Ventricular Assist Devices (VADs) in ICU

Quick Answer

Ventricular assist devices (VADs) are mechanical pumps that provide circulatory support for patients with advanced heart failure refractory to medical therapy. Modern continuous-flow LVADs (HeartMate 3, HVAD) have largely replaced pulsatile devices, providing 1-year survival of 80-85% (PMID: 35052322). Indications include bridge to transplant (BTT, 25%), bridge to candidacy (BTC, 45%), destination therapy (DT, 25%), and bridge to recovery (BTR, less than 5%). INTERMACS profiles 1-7 stratify severity, with profiles 1-3 having highest perioperative mortality but also greatest benefit. Key components include inflow cannula (LV apex), centrifugal/axial pump, outflow graft (ascending aorta), percutaneous driveline, and external controller/batteries. Continuous-flow hemodynamics require understanding of pulsatility index (target >2.5), MAP targets (70-80 mmHg), and absent/diminished pulse pressure. Anticoagulation (Warfarin INR 2-3 plus aspirin 81-325mg) balances thrombosis vs bleeding. Major complications include pump thrombosis (2-8%), GI bleeding/AVM (15-30%), driveline infection (10-30%), stroke (3-5%/year), RV failure (20-40%), and acquired von Willebrand disease (nearly universal). Landmark trials (REMATCH 2001, HeartMate II 2007, MOMENTUM 3 2017) established VAD superiority over medical therapy and HeartMate 3 superiority over axial-flow devices. Australian VAD programs at The Alfred (Melbourne) and St Vincent's Hospital (Sydney) implant ~50-80 devices/year.

---

CICM Exam Focus

What Examiners Expect

Second Part Written (SAQ):

VAD management and complications are increasingly examined as mechanical circulatory support expands

Common SAQ stems:

• "A 55-year-old male with an LVAD is admitted to ICU with suspected pump thrombosis. Outline your diagnostic approach and management."
• "Describe the physiological principles of continuous-flow LVAD support and how this affects patient assessment."
• "Outline the indications for ventricular assist device implantation and the INTERMACS classification system."
• "A patient with an LVAD presents with GI bleeding. Discuss the pathophysiology of bleeding complications in VAD patients and your management approach."
• "Describe the anticoagulation strategy for LVAD patients and the management of supratherapeutic INR."
• "Outline the assessment and management of right ventricular failure following LVAD implantation."

Recent SAQ themes (2020-2025):

• 2024: "Discuss the diagnosis and management of driveline infection in VAD patients."
• 2023: "A patient with HeartMate 3 presents in cardiogenic shock. Outline your approach to device interrogation and troubleshooting."
• 2022: "Describe the differences between pulsatile and continuous-flow VADs, including hemodynamic implications."
• 2021: "Outline the post-operative ICU management of a patient following LVAD implantation."
• 2020: "Discuss the management of cardiac arrest in a patient with an LVAD."

Expected depth:

• INTERMACS profiles 1-7 with clinical descriptions and outcomes
• Device types (HeartMate 3, HVAD, Impella) with key differences
• Continuous-flow physiology and hemodynamic assessment
• Anticoagulation targets and management
• Recognition and management of all major complications
• Evidence base from landmark trials (REMATCH, HeartMate II, MOMENTUM 3)

Second Part Hot Case:

Typical VAD presentations:

• Post-LVAD implantation Day 1-3: Bleeding, RV failure, vasoplegic shock
• LVAD patient with suspected pump thrombosis: High LDH, hemolysis markers
• LVAD patient with GI bleeding: Scope findings, acquired vWD
• LVAD patient with stroke: Ischemic vs hemorrhagic, anticoagulation management
• LVAD patient with driveline infection: Wound assessment, sepsis workup
• LVAD patient in cardiac arrest: Resuscitation modifications

Examiners assess:

• Understanding of continuous-flow hemodynamics (no pulse, BP measurement)
• Systematic approach to device assessment (alarms, parameters, power/flow)
• Integration of clinical assessment with device parameters
• Recognition of complications and appropriate management
• Communication with VAD coordinator and cardiac surgery team
• Understanding of limitations (no defibrillation via device, chest compressions controversial)

Second Part Viva:

Expected discussion areas:

• Indications (BTT, BTC, DT, BTR) and patient selection
• INTERMACS classification and prognostic implications
• Device types and mechanisms (centrifugal vs axial flow)
• Hemodynamic assessment in continuous-flow VAD patients
• Anticoagulation strategy and INR targets
• Pump thrombosis: diagnosis, risk factors, management
• GI bleeding and acquired von Willebrand disease
• Driveline infection: prevention, diagnosis, management
• RV failure: prediction, management, need for RVAD
• Stroke: prevention, diagnosis, acute management
• Cardiac arrest and resuscitation in VAD patients
• Australian VAD programs and patient referral

Examiner expectations:

• Comprehensive understanding of VAD physiology
• Ability to interpret device parameters (flow, power, pulsatility index)
• Recognition of complication patterns
• Evidence-based discussion of landmark trials
• Practical approach to ICU management
• Understanding of multidisciplinary team involvement

Common Mistakes

• Not understanding continuous-flow hemodynamics (expecting palpable pulse)
• Using incorrect BP measurement technique (Doppler systolic, not auscultation)
• Not recognizing pump thrombosis markers (LDH, plasma-free Hb, power changes)
• Forgetting acquired von Willebrand disease as cause of GI bleeding
• Incorrect INR targets (2.0-3.0 for HeartMate 3, not higher)
• Not involving VAD coordinator/cardiac surgery in management decisions
• Incorrect approach to cardiac arrest (chest compressions controversial, no internal defibrillation)
• Confusing HeartMate 3 (centrifugal, fully magnetically levitated) with HeartMate II (axial flow)
• Not knowing INTERMACS profiles and their prognostic significance
• Forgetting RV failure as major post-implant complication (20-40%)

---

Key Points

Must-Know Facts

1. LVAD Indications: Bridge to transplant (BTT, 25%), bridge to candidacy/decision (BTC, 45%), destination therapy (DT, 25%), bridge to recovery (BTR, less than 5%); all require NYHA III-IV despite optimal medical therapy, EF less than 25%, peak VO2 less than 14 mL/kg/min or inotrope-dependence (PMID: 23747642)

2. INTERMACS Profiles: Profile 1 (critical cardiogenic shock, "crash and burn"), Profile 2 (progressive decline on inotropes, "sliding fast"), Profile 3 (stable on inotropes), Profile 4 (resting symptoms on oral therapy), Profile 5 (exertion intolerant), Profile 6 (exertion limited), Profile 7 (advanced NYHA III); Profiles 1-2 have highest perioperative mortality (30-40%) but greatest survival benefit with VAD (PMID: 30586764)

3. HeartMate 3 Technology: Third-generation centrifugal-flow LVAD with fully magnetically levitated rotor; wide blood-flow gaps (0.5mm) reduce shear stress; artificial pulse (speed modulation ±2000 RPM every 2 seconds) reduces stasis; 2-year freedom from pump thrombosis 98.6% vs HeartMate II 89.4% (PMID: 28211672)

4. Continuous-Flow Hemodynamics: Absent or diminished pulse pressure (5-15 mmHg); MAP target 70-80 mmHg (measured by Doppler); pulsatility index (PI) = (max flow - min flow) / mean flow, target 2.5-4.5; low PI (less than 1.5) suggests hypovolemia, RV failure, or suction; high PI (>6) suggests aortic insufficiency or tamponade (PMID: 23680030)

