CORONARY BLOOD FLOW
-Q proportional to P/R
-predominance of coronary perfusion takes place during diastole, compression of branches occurs during systole
-also depends on coronary vascular resistance: influenced by external compression and intrinsic regulation
-subendothelium subjected to greater force during systole contraction, most vulnerable to ischemic damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the factors that influence coronary vascular resistance.

A
  • heart can’t increase oxygen extraction since at basal state already extracts most of oxygen, so increase in blood flow must be used to meet additional oxygen requirement
    1. local metabolites
  • adenosine is potent vasodilator (produced by accumulation of ADP and AMP which degrade to adenosine). Decreases Ca2+ entry into cells
    2. Endothelial factors
  • vasodilators: NO, protacyclin, EDHF (endothelium derived hyper polarizing factor)
  • vasoconstrictor: Endothelin-1
    3. Neural factors
  • sympathetic receptors have major role
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List and describe the major determinants of myocardial oxygen demand.

A
  1. Afterload-resistance
  2. Preload-stretch
  3. heart rate
    - increased hr, more contractions, more ATP consumed, more oxygen needed
  4. contractility
    - greater force of contraction requires greater oxygen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe wall stress and LaPlace’s principle

A

-Laplace= P x r/2h
P=intraventricular pressure, r=radius of ventricle
h=ventricular wall thickness
-raises wall stress: aortic stenosis, hypertension (increase P), mitral/aortic regurg (raise r)
-reduce wall stress: hypertrophy (increase h, force spread over greater muscle mass), drugs that reduce LV filling and size
-myocardial oxygen consumption more affected by aortic pressure/rate/inotropy than stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the pathophysiology of ischemia in atherosclerosis?

A
  1. fixed vessel narrowing with reduction in coronary vessel perfusion distal to plaque
  2. abnormal vascular tone due to endothelial cell dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Determinants of coronary blood flow.

A
Poiseuille's law
A=deltaPpi r^4/ (8nL)
or resistance can be expressed as: 
R=8nL/(pi r^4) 
n=viscosity, L =vessel length
-consequences of stenosis by plaque depends on length of vessel and reduction of radius (degree of narrowing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Determinants of coronary blood flow: vasomotor tone and coronary flow reseve

A

-if stenosis narrow lumen diameter 60%, resting blood flow normal, but maximal blood flow reduced that even with fully dilated distal resistance vessels. So when O2 demand increases during physical exertion, coronary flow reserve isn’t enough, oxygen demand is greater than supply, results in myocardial ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe consequences of myocardial ischemia.

A

Depends on severity and duration of oxygen supply and demand imbalance.

  • stunned myocardium: after severe acute, transient ischemia, tissue has prolonged systolic dysfunction even after return of normal blood flow. Gradual recovery of contractile function.
  • hibernating myocardium: chronic ventriuclar contractile dysfunction due ot persistently reduced blood supply. Multivessel CAD usually causes. If blood flow restored, can reverse damage.
  • myocardial infarct: irreversible necrosis, >20-30 min of total occlusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe clinical syndromes of ischemia.

A
  1. stable angina: lumen narrows by plaque, inappropriate vasoconstriction. May have sufficient oxygen at rest, but has chest discomfort with physical exertion
  2. unstable angina: sudden increase and duration of ischemic episodes in last 2 months, occurring with less exertion or even at rest. >90% stenosis, May have plaque rupture, platelet aggregation, thrombus formation, or unopposed vasoconstriction.
  3. Varient angina: intense vasospasm reduces coronary O2 supply and results in angina. At rest. No overt plaques, may be due to endothelial dysfunction.
  4. Silent ischemia: no angina, but other manifestations. detected by stress testing, or EKG monitoring.
  5. Syndrome X: angina with ischemia inducible on stress testing but no evidence of significant coronary obstruction on angiogram. Microvascular dysfunction in resistant vessels along with increased pain perception. Good prognosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe clinical history of chronic stable angina.

