Valvular Emergencies in ICU

Quick Answer: Valvular emergencies present as acute haemodynamic compromise requiring urgent ICU management and often emergent cardiac surgery. Acute aortic regurgitation (AR) from endocarditis, aortic dissection, or trauma causes rapid LV failure without compensatory dilatation—IABP is absolutely contraindicated. Acute mitral regurgitation (MR) from papillary muscle rupture (post-MI) or chordal rupture presents with flash pulmonary oedema and requires urgent surgical repair. Prosthetic valve thrombosis (PVT) is managed with fibrinolysis for non-obstructive or right-sided thrombosis, and surgery for left-sided obstructive PVT with haemodynamic compromise. Infective endocarditis (IE) requires multidisciplinary assessment with surgery indicated for heart failure, uncontrolled infection, or large mobile vegetations greater than 10 mm. Critical aortic stenosis decompensation requires afterload maintenance (avoid hypotension), avoidance of tachycardia, and consideration of TAVI as bridge or definitive therapy. Australian context is critical for rheumatic heart disease (RHD) in Aboriginal and Torres Strait Islander populations where prevalence is 50-100× higher than non-Indigenous Australians. [1-5]

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CICM Exam Focus

Written Examination (SAQ)

High-yield topics for CICM Second Part Written:

1. Acute Valvular Regurgitation

   • Pathophysiology of acute vs chronic regurgitation
   • Haemodynamic consequences and LV compensation
   • Why IABP is contraindicated in severe AR
   • Surgical indications and timing

2. Prosthetic Valve Emergencies

   • Mechanical vs bioprosthetic valve differences
   • Thrombosis vs pannus: differentiation and management
   • Fibrinolysis protocols and contraindications
   • Emergency surgical indications

3. Infective Endocarditis Complications

   • Modified Duke criteria
   • Embolic complications (stroke, splenic abscess)
   • Perivalvular abscess and conduction disturbances
   • Surgical indications per ESC guidelines

4. Critical Aortic Stenosis Management

   • Haemodynamic goals (afterload, preload, rate)
   • Why vasodilators are relatively contraindicated
   • TAVI as bridge to definitive therapy
   • Anaesthetic considerations

5. Rheumatic Heart Disease

   • Australian Indigenous health context
   • Acute rheumatic fever diagnosis (Jones criteria)
   • Secondary prophylaxis protocols
   • Multivalvular disease management

Hot Case Presentations

Typical scenarios:

• Post-MI papillary muscle rupture with cardiogenic shock
• Prosthetic mitral valve with elevated gradients and fever
• Young Aboriginal patient with acute pulmonary oedema and RHD
• Post-aortic dissection repair with severe AR
• IE with new AV block and perivalvular abscess

Key examination findings to elicit:

• Murmur characteristics (timing, radiation, intensity)
• Signs of heart failure (JVP, crackles, oedema)
• Peripheral stigmata of IE (splinter haemorrhages, Janeway lesions)
• Signs of embolic phenomena (focal neurology, splenomegaly)

Viva Voce

Scenario-based questions:

• Approach to acute pulmonary oedema with new murmur post-MI
• Management of prosthetic valve with elevated gradients
• Decision-making: fibrinolysis vs surgery for PVT
• IE with embolic stroke: timing of surgery
• Haemodynamic management of critical AS awaiting TAVI

Key discussion points:

• Pathophysiology of acute vs chronic valvular lesions
• Role of TOE vs TTE in valvular emergencies
• IABP indications and contraindications
• Surgical timing: emergent vs urgent vs elective
• Indigenous health considerations in RHD

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Key Points

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Epidemiology

Valvular Heart Disease in ICU

Incidence:

• Valvular heart disease accounts for 10-25% of cardiac ICU admissions globally [26]
• Acute valvular emergencies requiring emergency surgery: 2-5% of all cardiac surgery [27]
• Prosthetic valve thrombosis: 0.5-8% per patient-year for mechanical valves, higher with inadequate anticoagulation [10]
• Infective endocarditis: 3-10 per 100,000 person-years, increasing with prosthetic valves and device use [28]

Australian/New Zealand Context:

• Rheumatic heart disease prevalence in Aboriginal and Torres Strait Islander populations: 8.6 per 1,000 (vs 0.15 per 1,000 in non-Indigenous) [18]
• RHD-related cardiac surgery in Australia: Aboriginal patients 8× more likely than non-Indigenous [29]
• Mean age at first RHD surgery in Indigenous Australians: 21 years (vs 67 years non-Indigenous) [30]
• Northern Territory has highest RHD burden globally for high-income countries [31]

Mortality Data

Acute Aortic Regurgitation:

• Medical management mortality: 75% within 48 hours [6]
• Emergent surgical repair mortality: 15-25% [32]
• Post-aortic dissection AR surgical mortality: 25-35% [33]

Acute Mitral Regurgitation:

• Papillary muscle rupture without surgery: 75% mortality within 24 hours [8]
• Emergent mitral valve surgery: 20-40% operative mortality [9]
• Post-MI MR (any severity) associated with 2-3× increased 30-day mortality [34]

Prosthetic Valve Thrombosis:

• Obstructive PVT mortality: 10-15% with surgery, 5-10% with fibrinolysis [10]
• Non-obstructive PVT: low mortality with anticoagulation optimisation [11]

Infective Endocarditis:

• Overall in-hospital mortality: 15-25% [28]
• IE with cardiogenic shock: 40-60% mortality [35]
• IE with stroke: 20-40% mortality [36]
• Prosthetic valve endocarditis (PVE): 20-40% in-hospital mortality [37]

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Acute Aortic Regurgitation

Aetiology

Acute AR presents differently from chronic AR due to lack of compensatory LV dilatation:

PMID: 26320853 - ESC Guidelines on Valvular Heart Disease 2021 [38]

Pathophysiology

Acute vs Chronic AR - Critical Distinction:

Chronic AR:

• Gradual volume overload allows LV eccentric hypertrophy and dilatation
• LV end-diastolic volume increases (up to 200-300 mL)
• LV compliance increases, maintaining normal filling pressures
• Forward stroke volume maintained by increased total stroke volume
• Patients may remain asymptomatic for decades

Acute AR:

• Sudden volume overload on non-dilated, non-compliant LV
• LV cannot accommodate regurgitant volume
• Rapid rise in LV end-diastolic pressure (LVEDP) → approaches aortic diastolic pressure
• Early closure of mitral valve (protective but reduces preload)
• Rapid rise in left atrial pressure → pulmonary oedema
• Compensatory tachycardia limits diastolic filling time (partially protective)
• Systemic vasoconstriction reduces forward flow

Haemodynamic Consequences:

• Narrow pulse pressure (unlike chronic AR with wide pulse pressure)
• Elevated pulmonary capillary wedge pressure (often greater than 25 mmHg)
• Low cardiac output despite hyperdynamic LV
• Rapid progression to cardiogenic shock

Clinical Features

Symptoms:

• Acute dyspnoea (flash pulmonary oedema)
• Chest pain (coronary malperfusion, dissection)
• Syncope (low cardiac output)
• Symptoms of underlying cause (fever in IE, back pain in dissection)

Signs:

• Tachycardia (often greater than 100 bpm)
• Hypotension with narrow pulse pressure
• Short, soft diastolic murmur (not the classical long decrescendo of chronic AR)
• Absent peripheral signs (no water-hammer pulse, Corrigan's sign, pistol-shot femorals)
• Signs of pulmonary oedema (crackles, hypoxia)
• Soft S1 (early mitral valve closure due to elevated LVEDP)
• Austin Flint murmur may be present (low-pitched diastolic rumble from functional MS)

Clinical Pearl: The murmur in acute severe AR is often shorter and softer than chronic AR because rapid equalisation of aortic and LV pressures shortens regurgitation time.