5. Anticoagulation Strategy: Warfarin INR target 2.0-3.0 (HeartMate 3), 2.0-2.5 (HVAD); aspirin 81-325mg daily (some centers use 81mg); no heparin bridging for minor procedures if INR >1.5; balance between pump thrombosis (2-8%) and bleeding complications (30-40%) (PMID: 31865801)

6. Pump Thrombosis Markers: LDH >2.5× ULN (sensitivity 90%), plasma-free Hb >40 mg/dL, increased power consumption >10W (HeartMate), decreased pump flow, dark urine, symptoms of heart failure; incidence 2-8% for HeartMate 3, was 10-15% for HeartMate II (PMID: 24987394)

7. GI Bleeding/Acquired vWD: Occurs in 15-30% of LVAD patients; high shear stress causes acquired von Willebrand disease (loss of high-molecular-weight multimers); AVMs develop due to pulselessness and angiodysplasia; management includes octreotide, thalidomide (off-label), pump speed reduction, endoscopic therapy (PMID: 25042534)

8. Driveline Infection: Occurs in 10-30% of LVAD patients; most common late infection; organisms: S. aureus (40%), S. epidermidis, Pseudomonas, Candida; prevention: immobilization, tunneling, patient education; treatment: long-term suppressive antibiotics, surgical debridement, rarely pump exchange (PMID: 28259619)

9. RV Failure Post-LVAD: Occurs in 20-40% of LVAD recipients; LVAD unloading increases venous return to RV, shifts septum leftward, worsens RV geometry; predictors: RA/PCWP ratio >0.63, severe TR, RV dysfunction on echo, high creatinine, need for RVAD in 5-10%; managed with inotropes, pulmonary vasodilators, volume optimization, temporary RVAD if refractory (PMID: 23849541)

10. MOMENTUM 3 Trial (2017, 2022): Randomized 1028 patients to HeartMate 3 vs HeartMate II; primary endpoint (survival free of disabling stroke or reoperation for device malfunction): HeartMate 3 77.9% vs HeartMate II 71.8% at 2 years (p=0.04); 5-year survival 58.4% vs 43.7%; pump thrombosis 98.6% freedom vs 89.4% (PMID: 28211672, 35052322)

Memory Aids

Mnemonic LVAD-FLOW: Key management principles

• L: Low MAP target (70-80 mmHg)
• V: Validate with Doppler BP (not auscultation)
• A: Anticoagulation (INR 2-3, aspirin)
• D: Driveline care (immobilize, inspect daily)
• F: Flow and power monitoring (watch trends)
• L: LDH for pump thrombosis (>2.5× ULN)
• O: Optimize RV (avoid fluid overload, pulmonary vasodilators)
• W: Watch for bleeding (GI most common)

Mnemonic INTERMACS: Profiles 1-4 (most exam-relevant)

• 1: "Crashing"
• Critical shock, need urgent MCS
• 2: "Sliding"
• Progressive decline despite inotropes
• 3: "Stable"
• Inotrope-dependent but stable
• 4: "Symptomatic"
• Resting symptoms, oral therapy

Mnemonic THROMBOSIS: Pump thrombosis markers

• T: Trending power increase
• H: Hemoglobin (plasma-free) elevated
• R: Red urine (hemoglobinuria)
• O: Output (pump flow) decreased
• M: Multimer loss (vWF) - related but more for bleeding
• B: Bilirubin elevated (hemolysis)
• O: Onset of heart failure symptoms
• S: Symptoms recurrence (dyspnea, edema)
• I: Increased LDH >2.5× ULN
• S: Suction events excluded

---

Definition and Epidemiology

Definition

A ventricular assist device (VAD) is a mechanical circulatory support (MCS) pump that augments or replaces the function of a failing ventricle by continuously drawing blood from the ventricle and propelling it into the arterial circulation.

VAD Classifications:

By Ventricle Supported:

• LVAD (Left Ventricular Assist Device): Most common; supports left ventricle
• RVAD (Right Ventricular Assist Device): Supports right ventricle; RA→PA
• BiVAD (Biventricular Assist Device): Both ventricles; separate or total artificial heart

By Duration:

• Short-term/Temporary: Days to weeks; percutaneous (Impella, TandemHeart) or surgical (CentriMag)
• Durable/Long-term: Months to years; surgically implanted (HeartMate 3, HVAD)

By Flow Type:

• Pulsatile-flow (First generation): Volume-displacement pumps; obsolete (HeartMate XVE, Novacor)
• Continuous-flow (Second/Third generation): Axial or centrifugal pumps; current standard
  • "Axial-flow (Second generation): HeartMate II, Jarvik 2000"
  • "Centrifugal-flow (Third generation): HeartMate 3 (fully magnetically levitated), HVAD (hybrid magnetic-hydrodynamic)"

Current Durable LVAD Devices:

*HVAD voluntarily withdrawn from market June 2021 due to neurological adverse events; existing patients continue on device

Temporary/Short-Term MCS Devices:

Epidemiology

Global VAD Implants:

• United States: ~3,500 primary LVAD implants/year (INTERMACS 2023); HeartMate 3 >95% of new implants (PMID: 37148016)
• Europe: ~2,000 implants/year (EUROMACS)
• Australia/New Zealand: ~50-80 implants/year across 4-5 centres

Australian VAD Programs (PMID: 35587227):

INTERMACS Registry Data (2023) (PMID: 37148016):

• Total implants >30,000 in registry
• Indication distribution: BTT 20-25%, BTC/decision 45%, DT 25-30%, BTR less than 5%
• INTERMACS profile at implant: Profile 1 (3%), Profile 2 (15%), Profile 3 (40%), Profile 4 (25%), Profile 5-7 (17%)
• 1-year survival: 82-85% (HeartMate 3)
• 2-year survival: 75-80%
• 5-year survival: 55-60%

Outcomes by INTERMACS Profile (PMID: 30586764):

Indigenous Health Considerations:

Aboriginal and Torres Strait Islander Populations:

• Higher rates of cardiomyopathy due to rheumatic heart disease, ischemic heart disease
• Often present later with more advanced heart failure (INTERMACS 1-2)
• Limited access to VAD centres (all metropolitan); require extended stays away from Country
• Cultural considerations:
  • Involve Aboriginal Hospital Liaison Officers (AHLOs) early
  • Extended family involvement in decision-making
  • Concerns about return to Country with chronic medical device
  • Importance of connection to land during recovery
• Post-implant challenges:
  • Remote follow-up difficult (driveline care, INR monitoring, device checks)
  • Telehealth and outreach programs essential
  • Training local health workers in VAD recognition/troubleshooting
  • RFDS protocols for VAD patient retrieval

Maori Health Considerations (New Zealand):

• Whanau (family) involvement in all discussions
• Kaumatua (elder) consultation may be appropriate
• Cultural safety in explaining invasive permanent device
• Considerations about mauri (life force) and device technology
• Access from remote areas to specialist centres (Auckland, Christchurch)

---

Applied Basic Sciences

Cardiovascular Physiology

Normal Cardiac Physiology (Review):

