Pathoma - Ischemic heart disease Flashcards
What are the EKG changes on sudendothelial vs. transmural damage
Subendothelial - ST depression
Transmural - ST elevation
How do you relieve angina
Nitroglycerin (will cause vasodilation, thus decreasing preload and decreasing the work on the heart)
What is the major cause of stable vs. unstable angina
Stable - atherosclerosis of coronary artery with >70% stenosis
Unstable - rupture of atherscleroti plaque with thrombosis leading to incomplete artery occlusion
What is Prinzmetal angina
Episodic chest pain unrelated to exertion
Due to coronary artery vasospasm
What are the EKG changes you will see in the different type of angina (stable, unstable, prinzmetal)
Stable - ST depression
Unstable - ST depression
Prinzmetal - ST elevation (vasospasm will completely occlude the coronary artery, affecting all 3 layers of the wall - transmural)
Causes of mycardial infarction
Rupture of atherosclerotic plaque with complete occlusion of coronary artery
Coronary artery vasospasm (Prinzmetal or cocaine)
Emboli
Vasculitis (e.g. Kawasaki)
What are the 3 major arteries involved in mycoardial infarction and what part of the heart will they cause infarction of?
(1) Left anterior descending (LAD) - anterior wall and anterior septum of LV
(2) R coronary artery (RCA) - posterior wall, posterior septum, and papillary muscles of the LV
(3) L circumflex artery - lateral wall of the LV
Laboratory tests to detect elevated cardiac enzymes and when the rise, peak, and fall
Troponin (gold standard) - Rises 2-4 h; peak 24 h; normal by 7-10 days
Creatinine kinase MB (CK-MB) - Rises 4-6 h; peak 24 h; normal by 72 h
CK-MB can be used to detect reinfarction that occurs days after initial MI
What is contraction band necrosis?
Reperfusion complication following fibrinolysis or angioplasty after MI
Return of blood leads to return of Ca2+ which causes contraction –> contraction band necrosis
Describe reperfusion injury
Return of blood to necrotic mycocytes will also cause return of O2; O2 may lead to free radicals, further damaging myocytes
Describe the timeline of microscopic changes following an MI
1 day - coagulative necrosis
(1 DAY)
1-3 days - neutrophils
4-7 days - macrophages
(1 WEEK)
1-3 weeks - granulation tissue
(1 MONTH)
Months - fibrosis
Describe the timeline of gross changes following an MI
1 day - dark discoloration (due to coagulative necrosis)
1-7 days - yellow pallor (due to WBC of inflammation - first neutrophils then macrophages)
1-3 weeks - Red border (blood vessels from normal tissue growing into necrotic area to form granulation tissue)
Months - white scar (due to fibrosis)
What are the complications of the first 4 hours following an MI?
Cardiogenic shock (heart cannot provide blood to organs)
Congestive heart failure
Arrhythmia
What are the complications 4-24 h following an MI?
Arrhythmia
What are the complications 1-3 days following an MI?
Think of neutrophils:
Fibrinous pericarditis if infarct was transmural (chest pain with friction rub)
What are the complications 4-7 days following an MI?
Think of macrophages:
Rupture possible:
- Ventricle free wall (cardiac tamponade)
- Interventricular septum (shunt)
- Papillary muscle (mitral insufficiency)
What are the complications of the months following an MI?
Think of scar:
Aneurysm (scar is weaker than myocardium)
Mural thrombus
Dressler syndrome (antibodies against pericardium 2 weeks after MI)
Most common cause of sudden cardiac death
Acute ischemia (90% of patients have pre-existing severe atherosclerosis)
Less common causes:
- Mitral valve prolapse
- Cardiomyopathy
- Cocaine abuse
What are some causes of L-sided CHF
Ichemia
HTN (hypertrophic heart is harder to oxygenate)
Dilated cardiomyopathy (stretched muscle cannot contract as well)
Myocardial infarction
Restrictive cardiomyopathy (heart cannot fill appropriately)
Describe “heart failure” cells
L-sided CHF leads to pulmonary congestion –> engorged capillaries burts into air sac –> macrophages consume blood –> iron piles up in macrophages –> hemosiderin-laden macrophages
Describe how LHF auto-exacerbates?
Decreased CO = decreased flow to kindey = activation of RAAS = fluid retention = increased work on heart
What are the 3 most common causes of R heart failure
L-heart failure
L-to-R shunt
Chronic lung disease (cor pulmonale)
What are the organs/vessels that will be most affected by congestion caused by RHF
JVD
Painful hepatosplenomegaly with “nutmeg” liver
Pitting edema
