Chapter 16_2 flashcards

Question 1

Unstable Angina (UA): Definition & Significance

Answer 1

Cardiac chest pain occurring for the first time, or new/different from previous episodes, not relieved by rest. An ACS that can lead to MI; requires immediate treatment.

Question 2

Unstable Angina: Etiology & Common Cause

Answer 2

Most common etiology: Myocardial ischemia due to coronary artery arteriosclerosis with plaque accumulation obstructing blood flow (often LAD). Can also be due to coronary artery spasm (Prinzmetal’s) or microvascular dysfunction (INOCA).

Question 3

Unstable Angina: Pathophysiology (Exertional)

Answer 3

During exertion, heart muscle needs more O2. Arteriosclerotic coronary arteries cannot supply enough -> ischemia -> anaerobic metabolism -> lactic acid & adenosine accumulation -> anginal pain.

Question 4

Unstable Angina: Clinical Presentation (Classic)

Answer 4

Retrosternal chest discomfort (pressure, choking, squeezing, heaviness), often radiating to left shoulder/arm, jaw, back, neck, or epigastric region. Precipitated by exertion/stress, lasts 1-5 min, relieved by rest/nitrates. Pain not affected by respirations/cough/position.

Question 5

Anginal Equivalents (Often in Women)

Answer 5

Symptoms of myocardial ischemia other than classic chest pain: Episodic dyspnea, dizziness, lightheadedness, fainting, pain in jaw/epigastric region/back with exertion or stress.

Question 6

Levine’s Sign

Answer 6

Clenching a fist over the sternum when experiencing anginal pain; consistent with angina pectoris and MI.

Question 7

Diagnosis of Angina: Key Tests

Answer 7

ECG (may show ST depression/elevation), hs-cTn (to rule out MI - will be negative in UA), exercise stress test (with ECG, echo, or radionuclide imaging), coronary angiography (gold standard for CAD), CCTA.

Question 8

Treatment of Unstable Angina (Initial)

Answer 8

Oxygen (if SaO2 <95%), Nitrates (sublingual, IV - potent vasodilators), Aspirin (antiplatelet). Goal: relieve symptoms, slow disease progression, prevent MI.

Question 9

Prinzmetal’s (Variant/Vasospastic) Angina: Cause & Characteristics

Answer 9

Caused by coronary artery vasospasm, obstructing blood flow. Chest pain often occurs at rest, typically early morning. Not usually related to exertion. May have ST elevation on ECG during spasm.

Question 10

Microvascular Angina (INOCA): Definition & Criteria

Answer 10

Ischemia with No Obstructive Coronary Artery disease (<50% stenosis or FFR >0.80). Due to coronary microvascular dysfunction. Criteria: Ischemic symptoms, objective ischemia documentation, absence of obstructive CAD, confirmed reduced coronary flow reserve/inducible microvascular spasm.

Question 11

Chronic Stable Angina: Definition & Characteristics

Answer 11

Recurring episodes of chest pain caused by transient myocardial ischemia, typically due to fixed atherosclerotic coronary obstruction. Pain pattern is predictable, similar to past episodes, relieved by rest/prescribed NTG.

Question 12

Myocardial Infarction (MI): Definition & Types (ECG-based)

Answer 12

Acute coronary syndrome with prolonged ischemia causing irreversible myocardial cell death (necrosis). ECG types: STEMI (ST-segment elevation MI, often transmural) or NSTEMI (Non-ST segment elevation MI, often subendocardial).

Question 13

MI Classification (Universal Definition Types 1-5)

Answer 13

Type 1: Spontaneous MI (plaque rupture/thrombus). Type 2: MI due to O2 supply/demand imbalance (not atherothrombotic). Type 3: MI resulting in death before biomarkers measured. Type 4: MI due to PCI/stent. Type 5: MI due to CABG.

Question 14

Factors Influencing MI Damage Extent

Answer 14

1. Location/level of coronary artery occlusion. 2. Length of time artery has been occluded (>30 min ischemia usually causes irreversible damage). 3. Heart’s availability of collateral circulation.

Question 15

MI Pathophysiology: Cellular Changes & Markers

Answer 15

Prolonged ischemia -> anaerobic metabolism -> ATP depletion, Na+/K+ pump failure -> K+ efflux, Na+ influx, lactic acid accumulation -> ST changes on ECG. Cell membrane rupture releases intracellular contents (CPK-MB, cardiac troponins) into bloodstream.

Question 16

MI Diagnosis: Cardiac Biomarkers

Answer 16

High-sensitivity cardiac troponin I (hs-cTnI) is preferred, rises 4-8h, peaks, remains elevated for days (confirmatory). CPK-MB (cardiac enzyme) rises within 4h, peaks 18-24h, subsides in 3-4 days. Serial measurements track progression.

Question 17

MI Diagnosis: ECG Changes

Answer 17

STEMI: ST segment elevation. NSTEMI: ST depression or T-wave inversion. Pathological Q waves may develop later, indicating prior MI. ECG alone cannot confirm MI.