• Cardiac output (CO) = Heart rate (HR) × Stroke volume (SV)
• Stroke volume determined by: Preload (Frank-Starling), afterload (wall stress), contractility
• Normal CO: 4-8 L/min; normal cardiac index (CI): 2.5-4.0 L/min/m²
• MAP = CO × SVR = DBP + 1/3(SBP - DBP)
• In heart failure: Reduced SV → compensatory ↑HR, ↑SVR, neurohormonal activation

Continuous-Flow VAD Physiology (PMID: 23680030):

Unlike the native heart or pulsatile VADs, continuous-flow devices provide non-pulsatile or minimally pulsatile flow:

Flow Generation:

• Axial-flow pumps (HeartMate II): Archimedes screw mechanism; blood flows along axis of rotation
• Centrifugal-flow pumps (HeartMate 3, HVAD): Blood enters centrally, exits peripherally; generates centrifugal force

Pressure-Flow Relationship:

• VAD flow is afterload-sensitive: Higher MAP → lower pump flow (for fixed pump speed)
• VAD flow is preload-sensitive: Low LV volume → reduced flow, suction events
• Flow = f(Pump speed, Δ Pressure across pump)
• ΔP = Pressure head = Aortic pressure - LV pressure

Continuous-Flow Hemodynamics:

HeartMate 3 Artificial Pulse (PMID: 28211672):

• Speed modulation: ±2000 RPM every 2 seconds
• Creates systolic-diastolic variation in flow
• Reduces blood stasis within pump
• May reduce pump thrombosis and arteriovenous malformations
• Partially restores pulse pressure (10-20 mmHg)

Pulsatility Index (PI):

PI = (Max Flow - Min Flow) / Mean Flow

Device Parameters and Alarms:

HeartMate 3 Parameters:

• Pump Speed: 3000-9000 RPM; typically 5000-6000 RPM
• Pump Flow: Estimated 3-10 L/min (calculated from power and speed)
• Power: 3-7 Watts typical; >10W suggests thrombosis
• Pulsatility Index: 2.5-4.5 optimal

HVAD Parameters:

• Pump Speed: 1800-4000 RPM
• Pump Flow: 3-10 L/min
• Power: 3-6 Watts typical

Critical Alarms:

• High power/low flow: Pump thrombosis, inflow obstruction
• Low flow: Hypovolemia, suction, RV failure
• Red heart (HeartMate): Critical alarm requiring immediate attention
• Battery low: less than 15 minutes remaining; immediate power source change

Anatomy

LVAD Surgical Anatomy:

Inflow Cannula Placement (LV apex):

• LV apex provides direct, unobstructed access to LV cavity
• Positioned lateral to LAD, avoiding papillary muscles
• Apical coring device removes LV tissue, creates connection
• Inflow cannula (sewing ring) sutured to LV apex
• Malposition → suction events, poor flows

Outflow Graft Placement (Ascending aorta):

• Dacron graft anastomosed to ascending aorta (typically right lateral aspect)
• End-to-side anastomosis
• Graft length optimized to prevent kinking
• Graft stenosis is rare complication

Driveline Tunnel:

• Percutaneous cable exits right upper quadrant or left lower quadrant
• Tunneled subcutaneously to minimize infection
• Velour-covered portion promotes tissue ingrowth (skin exit site)
• Smooth silicone portion for internal course
• Immobilization critical to prevent trauma and infection

Pump Pocket:

• HeartMate 3/II: Pre-peritoneal or intra-peritoneal pocket
• HVAD: Intrapericardial (smaller device)
• Pocket hematoma or infection are complications

Pathophysiology

End-Stage Heart Failure (PMID: 34446049):

Hemodynamic Derangements:

• Reduced cardiac output (CI less than 2.0 L/min/m²)
• Elevated filling pressures (PCWP >20 mmHg, CVP >15 mmHg)
• Low MAP (less than 60-70 mmHg)
• Reduced mixed venous O2 saturation (less than 60%)
• Cardiorenal syndrome (GFR decline)
• Hepatic congestion (elevated bilirubin, transaminases)

Neurohormonal Activation:

• RAAS activation → sodium/water retention, vasoconstriction
• Sympathetic nervous system activation → tachycardia, arrhythmias
• Natriuretic peptide elevation (BNP/NT-proBNP)
• Inflammatory cytokine elevation

LVAD Effects on Physiology (PMID: 22546867):

Beneficial Effects:

• Improved cardiac output and tissue perfusion
• Reduced LV end-diastolic pressure and volume
• Improved end-organ function (renal, hepatic)
• Reverse remodeling (in some patients)
• Neurohormonal normalization
• Improved exercise capacity and quality of life

Adverse Physiological Effects:

• Altered aortic root hemodynamics → aortic insufficiency (10-30%)
• Reduced pulsatility → arteriovenous malformations
• High shear stress → acquired von Willebrand disease
• Chronic anticoagulation → bleeding risk
• Foreign surface → thrombosis risk
• Percutaneous driveline → infection risk

Acquired von Willebrand Disease (PMID: 25042534):

Mechanism:

1. High shear stress (>5000 dynes/cm²) in pump causes unfolding of vWF multimers
2. Exposed ADAMTS13 cleavage sites → proteolysis of large vWF multimers
3. Loss of high-molecular-weight vWF multimers (HMW-vWF)
4. HMW-vWF essential for primary hemostasis, especially at high shear (arterial)
5. Results in bleeding diathesis, particularly GI bleeding

Findings:

• Reduced vWF:RCo/vWF:Ag ratio (less than 0.7)
• Loss of HMW multimers on gel electrophoresis
• Prolonged closure time on PFA-100
• Nearly universal in continuous-flow LVAD patients

Angiodysplasia/AVM Formation (PMID: 25042534):

Mechanism:

1. Loss of pulsatility → altered angiogenesis signaling
2. Reduced pulse pressure → mucosal hypoperfusion
3. Mucosal hypoxia → VEGF and HIF-1α upregulation
4. Angiogenesis → arteriovenous malformations
5. Fragile vessels prone to bleeding
6. Combined with acquired vWD → high GI bleeding risk

Right Ventricular Failure Post-LVAD (PMID: 23849541):

Incidence: 20-40% of LVAD recipients

Mechanisms:

1. Increased venous return to RV (reduced LV obstruction)
2. Leftward septal shift (LV unloading) → impaired RV septal contribution
3. Reduced RV perfusion (low diastolic pressure)
4. Pre-existing RV dysfunction unmasked
5. Perioperative factors: CPB, volume loading, transfusion

Predictors (RVAD Risk Score):

• Elevated CVP/PCWP ratio >0.63
• Severe tricuspid regurgitation
• RV dysfunction on echo (TAPSE less than 14mm, RV FAC less than 30%)
• Elevated creatinine
• Need for inotropes/IABP pre-operatively
• Bilirubin >2.0 mg/dL

Pharmacology

Anticoagulation Pharmacology:

Warfarin (PMID: 31865801):

• Mechanism: Vitamin K epoxide reductase inhibitor; reduces factors II, VII, IX, X, protein C/S
• Target INR: 2.0-3.0 (HeartMate 3), 2.0-2.5 (HVAD)
• Onset: 3-5 days (factor half-lives)
• Duration: 2-5 days after cessation
• Reversal: Vitamin K (slow), PCC/FFP (immediate)
• Monitoring: INR (target range differs by device)

Aspirin:

