Flashcards in Ischemic Heart Disease Deck (27):
Heart is unable to pump blood sufficiently to meet the neds of tissue
-ventricle unable to fill with or eject blood
-"congestive heart failure"
-usually progressive condition with poor prognosis
Systolic heart failure
deterioration of myocardial contraction
Diastolic heart failure
Inability of heart chamber to relax, expand, and adequately fill during diastole
Left sided heart failure
Signs and Symptoms
3. Aortic/mitral valve disease
4. Nonischemic myocardial diseases
1. Damming of blood in pulmonary circulation
2. Diminished peripheral blood flow
Signs and Symptoms:
-shortness of breath
Right sided heart failure:
Signs and Symptoms
1. Left sided heart failure (#1 cause)
2. cor pulmonale-lung disease or primary pulmonary hypertension
Signs and symptoms:
-peripheral edema, ascites
What is stable angina pectoris?
-chronic stenosing coronary atherosclerosis (>75% reduction of lumen area)
1. increased cardiac demand and workload needs unmet
-substernal chest pressure
2. physical activity, emotional excitement
-relieved with rest
-ST segment depression-subendocardial ischemia
What is unstable angina pectoris?
Atherosclerotic plaque disruption-->partially occluding thrombus
-thrombogenic plaque components, subendothelial basement membrane exposed
-platelet activation, aggregation
-frequent, less effort, at rest, longer duration
ST segment depression-subendocardial ischemia
What makes plaques vulnerable?
1. lipid rich atheromas
2. thin fibrous caps
What is prinzmetal variant angina?
coronary artery spasm
unrelated to physical activity, heart rate, or bp
-responds to vasodilators
ST segment elevation-transmural ischemia
How does a myocardial infarction happen?
Platelet adhesion, aggregation activation
-->occlusive thrombus formation
TIme of infarction is reversible what time is irreversible?
30 irreversible, coagulative necrosis
What are transmural vs. nontransmural infarcts?
transmural: occlusive thrombus
nontransmural: subendocardial infarct or microinfarcts
no gross or light microscopic changes
microscopic changes: coagulative necrosis
-start losing nuclei and eosinophilia
Gross: dark mottling
Microscopic: ongoing coagulation necrosis
-pyknosis of nuclei
Microscopic: loss of nuclei and myocytes
-myocyte disintegration, phagocytosis of dead cells
well developed phagocytosis and early granulation tissue
How do patients with an MI present?
-crushing substernal chest pain, dyspnea, diaphoresis
-tachycardia, pulmonary congestion and edema
-10-15% silent : elderly, diabetic
What labs do you look at?
myoglobin-peaks early but insensitive
CK-MB-goes down faster
Troponin-peaks lasts long time
What does Triphenyltetrozolium chloride stain stain for?
Infarcted myocardium does not stain due to enzyme depletion
What are the treatments to myocardial infarction?
Aspirin and other antiplatelet agents
What can happen with reperfusion?
reperfusion injury-restoration of blood flow leads to local myocardial damage
-free radical prodcution
-myocyte hypercontracture, increased Ca
-leukocyte aggregation-->proteases, elastases
What are some complications of myocardial infarction?
1. cardiogenic shock
-severe pump failure
-10-15% of patients
-large infarcts (>40% of ventricle)
3. myocardial rupture
-free wall-hemopericaridum, cardiac temponade
4. Acute pericarditis
5. Ventricular aneurysm
6. progressive heart failure