Comprehensive Cardiovascular Review Notes
Electrocardiography & Arrhythmia Management
- Standard ECG calibration: 1mV and 200ms (1 big box = 5 small boxes = 200ms).
- Wide QRS complex definition: ≥3 small boxes.
- QTc reference thresholds: Females = 460ms; Males = 450ms (460−10ms).
- A 6-second ECG strip contains 150 small boxes.
- ECG Rhythm Identification Rules:
- Absence of P wave + fast HR + narrow QRS + irregular rhythm = Atrial Fibrillation.

- Absence of P wave + fast HR + wide QRS + regular rhythm = Ventricular Tachycardia.

- Narrow QRS + regular rhythm = Supraventricular Tachycardia (Initial treatment: adenosine; Alternative: verapamil).
- Multiple discrete P wave morphologies + pulmonary disease context = Multifocal Atrial Tachycardia.
- Atrioventricular (AV) Blocks: Constant or fixed PR interval followed by a dropped QRS complex = 2nd-degree AV Block Mobitz Type II.
- Cardiac Resuscitation Management:
- Unconsciousness with BP = 0mmHg and HR = 0bpm: Immediate CPR before epinephrine administration.
- Symptomatic Junctional Bradycardia: Initial drug is Atropine (followed by Transcutaneous Pacing, Dopamine, or Epinephrine).
- Electrophysiology: L-type Ca2+ channels open during Phase 0; Funny channels operate during Phase 4.
- Reversible causes of cardiac arrest (5Ts and 5Hs): Thrombosis can be either coronary or pulmonary.
Diseases of the Aorta & Vascular Disorders
- Aortic Anatomy & Landmarks:
- Arch of the aorta begins at the right brachiocephalic artery.
- Anatomical levels: T4 (nipple line), T6 (xiphoid process), T8 (IVC aperture), T10 (esophageal hiatus), T12 (aorta hiatus - descending thoracic aorta termination), L4 (aortic bifurcation).
- Aortic Aneurysms:
- Saccular aneurysm: Asymmetric outpouching involving all vascular wall layers.
- Abdominal Aortic Aneurysm (AAA): Majority originate from the infrarenal artery.
- AAA rapid growth definition: 1cm/year.
- 5-year rupture risk for AAA >7cm: >80%.
- Preferred screening modality: Abdominal ultrasound (UTZ).
- Aortic Dissection:
- Condition characterized by an intimal tear.
- Stanford Classification: Type A (originates in ascending aorta), Type B (originates in descending aorta).
- DeBakey Classification: Type 1 (involves whole aorta), Type 2 (involves up to aortic arch), Type 3 (involves up to descending thoracic aorta).
- Type B3 involves up to the descending thoracic aorta.
- Major complication: Pseudoaneurysm.
- Blood Pressure Measurement: Target SBP inflation level is increased by 30mmHg above palpated loss of pulse.
Hypertension Mechanisms & Management
- Mechanisms of Hypertension:

- Intravascular volume: Pressure-natriuresis impairment leading to NaCl imbalance and volume expansion.
- Autonomic Nervous System (ANS): Increased sympathetic outflow and decreased baroreceptor activity reset to higher pressure.
- RAAS: Increased renin and angiotensin II, decreased AT1 activity, increased aldosterone.
- Vascular mechanism: Increased NHE activity, impaired endothelium-dependent vasodilation, increased stiffness, decreased lumen, and increased SVR.
- BP Targets & Thresholds: Target BP is generally <130/80mmHg. Ambulatory thresholds follow the CAN mnemonic: Conventional (140/90mmHg), Average (130/80mmHg), Nighttime (120/70mmHg).
- First-Line Anti-hypertensive Therapy: ACE inhibitors (perindopril), ARBs (losartan), Calcium-channel blockers (CCBs), Thiazide diuretics.
- Beta-blockers (bisoprolol), loop diuretics (furosemide), and alpha-1 blockers (terazosin) are NOT first-line.
- Beta-Blocker Classification: Drug names starting with letters A through N are β1-selective; O onwards are non-selective. Suffixes
-ilol or -alol indicate mixed α/β blockers (e.g., carvedilol).
Pulmonary Embolism & Deep Vein Thrombosis
- Clinical Symptoms: Lower calf cramp ("Charley horse") is the most common symptom of DVT; unexplained breathlessness is the most common symptom of PE.
- Homan Sign: Discomfort behind the knee on forced foot dorsiflexion; lacks sensitivity and specificity for DVT.
- PE Pathophysiology: Most common gas exchange abnormalities are arterial hypoxemia and increased alveolar-arterial O2 tension gradient. Also causes increased pulmonary vascular resistance and alveolar hyperventilation.
- Diagnostic Findings:
- ECG: S1Q3T3 pattern (S wave in lead I, Q wave in lead III, inverted T wave in lead III) alongside sinus tachycardia.
- Chest X-ray: Hampton sign (triangular wedge-shaped opacity).
- Biomarkers & Imaging: D-dimer upper limit = 500ng/mL. Venous ultrasonography is the principal imaging modality for DVT.
- PE Risk Classification: Low-risk PE presents with normotension without RV dysfunction (65–75% of cases). Submassive PE features normotension with RV dysfunction (20–25% of cases).
Ischemic Heart Disease & Acute Coronary Syndromes
- Clinical Examination:
- Levine sign: Patient places a clenched fist over the sternum and leans forward during chest pain.
- Atherosclerosis signs: Xanthelasmas and xanthomas.
- Hypertensive changes: Fundoscopic examination showing increased light reflex and arteriovenous (AV) nicking.
- Palpation/Auscultation: LV dyskinesia on palpation; apical systolic murmur of mitral regurgitation on auscultation.
- Myocardial Oxygen Determinants:
- Oxygen Demand: Heart rate, myocardial contractility, myocardial wall tension (preload, afterload, ventricular size).
- Oxygen Supply: Blood oxygen-carrying capacity (inspired O2, hemoglobin, pulmonary function) and coronary blood flow (vessel diameter, patency, vascular resistance, perfusion pressure, diastolic filling time).
- Functional Classification: NYHA Class I represents patients who are asymptomatic during ordinary activity (able to walk >4 blocks or climb >3 flights of stairs).
- Acute Management & STEMI Criteria:
- Initial anti-ischemic drugs: Sublingual isosorbide dinitrate and beta-blockers.
- Coronary Anatomy: Inferior wall MI involves the Right Coronary Artery (RCA).
- Revascularization Target Times: Door-to-needle time (thrombolysis) ≤30mins; Door-to-balloon time (PCI) ≤90mins. Exact lesion dimensions are required prior to revascularization.