• Mechanism: Irreversible COX-1 inhibition; reduces TXA2
• Dose: 81-325 mg daily (most centers use 81mg post-MOMENTUM 3)
• Duration: Platelet lifespan (~10 days)
• Reversal: Platelet transfusion if bleeding

Heparin (Bridging):

• Used in immediate post-operative period
• Transition to warfarin when INR therapeutic
• No bridging needed for minor procedures if INR >1.5

Inotropes for RV Support:

Pulmonary Vasodilators for RV Support:

---

Indications

Treatment Strategies (PMID: 23747642)

Bridge to Transplant (BTT):

• Patient listed for heart transplant
• VAD provides support while awaiting donor organ
• ~25% of current LVAD implants
• Goal: Maintain end-organ function, improve functional status
• Success: >90% transplant rate if survives to offer

Bridge to Candidacy/Decision (BTC/BTD):

• Patient currently not transplant candidate (too sick or contraindication)
• VAD provides time to reassess eligibility
• ~45% of current LVAD implants
• May become transplant candidate after end-organ recovery
• May become destination therapy if transplant contraindication permanent

Destination Therapy (DT):

• Not candidate for transplant (age, comorbidities)
• VAD is definitive long-term therapy
• ~25-30% of current LVAD implants
• Originally established by REMATCH trial (PMID: 11717165)
• Survival now approaches transplant at 2-5 years

Bridge to Recovery (BTR):

• Goal is myocardial recovery allowing device explant
• less than 5% of LVAD implants achieve sustained recovery
• Most common in: Acute myocarditis, peripartum cardiomyopathy, recent-onset DCM
• Requires aggressive medical therapy, monitoring, explant protocol

INTERMACS Classification (PMID: 20488969, 30586764)

Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS):

Modifiers:

• A: Arrhythmia (ICD shocks, VT)
• TCS: Temporary Circulatory Support (IABP, Impella, VA-ECMO)
• FF: Frequent Flyer (recurrent hospitalizations)

Outcomes by Profile (INTERMACS 2023):

• Profile 1: Highest operative mortality (15-25%), but greatest benefit vs medical therapy
• Profile 2-3: Best risk-benefit ratio; most common implant profiles
• Profile 4-5: Lower operative mortality, less clear benefit; must balance risks
• Profile 6-7: Generally not offered LVAD unless rapid decline

Patient Selection Criteria

Indications for Durable LVAD (ISHLT 2013) (PMID: 23856341):

Class I Indications (Benefit clearly established):

1. INTERMACS Profile 1-3 (inotrope-dependent or cardiogenic shock)
2. LVEF ≤25%
3. Peak VO2 less than 14 mL/kg/min (or less than 50% predicted)
4. NYHA Class IIIB-IV despite optimal GDMT
5. Inotrope dependence
6. End-organ dysfunction secondary to low output

Class IIa Indications (Reasonable to consider):

1. INTERMACS Profile 4-5 with frequent HF hospitalizations
2. Exercise intolerance with progressive decline
3. Refractory angina (select cases with ischemic CM)

Contraindications:

Absolute Contraindications:

• Irreversible multi-organ failure (except cardiac)
• Active uncontrolled sepsis (source control inadequate)
• Severe irreversible cognitive impairment
• Inadequate psychosocial support/compliance concerns
• Active malignancy with limited prognosis (less than 2 years)
• Severe peripheral vascular disease precluding femoral cannulation (Impella) or limiting ambulation
• Active substance abuse with no engagement in treatment

Relative Contraindications (May be overcome):

• Age >70-75 (destination therapy); considered case-by-case
• BMI less than 18 or >40 (higher complications)
• Significant RV dysfunction (may require BiVAD)
• Severe aortic insufficiency (requires concurrent repair)
• Mechanical aortic valve (requires conversion to bioprosthetic)
• LV thrombus (anticoagulation, surgical excision)
• Renal dysfunction (Cr >3.0, dialysis-dependent - higher mortality)
• Hepatic dysfunction (INR >2.5, bilirubin >3.0 - higher mortality)
• Coagulopathy
• Pulmonary disease (FEV1 less than 50%, need for home O2)
• Recent stroke (less than 30-90 days)
• Active psychiatric illness (uncontrolled)

---

Device Types

Durable (Long-Term) LVADs

HeartMate 3 (Abbott) - Current Standard (PMID: 28211672):

Key Advantages:

• Fully magnetically levitated rotor - no mechanical wear
• Widest blood flow gaps - reduced shear stress
• Artificial pulse feature - reduces stasis, may reduce AVM
• Lowest pump thrombosis rate (less than 2% at 2 years)
• Best survival outcomes (MOMENTUM 3)

HVAD (HeartWare) (Medtronic) - Discontinued (PMID: 28526653):

Status: Voluntarily withdrawn June 2021 due to:

• Higher neurological adverse events vs HeartMate 3
• Increased mortality signal in post-market surveillance
• Existing patients continue on device with enhanced monitoring

HeartMate II (Abbott) - Second Generation (PMID: 17967141):

Historical significance:

• First widely successful continuous-flow LVAD
• Established superiority of continuous over pulsatile flow
• Now second-line to HeartMate 3 (higher thrombosis)

Temporary/Short-Term MCS

Impella Devices (Abiomed) (PMID: 28430099):

Mechanism:

• Microaxial pump on catheter
• Positioned across aortic valve (LV→aorta)
• Archimedes screw propels blood from LV to ascending aorta
• Unloads LV, reduces myocardial oxygen demand

Complications:

• Hemolysis (high shear)
• Limb ischemia (large femoral sheath)
• Aortic valve injury
• Device migration

CentriMag (Abbott) (PMID: 23294751):

Indications:

• Post-cardiotomy shock
• Bridge to decision
• Bridge to durable VAD or transplant
• Right ventricular support post-LVAD

RVAD Options:

For isolated RV failure post-LVAD:

• Impella RP (percutaneous, RA→PA)
• CentriMag (surgical, RA→PA)
• Protek Duo (dual-lumen percutaneous, RA→PA)

BiVAD Considerations:

• Required in 5-10% of patients
• Higher mortality than isolated LVAD
• Options: Two durable LVADs (rare), durable LVAD + temporary RVAD, total artificial heart
• Total Artificial Heart (TAH): SynCardia TAH - orthotopic biventricular replacement

---

Components

Inflow Cannula

Design:

• Connects pump to LV apex
• Sewing ring sutured to LV epicardium
• Short, rigid or flexible segment enters LV cavity
• Positioned to avoid papillary muscles and septum

HeartMate 3 Inflow Cannula:

• Inflow tip with sintered titanium surface
• Promotes endothelialization
• Gore-Tex felt sewing ring

Complications:

• Inflow obstruction (thrombus, tissue ingrowth)
• Malposition (suction events)
• Dehiscence (rare, catastrophic)

Pump

Centrifugal Pump (HeartMate 3):

• Spinning rotor creates centrifugal force
• Blood enters centrally, exits peripherally
• Fully magnetically levitated - no contact points
• Lower shear stress than axial flow

Axial Pump (HeartMate II):

• Archimedes screw mechanism
• Blood flows along axis of rotation
• Mechanical bearings (ruby contacts)
• Higher shear stress, higher thrombosis risk

Outflow Graft

Design:

• Dacron graft (often reinforced)
• Anastomosed to ascending aorta (end-to-side)
• Length optimized to prevent kinking

Complications:

• Anastomotic stenosis (rare)
• Kinking (positional)
• Aortic insufficiency development

Driveline

Design:

• Percutaneous cable connecting pump to external controller
• Two portions:
  • "Velour-covered (at skin exit): Promotes tissue ingrowth"
  • "Smooth silicone (internal): Tunneled subcutaneously"
• Contains electrical cables and (in some devices) speed signal wire

Exit Site:

• Right upper quadrant (most common)
• Left lower quadrant (alternative)
• Distance from belt line, incisions, ostomies

Care:

• Daily inspection for signs of infection
• Immobilization with abdominal binder or anchor device
• Sterile dressing changes (frequency per protocol)
• Showering with protective measures (after healing)

Complications:

• Infection (10-30%) - most common late complication
• Trauma/fracture (rare with immobilization)
• Lead fracture

Controller

HeartMate 3 Controller:

• Pocket-sized computer
• Displays: Power, flow, pulsatility index, alarms
• Two power inputs (batteries or AC power)
• Audible and visual alarms
• Data logging for interrogation

Power Sources:

• Two 14-volt lithium-ion batteries (each 4-6 hours)
• AC power adapter (home, car, hospital)
• Always requires two power sources connected

Alarms:

---

Continuous-Flow Hemodynamics

Blood Pressure Assessment (PMID: 23680030)

Doppler Blood Pressure Measurement:

• Auscultatory method unreliable (no Korotkoff sounds)
• Doppler opening pressure = MAP (or slightly above systolic)
• Technique:
  1. Apply BP cuff to arm
  2. Place Doppler probe over brachial/radial artery
  3. Inflate cuff until Doppler signal disappears
  4. Slowly deflate cuff
  5. Record pressure when Doppler signal returns = "Doppler opening pressure"
• This approximates MAP in most patients
• Target: 70-80 mmHg

Why Pulse Is Absent/Diminished:

• Continuous-flow pump maintains relatively constant flow
• Native heart contributes only minor additional stroke volume
• Results in minimal pulse pressure (5-15 mmHg)
• Arterial line shows flat or minimally oscillating waveform

Consequences of Absent Pulsatility:

• Pulse oximetry may fail (algorithm requires pulsatility)
• NIBP cuffs may fail
• End-organ effects (? increased AVM formation)
• Baroreflex alterations

Pulsatility Index (PI)

Definition: PI = (Maximum Flow - Minimum Flow) / Mean Flow

Normal Range: 2.5-4.5 (may vary by device)

Interpretation:

Suction Events:

• Occur when LV volume too low for pump speed
• Causes: Hypovolemia, RV failure, arrhythmia, high pump speed
• Results: Intermittent flow reduction, arrhythmias, hemolysis
• Management: Volume, reduce pump speed, treat underlying cause

Device Parameter Monitoring

HeartMate 3 Parameters:

Flow Calculation:

• HeartMate devices estimate flow from power and speed
• Not directly measured (no flow meter)
• Accuracy affected by hematocrit, viscosity
• Trend more important than absolute value

Power Trends:

• Increasing power over days-weeks may indicate thrombosis
• Sudden high power = acute thrombosis
• Correlate with LDH, plasma-free Hb

---

Anticoagulation

Rationale (PMID: 31865801)

Thrombotic Risk Factors:

• Foreign surface exposure (pump components, graft)
• Altered blood flow patterns (stasis zones)
• Shear-induced platelet activation
• Hypercoagulable state of heart failure

Bleeding Risk Factors:

• Acquired von Willebrand disease (nearly universal)
• Anticoagulation therapy
• Angiodysplasia/AVM formation
• Altered hemostasis

Anticoagulation Regimen

Immediate Post-Operative Period:

1. Heparin infusion started when chest tube output stable (usually POD 1-2)
2. Target aPTT 50-70 seconds (or anti-Xa 0.3-0.5)
3. Warfarin started when tolerating oral intake
4. Heparin continued until INR therapeutic (2 consecutive days)

Long-Term Anticoagulation:

MOMENTUM 3 Sub-Analysis:

• Lower aspirin dose (81mg) had similar thrombosis rates, less bleeding
• Many centers now use ASA 81mg with HeartMate 3

INR Monitoring:

• Weekly initially, then every 2-4 weeks when stable
• Home INR monitoring encouraged
• Target INR achieved ~50-60% of time in most patients

Anticoagulation Management Challenges

Supratherapeutic INR (>3.5):

1. Hold warfarin
2. Check for bleeding symptoms
3. If INR 3.5-5.0 with no bleeding: Hold warfarin, recheck in 1-2 days
4. If INR 5.0-9.0 with no bleeding: Hold warfarin, consider low-dose vitamin K (1-2.5mg PO)
5. If INR >9.0 or any bleeding: Vitamin K 2.5-5mg PO/IV, consider PCC if serious bleeding
6. Avoid over-correction (thrombosis risk)

Subtherapeutic INR (less than 2.0):

1. Assess compliance, diet, drug interactions
2. If stable and slightly low: Increase weekly dose by 10-15%
3. If significantly low (less than 1.5) or high thrombosis risk: Consider heparin bridging
4. In HeartMate 3, transient low INR less concerning due to low thrombosis rate

Bridging for Procedures:

• Minor procedures (dental, skin): Continue warfarin if INR less than 3.0
• Low bleeding risk (endoscopy without biopsy): Hold warfarin, no bridging
• Moderate bleeding risk: Hold warfarin, bridge with heparin
• High bleeding risk (major surgery): Hold warfarin, bridge with heparin, FFP/vitamin K to normalize INR

---

Complications

Pump Thrombosis (PMID: 24987394)

Incidence:

• HeartMate 3: 1-2% at 2 years (exceptionally low)
• HeartMate II: 8-12% (led to product changes)
• HVAD: 4-8%

Risk Factors:

• Subtherapeutic anticoagulation
• Infection (activates coagulation)
• Suction events
• Device malposition
• Atrial fibrillation (reduced LV filling)
• Low pump speed

Presentation:

• Recurrent heart failure symptoms (dyspnea, edema)
• Hemolysis (dark urine, jaundice, anemia)
• Device alarms (high power, low flow)
• Hemodynamic instability

Diagnostic Markers:

Management Algorithm:

1. Mild hemolysis, stable patient:

   • Optimize anticoagulation (heparin infusion, target aPTT 60-80)
   • IV fluids to maintain volume
   • Close monitoring (LDH q6-12h)
   • Consider thrombolytics if not improving

2. Moderate hemolysis, stable:

   • Admit to ICU
   • IV heparin (higher targets)
   • Consider t-PA infusion (controversial, risk of ICH)
   • Prepare for surgical options

3. Severe hemolysis or hemodynamic instability:

   • Surgical pump exchange (preferred)
   • Consider thrombolysis if not surgical candidate
   • ECMO bridge if needed

Thrombolytic Therapy (Controversial):

• t-PA 50mg over 4-6 hours infusion
• Or t-PA 25mg bolus, may repeat
• High risk of intracranial hemorrhage (5-10%)
• Reserved for non-surgical candidates or deteriorating patients

Gastrointestinal Bleeding (PMID: 25042534)

Incidence: 15-30% of LVAD patients (most common bleeding site)

Pathophysiology:

1. Acquired von Willebrand disease (nearly universal)
2. Angiodysplasia formation (loss of pulsatility)
3. Anticoagulation therapy
4. Uremic platelet dysfunction (if AKI)

