Ischemic Heart Disease (IHD) Flashcards
What is stable angina?
Chest pain that arises with exertion or emotional stress
What causes stable angina?
Atherosclerosis of coronary rates with > 70% stenosis (causes symptoms); decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion.
What type of injury is stable angina?
Represents reversible injury (cellular swelling) to myocytes (no necrosis)
What does stable angina present as?
Chest pain (
What does the EKG show for stable angina?
ST-segment depression due to subendocardial ischemia
What relieves stable angina?
Rest or Nitroglycerin (vasodilator of veins –> decreases preload!)
What is unstable angina?
Chest pain that occurs at rest
What causes unstable angina?
Due to rupture of an atherosclerotic plaque with thrombosis and INCOMPLETE occlusion of a coronary artery
What type of injury is unstable angina?
Reversible injury to myocytes (no necrosis)
What does the EKG show for unstable angina?
ST segment depression due to subendocardial ischemia
What is used to treat unstable angina?
Nitroglycerin
What does unstable angina put you at high risk for?
Myocardial infarction
What is Prinzmetal angina?
Episodic chest pain unrelated to exertion
What causes Prinzmetal angina?
Coronary artery vasospasm
What type of injury does Prinzmetal angina cause?
Reversible injury to myocytes (no necrosis)
What does the EKG show in Prinzmetal angina?
ST-segment elevation due to transmural ischemia (entire wall damage/block in blood flow)
What can you use to treat Prinzmetal angina?
Nitroglycerin or Calcium channel blockers (relives vasospasm by blocking Ca2+)
What is myocardial infarction?
Necrosis of cardiac myocytes
What causes myocardial infarction?
Usually due to rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery
(other causes include coronary artery vasospasm (due to Prinzmetal angina or cocaine use), emboli, and vasculitis (Kawasaki disease))
What are symptoms of MI?
Severe, crushing chest pain (>20 min) that radiates to left arm or jaw, diaphoresis and dyspnea (SOB - pulmonary congestion, anemia), symptoms NOT relieved by nitroglycerin
What does infarction usually involve with MI?
LV (RV and atria are usually spared)
What does an LAD occlusion cause?
Infarction of the anterior wall and anterior septum of LV
What is the most commonly involved artery in MI?
LAD - 45% of cases!
What does occlusion of the RCA cause?
Infarction of posterior wall, posterior septum and papillary muscles of LV (second most common infarct here)
What does occlusion of the left circumflex cause?
Infarction of the lateral wall of the LV.
What does the initial phase of infarction cause?
Subendocardial necrosis involving
What happens after continued ischemia?
Transmural necrosis involving most of the myocardial wall (transmural infarction)
-EKG shows ST-segment elevation
What is Troponin?
Most sensitive and specific marker (gold standard) for MI.
What is the timeline for Troponin?
Levels rise 2-4 hours after infarction, peak at 24 hours, and return to normal by 7-10 days.
What is CK-MB?
Useful for detecting re-infarction that occurs days after initial MI.
-CK-MB levels rise 4-6 hours after infarction, peak at 24 hours, return to normal by 72 hours
What are the six treatments used for MI?
- Aspirin and/or heparin - limits thrombosis
- Supplemental O2 - minimizes ischemia
- Nitrates - vasodilate veins and coronary arteries (veins –> dec preload)
- Beta-blocker - Slows HR, decreasing O2 demand, and risk for arrhythmia
- ACE inhibitor
- Fibrinolysis or angioplasty - opens blocked vessel
What two adverse side effects can reperfusion cause?
- Contraction band necrosis
2. Reperfusion injury
What is contraction band necrosis?
Reperfusion of irreversibly-damaged cells results in calcium influx, leading to hyper contraction of myofibrils
What is reperfusion injury?
-Return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes (why we continue to see elevated enzymes)
What changes do you see in MI after
No gross changes
No microscopic changes
Complications: Cardiogenic shock (massive infarction), congestive heart failure, and arrhythmia
What do you see in MI after 4-24 hours?
Gross: Dark discoloration
Microscopic: Coagulative necrosis (nuclei removed from cells)
Complications: Arrhythmia
What do you see in MI after 1-3 days?
Gross: Yellow Pallor
Microscopic: Neutrophils
Complications: Fibrinous pericarditis (transmural)- presents as chest pain with friction rub!
What do you see in MI after 4-7 days?
Gross: Yellow Pallor
Microscopic: Macrophages (eat debris - cause wall weakness)
Complications: Rupture of ventricular free wall (cardiac tamponade), inter ventricular septum (leads to shunt), or papillary muscle (leads to mitral insufficiency)
What do you see in MI after 1-3 weeks?
Gross: Red border emerges as granulation tissue enters from edge of infarct.
Microscopic: Granulation tissue with plump fibroblasts, collagen, and blood vessels
What do you see in MI after Months?
Gross: White scar (not as strong as myocardium)
Microscopic changes: Fibrosis
Complications: Aneurysm (dilation of wall), mural thrombus or Dressler syndrome
What is Dressler syndrome?
Pericarditis caused by autoimmune antibodies against pericardium (6-8 weeks after infarction)
What is sudden cardiac death?
Unexpected death due to cardiac disease; occurs without symptoms or
What usually causes sudden cardiac death?
Fatal ventricular arrhythmia
What is the most common etiology for sudden cardiac death?
Acute ischemia - 90% of patients have preexisting severe atherosclerosis
What are less common causes of sudden cardiac death?
Mitral valve prolapse
Cardiomyopathy
Cocaine abuse (w/vasospasm)
What is Chronic Ischemic Heart Disease?
Poor myocardial function due to chronic ischemic damage (with or without infarction); progresses to congestive heart failure (CHF)