Investigations

Transthoracic Echocardiography (TTE):

• Normal or mildly dilated LV (unlike chronic AR)
• Hyperdynamic LV function (EF often preserved initially)
• Dense, holodiastolic regurgitant jet
• Premature mitral valve closure (M-mode)
• Pressure half-time less than 200 ms (severe AR)
• Diastolic mitral regurgitation (reversal of transmitral flow)

Transoesophageal Echocardiography (TOE):

• Essential for mechanism identification
• Aortic root assessment (dissection, abscess)
• Vegetation detection
• Prosthetic valve dysfunction

CT Aortography:

• Mandatory if dissection suspected
• Define extent of dissection
• Plan surgical approach

Cardiac Catheterisation:

• Rarely needed with modern echo
• May show elevated LVEDP, equalisation of aortic diastolic and LV end-diastolic pressures

Management

Immediate Resuscitation:

• High-flow oxygen, non-invasive ventilation if tolerated
• Arterial line for BP monitoring
• Central venous access
• Urgent surgical consultation

Medical Stabilisation (Bridge to Surgery):

IABP is ABSOLUTELY CONTRAINDICATED:

• Diastolic augmentation increases regurgitant volume
• Worsens pulmonary oedema
• May precipitate circulatory collapse

VA-ECMO:

• May be considered as bridge to surgery in refractory cardiogenic shock
• Increases afterload (must consider in AR context)
• Should be combined with LV venting strategy if prolonged

Surgical Intervention:

• Emergent surgery (within hours) is treatment of choice
• Aortic valve replacement (mechanical or bioprosthetic)
• Valve-sparing root replacement if feasible
• Bentall procedure for aortic root pathology
• Operative mortality: 15-25% for acute AR [32]

PMID: 23391586 - Acute Aortic Regurgitation [6]

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Acute Mitral Regurgitation

Aetiology

Papillary Muscle Rupture

Anatomy and Vulnerability:

• Posteromedial papillary muscle: Single blood supply from posterior descending artery (PDA)
• Anterolateral papillary muscle: Dual supply from LAD and LCx
• Posteromedial rupture 6-12× more common than anterolateral [8]
• Occurs in 1-3% of acute MI, usually 2-7 days post-infarction

Types of Rupture:

• Complete rupture: Flail leaflet, acute severe MR, cardiogenic shock
• Partial rupture: Severe MR, may be initially stable
• Papillary muscle dysfunction (without rupture): Moderate MR, more stable

Clinical Pearl: Papillary muscle rupture can occur with relatively small infarcts because the papillary muscle is an end-arterial structure. Unlike ventricular septal rupture, it doesn't require extensive myocardial necrosis.

Pathophysiology

Acute vs Chronic MR:

Chronic MR:

• Gradual volume overload → LA dilatation
• LA compliance increases → normal LA pressures
• LV eccentric hypertrophy maintains forward output
• Patients often asymptomatic for years

Acute MR:

• Sudden volume overload on non-compliant LA
• Rapid rise in LA pressure → pulmonary oedema
• LA pressure may exceed 30-40 mmHg
• V-waves greater than 50 mmHg on PCWP tracing (giant V-waves)
• Reduced forward cardiac output → cardiogenic shock
• LV hyperdynamic but ineffective (ejecting into low-pressure LA)

Haemodynamic Profile:

• Low systemic BP
• High PCWP with giant V-waves
• Low cardiac output/cardiac index
• High systemic vascular resistance (compensatory)
• Pulmonary hypertension (reactive)

Clinical Features

Symptoms:

• Acute severe dyspnoea (flash pulmonary oedema)
• Chest pain (if ongoing ischaemia)
• Haemoptysis (pink frothy sputum)
• Syncope (low output)

Signs:

• Tachycardia
• Hypotension with cool extremities
• Loud pansystolic murmur (apex, radiating to axilla) - BUT may be soft or absent in severe MR with low cardiac output
• S3 gallop (volume overload)
• Pulmonary oedema (crackles throughout)
• Signs of RV failure if severe

Clinical Pearl: The murmur of acute severe MR may be deceptively soft because:

1. Large regurgitant orifice allows rapid pressure equalisation
2. Low cardiac output reduces flow velocity
3. Tachycardia shortens systole

Investigations

Transthoracic Echocardiography:

• Flail mitral leaflet (ruptured papillary muscle or chordae)
• Severe MR with eccentric jet
• Hyperdynamic LV (may have regional wall motion abnormality from MI)
• Normal or small LA (not dilated as in chronic MR)
• Pulmonary vein flow reversal

Transoesophageal Echocardiography:

• Superior for mechanism delineation
• Essential for surgical planning
• Detects subtle chordal or papillary muscle pathology

Pulmonary Artery Catheter:

• Giant V-waves on PCWP tracing (greater than 50 mmHg)
• Elevated PCWP (greater than 25 mmHg)
• Low cardiac output (CI less than 2.0 L/min/m²)

Coronary Angiography:

• If aetiology is post-MI and revascularisation considered
• May identify culprit vessel for combined CABG

Management

Immediate Resuscitation:

• High-flow oxygen, intubation often required
• Arterial line, central venous access
• Vasodilator therapy to reduce afterload and regurgitant fraction
• Urgent surgical consultation

Medical Stabilisation:

IABP in Acute MR:

• Indicated (unlike AR) - diastolic deflation reduces afterload
• Increases forward cardiac output
• Reduces regurgitant volume
• Improves coronary perfusion
• Bridge to surgery

Surgical Intervention:

• Emergent surgery is definitive treatment
• Mitral valve repair preferred if anatomically feasible (better long-term outcomes)
• Mitral valve replacement if repair not possible (extensive destruction)
• Combined CABG if significant coronary disease
• Operative mortality: 20-40% for post-MI papillary muscle rupture [9]

PMID: 25863668 - Papillary Muscle Rupture [8]

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Acute Aortic Stenosis Decompensation

Critical Aortic Stenosis

Definition:

• Severe AS: Valve area less than 1.0 cm² (or less than 0.6 cm²/m² indexed), mean gradient greater than 40 mmHg, peak velocity greater than 4 m/s
• Critical AS: Subset of severe AS with symptoms or LV decompensation

Natural History:

• Symptomatic severe AS: 50% mortality at 2 years without intervention [14]
• Sudden death risk: 1-2% per year in asymptomatic severe AS
• Once symptoms develop: 25% mortality per year without surgery

Precipitants of Decompensation

Pathophysiology of Decompensation

Chronic Compensation:

• Pressure overload → concentric LV hypertrophy
• Thick LV wall maintains normal wall stress (Law of Laplace)
• Diastolic dysfunction develops (stiff LV)
• Preload-dependent physiology

Decompensation:

• LV systolic dysfunction develops (afterload mismatch)
• Rising LVEDP → pulmonary congestion
• Reduced cardiac output → symptoms
• Subendocardial ischaemia (increased demand + reduced supply)
• May develop low-flow, low-gradient AS

Haemodynamic Fragility:

• Preload-dependent: Stiff LV requires high filling pressures
• Afterload-sensitive: Cannot increase stroke volume against sudden afterload reduction
• Rate-dependent: Fixed stroke volume; CO = HR × SV (limited reserve)
• Coronary flow reserve reduced (hypertrophied myocardium)

Clinical Features

Symptoms of Decompensation:

• Dyspnoea (most common presenting symptom of severe AS)
• Angina (supply-demand mismatch, even without CAD)
• Syncope (especially exertional - unable to increase CO)
• Orthopnoea/PND (elevated filling pressures)

Signs:

• Slow-rising, low-volume pulse (parvus et tardus)
• Narrow pulse pressure
• Harsh crescendo-decrescendo systolic murmur (RUSB, radiating to carotids)
• Soft or absent S2 (calcified, immobile aortic valve)
• S4 gallop (stiff LV)
• Signs of heart failure (JVP, oedema, crackles)
• Heaving, sustained apex beat (LVH)

Clinical Pearl: In severe LV dysfunction, the murmur may be soft despite critical stenosis (low-flow state).