Presentation:

• Melena, hematochezia, hematemesis
• Anemia (may be occult blood loss)
• INR may be therapeutic or elevated

Anatomic Distribution:

• Upper GI: 30-40% (gastric AVMs, duodenal)
• Small bowel: 30-40% (AVMs, most common in continuous-flow)
• Lower GI: 20-30% (colonic AVMs)

Management:

Acute Management:

1. Resuscitation (IV fluids, blood transfusion, correct coagulopathy)
2. Hold anticoagulation (assess thrombosis risk)
3. PPI if upper GI suspected
4. Urgent endoscopy (EGD, colonoscopy)
5. Capsule endoscopy or push enteroscopy for small bowel
6. Interventional radiology (angiography, embolization) if endoscopy fails

Endoscopic Therapy:

• Argon plasma coagulation for AVMs
• Clips, thermal therapy
• May require multiple sessions

Medical Therapies (Evidence Limited):

• Octreotide: Reduces splanchnic blood flow; 100-200 mcg SQ TDS or LAR 20-30mg monthly (PMID: 25747988)
• Thalidomide: Anti-angiogenic; 50-100mg daily; efficacy in case series (PMID: 29107577)
• Danazol: Anabolic steroid; may improve vWF levels
• DDAVP: Limited effect due to vWF deficiency (not synthesis problem)

Device Management:

• Reduce pump speed (increases pulsatility, may improve vWF)
• Balance with adequate hemodynamic support
• Consider pump exchange if recurrent refractory bleeding

Anticoagulation Resumption:

• Case-by-case decision
• May restart at lower INR target (2.0-2.5)
• Some patients managed without warfarin (aspirin only) - controversial
• Higher pump thrombosis risk must be balanced

Driveline Infection (PMID: 28259619)

Incidence: 10-30% of LVAD patients (most common infection)

Risk Factors:

• Poor driveline immobilization
• Obesity
• Diabetes
• Poor hygiene/compliance
• Trauma to exit site

Classification:

• Superficial: Exit site only, cellulitis, no systemic signs
• Deep: Tunnel infection, abscess, systemic sepsis
• Pocket infection: Pump pocket involved (HeartMate II more than HeartMate 3)
• Endovascular: Bacteremia, endocarditis (rare)

Organisms:

• Staphylococcus aureus (40%): MSSA and MRSA
• Coagulase-negative staphylococci (20%)
• Pseudomonas aeruginosa (15%)
• Enterobacteriaceae (10%)
• Candida species (5%)
• Polymicrobial (10%)

Presentation:

• Exit site erythema, warmth, tenderness
• Purulent drainage
• Fever, elevated WBC
• Positive blood cultures (if systemic)
• Subcutaneous swelling (tunnel infection)

Diagnosis:

• Wound cultures (deep swab or aspirate)
• Blood cultures (if systemic signs)
• CT scan with contrast (abscess, tunnel involvement, pocket)
• Inflammatory markers (CRP, procalcitonin)
• Echocardiography (endocarditis if prolonged bacteremia)

Management:

Superficial Infection:

• Optimize driveline care
• Oral antibiotics (fluoroquinolone + TMP-SMX or linezolid)
• Daily dressing changes
• Close follow-up

Deep/Tunnel Infection:

• IV antibiotics (vancomycin + anti-Pseudomonal, minimum 4-6 weeks)
• Surgical debridement (may require OR)
• Vacuum-assisted closure (VAC) therapy
• Consider driveline relocation

Pocket Infection:

• Prolonged IV antibiotics
• Surgical drainage/debridement
• May require pump exchange

Chronic Suppressive Therapy:

• Often required indefinitely
• Oral antibiotics based on cultures
• Prevents progression to systemic infection

Prevention:

• Driveline immobilization with abdominal binder
• Patient education on exit site care
• Sterile technique for dressing changes
• Early recognition and treatment of exit site changes

Stroke (PMID: 30638371)

Incidence: 3-5% per year (ischemic or hemorrhagic)

Types:

• Ischemic stroke (60-70%): Thromboembolism from pump, paradoxical embolism
• Hemorrhagic stroke (30-40%): Anticoagulation-related, AVM bleeding

Risk Factors:

• Atrial fibrillation
• Subtherapeutic anticoagulation (ischemic)
• Supratherapeutic anticoagulation (hemorrhagic)
• Pump thrombosis
• Infection (increases thromboembolic risk)
• Previous stroke/TIA
• Uncontrolled hypertension

Prevention:

• Maintain therapeutic INR
• Treat atrial fibrillation (rate or rhythm control)
• Monitor for pump thrombosis
• Treat infections aggressively
• Blood pressure control (MAP 70-80 mmHg)

Acute Stroke Management:

Ischemic Stroke:

• Urgent CT head (exclude hemorrhage)
• CT angiography (if large vessel occlusion suspected)
• IV thrombolysis (t-PA): Generally avoided due to bleeding risk and anticoagulation, but considered case-by-case
• Mechanical thrombectomy: Preferred for large vessel occlusion (LVO)
• Optimize anticoagulation post-stroke

Hemorrhagic Stroke:

• Reverse anticoagulation (PCC, FFP, vitamin K)
• Neurosurgical consultation (evacuation if indicated)
• BP control (target MAP 70-80)
• ICU monitoring
• Restart anticoagulation cautiously when stable (days-weeks, individualized)

Right Ventricular Failure (PMID: 23849541)

Incidence: 20-40% early post-LVAD implantation; 5-10% require RVAD

Pathophysiology:

1. Increased venous return to RV (LV no longer "dam")
2. Leftward septal shift (LV unloading) reduces RV septal contribution
3. Reduced RV perfusion (low aortic diastolic pressure)
4. Pre-existing RV dysfunction unmasked
5. Perioperative factors (CPB, transfusion, volume loading)

Predictors (Pre-Operative Risk Scores):

Clinical Features:

• Elevated CVP (>15 mmHg)
• Low pump flows despite adequate speed
• Low pulsatility index
• Renal dysfunction (cardiorenal syndrome)
• Hepatic dysfunction (elevated bilirubin, transaminases)
• Peripheral edema, ascites

Management:

Medical Management:

1. Optimize RV preload (avoid over-distension and under-filling)
   • Diuresis if volume overloaded
   • Volume if underfilled
2. Reduce RV afterload
   • Inhaled nitric oxide (10-40 ppm)
   • Inhaled epoprostenol (10-50 ng/kg/min)
   • Sildenafil (oral when tolerating)
3. Inotropic support
   • Milrinone (inotropy + pulmonary vasodilation)
   • Dobutamine
   • Epinephrine (low dose)
4. Optimize systemic perfusion
   • Norepinephrine (maintains RV coronary perfusion)
5. Maintain sinus rhythm
   • AF/flutter compromises RV filling

RVAD Indications:

• Refractory RV failure despite maximal medical therapy
• Escalating inotropes
• Worsening end-organ function
• Inability to separate from CPB

RVAD Options:

• Impella RP (percutaneous, RA→PA)
• CentriMag (surgical)
• Temporary surgical RVAD

Weaning RVAD:

• Gradual flow reduction with hemodynamic monitoring
• Wean inotropes, pulmonary vasodilators first
• Most temporary RVADs explanted within 2-4 weeks
• 50-70% of temporary RVAD patients successfully weaned

