ICU · cardiovascular

Acute severe valvular emergencies — critical aortic stenosis, acute mitral regurgitation, acute aortic regurgitation (comprehensive ICU management)

Also known as Critical aortic stenosis · Acute mitral regurgitation · Acute aortic regurgitation · Papillary muscle rupture · Acute MR · Acute AR · Valvular cardiogenic shock · Balloon aortic valvuloplasty · BAV · TAVI · TAVR · Transcatheter aortic valve implantation · Surgical aortic valve replacement · SAVR · PARTNER 3 · Evolut Low Risk · Prosthetic valve thrombosis · Paravalvular leak · MitraClip · TEER · Flail leaflet · Aortic stenosis symptom triad · AS syncope angina heart failure

Acute valvular emergencies present as cardiogenic shock, flash pulmonary oedema, syncope, or cardiac arrest, and they are defined by THREE NATIVE-VALVE LESIONS plus prosthetic valve failure. (1) CRITICAL AORTIC STENOSIS (AVA <1.0 cm², mean gradient >40 mmHg, peak velocity >4 m/s; critical/shock when AVA ~0.6 and gradient ~50): a FIXED LV outflow obstruction with a stiff hypertrophied ventricle that is PRELOAD-, AFTERLOAD- and ATRIAL-KICK dependent. The AS symptom triad is ANGINA (5-yr survival), SYNCOPE (3-yr), HEART FAILURE (2-yr) — prognosis without AVR is dismal. Haemodynamic goal: SLOW heart rate (60-80, long diastolic filling time), HIGH SVR (noradrenaline — never vasodilate), ADEQUATE PRELOAD (cautious diuresis only), and MAINTAIN SINUS RHYTHM (AF is devastating — synchronised DC cardioversion if unstable). AVOID nitrates/GTN, ACEi/ARB, high-dose beta-blockers, and over-diuresis. Definitive therapy is AORTIC VALVE REPLACEMENT (surgical AVR or TAVI); balloon aortic valvuloplasty (BAV) or VA-ECMO bridge the unstable patient. (2) ACUTE MITRAL REGURGITATION (papillary muscle rupture 2-7 days post-inferior MI, chordal rupture, endocarditis, trauma): sudden volume overload of a small non-compliant LA - flash pulmonary oedema + shock; the murmur may be SOFT or ABSENT (rapid LA pressure equalisation) — never be reassured by a quiet chest. Echo (flail leaflet, eccentric jet) is diagnostic. Haemodynamic goal: LOW SVR/afterload reduction (nitroprusside; IABP gives mechanical unloading) + inotrope (dobutamine/milrinone); definitive therapy is URGENT MV repair/replacement, or MitraClip (TEER) in the prohibitive-surgical-risk patient. (3) ACUTE AORTIC REGURGITATION (Type A dissection, endocarditis, trauma): diastolic run-off into a non-compliant LV - rapidly rising LVEDP - acute pulmonary oedema + shock; the wide pulse pressure, water-hammer pulse and Austin-Flint murmur of CHRONIC AR are usually ABSENT in acute AR (LV has not adapted; pulse pressure may be normal, murmur SHORT). Haemodynamic goal: LOW SVR + HIGH HEART RATE (tachycardia is protective — shorter diastole = less regurgitation) + vasopressor (noradrenaline to raise diastolic/coronary perfusion); AVOID pure beta-blockers in isolated acute AR (abolishes the compensatory tachycardia) and AVOID IABP (diastolic augmentation WORSENS the regurgitant volume) — except that in Type A dissection WITH AR, beta-blockers ARE first-line (to reduce dp/dt shear) and the AR is corrected by emergency surgery. Definitive therapy is URGENT SURGICAL AVR. (4) PROSTHETIC VALVE DYSFUNCTION: thrombosis (mechanical valve — obstructive: rtPA/systemic thrombolysis or surgery; non-obstructive: heparin ± lysis), pannus, dehiscence (paravalvular leak), structural deterioration (bioprosthesis), and prosthetic endocarditis — any unexplained shock/pulmonary oedema in a prosthetic-valve patient demands urgent echo (± fluoroscopy for leaflet motion). In ALL acute valvular emergencies the ECHOCARDIOGRAM is diagnostic and must be obtained EARLY; standard 'heart failure' therapy (nitrates, aggressive diuresis, IABP, negative inotropes) can be CATASTROPHIC if applied without knowing the lesion.