Investigations

Transthoracic Echocardiography:

• Valve area (continuity equation): less than 1.0 cm² (severe), less than 0.6 cm² (critical)
• Mean gradient: greater than 40 mmHg (severe)
• Peak velocity: greater than 4 m/s (severe)
• LV function (may be preserved or reduced)
• LV wall thickness (concentric hypertrophy)
• Diastolic function assessment

Low-Flow, Low-Gradient AS:

• AVA less than 1.0 cm², mean gradient less than 40 mmHg, EF less than 50%
• Dobutamine stress echo to differentiate:
  • "True severe AS: AVA remains less than 1.0 cm² with increased gradient"
  • "Pseudo-severe AS: AVA increases greater than 1.0 cm² (LV dysfunction, not true severe AS)"
• Stroke volume index less than 35 mL/m² = low flow

CT Calcium Score:

• Aortic valve calcium score greater than 2000 AU (men) or greater than 1200 AU (women) confirms severe AS
• Useful when echo gradient and area discordant

PMID: 27206819 - ESC/EACTS Guidelines on Valvular Heart Disease 2017 [14]

Haemodynamic Management

Core Principles:

Vasodilator Use:

• Traditionally contraindicated (unable to increase stroke volume to compensate for afterload reduction)
• Judicious use with invasive monitoring may be tolerated if:
  • Severe heart failure with elevated filling pressures
  • Careful titration with arterial line
  • Inotropic support available

PMID: 10639539 - Vasodilators in Aortic Stenosis [15]

Inotropic Support:

• Dobutamine: increases contractility, may reduce SVR (beneficial and detrimental)
• Milrinone: may cause excessive vasodilation
• Adrenaline: maintains SVR, potent inotropy

Atrial Fibrillation Management:

• Loss of atrial kick critical in AS (25% of LV filling)
• Urgent rate control (beta-blockers, digoxin, amiodarone)
• Cardioversion if haemodynamically unstable
• Avoid excessive negative inotropy

Bridging Strategies

TAVI as Bridge or Definitive Therapy:

• Increasingly used in high-risk surgical patients
• Can be performed urgently/emergently in select cases
• 30-day mortality: 3-5% in contemporary series [39]
• Procedural stroke: 2-4%

Balloon Aortic Valvuloplasty (BAV):

• Palliative or bridge to SAVR/TAVI
• Restenosis rate: 50% at 6 months
• Limited role in acute decompensation
• May provide haemodynamic stabilisation

Mechanical Circulatory Support:

• IABP: limited benefit (afterload reduction not tolerated)
• VA-ECMO: may be used as bridge to TAVI in cardiogenic shock
• Impella: can support LV while reducing afterload

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Prosthetic Valve Dysfunction

Types of Prosthetic Valves

Mechanical Valves:

• Bileaflet (St. Jude, On-X): Most common currently
• Single disc (Bjork-Shiley): Historical
• Ball-and-cage (Starr-Edwards): Historical
• Require lifelong anticoagulation (INR 2.5-3.5 for mitral, 2.0-3.0 for aortic)
• Durability: 20-30+ years

Bioprosthetic Valves:

• Porcine (Hancock, Mosaic)
• Bovine pericardial (Carpentier-Edwards, Magna)
• Usually no long-term anticoagulation (aspirin only after 3-6 months)
• Structural valve deterioration: 10-20 years (faster in younger patients)

TAVI Valves:

• Balloon-expandable (Edwards SAPIEN)
• Self-expanding (Medtronic CoreValve)
• Increasing use, durability data evolving

Causes of Prosthetic Valve Dysfunction

Thrombosis vs Pannus

Differentiation is Critical (Determines Management):

PMID: 27180098 - Prosthetic Valve Thrombosis vs Pannus [40]

Diagnosis

Clinical Features:

• New or worsening dyspnoea
• Signs of heart failure
• Embolic events (stroke, peripheral)
• Change in valve click sound (mechanical valves)
• New murmur

Investigations:

TTE:

• Elevated gradients (compare to baseline)
• Peak gradient greater than 50% above baseline suggests dysfunction
• Reduced effective orifice area
• Limited for prosthetic valves (shadowing)

TOE:

• Superior for prosthetic valve assessment
• Visualises thrombus, pannus, vegetation
• Assesses leaflet motion
• Detects paravalvular leak

Fluoroscopy:

• Assesses leaflet motion in mechanical valves
• Reduced excursion indicates obstruction
• Cannot differentiate thrombus from pannus

CT:

• Can visualise thrombus (hypoattenuating)
• Leaflet calcification in bioprosthetic
• Reduced leaflet motion on cine imaging

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Prosthetic Valve Thrombosis

Risk Factors

• Subtherapeutic anticoagulation (most important)
• Mitral position (lower flow, larger valves)
• Older valve designs
• Hypercoagulable states
• Atrial fibrillation
• Low cardiac output states
• Pregnancy

Classification

Obstructive PVT:

• Significant increase in gradients
• Clinical symptoms of heart failure or cardiogenic shock
• Haemodynamic compromise

Non-obstructive PVT:

• Small thrombus without significant gradient increase
• Often incidental finding
• Lower embolic risk

Management Algorithm

PMID: 25063007 - ACC/AHA Valve Guidelines 2014 [10]

Left-Sided Obstructive PVT:

Haemodynamically Unstable (Cardiogenic Shock):

• Emergency surgery is first-line (Class I)
• Fibrinolysis if surgery not immediately available or very high surgical risk

Haemodynamically Stable:

• Surgery preferred (Class IIa) - lower embolic risk than fibrinolysis
• Fibrinolysis reasonable alternative (Class IIb) if:
  • High surgical risk
  • Small thrombus (less than 0.8 cm²)
  • No contraindications to fibrinolysis
  • Consider if recent onset (less than 2 weeks)

Right-Sided PVT:

• Fibrinolysis first-line (Class IIa)
• Lower systemic embolic risk
• Surgery reserved for fibrinolysis failure

Non-Obstructive PVT:

• Anticoagulation optimisation (IV UFH to PTT 2-2.5× control)
• Serial imaging (TOE every 1-2 weeks)
• If thrombus persists/enlarges despite anticoagulation: surgery or fibrinolysis

Fibrinolysis Protocol

Agents:

• Alteplase (tPA): 10 mg bolus + 90 mg over 90 min (standard)
• Low-dose, slow-infusion protocol: 25 mg over 6-25 hours (lower bleeding risk)
• Tenecteplase: Weight-based bolus (less data for PVT)

PMID: 23611578 - Low-Dose Fibrinolysis for PVT [41]

Contraindications to Fibrinolysis:

• Recent stroke (within 3 months)
• Active bleeding
• Recent major surgery (within 10 days)
• Large thrombus greater than 0.8 cm² (high embolic risk)
• Left atrial thrombus
• History of haemorrhagic stroke