- STEMI ECG Criteria: New ST-elevation at J-point in ≥2 contiguous leads: ≥0.1mV (1mm) in all leads except V2–V3. In leads V2–V3: ≥0.2mV in men ≥40 years, ≥0.25mV in men <40 years, and ≥0.15mV in women.
Heart Failure, Cardiomyopathies & Peripheral Vascular Disease
- Heart Failure Pathophysiology & Management:
- High-Output Heart Failure (HOHF): Results from persistent tachycardia or hypermetabolic conditions (e.g., thyrotoxicosis, chronic lung disease, aging); hypertension does not cause HOHF.
- Ventricular Remodeling: Post-injury changes in LV mass, volume, and shape; includes both concentric and eccentric hypertrophy.
- Endogenous Counter-regulatory Hormones: ANP and PGE2 oppose RAAS and SNS activation.
- Electrolyte Abnormalities in MI: Common changes include hypomagnesemia, hyponatremia, hypercalcemia, and hypophosphatemia.
- GDMT Four First-Line Classes: ARNIs/ARBs, MRAs (spironolactone), SGLT2 inhibitors (dapagliflozin), and proven mortality-benefit beta-blockers (bisoprolol, carvedilol, metoprolol succinate). Metoprolol tartrate does NOT carry proven mortality benefit in HF.
- Peripheral Vascular Disease & Cardiomyopathies:
- Severe Raynaud Phenomenon: First-line medical therapy is a dihydropyridine CCB (nifedipine). Beta-blockers and non-DHP CCBs (diltiazem) are avoided.
- Peripheral Artery Disease (PAD): Calf claudication indicates femoral-popliteal involvement. Skin moisturization is a key supportive measure.
- Restrictive Cardiomyopathy: Most common cause is infiltrative disease (specifically amyloidosis, which most commonly presents as heart failure).
- Dilated Cardiomyopathy: Characterized by EF <50%; endomyocardial biopsy provides definitive diagnosis.
- Peripartum Cardiomyopathy: Occurs in the 3rd trimester up to 2 weeks post-delivery; diagnosis is invalid if HF presents early in pregnancy.
- Hypertrophic Cardiomyopathy (HOCM): Risk of sudden cardiac death is driven by LV systolic dysfunction; physical examination shows pulsus bisferiens.
Congenital, Valvular & Pericardial Diseases
- Physical Examination Findings: Right Ventricular Heave is assessed by placing the heel of the hand on the left parasternal border.
- Congenital Heart Disease (CHD) Associations:
- Down Syndrome: Atrioventricular (AV) canal defect / primum ASD.
- DiGeorge Syndrome: Conotruncal anomalies.
- Williams Syndrome: Supravalvular aortic stenosis.
- Noonan Syndrome: Dysplastic pulmonary valve.
- Atrial Septal Defects & Shunts:
- Secundum ASD: Associated with Patent Foramen Ovale (PFO) and fixed split S_2$.\n * Primum ASD: Associated with cleft mitral valve and AV abnormalities.\n * Sinus Venosus ASD: Associated with PAPVR and Scimitar sign.\n * Patent Ductus Arteriosus (PDA): Continuous murmur best heard below the left clavicle causing LA and LV enlargement. Most common shunt is VSD.\n* Pericardial Disease:\n * Cardiac Tamponade: Characterized by Pulsus Paradoxus. Hemodynamically compromised patients require urgent pericardiocentesis.\n * Acute Pericarditis: Diagnostic criteria include chest pain, pericardial friction rub, and diffuse concave ST-elevation with PR depression (in contrast to convex ST-elevation in MI). Elevated CRP is supportive but not a primary diagnostic criterion. Colchicine reduces recurrence rates. Viral infection is the most common cause in developed countries.\n* Valvular Heart Disease:\n * Pulmonic Stenosis (PS): Produces right-sided findings exclusively (RVH, RAE, RAD, RBBB). Murmur does not decrease during squatting.\n * Mitral Stenosis (MS): Displays "hockey stick" and "fish mouth" appearance on echocardiogram; antiplatelets (aspirin/clopidogrel) are not part of treatment.\n * Aortic Stenosis (AS): 70−year−oldwithcrescendo−decrescendosystolicmurmuratright2nd ICS is most commonly due to calcific degenerative etiology, leading to LV and ascending aorta enlargement.\n * Tricuspid Regurgitation (TR): Systolic murmur with Carvallo sign (intensifies on inspiration).\n * Pulmonic Regurgitation (PR): Diastolic Graham-Steell murmur heard at the left lower sternal border (intensifies on inspiration).\n * Tricuspid Stenosis (TS): Defined as severe if valve area is \le 1\,cm^2orpressurehalf−timeis\ge 190\,ms$$.