Chapter 4: Part 2 Pathos

Q1: What is the difference between valvular stenosis and regurgitation?

Stenosis means the valve does not open completely, narrowing blood flow and increasing resistance.

Regurgitation means the valve does not close completely, allowing blood to flow backward.
Both cause increased cardiac workload, leading to hypertrophy and decreased cardiac output

Q2: How do valvular disorders affect cardiac output (CO)?

• Stenosis decreases forward flow → ↓ CO.

• Regurgitation causes volume overload → ↓ effective ejection.

• The heart must work harder → leads to hypertrophy and dilation → overall decreased CO

Q3: What are common causes and treatments of valvular disorders?

• Causes: Congenital defects, infection (endocarditis), MI, cardiomyopathy, heart failure.

• Treatment: Reduce workload by lowering afterload and preload, oxygen therapy, preventing clots, and surgical repair or valve replacement

Q4: What are the basic components of the heart’s electrical system?

• Sinoatrial (SA) node: Natural pacemaker, initiates impulse.

• Atrioventricular (AV) node: Delays impulse before ventricles contract.

• Impulse travels to bundle branches and Purkinje fibers for ventricular contraction

Q5: What are the main components of an ECG waveform?

• P wave: Atrial depolarization

• PR interval: Delay at AV node

• QRS complex: Ventricular depolarization

• ST segment: Early ventricular repolarization

T wave: Ventricular repolarization

Q6: What are the normal and abnormal adult heart rates?

• Normal Sinus Rhythm: 60–100 bpm

• Bradycardia: <60 bpm (can ↓ CO if too slow)

• Tachycardia: >100 bpm (↓ filling time → ↓ CO)

Q7: How do electrical alterations affect cardiac output?

Abnormal rhythms disrupt effective contraction and filling → ↓ stroke volume and CO

Q8: Describe atrial fibrillation (A-fib) and its effects.

• No P wave; irregularly irregular rhythm; atria quiver instead of contracting.

• Blood flow into ventricles is reduced → ↓ CO.

• Major risk: Clot formation → embolic stroke.

• Treatment: Medications, cardioversion, ablation, pacemaker

Q9: What are PVCs, ventricular tachycardia, and ventricular fibrillation?

• PVCs: Premature ventricular contractions → ↓ filling time → ↓ CO.

• V-tach: >100 bpm from ventricles; ↓ CO, may deteriorate to V-fib.

• V-fib: Fatal; no pulse, ventricles quivering; requires defibrillation

Q10: What causes heart failure (HF)?

Congenital defects, myocardial ischemia/infarction, hypertension, valvular disease, dysrhythmias, thyroid or renal disease

Q11: What is the difference between left-sided and right-sided heart failure?

• Left-sided HF: Blood backs into lungs → pulmonary congestion, dyspnea, crackles, fatigue.

• Right-sided HF: Blood backs into systemic circulation → edema, weight gain, jugular vein distention

Q12: What compensatory mechanisms worsen HF over time?

• Sympathetic nervous system activation: Increases HR and workload.

• RAAS activation: Increases preload and afterload → fluid retention → worsens HF.

• Hypertrophy: Thickens muscle but decreases efficiency

Q13: How is heart failure managed?

• Lifestyle: Low-sodium diet, daily weights, fluid monitoring.

• Medications: Diuretics, ACE inhibitors, nitrates, beta-blockers.

• Advanced care: Oxygen, artificial devices, or heart transplant

Q14: What is cardiac hypertrophy and what causes it?

• Definition: Increased size of cardiac muscle cells (especially LV).

• Causes: Hypertension, aortic stenosis, obesity, genetic factors.

• Effect: Stiff ventricle → ↓ filling → ↓ CO

Q15: How does the RAAS system worsen cardiac hypertrophy?

Reduced blood flow to kidneys → ↑ renin → ↑ angiotensin II & aldosterone → vasoconstriction & fluid retention → ↑ afterload → more stress on LV → worsened hypertrophy

Q16: What is the role of cholesterol in the body?

It helps form hormones and cell membranes, but excess leads to plaque buildup in arteries (atherosclerosis)

Q17: What are normal cholesterol values?

• Total cholesterol: <200 mg/dL

• Borderline high: 200–239 mg/dL

• High: ≥240 mg/dL

Q18: What is the difference between LDL, HDL, and triglycerides?

• LDL (“bad”) → deposits cholesterol in vessels.

• HDL (“good”) → removes cholesterol from blood.

• Triglycerides → stored fats, also contribute to plaque formation

Q19: What are risk factors and prevention strategies for dyslipidemia?

• Risk factors: Obesity, poor diet, diabetes, hypothyroidism, sedentary lifestyle, alcohol, smoking.

• Prevention: Low-fat/high-fiber diet, exercise, quit smoking, weight loss, increase HDL with omega-3 and whole grains

Q20: What causes PAD?

Atherosclerosis in peripheral arteries → ↓ oxygen delivery to limbs

Q21: What are symptoms and complications of PAD?

• Symptoms: Leg pain with exertion (intermittent claudication), cool/pale skin, decreased pulses, slow cap refill.

• Complications: Ulcers, necrosis, gangrene

Q22: How is PAD treated?

Lifestyle modification, cholesterol management, angioplasty, stent, or bypass graft

Q23: What is the pathophysiology of CAD?

Atherosclerosis in coronary arteries → ↓ blood flow → ischemia → angina or myocardial infarction

Q24: What are the major risk factors for CAD?

• Modifiable: High LDL, hypertension, diabetes, obesity, smoking, inactivity.

• Non-modifiable: Age, gender, family history, ethnicity

Q25: What are symptoms of angina and MI?

• Angina: Chest pressure/tightness radiating to shoulder, neck, or jaw, relieved by rest or nitro.

• MI: Prolonged pain (>15 min), not relieved by rest, may cause nausea, diaphoresis, or SOB.

• Women may have atypical symptoms like back or abdominal pain

Q26: How is MI diagnosed and treated?

• Diagnosis: EKG (ST elevation, Q wave), cardiac enzymes (troponin ↑).

• Treatment:

  • MONA: Morphine, Oxygen, Nitroglycerin, Aspirin

  • Restore blood flow (PCI, CABG, thrombolytics)

  • Lifestyle modifications after recovery

Q27: What is hypertension and how is it classified?

• Definition: BP >130/80 mmHg.

• Stage 1: 140–159/90–99

• Stage 2: >160/100

• Malignant HTN: >180/120 = emergency

Q28: What are risk factors for hypertension?

Age, family history, race, obesity, smoking, high-sodium diet, alcohol, stress, low potassium intake

Q29: Why is hypertension called the “silent killer”?

It is often asymptomatic until serious complications occur, such as stroke, renal damage, or heart failure

Q30: What are complications of uncontrolled hypertension?

Atherosclerosis, aneurysm, heart failure, stroke, renal failure, vision loss, memory issues

Q31: How is hypertension prevented and managed?

• Prevention: Low-salt diet, limit saturated fats, regular exercise, stress control, smoking cessation.

• Treatment: BP medications (diuretics, ACE inhibitors, beta-blockers), monitor BP regularly

Q32: What is pregnancy-induced hypertension (PIH)?

• Characterized by elevated BP, proteinuria, and edema.

• Can progress to eclampsia with seizures.

• Treatment: Bed rest, magnesium sulfate, close monitoring