Monitoring:

• Serial TOE to assess thrombus resolution
• Neurological observations (stroke risk)
• Haemoglobin, fibrinogen monitoring

Success Rate:

• 70-90% thrombus resolution [10]
• Embolic events: 10-15%
• Major bleeding: 5-10%
• Mortality: 5-10%

Surgical Management

Indications:

• Left-sided obstructive PVT with haemodynamic instability
• Fibrinolysis failure
• Contraindication to fibrinolysis
• Large thrombus (greater than 0.8 cm²)
• Recurrent PVT

Surgical Options:

• Thrombectomy with valve preservation
• Valve replacement
• Operative mortality: 10-15%

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Infective Endocarditis

Modified Duke Criteria

PMID: 10770721 - Modified Duke Criteria [42]

Major Criteria:

1. Positive blood cultures:

   • Typical organisms in 2 separate cultures (Viridans streptococci, S. bovis, HACEK, S. aureus, community-acquired enterococci without primary focus)
   • Persistently positive blood cultures (greater than 12 hours apart or all 3/majority of 4+ cultures positive)
   • Single positive Coxiella burnetii culture or anti-phase 1 IgG antibody titre greater than 1:800

2. Evidence of endocardial involvement:

   • Positive echocardiogram (vegetation, abscess, new partial dehiscence of prosthetic valve)
   • New valvular regurgitation

Minor Criteria:

1. Predisposition (cardiac lesion, IV drug use)
2. Fever greater than 38°C
3. Vascular phenomena (emboli, Janeway lesions, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage)
4. Immunological phenomena (glomerulonephritis, Osler nodes, Roth spots, positive rheumatoid factor)
5. Microbiological evidence (positive blood culture not meeting major criteria, serological evidence)

Definite IE:

• 2 major criteria, OR
• 1 major + 3 minor, OR
• 5 minor criteria

Possible IE:

• 1 major + 1 minor, OR
• 3 minor criteria

Complications

Cardiac:

• Heart failure (most common indication for surgery)
• Perivalvular abscess (30-40% of native valve, 50-60% of prosthetic valve IE)
• Conduction disturbances (abscess extension)
• Fistulae

Embolic:

• Stroke (15-30%) - most common in S. aureus IE
• Systemic emboli (20-40%)
• Mycotic aneurysms
• Splenic abscess

Immunological:

• Glomerulonephritis
• Arthritis

PMID: 26320109 - ESC IE Guidelines 2015 [12]

Perivalvular Abscess

High-risk Features:

• Aortic valve involvement
• Prosthetic valve endocarditis
• S. aureus infection
• Prior IE

Clinical Features:

• Persistent fever despite appropriate antibiotics
• New conduction disturbances:
  • PR prolongation (first-degree AV block)
  • New bundle branch block
  • High-grade AV block
• Pericarditis

Diagnosis:

• TOE: Abscess cavity, fistula
• Sensitivity: 90% (vs 50% for TTE) [22]
• CT if TOE equivocal

Management:

• Urgent surgical indication (Class I)
• Radical debridement
• Patch reconstruction if needed
• May require aortic root replacement

Surgical Indications in IE

PMID: 22547425 - Early Surgery in IE [13]

Class I Indications (Strong Recommendation):

1. Heart Failure:

   • Severe aortic or mitral regurgitation with pulmonary oedema or cardiogenic shock
   • Valve obstruction

2. Uncontrolled Infection:

   • Persistent positive blood cultures despite appropriate antibiotics greater than 7-10 days
   • Perivalvular abscess
   • Infection by resistant organisms (fungi, Brucella, Coxiella)
   • Prosthetic valve IE caused by Staphylococci or non-HACEK gram-negatives

3. Prevention of Embolism:

   • Vegetation greater than 10 mm with one or more embolic events despite appropriate antibiotics
   • Vegetation greater than 15 mm (even without prior embolism) - Class IIa
   • Vegetation greater than 10 mm with severe stenosis/regurgitation and low surgical risk

Timing of Surgery:

• Emergent (within 24 hours): Cardiogenic shock, valve obstruction
• Urgent (within days): Uncontrolled infection, abscess, large vegetation with embolic risk
• Elective (within 1-2 weeks): Stable patient, vegetation less than 10 mm, completed antibiotics

Stroke and Surgery Timing

PMID: 23095164 - Surgery After Stroke in IE [36]

• Haemorrhagic stroke: Surgery should be delayed 4 weeks if possible
• Large ischaemic stroke: Delay 2-4 weeks to reduce haemorrhagic transformation risk
• Small ischaemic stroke or TIA: Surgery can proceed with acceptable risk
• CT/MRI should be performed to characterise lesion size and type
• Multidisciplinary decision (cardiology, cardiac surgery, neurology, infectious diseases)

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Haemodynamic Management of Valvular Emergencies

Lesion-Specific Haemodynamic Goals

Vasodilator Therapy

Nitroprusside:

• Mechanism: Arterial and venous dilation via NO release
• Dose: 0.5-5 mcg/kg/min
• Indications: Acute AR, acute MR with adequate BP
• Cautions: Cyanide toxicity (greater than 48 hours), hypotension

GTN (Nitroglycerin):

• Mechanism: Predominantly venodilation (preload reduction)
• Dose: 10-200 mcg/min
• Useful if hypertensive or significant pulmonary congestion

Nesiritide (BNP analogue):

• Limited availability in Australia
• May have role in acute heart failure from valvular disease

Inotropic Support

Dobutamine:

• Mechanism: Beta-1 agonist (inotropy) + mild beta-2 (vasodilation)
• Dose: 5-20 mcg/kg/min
• Preferred in most valvular emergencies
• Increases myocardial oxygen demand

Milrinone:

• Mechanism: PDE-III inhibitor (inotropy + vasodilation)
• Dose: 0.375-0.75 mcg/kg/min (loading 50 mcg/kg over 10 min optional)
• Useful in RV failure
• Caution: May cause excessive hypotension

Adrenaline/Noradrenaline:

• Used if hypotension refractory to vasodilators + dobutamine
• Increases afterload (detrimental in AR/MR)
• May be necessary to maintain coronary perfusion in AS

Levosimendan:

• Calcium sensitiser + K-ATP channel opener
• May be useful in decompensated valvular disease
• Limited ICU experience in acute valvular emergencies

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IABP in Valvular Disease

Mechanism of Action

• Diastolic inflation: Increases coronary perfusion pressure
• Systolic deflation: Reduces LV afterload, decreases myocardial oxygen demand

Indications in Valvular Disease

BENEFICIAL:

• Acute mitral regurgitation: Afterload reduction decreases regurgitant fraction
• Ischaemic MR pending revascularisation: Bridge to surgery
• Cardiogenic shock from AS (limited benefit, may worsen if significant AR)

CONTRAINDICATED:

• Aortic regurgitation (any severity): Diastolic augmentation worsens regurgitation
• Severe peripheral vascular disease
• Aortic dissection

IABP Timing

• Inflation: At dicrotic notch (aortic valve closure)
• Deflation: Just before systole (reduces afterload)
• Optimal timing assessed by arterial waveform

PMID: 21115682 - IABP in Valvular Disease [20]

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Mechanical Circulatory Support Selection

VA-ECMO in Valvular Emergencies

Advantages:

• Full haemodynamic support
• Not dependent on native cardiac function
• Can support biventricular failure

Disadvantages in Valvular Disease:

• Increases LV afterload (may worsen AR/MR)
• LV distension without venting → pulmonary oedema
• Requires LV venting strategy (Impella, septostomy, direct LV vent)