Question 18

MI Initial Treatment (Therapeutic Interventions)

Answer 18

MONA (historically, but O2 only if SaO2 <95%): Morphine (pain/anxiety), Oxygen, Nitrates (vasodilation), Aspirin (antiplatelet). Also: Beta-blockers (decrease myocardial O2 demand), ACE inhibitors (decrease BP/resistance).

Question 19

MI Reperfusion Therapy: PCI vs. Thrombolytics

Answer 19

Goal: Restore blood flow quickly. PCI (Percutaneous Coronary Intervention - angioplasty/stent): Preferred if available within 90 min for STEMI; superior outcomes. Thrombolytic agents (tPA): Dissolve clot; best if given within 12h of STEMI symptoms (strict contraindications due to bleeding risk).

Question 20

Coronary Artery Bypass Graft (CABG)

Answer 20

Surgical procedure creating new routes around occluded coronary arteries using grafts (e.g., saphenous vein, internal mammary artery). Can be “on-pump” (cardiopulmonary bypass) or “off-pump”.

Question 21

Reperfusion Injury (“Myocardial Stunning”)

Answer 21

Damage to ischemic myocardial tissue upon restoration of blood flow/oxygen, possibly due to oxidized free radicals from WBCs. Can cause arrhythmias and reduced contractility.

Question 22

Post-MI Complication: Dysrhythmias (Reentry Mechanism)

Answer 22

Ischemic/infarcted tissue doesn’t conduct impulses normally, causing impulses to slow, block, or change direction (reentry), leading to ectopic pacemakers and arrhythmias (e.g., PVCs, VT, VF).

Question 23

Post-MI Complication: Atrioventricular (AV) Block

Answer 23

SA atrial impulse fails to conduct to ventricles (often with anterior/inferior MI affecting AV node blood supply). ECG shows prolonged PR interval, bradycardia.

Question 24

Post-MI Complication: Atrial Fibrillation (AF)

Answer 24

Absence of coordinated atrial contractions (multiple irregular P waves). Can cause rapid ventricular response, decompensation, and increased risk of embolic stroke due to atrial stasis/clot formation.

Question 25

Post-MI Complication: Premature Ventricular Contractions (PVCs)

Answer 25

Ventricle beats independently; wide, bizarre QRS on ECG. Sporadic/infrequent may not need treatment. Frequent or couplets (2 sequential) increase risk of VT.

Question 26

Post-MI Complication: Ventricular Tachycardia (VT)

Answer 26

Series of widened QRS waves (>100 bpm) without P/T waves. Rapid, ineffective ventricular contractions -> severely diminished CO. Can lead to VF.

Question 27

Post-MI Complication: Ventricular Fibrillation (VF)

Answer 27

Ventricle quivers, no effective pumping (cardiac arrest). ECG shows bizarre waves. Often precipitated by PVC on T wave. Requires immediate defibrillation.

Question 28

Post-MI Complication: Papillary Muscle Rupture

Answer 28

Rupture of papillary muscle (often in LV MI) -> mitral valve incompetence (mitral insufficiency/regurgitation murmur) -> blood backup into LA/pulmonary circulation -> pulmonary edema.

Question 29

Post-MI Complication: Thromboembolism

Answer 29

Stagnant blood in poorly contracting heart chambers can form clots, which can embolize to pulmonary or systemic circulation.

Question 30

Post-MI Complication: Ventricular Aneurysm & Rupture

Answer 30

Weakened, bulging area of infarcted heart wall susceptible to rupture due to pressure. Rupture -> sudden drop in BP, shock, often fatal.

Question 31

Post-MI Complication: Pericarditis & Dressler's Syndrome

Answer 31

Pericarditis: Inflammation of pericardium (2-3 days post-MI). Sharp, stabbing chest pain (worse with inspiration), pericardial friction rub. Dressler's Syndrome: Hypersensitivity reaction to MI tissue necrosis (weeks-months post-MI), includes pericarditis, pleuritis, pneumonitis.

Question 32

Post-MI Complication: Heart Failure

Answer 32

Weakening of ventricles due to MI impairs pumping action -> blood volume accumulates -> hydrostatic pressure builds backward -> pulmonary edema (LV failure) or systemic edema (RV failure).

Question 33

Post-MI Complication: Cardiogenic Shock

Answer 33

Severe impairment of myocardium (often from extensive MI) -> LV pump failure -> diminished CO -> multiple organ hypoperfusion, cellular hypoxia, refractory hypotension. High mortality.

Question 34

Infective Endocarditis (IE): Definition & Common Pathogen

Answer 34

Noncontagious infection of cardiac endothelium, most commonly affecting heart valves. Main cause: Bacteria, esp. *Staphylococcus aureus*. Fungi can also cause.

Question 35

IE: Risk Factors

Answer 35

Damaged valves, turbulent blood flow, prosthetic valves, pacemakers, intravascular devices (central lines), IV drug use (IVDA), dental procedures, GABHS infections.

