MHD: Ischemic Heart Disease Flashcards
What is the leading cause of death/disability in the US?
Heart disease
What is heart failure?
A progressive condition where the heart is unable to pump blood sufficiently to meed the demand of tissues
What is the difference between systolic and diastolic heart failure?
In systolic heart failure, the heart is unable to properly contract to eject blood out. Diastolic failure has to do with stiffened ventricles that are unable to properly relax.
Which side of the hear is most often involved with heart failure: left, right or both?
Both. Usually left sided heart failure leads to right sided heart failure causing biventricular failure.
How is aortic stenosis related to diastolic heart failure?
Stenosis causes LV hypertrophy, which makes the LV stiffer leading to diastolic failure due to decreased filling
Where does blood “back up” into in right sided heart failure?
Portal venous circulation leading to peripheral edema, ascites, portal hypertension
Where does blood “back up” into in left sided heart failure?
Pulmonary circulation
What is the main cause of right heart failure?
Left heart failure
What is cor pulmonale?
Right heart failure without left heart failure, usually caused by lung disease, pulmonary hypertension
What condition has the same risk factors as ischemic heart disease?
Atherosclerosis
-hypertension, hyperlipidemia, diabetes, smoking, increased age, male gender
What are the 4 clinical presentations of ischemic heart disease?
Angina pectoris
Acute myocardial infarction
Chronic ischemic heart disease/heart failure
Sudden cardiac death
What are the 3 types of angina pectoris?
Stable, unstable, and Prinzmetal variant
Describe stable angina pectoris
Stenosis (>75% reduction) due to coronary artherosclerosis prevents adequate O2 supply during increased cardiac demand.
Presents as chest pressure on exertion that goes away with rest
Describe unstable angina pectoris
Caused by atherosclerotic plaque disruption (fissure/ulceration of fibrotic cap) that triggers platelet activation, aggregation and vasospasm
Partially occluding thrombus causes chest pain, even at rest.
Describe the composition of vulnerable plaques
Lipid rich with thin fibrous caps
True or false: stable and unstable angina can cause myocardial infarction
False. Both stable and unstable angina cause ischemia, not infarction.
What is prinzmetal variant angina?
Caused by coronary artery spasm that is unrelated to physical activity, heart rate, blood pressure.
Responds to vasodilators
Describe the pathogenesis of myocardial infarction
Plaque disruption leads to platelet adhesion, aggregation, activation, vasospasm and coagulation.
An occlusive thrombus forms leads to a true infarct
How quickly after occlusion does myocardial infarction become irreversible?
After 30 minutes, damage is irreversible, coagulative necrosis begins
What is a transmural infarction
An infarction involving the full thickness of the myocardial wall
Describe the location of a non-transmural infarct
Usually subendocardial infarction
The endocardium is most susceptible to ischemic damage due to distance from coronary arterial O2 supply
Describe the gross/microscopic changes associated with MI after 1/2-4 hours
No gross or microscopic changes
Describe the gross/microscopic changes associated with MI after 4-12 hours
Coagulation necrosis begins, is visible histologically as eosinophilic cytoplasm, pyknotic nuclei.
No gross changes visible.
Describe the gross/microscopic changes associated with MI after 12-24 hours
Gross changes visible: dark mottling due to hemorrhage into infarcted tissues
Ongoing coagulation necrosis, pyknosis of nuclei
Describe the gross/microscopic changes associated with MI after 1-3 days
Gross: mottled tissue
Histology: loss of nuclei and myocytes, neutorphils infiltrating
Describe the gross/microscopic changes associated with MI after 3-7 days
Gross: yellow appearing tissue
Histology: myocytes disintegrated via phagocytosis
Describe the gross/microscopic changes associated with MI after 7-10 days
Histology: granulation tissue begins to form
Describe the gross/microscopic changes associated with MI after 10-14 days
Histology: granulation tissue formed (mature collagen visible on trichrome stain)
Describe the gross/microscopic changes associated with MI after 2-8 weeks
Scar formation visible on trichrome stain (blue-stained collagen) and gross specimen (white scarring)
Describe the clinical presentation of myocardial infarction
Crushing substernal chest pain, dyspnea, diaphoresis
Tachycardia, pulmonary congestion, edema
Silent in 10-15% of patients
What laboratory tests are used to detect recent MI?
Creatinine kinase and troponin
What is the classical EKG finding of MI?
ST segment elevation
List the treatments of MI
Aspirin and other antiplatelet drugs Heparin Thrombolytic therapy Beta blockers ACE inhibitors Nitrates Oxygen
“A BATH, NO?”
What mechanisms are responsible for reperfusion injury?
Free radical production
Myocyte hypercontracture, increased Ca
Leukocyte aggregation
Mitochondrial dysfunction
What is cardiogenic shock?
A major complication of MI in which the heart is no longer able to supply enough blood to the rest of the body
What is an arrhythmia?
A disturbance of electrical conduction that can be caused by MI
Describe the vulnerable state of the heart following an MI that leads to myocardial rupture
3-7 days following infarction, the myocytes are dead and neutrophils have invaded. Neither provide any support, which makes the wall very weak
What is sudden cardiac death?
Fatal arrhythmia due to structural heart disease. Almost always related to sever atherosclerotic heart disease, not acute infarction
