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14 Cards in this Set

  • Front
  • Back
Clinical Spectrum of CAD
ATHEROMA
Asymptomatic
Exertional angina
Angina at rest
THROMBUS
Angina at rest
Unstable angina
Acute MI

CHF
Death
Normal Coronary Physiology
-Myocardium extracts all the oxygen from the blood so to increase delivery there must be increased coronary flow

-Coronary flow can increase during exercise by about 4x baseline values

-Exercise-induced fatigue is not a cardiac problem
Normal Coronary Physiology during Exercise
During exercise coronary blood flow must go up
Remember:
Pressure = Flow X Resistance

-The mechanism of increased flow is by means of decreased coronary vascular resistance

-Coronary reserve is the amount flow can go up from baseline until it is maximized
Determinants of Oxygen Demand
1) Heart rate
2) Contractility
3) Wall Stress:
Law of LaPlace
s = Pressure x Radius/2 Wall thickness
Process by which Coronary Artery Disease leads to symptoms:
Presence of occlusive lesion requires:

1)Vasodilation at rest to maintain baseline flow

2)Vasodilator reserve is reduced

3)Thus, with exercise the demand for oxygen exceeds the vessel’s ability to supply flow

4)When there is a supply/demand imbalance the patient develops ischemia:

5) Symptoms: pain, reduced function, ECG changes
Angina Pectoris is a consequence of what changes in myocardial oxygen demand and supply?
Angina Pectoris is a consequence of myocardial oxygen demand exceeding supply

-Supply limited by fixed atherosclerotic lesion (coronary blood flow)

-Demand increased by coronary vasoconstriction/ vasospasm (HR, contractility, systolic bp, LV thickness, LV volume)
Describe the symptoms of Angina Pectoris
1) Dull, pressure-like chest pain

2) Exertional in nature, relieved by rest

3) May radiate to arm, neck, shoulders

4) May be associated with:
-shortness of breath
-diaphoresis
-nausea/vomiting

5) Usually lasts ~ 5 minutes

6) May be relieved quickly by nitroglycerin
What is the significance of the defined threshold assoc. with Angina Pectoris?
Usually has a defined threshold:

-The double product =
Heart rate X blood pressure

-Threshold is generally stable for a given patient

-When the threshold is variable this must be explained - could be due to vasomotion, anemia, or other causes
Effect of vasospasm with an atherosclerotic lesion (40% obstruction)
1) Momentary vasospasm ->
2) Transient Increased obstruction (up to 80%)->
3)Ischemia of downstream tissues
Clinical Improtance of Coronary Vasospasm
1) Rest Angina

2) Lower exertional threshold for angina

3) Possible precipitant of acute MI
Unstable Angina defined
Stable angina versus unstable angina

1) USA: Progressive severity of pain, reduction in threshold for onset of pain

2) UA associated with endothelial disruption and partially occlusive thrombus in the coronary artery

3) Step change in size of vessel leads to acute exacerbation of symptoms
Diagnosis and Treatment of Unstable Angina
1) Absolute contraindication to exercise stress testing

2) ECG: If associated with ST elevation constitutes a medical emergency: MI in the making

3) Treatment includes nitrates, antiplatelet agents, anticoagulation

4) Patient should be taken to cardiac catheterization
Acute MI Diagnosis
1) Typical Chest Pain

2) Evolving ECG changes: T wave inversion, ST segment elevation, Q waves

3) Elevation of cardiac enzymes: CPK-MB
True Aneurysm Defined
1) A true aneurysm is a well-defined, thin-walled fibrotic segment of the ventricle that protrudes beyond the remainder of the cardiac surface\

2) Represents healed myocardial injury

3) Abnormal segments may display absence of motion(akinesis) or paradoxical expansion during mechanical systole (dyskinesis)