Pathoma - Ischemic heart disease

Question 1

What are the EKG changes on sudendothelial vs. transmural damage

Answer 1

Subendothelial - ST depression

Transmural - ST elevation

Question 2

How do you relieve angina

Answer 2

Nitroglycerin (will cause vasodilation, thus decreasing preload and decreasing the work on the heart)

Question 3

What is the major cause of stable vs. unstable angina

Answer 3

Stable - atherosclerosis of coronary artery with >70% stenosis

Unstable - rupture of atherscleroti plaque with thrombosis leading to incomplete artery occlusion

Question 4

What is Prinzmetal angina

Answer 4

Episodic chest pain unrelated to exertion

Due to coronary artery vasospasm

Question 5

What are the EKG changes you will see in the different type of angina (stable, unstable, prinzmetal)

Answer 5

Stable - ST depression

Unstable - ST depression

Prinzmetal - ST elevation (vasospasm will completely occlude the coronary artery, affecting all 3 layers of the wall - transmural)

Question 6

Causes of mycardial infarction

Answer 6

Rupture of atherosclerotic plaque with complete occlusion of coronary artery

Coronary artery vasospasm (Prinzmetal or cocaine)

Emboli

Vasculitis (e.g. Kawasaki)

Question 7

What are the 3 major arteries involved in mycoardial infarction and what part of the heart will they cause infarction of?

Answer 7

(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

Question 8

Laboratory tests to detect elevated cardiac enzymes and when the rise, peak, and fall

Answer 8

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

Question 9

What is contraction band necrosis?

Answer 9

Reperfusion complication following fibrinolysis or angioplasty after MI

Return of blood leads to return of Ca2+ which causes contraction –> contraction band necrosis

Question 10

Describe reperfusion injury

Answer 10

Return of blood to necrotic mycocytes will also cause return of O2; O2 may lead to free radicals, further damaging myocytes

Question 11

Describe the timeline of microscopic changes following an MI

Answer 11

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

Question 12

Describe the timeline of gross changes following an MI

Answer 12

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)

Question 13

What are the complications of the first 4 hours following an MI?

Answer 13

Cardiogenic shock (heart cannot provide blood to organs)

Congestive heart failure

Arrhythmia

Question 14

What are the complications 4-24 h following an MI?

Answer 14

Arrhythmia

Question 15

What are the complications 1-3 days following an MI?

Answer 15

Think of neutrophils:

Fibrinous pericarditis if infarct was transmural (chest pain with friction rub)

Question 16

What are the complications 4-7 days following an MI?

Answer 16

Think of macrophages:

Rupture possible:

• Ventricle free wall (cardiac tamponade)
• Interventricular septum (shunt)
• Papillary muscle (mitral insufficiency)

Question 17

What are the complications of the months following an MI?

Answer 17

Think of scar:

Aneurysm (scar is weaker than myocardium)

Mural thrombus

Dressler syndrome (antibodies against pericardium 2 weeks after MI)

Question 18

Most common cause of sudden cardiac death

Answer 18

Acute ischemia (90% of patients have pre-existing severe atherosclerosis)

Less common causes:

• Mitral valve prolapse
• Cardiomyopathy
• Cocaine abuse

Question 19

What are some causes of L-sided CHF

Answer 19

Ichemia

HTN (hypertrophic heart is harder to oxygenate)

Dilated cardiomyopathy (stretched muscle cannot contract as well)

Myocardial infarction

Restrictive cardiomyopathy (heart cannot fill appropriately)

Question 20

Describe “heart failure” cells

Answer 20

L-sided CHF leads to pulmonary congestion –> engorged capillaries burts into air sac –> macrophages consume blood –> iron piles up in macrophages –> hemosiderin-laden macrophages

Question 21

Describe how LHF auto-exacerbates?

Answer 21

Decreased CO = decreased flow to kindey = activation of RAAS = fluid retention = increased work on heart

Question 22

What are the 3 most common causes of R heart failure

Answer 22

L-heart failure

L-to-R shunt

Chronic lung disease (cor pulmonale)

Question 23

What are the organs/vessels that will be most affected by congestion caused by RHF

Answer 23

JVD

Painful hepatosplenomegaly with “nutmeg” liver

Pitting edema