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22 Cards in this Set

  • Front
  • Back
Compare systolic and diastolic heart failure:
Systolic: result of progressive deterioration of myocardial contraction where damaged myocardium contracts weakly and chambers to not empty adaquately. This is caused by ischemic injury, pressure, or volume overload

Diastolic heart failure: is caused when heart chambers do not sufficiently relax, expand, and fill during diastole. This is caused by left ventricular hypertrophy, myocardial disease, or constrictive pericarditis.
Compare and contrast effects of left and right sided heart failure.
Left sided: results in damming of blood in pulmonary circulation causing pulmonary edema and congestion. Also causes decreased peripheral blood flow causing renal hypoperfusion, m. fatigue, and cerbral hypoperfusion.

Right sided - this causes engorgement of systemic and portal venous circulation. This can cause peripheral edema, pleural effusions, ascites, hepatic congestion, congestive splenomegaly, and renal congestion.
Explain the CO and ejection fraction of diastolic heart failure.
CO is reduced but the ejection fraction may be normal.
What is ischemic heart disease?
The imbalance between the supply and demand of the heart for oxygenated blood either through reduced coronary blood flow or increased mycardial demand exceeding vascular supply.
Describe stable angina pectoris:
This is transcient myocardial ischemia without necrosis caused by a fixed coronary artery stenoses. It comes on with stress or activity and is relieved with rest and vasodilation.
Describe unstable angina pectoris:
This is seen as a preinfarction angina that is caused by an atherosclerotic plaque that has been disrupted caused a partially occluding platelet aggregation or thrombus. This angina is produced with less effort (no stress needed) and lasts longer than stable angina.
What is Prinzmental angina?
This is angina caused, not by coronary artery disease, but instead by coronary artery vasospasms that occurs at rest.
Myocardial infarction

What causes a transmural infarction?
Ischemic necrosis involving the full thickness of the ventricle. This is caused by an OCCLUSIVE coronary thrombus overlying a disrupted atherosclerotic plaque. But in 10% of the cases there is no evidence of atherosclerotic plaque disruption or thrombos
Myocardial infarction

What is a Subendocardial (nontransmural) infarct?
It is ischemic necrosis limited to the inner one third - one half of the ventricular wall. This is caused by diffuse stenosing coronary atherosclerosis and reduction of coronary flow and is RARELY evidence of plaque disruption. This can be caused by prolonged and severe hypertenstion.

What are the gross and microscopic changes in myocardium 30 min - 4 hrs post infarct?
At 30min to 4 hrs there are no gross or microscopic changes
What are the gross and microscopic changes in myocardium 4-12 hrs post infarct?
Beginning of coagulation necrosis can be seen with the myocardial fibers becoming more wavy

What are the gross and microscopic changes in myocardium 12-24 hrs post infarct?
You can see gross dark myocardial mottling. And can see ongoing coagulation necrosis and pynknosis of nuclei.

What are the gross and microscopic changes in myocardium 1-3 days post infarct?
There is a loss of myocardial nuclei and myocytes and neutrophils begin to infiltrate.

What are the gross and microscopic changes in myocardium 3-7 days post infarct?
There is yellow-tan softening of the tissue from myocyte disintegration and the phagocytosis of dead cells. There is now tremendous infiltration of neutrophils.

What are the gross and microscopic changes in myocardium 7-10 days post infarct?
Can see phagocytosis and early granulation tissue with fibrotic tissue and alot of vascular tissue.
What are the gross and microscopic changes in myocardium 10-14 days post infarct?
Graulation tissue and more blood vessel and deposition of fibrosis.
What are the gross and microscopic changes in myocardium 2-8 wks post infarct?
Scar formation.
What are the seven treatments of a myocardial infarction?
1. heparin
2. antiplatelet agents
3. oxygen
4. thrombolytic therapy
5. beta blockers
6. nitrates
7. morphine
What are two of the complications of MIs that can result after the infarct? When do they occur?
1. Myocardial rupture (days 3-7)
2. Pericarditis (days 2-3 after transmural infarct)
What is Left Sided hypertensive heart disease?
Heart disease caused by the adaptive response to pressure overload.
Why is left ventricular hypertrophy from left sided hypertensive heart disease so damaging? (5)
It causes an:
1. increase rate of myocyte protein synthesis
2. increased size of myocytes
3. increased number of sarcomeres and mitochondria
4. increased mass and size of heart
5. increased metabolic requirements for newly enlarged heart which can cause cardiac dysfunction
What is pulmonary (right sided) hypertensive heart disease? aka?
Cor Pulmonale-
Caused by disorders of the lungs and pulmonary vasculature (ex COPD, pulmonary fibrosis, PE, sleep apnea, obesity). This causes right ventricular hypertrophy, dilatation, right sided heart failure, hepatomegaly, splenomegaly, and peripheral edema.