Indications:

• Cardiogenic shock refractory to medical therapy
• Bridge to surgery or decision
• Post-cardiotomy failure

Impella

Impella CP/5.0/5.5:

• Transvalvular LV-to-aorta pump
• Provides 3.5-5.5 L/min flow
• Reduces LV preload

Contraindications:

• Aortic stenosis (cannot cross valve)
• Mechanical aortic valve (cannot cross)
• Aortic regurgitation (increases regurgitation)
• LV thrombus

May be used:

• Acute MR (unloads LV)
• Bridge to TAVI (off-label)

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Surgical Considerations

Timing of Surgery

PMID: 24016455 - Surgical Timing in Valvular Emergencies [43]

Preoperative Optimisation

Haemodynamic Stabilisation:

• Inotropes/vasodilators as indicated
• IABP if appropriate (MR)
• VA-ECMO if refractory shock

Metabolic Optimisation:

• Correct electrolytes (especially K+, Mg2+)
• Optimise renal function
• Correct coagulopathy

Infection Control (IE):

• Blood cultures before antibiotics
• Appropriate empiric antibiotics
• Source control of extracardiac foci

Risk Stratification

EuroSCORE II:

• Validated for cardiac surgery risk prediction
• Includes emergency surgery as high-risk factor
• Estimates operative mortality

STS Score:

• Alternative risk calculator
• Valve-specific modules available

High-Risk Features:

• Cardiogenic shock
• Renal failure (dialysis)
• Respiratory failure
• Advanced age
• Prior cardiac surgery (redo)
• Active endocarditis
• Emergency surgery

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Rheumatic Heart Disease

Australian Indigenous Health Context

Epidemiology:

• RHD prevalence in Aboriginal and Torres Strait Islander Australians: 8.6 per 1,000 [18]
• Non-Indigenous Australian prevalence: 0.15 per 1,000
• 50-100× disparity - one of the highest rates globally
• Highest burden in Northern Territory, Far North Queensland, Kimberley region
• Mean age at first valve surgery: 21 years (vs 67 years non-Indigenous)

PMID: 27198622 - RHD in Indigenous Australians [18]

Acute Rheumatic Fever (ARF)

Jones Criteria (2015 Revision) - High-Risk Populations:

PMID: 25917121 - Jones Criteria Revision [44]

Major Criteria (Low-Risk):

1. Carditis (clinical or subclinical)
2. Polyarthritis
3. Chorea
4. Erythema marginatum
5. Subcutaneous nodules

Major Criteria (High-Risk Populations, including Australian Indigenous):

1. Carditis (clinical or subclinical)
2. Polyarthritis, monoarthritis, or polyarthralgia (modified)
3. Chorea
4. Erythema marginatum
5. Subcutaneous nodules

Minor Criteria:

• Fever (≥38.5°C low-risk; ≥38°C high-risk)
• Polyarthralgia (low-risk only)
• Monoarthralgia (high-risk only)
• Elevated ESR (≥60 mm/hr low-risk; ≥30 mm/hr high-risk) or CRP (≥30 mg/L)
• Prolonged PR interval

Definite ARF:

• Evidence of recent GAS infection + 2 major OR 1 major + 2 minor criteria

Valvular Involvement in RHD

Mitral Valve (Most Common - 90%):

• Mitral regurgitation (acute, most common in initial episode)
• Mitral stenosis (chronic, from repeated episodes)
• Mixed lesion

Aortic Valve (30-40%):

• Usually combined with mitral involvement
• Aortic regurgitation more common than stenosis

Tricuspid/Pulmonary:

• Less common, usually with severe left-sided disease

Management of RHD Emergencies

Acute Pulmonary Oedema in RHD:

• Often triggered by intercurrent illness, AF, pregnancy
• Management principles as per MS/MR
• Diuretics, rate control for AF
• Consider urgent intervention if refractory

Secondary Prophylaxis:

• Benzathine penicillin G 1.2 million units IM every 4 weeks (3 weeks in high-risk)
• Duration: Until age 21-40 depending on severity and recurrence
• Reduces recurrence from 50% to less than 5%

PMID: 22927445 - RHD Prophylaxis [19]

Australian Guidelines:

• RHDAustralia (www.rhdaustralia.org.au) provides national guidelines
• Register-based recall systems for secondary prophylaxis
• Culturally appropriate care delivery

Cultural Considerations

Aboriginal and Torres Strait Islander Patients:

• Involve Aboriginal Health Workers (AHW) and Aboriginal Liaison Officers (ALO)
• Recognise family structures and decision-making processes
• Consider "sorry business" and cultural obligations
• Use interpreters for language barriers
• Respect kinship systems in consent discussions
• Engage with community when possible

Māori Patients (New Zealand):

• Involve whānau (extended family) in discussions
• Respect tikanga (cultural practices)
• Engage Māori Health Workers
• Consider cultural practices around illness and death

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SAQ Practice Questions

SAQ 1: Post-MI Mitral Regurgitation

A 68-year-old man is admitted to ICU 4 days after an inferior STEMI treated conservatively (thrombolysis, not PCI). He develops sudden severe dyspnoea with pink frothy sputum. BP 85/60 mmHg, HR 115 bpm, SpO2 82% on 15 L/min oxygen. A loud pansystolic murmur is heard at the apex.

Question (15 marks): a) What is the most likely diagnosis and underlying mechanism? (3 marks) b) Describe the pathophysiology explaining his clinical presentation. (4 marks) c) Outline your initial management priorities. (4 marks) d) Discuss the role of mechanical circulatory support and definitive management. (4 marks)

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Model Answer:

a) Diagnosis and Mechanism (3 marks):

• Diagnosis: Acute severe mitral regurgitation secondary to papillary muscle rupture (1 mark)
• Mechanism: Infarction of the posteromedial papillary muscle (single blood supply from PDA in inferior MI) leading to necrosis and rupture 4 days post-MI (1 mark)
• The posteromedial papillary muscle is 6-12× more vulnerable than anterolateral due to single blood supply (1 mark)

b) Pathophysiology (4 marks):

• Sudden severe MR causes acute volume overload on a non-compliant left atrium (1 mark)
• Non-dilated LA cannot accommodate regurgitant volume → rapid rise in LA pressure (greater than 30-40 mmHg) (1 mark)
• Transmission of elevated LA pressure to pulmonary veins → acute pulmonary oedema (flash pulmonary oedema) (1 mark)
• Reduced forward cardiac output as blood preferentially regurgitates into low-pressure LA → cardiogenic shock despite hyperdynamic LV (1 mark)

c) Initial Management (4 marks):

• Airway/Breathing: Immediate intubation and mechanical ventilation for severe hypoxia and work of breathing (1 mark)
• Circulation: Arterial line, vasodilator therapy (nitroprusside 0.5-5 mcg/kg/min) to reduce afterload and regurgitant fraction (1 mark)
• Inotropic support: Dobutamine 5-15 mcg/kg/min to augment forward flow (0.5 marks)
• IABP insertion: Reduces afterload, increases coronary perfusion; appropriate bridge to surgery in acute MR (unlike AR where contraindicated) (1 mark)
• Urgent cardiothoracic surgical consultation (0.5 marks)

d) Mechanical Circulatory Support and Definitive Management (4 marks):

• IABP: First-line MCS in acute MR - diastolic deflation reduces afterload, increases forward cardiac output, and reduces regurgitant volume. Bridge to surgery (1 mark)
• VA-ECMO: May be required if refractory shock despite IABP; requires LV venting to prevent distension (0.5 marks)
• Definitive treatment: Emergent mitral valve surgery is life-saving (1 mark)
• Mitral valve repair preferred if anatomically feasible (better long-term outcomes); replacement if repair not possible (0.5 marks)
• Combined CABG if significant coronary disease; operative mortality 20-40% but medical mortality is 75% at 24 hours without intervention (1 mark)

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SAQ 2: Prosthetic Valve Thrombosis

A 52-year-old woman with a mechanical mitral valve replacement (St. Jude bileaflet, implanted 8 years ago) presents with progressive dyspnoea over 2 weeks. She admits to erratic warfarin compliance. INR is 1.4. BP 100/70 mmHg, HR 95 bpm, JVP elevated, bilateral crackles. TTE shows mean transmitral gradient 18 mmHg (baseline 5 mmHg). TOE reveals a 0.5 cm² thrombus on the atrial surface with restricted leaflet motion.