A
  • Chest pain: pressure or discomfort, lasts a few minutes, diffuse in retrosternal area with radiation
  • abates when stressor is gone of nitroglycerin is taken
  • precipitated by exercise, anger, emotional excitement, large meal, cold weather
  • risk factors are risk factors for CAD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Differential diagnosis for chest pain.

A

Cardiac
-MI, CAD, coronary spasm, endothelial dysfunction, HTN,
-pericarditis: can last hours to days
GI
-GERD, peptic ulcer, esophageal spasm, biliary colic
MS
-costochondral syndrome, cervical radiculitis
If patient can point to pain with one finger, probably not cardiac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the physical examination of a patient with ischemic heart disease.

A
  • often normal
  • look for signs of extra cardiac atherosclerosis: signs of peripheral vascular disease (pulses), cerebrovascular disease
  • signs of HTN and diabetes: elevated bp, retinal vascular changes, S4 gallop
  • Possible findings during episode of angina: rales, mitral regurg, increased hr and bp, S4, dyskinetic apical impulse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe diagnostic studies for ischemic heart disease: ECG and standard exercise testing

A
  1. ECG: normal in half of patients with chronic stable angina. Becomes abnormal during episode of chest pain
    - subendocardial ischemia: ST depression (downsloping), ST depression (horizontal), T wave inversion
    - transmural ischemia: ST elevation
  2. Standard exercise testing
    - exercise until able to reach target heart rate is 85% max predicted hr (MHR), angina develops, ECG signs of Myocardial ischemia, or patient too fatigued
    - treadmill or bicycle
    - Positive test: chest pain or >1mm horizontal or downsloping ST depression
    - goal: ID high risk criteria and patients with normal stress test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe diagnostic studies for ischemic heart disease: stress test w/ imaging, phamacologic stress test

A
  1. Stress test+imaging
    - for baseline ECG abnormalities, or condition that interferes with interp of exercise EKG, can’t achieve 85% MPHR, high suspicion of CAD
    - use stress echocardiography or stress radionuclide myocardial perfusion imaging
  2. Pharmacologic stress test
    - for those who can’t exercise
    - adenosine to dilate arteries, dobutamine increases contractility and heart rate
    - nuclear detection of CAD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe diagnostic studies for ischemic heart disease: Coronary angiography

A
  • for high risk stress test (left main or 3 vessel CAD), high desk clinical criteria but can’t do noninvasive testing, patients with failure of medical therapy or unstable clinical presentation, survival of sudden death.
  • goal: identify patients who have survival benefit with revascularization (LT main,3 vessels disease or 2 vessel with proximal LAD and LV dysfunction)
17
Q

Describe natural history of chronic angina.

A

-stable angina/asymptomatic ischemia for years, intermittent ACS (non-ST elevation), then myocardial infarction and sudden death

18
Q

Describe the treatment of stable angina, including pharmacologic and PCI (percutaneous coronary intervention).

A
  1. Medical therapy:
    - reduce angina/ischemia: beta blockers, organic nitrates, calcium channel blockers
    - reduce risk of ACS and mortality:cut smoking, more exercise, diet change, txt for diabetes, HTN, hyperlipidemia
    - reduce risk of ACS and mortality: aspirin or aspirin alternatives (no dual anti platelet therapy), lipid lowering agents (statins), ACE inhibitors
  2. Coronary revascularization: reduces angina/ischemia, but doesn’t reduce MI risk
    - indications: high risk coronary anatomy, failure of medical therapy
    - PCI: balloon angioplasty, place stent
    - coronary artery bypass graft
19
Q

What is the CCS classification for grading the severity of angina?

A

I. no angina with ordinary physical activity. Angina with strenuous or prolonged exertion
II. early onset limitation of ordinary activity.
III. Marked limitation of ordinary activity
IV. inability to carry out any physical activity without chest discomfort. Angina during rest.