Question 36

IE Types & Common Organisms

Answer 36

Native Valve Endocarditis (NVE): *Streptococcus* spp. (viridans, bovis), *Enterococci*, *Staphylococcus* spp. Prosthetic Valve Endocarditis (PVE): *S. aureus*, *S. epidermidis* (often MRSA), *Corynebacterium*, fungi. IVDA Endocarditis: *S. aureus* (often tricuspid valve), Streptococci, fungi, Pseudomonas.

Question 37

IE: Pathophysiology (Vegetation Formation)

Answer 37

Microbes adhere to damaged endothelium/thrombi -> multiply -> attract WBCs/platelets -> release cytokines/coagulation factors -> fibrin deposition -> vegetation forms (microbes, fibrin, cellular components). Fragments can embolize (septic emboli).

Question 38

IE: Clinical Presentation & Classic Signs

Answer 38

Fever, chills, anorexia, weight loss, myalgias, arthralgias. New/worsening heart murmur (important!). Septic emboli -> ischemia/infarction in organs (stroke, kidney/spleen infarcts). Classic signs (from septic emboli, prolonged illness): Petechiae, Splinter hemorrhages (nails), Janeway lesions (painless, palms/soles), Osler's nodes (painful, fingertips), Roth spots (retina).

Question 39

IE: Diagnosis (Duke Criteria & Tests)

Answer 39

Duke Criteria (Major: positive blood cultures for typical IE organisms, evidence of endocardial involvement on echo. Minor: predisposing factor, fever, vascular/immunological phenomena, microbiological evidence). Requires =3 blood cultures (12h apart). Echocardiography (TEE preferred over TTE). Labs: CBC (anemia, leukocytosis), ESR, CRP.

Question 40

IE: Treatment & Prevention

Answer 40

IV antibiotics for 6 weeks or longer (based on culture/sensitivity). Surgery for valve repair/replacement if severe. Prophylactic antibiotics for at-risk patients before procedures causing bacteremia (dental, surgical).

Question 41

Myocarditis (Inflammatory Cardiomyopathy): Definition & Etiology

Answer 41

Inflammation of myocardium with myocyte degeneration/necrosis; not due to ischemia. Common cause: Viruses (influenza, herpes, hepatitis, coxsackievirus, adenovirus, parvovirus B19). Also bacteria, fungi, parasites, drugs, toxins, autoimmune diseases (SLE, sarcoid). Major cause of cardiac transplant rejection.

Question 42

Myocarditis: Clinical Presentation & Diagnosis

Answer 42

Range from asymptomatic to severe. Fever, myalgia, arthralgia, palpitations, dyspnea, chest pain. S3 gallop, pericardial friction rub possible. Diagnosis: CBC (leukocytosis), ESR, CRP, cTnI/cardiac enzymes (elevated -> damage). Viral antibody titers. Myocardial biopsy (gold standard if GCM suspected or ongoing uncertainty). ECG, Echo, Cardiac MRI.

Question 43

Myocarditis: Treatment

Answer 43

Reduce myocardial workload (activity restriction for =6 months). Treat underlying etiology (e.g., antivirals if applicable). Supportive for heart failure/arrhythmias (ACE inhibitors, inotropes). Immunosuppressants if autoimmune/GCM. Pacemaker, transplant in severe cases.

Question 44

Pericarditis: Definition & Pathophysiology

Answer 44

Inflammation of pericardium (sac surrounding heart) and epicardium. Capillaries become permeable -> plasma proteins/fibrinogen enter pericardial space -> fibrin-rich exudative edema -> scar tissue/adhesions may form.

Question 45

Pericardial Effusion & Cardiac Tamponade

Answer 45

Pericardial Effusion: Excess fluid (can be >200mL) in pericardial space, surrounding heart. Cardiac Tamponade: Fluid accumulation compresses heart, restricting chamber filling and reducing cardiac output.

Question 46

Pericarditis: Etiology (including Dressler's Syndrome)

Answer 46

Viruses (Coxsackievirus, influenza, EBV), bacteria, fungi, TB. Radiation, cardiac surgery, connective tissue disease (SLE, RA), renal failure, MI. Dressler's Syndrome: Post-MI autoimmune pericarditis (2-3 weeks after), immune complexes deposit in pericardium.

Question 47

Pericarditis: Clinical Presentation (Beck Triad, Pulsus Paradoxus)

Answer 47

Chest pain (sharp, sudden, worse with deep breath/cough/swallowing, radiates to neck/jaw/back). Fever, dyspnea. Pericardial friction rub (scratchy sound). Cardiac Tamponade signs: Beck Triad (hypotension, JVD, muffled heart sounds); Pulsus Paradoxus (SBP decrease =10 mmHg with inspiration).

Question 48

Pericarditis: Diagnosis & Treatment

Answer 48

ECG (ST elevations in multiple leads). Elevated BUN/creatinine (if renal failure). Possible elevated cTn/CPK-MB. Echocardiogram (for effusion/tamponade), CT, Cardiac MRI. Treatment: Depends on etiology. NSAIDs/aspirin for pain/inflammation, colchicine. Antibiotics if bacterial. Pericardiocentesis to drain effusion. Treat heart failure.