Question (15 marks): a) What is the diagnosis and what are the key features that confirm this? (3 marks) b) How do you differentiate thrombosis from pannus? (3 marks) c) Discuss the management options for this patient. (5 marks) d) What is the fibrinolysis protocol and what are the risks? (4 marks)

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Model Answer:

a) Diagnosis and Key Features (3 marks):

• Diagnosis: Obstructive prosthetic valve thrombosis (PVT) of mechanical mitral valve (1 mark)
• Key features confirming diagnosis:
  • Subtherapeutic anticoagulation (INR 1.4) with erratic compliance (0.5 marks)
  • Significantly elevated gradient (18 mmHg vs baseline 5 mmHg) - greater than 50% increase (0.5 marks)
  • TOE demonstrating thrombus on valve with restricted leaflet motion (0.5 marks)
  • Clinical deterioration with heart failure symptoms (dyspnoea, elevated JVP, crackles) (0.5 marks)

b) Differentiation of Thrombosis from Pannus (3 marks):

(0.5 marks per distinguishing feature, max 3 marks)

c) Management Options (5 marks):

• Immediate anticoagulation: IV unfractionated heparin to PTT 2-2.5× control (1 mark)
• Patient is haemodynamically stable (BP 100/70, HR 95) - allows time for decision-making (0.5 marks)
• Options:
  1. Surgery (valve replacement/thrombectomy): Lower embolic risk than fibrinolysis; preferred by some guidelines for left-sided obstructive PVT; operative mortality 10-15% (1 mark)
  2. Fibrinolysis: Reasonable alternative in this stable patient with small thrombus (0.5 cm²), recent onset, no contraindications; success rate 70-90%; embolic risk 10-15% (1 mark)
  3. Anticoagulation alone: NOT sufficient for obstructive PVT with clinical deterioration (0.5 marks)
• My approach: Given haemodynamic stability, small thrombus (less than 0.8 cm²), and recent onset, fibrinolysis is a reasonable first-line option with close monitoring; surgery if fibrinolysis fails or patient deteriorates (1 mark)

d) Fibrinolysis Protocol and Risks (4 marks):

• Standard protocol: Alteplase 10 mg bolus + 90 mg over 90 minutes (0.5 marks)
• Low-dose slow-infusion protocol: 25 mg alteplase over 6-25 hours - lower bleeding risk, similar efficacy; may be preferred in stable patients (1 mark)
• Monitoring: Serial TOE to assess thrombus resolution; neurological observations; haemoglobin and fibrinogen levels (0.5 marks)
• Risks:
  • "Systemic embolism (stroke, peripheral): 10-15% (0.5 marks)"
  • "Major bleeding (including intracranial): 5-10% (0.5 marks)"
  • "Death: 5-10% (0.5 marks)"
  • "Failure requiring surgery: 10-20% (0.5 marks)"
• Contraindications: Recent stroke (within 3 months), active bleeding, recent major surgery, large thrombus greater than 0.8 cm², left atrial thrombus

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Hot Case Scenarios

Hot Case 1: Post-MI Papillary Muscle Rupture

Setting: Cardiac ICU, Day 5

Patient: 72-year-old woman, Day 5 post-inferior STEMI (RCA occlusion, treated with primary PCI)

Current Situation:

• Intubated and ventilated 24 hours ago for flash pulmonary oedema
• IABP in situ
• Noradrenaline 0.15 mcg/kg/min, dobutamine 10 mcg/kg/min
• ABG: pH 7.32, PaCO2 38, PaO2 85, HCO3 19, lactate 3.8 mmol/L
• Echo: Flail posterior mitral leaflet, severe MR, LVEF 45%, moderate RV dysfunction

Examination Findings:

• Intubated, sedated (RASS -2)
• HR 105, BP 95/65 (MAP 75 with IABP augmentation), SpO2 94% on FiO2 0.6
• JVP elevated 8 cm
• IABP augmented waveform on arterial line
• Loud pansystolic murmur at apex radiating to axilla
• Bilateral coarse crackles
• Warm peripheries with brisk capillary refill (on inotropes)
• Abdomen soft, minimal ascites
• IABP catheter right femoral artery, dialysis catheter left femoral vein

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Examiner Questions and Model Answers:

Q: Please provide a one-minute summary of this patient.

A: "This is a 72-year-old woman, Day 5 post-inferior STEMI complicated by acute severe mitral regurgitation due to papillary muscle rupture. She developed cardiogenic shock with flash pulmonary oedema requiring intubation, IABP insertion, and inotropic support. She currently has features of ongoing shock with elevated lactate and vasoactive requirements. Key issues are:

1. Cardiogenic shock from acute severe MR - requires emergent surgical intervention
2. Haemodynamic instability requiring MCS and inotropes
3. Metabolic acidosis with elevated lactate indicating inadequate tissue perfusion
4. Moderate RV dysfunction complicating the picture
5. Surgical decision-making regarding timing and approach"

Q: Why is IABP appropriate in this case but contraindicated in aortic regurgitation?

A: "IABP works by inflating during diastole (increasing coronary perfusion) and deflating just before systole (reducing LV afterload). In acute MR, the afterload reduction during systolic deflation reduces the regurgitant fraction - blood preferentially flows forward into the aorta rather than backward into the LA. This increases effective cardiac output.

In aortic regurgitation, the problem occurs during diastole. Diastolic inflation of the IABP increases aortic diastolic pressure, which increases the pressure gradient driving blood backward through the incompetent aortic valve into the LV. This worsens the regurgitant volume and can precipitate cardiogenic shock."

Q: She has elevated lactate and metabolic acidosis. What are your next steps?

A: "The elevated lactate (3.8 mmol/L) and metabolic acidosis indicate inadequate tissue perfusion despite current support. My approach:

1. Optimise current support: Consider increasing dobutamine (up to 20 mcg/kg/min), ensure IABP timing is optimal
2. Assess for additional causes: Check for bleeding, evolving infection, other sources of hypoperfusion
3. Escalate MCS if needed: If refractory, consider VA-ECMO as bridge to surgery
4. Expedite surgical intervention: This patient has ongoing shock despite IABP - she requires emergent surgery. I would contact the cardiothoracic surgical team urgently to proceed with mitral valve repair or replacement
5. Pre-surgical optimisation: Correct electrolytes, ensure adequate haemoglobin (transfuse if Hb less than 80), correct coagulopathy"

Q: What are the surgical options and expected outcomes?

