Flashcards in Ischemic Heart Disease Deck (35):
What is congestive heart failure?
The ability of the heart to pump is unable to meet the needs of tissues
Systolic Heart Failure
Deterioration of myocardial contraction and so myocytes cannot generate enough force in contraction
Diastolic Heart Failure
Inability of heart chamber to relax, expand, and adequately fill during diastole
Right Sided Heart Failure
Leads to the engorgement of the systemic and portal venous circulation that can cause edema
Left Sided Heart Failure
Damning of blood in pulmonary circulation causes diminished peripheral blood flow that can lead to pulmonary edema
Biventricular Heart Failure
Shows symptoms of both right and left sided heart failure
What is the pathogenesis of heart failure?
It occurs as a result of decreased perfusion to the coronary arteries in a combination with increased myocardial demand.
What is the main cause of right side heart failure?
Left sided heart failure
What are the 3 types of angina?
What are the features of stable angina?
Large stenosis of the coronary artery due to atherosclerosis and in times of increased O2 demand such as exercise will cause chest pain that subsides with rest
What are the features of unstable angina?
The necrotic core of an atheroma is exposed due to an atherosclerotic plaque disruption that causes thrombus formation that can occlude coronary arteries even at rest.
What plaques are the most vulnerable for unstable angina?
Vulnerable plaques are ones with very thin fibrous caps
What are the features of Prinzmetal angina?
Coronary artery vasospasm cause chest pain that occurs even at rest
What is the pathogenesis of a myocardial infarction?
Plaque disruption leads to the formation of an occlusive thrombus that leads to infarction
What is another mechanism of MI that does not involve thrombus?
Cocaine can cause vasospasm that lead to an MI
What are the EKG changes with an MI?
Characteristically ST segment elevation on EKG
corresponding to distribution of occluded coronary artery
Ischemic necrosis limited to inner one third, or at most one half of ventricular wall AKA subendocardial
Ischemic necrosis involves full (or nearly full)
thickness of ventricle
What is often the cause of nontransmural infarcts?
In majority of cases there is diffuse stenosing coronary atherosclerosis and reduction of coronary flow with rarely evidence of plaque disruption or superimposed thrombus
What is often the cause of transmural infarcts?
Occlusive coronary thrombus overlying a disrupted atherosclerotic plaque
What is the first tissue of the heart to infarct?
What compounding factor can cause a circumferential subendocardial infarct?
Global hypotension - coronaries are not well perfused
MI Changes 30 minutes to 4 hours
o No gross or microscopic changes
MI Changes 4-12 hours
o Beginning coaglulation necrosis
MI Changes 12-24 hours
o Gross – dark myocardial mottling
o Microscopic – ongoing coagulation necrosis,
pyknosis of nuclei
MI Changes 1 to 3 days
o Loss of myocardial nuclei and myocytes
o Neutrophilic infiltrate
MI Changes 3-7 days
o Gross - yellow-tan softening
o Microscopic - myocyte disintegration, phagocytosis
of dead cells
MI Changes 7 to 10 days
o Well-developed phagocytosis and early granulation tissue
MI Changes 10 to 14 days
o Granulation tissue
MI Changes 2 to 8 weeks
o Scar formation
What is the main lab finding for MI?
What is reperfusion injury?
Restoration of blood flow leads to local myocardial damage
What is cardiogenic shock?
Severe pump failure and often occurs with large infarcts
What are some complications of MI?
- Myocardial Rupture
- Ventricular Aneurysm