Cardiovascular Medicine

Bedside anchors

• Slow-rising pulse → AS; collapsing pulse → AR; alternans → severe LV dysfunction.
• a wave = atrial contraction; absent in AF, cannon in AV dissociation.
• Tamponade: high JVP, pulsus paradoxus, blunted y; constriction: Kussmaul + rapid y + knock.
• S3 = rapid filling/volume; S4 = stiff ventricle + atrial kick; no S4 in AF.
• Diastolic murmur is pathological until proven otherwise.
• Inspiration generally increases right-sided murmurs.
• Standing/Valsalva: HCM louder; MVP click earlier.

Threshold anchors

• ESC office hypertension: ≥140/90; treated SBP goal 120–129 if tolerated.
• Severe MS: MVA ≤1.5 cm².
• Severe primary MR LV trigger: EF ≤60% or LVESD ≥40 mm.
• High-gradient severe AS: Vmax ≥4 m/s or mean gradient ≥40 mmHg; AVA typically ≤1.0 cm².
• Severe AR LV trigger: EF ≤50% or LVESD >50 mm/indexed >25 mm/m².
• HCM: wall thickness usually ≥15 mm; obstruction ≥30 mmHg; ≥50 mmHg treatment-relevant.
• Pulsus paradoxus: inspiratory SBP fall >10 mmHg.

Emergency anchors

• BP number alone ≠ hypertensive emergency; look for acute organ injury.
• Tamponade shock → urgent drainage; avoid preload-reducing treatment.
• Acute pulmonary oedema → NIV if suitable, oxygen if hypoxaemic, diuretic for overload, nitrate if hypertensive.
• Cardiogenic shock → define cause, norepinephrine for pressure, selected inotrope for output; do not treat EF alone.
• Acute severe MR/AR may be quiet and requires urgent echo/team escalation.

Chronic HF anchors

• Diagnose syndrome + objective cardiac abnormality; EF alone is insufficient.
• Search cause and trigger every time.
• Classic four pillars: beta blocker + RAAS inhibitor/ARNI + MRA + SGLT2 inhibitor.
• Diuretics improve congestion, not the underlying survival pathway.
• ESC 2026: HFrEF <50%; HFpEF ≥50%; older literature may retain ≤40/41–49/≥50.
• Normal EF does not exclude HF.