A: "Surgical options:

1. Mitral valve repair: Preferred if anatomically feasible - better long-term outcomes with lower thromboembolism risk and no need for anticoagulation. May involve chordal replacement and annuloplasty ring
2. Mitral valve replacement: Necessary if repair not possible (extensive papillary muscle destruction). Choice of bioprosthetic (no anticoagulation but durability concerns) vs mechanical (durability but lifelong warfarin)
3. Combined CABG: Should be considered given underlying CAD

Expected outcomes:

• Operative mortality for emergent mitral surgery post-MI papillary muscle rupture: 20-40%
• However, medical mortality is 75% at 24 hours without surgery
• Long-term survival in operative survivors is reasonable if they survive the perioperative period
• Given her age (72) and comorbidities, I would discuss goals of care with family while preparing for surgery"

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Hot Case 2: Infective Endocarditis with Perivalvular Abscess

Setting: ICU, Day 3

Patient: 45-year-old Aboriginal man from remote Northern Territory community

History:

• Presented 1 week ago with fever, night sweats, weight loss over 2 months
• Known RHD with prior mitral valve replacement (bioprosthetic, 6 years ago)
• Blood cultures positive for Staphylococcus aureus (MSSA)
• TOE: 15 mm vegetation on prosthetic mitral valve, moderate paravalvular regurgitation, aortic root abscess 1.2 cm

Current Situation:

• Transferred to tertiary ICU for surgical consideration
• Developed complete heart block requiring temporary pacing wire
• Currently: temp 38.2°C, HR 80 (paced), BP 105/65, on vancomycin + gentamicin
• Family (wife, mother, uncle as elder) present from community - 8-hour RFDS flight away

Examination Findings:

• Alert, oriented, mildly confused (GCS 14 - E4 V4 M6)
• Paced rhythm (transvenous pacemaker right IJ)
• JVP 6 cm, metallic prosthetic S1, soft early diastolic murmur (AR from abscess extension)
• Lungs clear
• Spleen palpable 3 cm below costal margin
• Multiple splinter haemorrhages both hands
• Janeway lesions on palms
• Right foot: cool, delayed capillary refill, absent dorsalis pedis pulse (embolic occlusion)

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Examiner Questions and Model Answers:

Q: Please summarise this case and identify the key issues.

A: "This is a 45-year-old Aboriginal man with prosthetic valve endocarditis (PVE) complicated by perivalvular abscess, complete heart block, and multiple systemic emboli. Key issues:

1. Prosthetic valve endocarditis with S. aureus - high-risk organism with high mortality
2. Perivalvular abscess with extension causing complete heart block - Class I surgical indication
3. Large vegetation (15 mm) - high embolic risk
4. Multiple embolic complications: Splenic (splenomegaly), cutaneous (Janeway lesions, splinter haemorrhages), suspected right foot arterial embolism
5. Acute limb ischaemia - right foot requiring vascular assessment
6. Temporary pacing dependence - will need permanent pacemaker
7. Remote Indigenous patient - cultural considerations for family communication and ongoing care
8. RHD background - reflects health disparity affecting Aboriginal Australians"

Q: What are the surgical indications in this case?

A: "This patient has multiple Class I indications for urgent surgery per ESC guidelines:

1. Perivalvular abscess: The aortic root abscess is an absolute indication for surgery - medical therapy alone cannot eradicate abscess cavities, and there is risk of fistula formation and further extension

2. New conduction disturbance: Complete heart block indicates abscess extension to conduction system - requires surgical debridement

3. Prosthetic valve endocarditis with Staphylococcus: PVE with staphylococcal infection has high mortality with medical therapy alone

4. Large vegetation (15 mm): Greater than 10 mm vegetation is an indication for surgery to prevent further embolism, especially as he already has multiple embolic events

5. Uncontrolled infection: Persistent fever despite antibiotics suggests inadequate source control

The timing should be urgent (within 48-72 hours) once his foot ischaemia is addressed and he is optimised."

Q: How would you approach communication with his family given the cultural context?

A: "Culturally appropriate communication is essential. My approach:

1. Involve Aboriginal Health Worker (AHW) and Aboriginal Liaison Officer (ALO) from the beginning - they can advise on cultural protocols and facilitate communication

2. Understand family structure: The uncle as elder may be the appropriate decision-maker in his culture. I would clarify who should be included in discussions

3. Arrange a family meeting in an appropriate space with adequate time, including:

   • Cardiothoracic surgeon
   • Intensivist (myself)
   • AHW/ALO
   • Interpreter if language barriers exist
   • All key family members the patient wishes to have present

4. Explain the situation clearly without medical jargon:

   • The infection has damaged the new valve and spread to surrounding heart
   • He needs surgery to clean out the infection and replace the valve
   • Without surgery, he is unlikely to survive
   • Surgery carries significant risk (20-30% mortality for PVE with abscess) but is his best chance

5. Acknowledge the remoteness: Discuss how family can stay connected if they need to return to community, explore options for accommodation in the city

6. Consider cultural practices: Ask if there are any cultural or spiritual practices they would like to observe

7. Allow time for family discussion - decisions may need to be made collectively

8. Document discussions carefully and ensure understanding is confirmed"

Q: What about the acute limb ischaemia?

A: "The right foot with absent dorsalis pedis pulse, delayed capillary refill, and coolness suggests acute arterial embolic occlusion. My approach:

1. Urgent vascular surgery consultation: This is a surgical emergency (6-hour window to prevent irreversible tissue loss)
2. Assess the 6 Ps: Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Poikilothermia
3. If Rutherford class I-IIa (viable, marginally threatened): Anticoagulation, monitoring, may need surgical embolectomy or catheter-directed therapy
4. If Rutherford class IIb (immediately threatened): Urgent revascularisation
5. Coordination with cardiac surgery: May need combined procedure or staged approach

The challenge is balancing:

• Limb-threatening ischaemia requiring urgent intervention
• Cardiac surgery for life-threatening endocarditis
• Risk of bleeding with anticoagulation in context of possible cerebral emboli

I would involve vascular surgery immediately for joint decision-making. If the limb is immediately threatened, embolectomy may need to precede cardiac surgery."

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Viva Scenarios

Viva 1: Acute Aortic Regurgitation

Examiner: "A 58-year-old man presents with sudden severe dyspnoea. He is hypotensive with a new diastolic murmur. Echo shows severe aortic regurgitation. Tell me about the pathophysiology of acute versus chronic aortic regurgitation."

Candidate: "Acute and chronic aortic regurgitation have fundamentally different pathophysiology due to the LV's ability to adapt:

Chronic AR:

• Gradual volume overload over months to years
• LV undergoes eccentric hypertrophy - sarcomeres replicate in series, increasing LV diameter
• This increases end-diastolic volume, sometimes to 200-300 mL
• LV compliance increases, so despite higher volumes, filling pressures remain near normal
• The increased end-diastolic volume allows increased total stroke volume (Frank-Starling), maintaining forward output
• Patients may remain asymptomatic for decades until LV decompensation

Acute AR:

• Sudden volume overload on a normal, non-dilated LV
• The LV cannot acutely increase its compliance or size
• The regurgitant volume causes rapid rise in LV end-diastolic pressure
• LVEDP may approach aortic diastolic pressure - this causes early closure of the mitral valve (protective but reduces preload)
• The elevated LVEDP transmits backward to the left atrium and pulmonary veins, causing acute pulmonary oedema
• Forward stroke volume falls dramatically
• Compensatory tachycardia occurs (shortens diastolic regurgitation time) and vasoconstriction maintains BP temporarily
• Without intervention, rapid progression to cardiogenic shock and death"

Examiner: "Why is the murmur different in acute versus chronic AR?"

Candidate: "The classical murmur of chronic AR is a long, decrescendo, high-pitched early diastolic murmur best heard at the left sternal edge with the patient leaning forward in expiration.

In acute severe AR, the murmur is typically shorter and softer for two reasons:

1. Rapid equalisation of aortic and LV diastolic pressures - the pressure gradient driving the murmur diminishes quickly during diastole, shortening the murmur duration
2. Lower cardiac output reduces flow velocity across the regurgitant orifice, making the murmur quieter

Similarly, the peripheral signs of chronic AR (water-hammer pulse, Corrigan's sign, pistol-shot femorals, de Musset's sign) are absent in acute AR because there isn't the wide pulse pressure that develops with chronic compensated AR. In fact, the pulse pressure in acute severe AR is often narrow due to low systolic pressure and relatively maintained diastolic pressure."

Examiner: "Why is IABP contraindicated in aortic regurgitation?"

Candidate: "IABP works by:

1. Inflating during diastole - increasing aortic diastolic pressure and coronary perfusion
2. Deflating just before systole - reducing LV afterload

In AR, the problem is regurgitation occurring during diastole. When the IABP inflates and increases aortic diastolic pressure, it increases the pressure gradient driving blood backward through the incompetent aortic valve into the LV.

This worsens the regurgitant volume, further overloads the already distended LV, increases LVEDP and pulmonary congestion, and can precipitate cardiovascular collapse.

For this reason, IABP is absolutely contraindicated in any degree of aortic regurgitation. This includes patients with acute Type A aortic dissection who may have varying degrees of AR from commissural detachment.

If mechanical circulatory support is needed in acute AR, VA-ECMO is the preferred option, though this also increases afterload and may require LV venting strategies."

Examiner: "What is the definitive management?"

Candidate: "Definitive management of acute severe AR is emergent cardiac surgery - typically within hours of diagnosis.

Preoperative stabilisation includes:

• Vasodilators (nitroprusside) to reduce afterload and improve forward flow
• Inotropes (dobutamine) to augment cardiac output
• Allowing tachycardia (reduces diastolic regurgitation time)
• Intubation and ventilation for respiratory failure

Surgical options depend on aetiology:

• Aortic valve replacement (mechanical or bioprosthetic) for isolated valve disease
• Bentall procedure (composite graft with valve) for aortic root pathology
• Valve-sparing root replacement (David or Yacoub procedure) if feasible
• Urgent repair of Type A dissection if that's the cause

Operative mortality for acute AR is 15-25%, but medical mortality is 75% within 48 hours, making surgery imperative."

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Viva 2: Critical Aortic Stenosis Management

Examiner: "You're called to review a 78-year-old man in the Emergency Department with severe dyspnoea. He has critical aortic stenosis and is hypotensive. Discuss your haemodynamic management."

Candidate: "This patient with critical AS and hypotension represents a challenging management scenario. The key is understanding AS pathophysiology:

Haemodynamic Principles in AS:

1. Fixed stroke volume: The stenotic valve limits output increase
2. Preload dependent: The hypertrophied, stiff LV requires high filling pressures
3. Afterload sensitive: Sudden afterload reduction cannot be compensated by increased stroke volume
4. Rate dependent: CO = HR × SV; with fixed SV, maintaining HR is important (but not tachycardia which reduces diastolic filling)
5. Sinus rhythm critical: Loss of atrial kick (25% of LV filling) is poorly tolerated

Initial Assessment:

• Determine precipitant (AF, infection, anaemia, dehydration, ischaemia)
• Check ECG for rhythm (AF requires urgent rate control or cardioversion)
• Arterial line for accurate BP monitoring
• Volume assessment (JVP, echo)

Haemodynamic Management:

For hypotension:

• Judicious fluid challenge: Small aliquots (250 mL) if hypovolaemic - the stiff LV needs adequate preload
• Vasopressors: Phenylephrine or noradrenaline to maintain afterload and coronary perfusion pressure
• Avoid excessive vasodilation: Vasodilators traditionally contraindicated as the patient cannot increase stroke volume to compensate

For atrial fibrillation:

• Urgent rate control (amiodarone preferred as less negative inotropy than beta-blockers)
• Consider DC cardioversion if unstable

Avoid:

• Aggressive diuresis (reduces preload)
• Pure vasodilators without monitoring
• Tachycardia (reduces diastolic filling and coronary perfusion)
• Beta-blockers in decompensated state (negative inotropy)

Inotropic support if needed:

• Dobutamine: increases contractility, reduces SVR (mixed effects)
• May need vasopressor to maintain afterload if using dobutamine"

Examiner: "The patient improves with fluids and vasopressors. His echo shows AVA 0.5 cm², mean gradient 25 mmHg, EF 35%. What is the significance of these findings?"

Candidate: "This is a case of low-flow, low-gradient severe AS - a challenging diagnostic and management situation.

The findings show:

• AVA 0.5 cm²: Severely reduced, in critical range
• Mean gradient 25 mmHg: Less than 40 mmHg, which is the threshold for severe AS
• EF 35%: Reduced systolic function

The discordance between severely reduced valve area and low gradient is due to low stroke volume - insufficient flow to generate a high gradient across the stenotic valve.

This could represent:

1. True severe AS with LV dysfunction ("classical low-flow, low-gradient AS"): Afterload mismatch has caused LV decompensation
2. Pseudo-severe AS: The valve isn't truly severely stenotic, but appears so because the weak LV can't open it fully

Distinguishing these requires dobutamine stress echocardiography:

• True severe AS: AVA remains less than 1.0 cm² at peak stress, gradient increases with increased flow
• Pseudo-severe AS: AVA increases greater than 1.0 cm² at peak stress (the valve opens better with higher flow)

Additionally, CT calcium scoring can help:

• Aortic valve calcium greater than 2000 AU (men) or greater than 1200 AU (women) supports true severe AS

This distinction is critical because patients with true severe AS benefit from aortic valve replacement (surgical or TAVI), while those with pseudo-severe AS have primarily cardiomyopathy as their issue."

Examiner: "Assuming true severe AS is confirmed, what are the treatment options?"

Candidate: "For confirmed true severe AS with LV dysfunction and heart failure symptoms:

Surgical Aortic Valve Replacement (SAVR):

• Traditional gold standard
• This patient (78 years, LV dysfunction, decompensated) would be moderate-to-high surgical risk
• Operative mortality varies with risk scores (STS/EuroSCORE)
• Requires sternotomy, cardiopulmonary bypass

TAVI (Transcatheter Aortic Valve Implantation):

• Now first-line for high-risk and often intermediate-risk patients
• Non-inferior to SAVR in low-to-intermediate risk patients in recent trials
• Lower procedural risk, especially in high-risk patients
• 30-day mortality 3-5% in contemporary series
• Can be performed urgently if patient stabilises
• May be appropriate as bridge in acutely decompensated patients

Balloon Aortic Valvuloplasty (BAV):

• Palliative procedure - restenosis within 6 months in 50%
• Can be bridge to definitive SAVR or TAVI
• May provide haemodynamic stabilisation in acute setting
• Not a definitive therapy

Medical therapy alone:

• Poor prognosis: 50% 2-year mortality without intervention
• May be appropriate for palliation if intervention declined/not suitable

For this patient, after stabilisation, I would pursue urgent TAVI as the preferred option given his age, LV dysfunction, and acute presentation."

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Related Topics

• Cardiogenic Shock
• Echocardiography in ICU
• ECMO and Mechanical Circulatory Support
• Acute Heart Failure
• Infective Endocarditis
• Post-Cardiac Surgery Care