Acquired von Willebrand Disease (PMID: 25042534)

Incidence: Nearly universal in continuous-flow LVAD patients

Pathophysiology:

• High shear stress (>5000 dynes/cm²) in pump
• vWF multimers unfold, exposing ADAMTS13 cleavage sites
• Proteolysis of large vWF multimers
• Loss of high-molecular-weight vWF multimers
• HMW-vWF essential for primary hemostasis at high shear

Laboratory Findings:

• Reduced vWF:RCo/vWF:Ag ratio (less than 0.7)
• Loss of HMW multimers on gel electrophoresis
• Prolonged PFA-100 closure time
• Often normal or elevated vWF:Ag (acute phase reactant)

Clinical Significance:

• Contributes to GI bleeding risk
• Epistaxis, mucosal bleeding
• May affect surgical hemostasis

Management:

• No specific treatment for the deficiency itself
• Reduce pump speed (increases pulsatility, may improve vWF)
• Manage bleeding episodes supportively
• vWF concentrates (Humate-P): Limited data, may be used for severe bleeding

---

Evidence Base

Landmark Trials

REMATCH Trial (2001) (PMID: 11717165):

Historical significance: Established LVAD as destination therapy option

HeartMate II Bridge-to-Transplant Trial (2007) (PMID: 17967141):

HeartMate II Destination Therapy Trial (2009) (PMID: 19920051):

ENDURANCE Trial (2017) (PMID: 28526653):

MOMENTUM 3 Trial (2017, 2019, 2022) (PMID: 28211672, 30571454, 35052322):

INTERMACS Registry Data (PMID: 30586764, 37148016)

Key Findings (2023 Report):

• 30,000 patients in registry

• 1-year survival: 82-85% (HeartMate 3)
• 2-year survival: 75-80%
• Leading causes of death: Multi-organ failure (21%), neurological (17%), infection (17%)
• Profile 1-2 patients: Higher early mortality, greater long-term benefit
• Trend toward earlier implantation (Profile 3-4)

Comparative Outcomes (PMID: 35052322)

---

Australian VAD Programs

Program Overview (PMID: 35587227)

The Alfred Hospital (Melbourne, Victoria):

• Australia's largest VAD program
• Established 1994
• ~25-35 implants/year
• Comprehensive transplant and VAD program
• Lead site for Australian VAD registry
• Destination therapy program established

St Vincent's Hospital (Sydney, NSW):

• Second-largest program
• Established 1996
• ~20-30 implants/year
• Strong transplant program with VAD as BTT
• Research focus on VAD outcomes

Royal Perth Hospital (Perth, WA):

• Regional service for Western Australia
• ~5-10 implants/year
• BTT primarily

Prince Charles Hospital (Brisbane, QLD):

• Queensland service
• ~5-10 implants/year
• Growing program

Australian Outcomes

Australian-Specific Data (PMID: 35587227):

• 1-year survival comparable to international data (~80%)
• Lower overall volumes than US (learning curve considerations)
• Higher proportion BTT (access to transplant)
• Remote follow-up challenges addressed with telehealth

ANZICS Considerations:

• Level III ICU capability for post-operative care
• VAD-trained intensivists essential
• Multidisciplinary team (cardiac surgery, cardiology, ICU, VAD coordinators)
• Retrieval considerations for interstate patients

Referral Pathway

Who to Refer:

• NYHA III-IV despite optimal medical therapy
• Recurrent HF hospitalizations
• Inotrope-dependence
• Declining renal/hepatic function secondary to cardiac output
• Peak VO2 less than 14 mL/kg/min
• LVEF less than 25%

Referral Information Required:

• Complete cardiac history
• Echocardiography (LV function, RV function, valve disease)
• Right heart catheterization data
• Cardiopulmonary exercise testing
• Renal and hepatic function
• Psychosocial assessment
• Insurance/funding status

---

Indigenous Health Considerations

Aboriginal and Torres Strait Islander Populations

Epidemiology:

• Higher rates of heart failure due to:
  • Rheumatic heart disease (10-15× higher)
  • Ischemic heart disease (earlier onset)
  • Hypertensive heart disease
  • Diabetes-related cardiomyopathy
• Often present with more advanced disease
• Younger age at presentation

Barriers to VAD Access:

• Geographic: VAD centers in metropolitan areas only
• Financial: Extended time away from home, family, work
• Cultural: Concerns about return to Country with device
• Health literacy: Complex device education
• Comorbidities: May affect candidacy

Cultural Considerations:

• Involve Aboriginal Hospital Liaison Officers (AHLOs) from first contact
• Extended family involvement in all discussions and decisions
• Respect for Elders in decision-making process
• Acknowledge connection to Country and challenges of being away
• Language services for non-English speakers
• Allow time for family consensus

Post-Implant Challenges:

• Remote follow-up difficult:
  • INR monitoring (point-of-care testing solutions)
  • Device checks (telehealth, outreach clinics)
  • Driveline care (training local health workers)
• Emergency access:
  • RFDS protocols for VAD patients
  • Telemedicine consultation with VAD centers
  • Pre-hospital provider education
• Community support:
  • Identify local support persons
  • Community education about device
  • Cultural safety in ongoing care

Strategies to Improve Access:

• Outreach clinics to regional centers
• Telehealth for device interrogation
• Training remote health workers in VAD basics
• Cultural safety training for VAD teams
• Aboriginal-specific support programs
• Accommodation support for extended stays

Maori Health Considerations (New Zealand)

Cultural Framework:

• Whanau (family): Central to decision-making
• Kaumatua (elders): May be consulted for major decisions
• Tikanga (customs): Respect for cultural practices
• Mauri (life force): Discussion about technology and mauri

Practical Considerations:

• Whanau involvement in all discussions
• Maori Health Workers as cultural liaisons
• Consider karakia (prayers) if requested
• Access from remote areas to specialist centers
• Support for family during extended treatment

---

ICU Management

Post-Implantation ICU Care

Immediate Post-Operative Period (0-24 hours):

Hemodynamic Targets:

• MAP 70-80 mmHg (Doppler BP)
• CVP 8-12 mmHg (avoid extremes)
• Pump flow 4-6 L/min
• Pulsatility index 2.5-4.5
• Urine output >0.5 mL/kg/hr

Monitoring:

• Invasive arterial line (recognizing altered waveform)
• CVP monitoring
• Pulmonary artery catheter (if RV concerns)
• Device parameters (flow, power, PI)
• Chest tube output (expect higher due to anticoagulation)
• Hourly neuro checks (stroke risk)
• Lactate (perfusion)

Common Post-Operative Issues:

Anticoagulation Initiation:

1. Check chest tube output stable (less than 100 mL/hr for 2-4 hours)
2. Check coagulation (PT, PTT, fibrinogen, platelets)
3. Start unfractionated heparin infusion (no bolus)
4. Target aPTT 50-70 sec initially
5. Transition to warfarin when tolerating oral intake
6. Continue heparin until INR therapeutic (2 consecutive days)

Troubleshooting Device Issues

Low Pump Flow:

High Power Alarm:

Controller Alarms:

Cardiac Arrest in VAD Patients (PMID: 26903073)

Key Considerations:

• No palpable pulse at baseline - cannot assess circulation this way
• Consciousness, capillary refill, end-tidal CO2 more useful

Assessment:

1. Assess consciousness - if unresponsive, assume cardiac arrest
2. Check device: Controller on? Batteries connected? Alarms?
3. Listen with Doppler over brachial/radial artery
4. Check end-tidal CO2 if intubated

Resuscitation Modifications:

Chest Compressions:

• Controversial: May dislodge cannula, damage device
• Current recommendation: May be performed if device failure confirmed
• If device functioning: Compressions may be ineffective (continuous-flow already providing output)
• Focus on correctable causes: Volume, arrhythmia, device issues

Defibrillation:

• Safe to defibrillate (external pads)
• VF/VT common causes of arrest
• Standard pad placement

Algorithm:

1. Call for help, VAD coordinator
2. Check device function (power, alarms)
3. If device appears functioning:
   • Consider arrhythmia (defibrillate if VF/VT)
   • Consider hypovolemia (IV fluids)
   • Consider tamponade (bedside echo, emergent drainage)
4. If device not functioning:
   • Chest compressions may be considered
   • Establish cause of device failure
   • Consider ECMO if available
5. Standard ACLS drugs (epinephrine, amiodarone)

Do NOT:

• Disconnect device power sources
• Attempt internal defibrillation via device
• Assume device alone provides adequate output in arrest

---

SAQ Practice

SAQ 1: Pump Thrombosis

Stem:

A 62-year-old male with ischemic cardiomyopathy and a HeartMate 3 LVAD implanted 8 months ago as destination therapy presents to the emergency department with increasing dyspnea, peripheral edema, and dark urine over the past 3 days. His INR 2 days ago was 1.8 (target 2.0-3.0). He is on warfarin and aspirin 81mg daily.

Observations: HR 95 bpm, Doppler BP 75 mmHg, RR 24, SpO2 (unreliable), afebrile.

Device parameters: Pump speed 5400 RPM, Power 11 Watts (baseline 5.5 W), Flow 3.2 L/min (baseline 5.0 L/min), PI 1.8 (baseline 3.2).

Questions:

(a) What is the most likely diagnosis? List 4 clinical and laboratory features that would support this diagnosis. (4 marks)

Model Answer:

Diagnosis: Pump thrombosis (1 mark)

Supporting features (1 mark each, max 4):

Clinical:

• Recurrent heart failure symptoms (dyspnea, edema)
• Dark urine (hemoglobinuria from hemolysis)
• Subtherapeutic INR (1.8) predisposing to thrombosis
• Elevated power consumption (11W, baseline 5.5W)
• Decreased pump flow (3.2 vs baseline 5.0 L/min)
• Low pulsatility index (1.8 vs baseline 3.2)

Laboratory:

• LDH >2.5× upper limit of normal (expect >600 U/L)
• Elevated plasma-free hemoglobin (>40 mg/dL)
• Elevated indirect bilirubin
• Decreased haptoglobin
• Reticulocytosis
• Hemoglobinuria on urinalysis

(b) Outline your immediate management of this patient. (6 marks)

Model Answer:

Immediate Assessment and Resuscitation (2 marks):

• High-flow oxygen, establish IV access
• Continuous cardiac monitoring
• Arterial line (recognizing altered waveform)
• Urgent laboratory studies: LDH, plasma-free Hb, haptoglobin, bilirubin, CBC, coagulation (INR, aPTT, fibrinogen), renal function, BNP
• Echocardiography (assess LV size, aortic valve opening, RV function)
• Contact VAD coordinator and cardiac surgery team

Anticoagulation Optimization (2 marks):

• Commence IV unfractionated heparin infusion (no bolus if stable)
• Target aPTT 60-80 seconds (higher than usual target)
• Hold warfarin until heparin therapeutic, then restart with overlap
• Continue aspirin unless active bleeding

Supportive Care (1 mark):

• IV fluids to maintain preload (avoid over-aggressive, risk of hemolysis worsening)
• Diuresis if volume overloaded
• Inotropic support if hemodynamically unstable

Definitive Management Planning (1 mark):

• Serial LDH, plasma-free Hb (q6-12h) to assess response
• If improving: Continue medical management
• If not improving/deteriorating: Consider thrombolysis (t-PA) or surgical pump exchange
• ICU admission for close monitoring

(c) The patient deteriorates despite 24 hours of heparin therapy. LDH is rising, and he is becoming hypotensive. Discuss the options for definitive management, including risks and benefits. (6 marks)

Model Answer:

Option 1: Surgical Pump Exchange (3 marks):

Benefits:

• Definitive treatment - removes thrombus and damaged pump
• Allows inspection of cannulae and outflow graft
• Lower neurological risk than thrombolysis
• Preferred option if patient surgical candidate

Risks:

• Major cardiac surgery (redo sternotomy)
• Cardiopulmonary bypass
• Bleeding risk
• Perioperative mortality (5-15%)
• RV failure risk

Indications: Hemodynamically unstable, failed thrombolysis, recurrent thrombosis

Option 2: Thrombolytic Therapy (t-PA) (3 marks):

Regimen options:

• t-PA 50mg infused over 4-6 hours
• Or t-PA 25mg bolus, may repeat in 6-24 hours

Benefits:

• Avoids major surgery
• Can be initiated rapidly in ICU
• May be successful in restoring pump function

Risks:

• Intracranial hemorrhage (5-10%)
• Major bleeding (10-20%)
• May not be effective
• May need surgical rescue

Indications: Patient not surgical candidate, bridge to surgery, moderate thrombosis with hemodynamic stability

Other Considerations:

• ECMO as bridge to decision if hemodynamically unstable
• Palliative care discussion if no further escalation appropriate
• Multidisciplinary team decision (cardiac surgery, VAD coordinator, intensivist, patient/family)

(d) What strategies might reduce the risk of pump thrombosis in LVAD patients? (4 marks)

Model Answer (1 mark each, max 4):

1. Anticoagulation compliance: Maintain therapeutic INR 2.0-3.0, regular monitoring, patient education, home INR monitoring

2. Aspirin therapy: Continue aspirin 81-325mg daily unless contraindicated

3. Device selection: HeartMate 3 has lowest thrombosis risk (less than 2% at 2 years vs HeartMate II 10%)

4. Infection prevention/treatment: Infections increase thromboembolic risk; aggressive treatment, driveline care

5. Optimal pump speed: Avoid too low speed (stasis), avoid suction events (damage)

6. Blood pressure control: Maintain MAP 70-80 mmHg to ensure adequate flow

7. Hydration: Avoid dehydration (increases viscosity, reduces flow)

8. Atrial fibrillation management: Rate/rhythm control to optimize LV filling

---

SAQ 2: Right Ventricular Failure Post-LVAD

Stem:

A 48-year-old female with non-ischemic dilated cardiomyopathy underwent HeartMate 3 LVAD implantation 18 hours ago as bridge to transplant. Pre-operatively, she was INTERMACS Profile 2 on dobutamine 7.5 mcg/kg/min with LVEF 12%, moderate RV dysfunction, and moderate-severe tricuspid regurgitation. She is now failing to wean from cardiopulmonary bypass and is on multiple vasoactive agents.

Current medications: Norepinephrine 0.25 mcg/kg/min, epinephrine 0.08 mcg/kg/min, vasopressin 0.04 units/min, milrinone 0.4 mcg/kg/min.

Hemodynamics: HR 110 bpm (sinus), MAP 55 mmHg, CVP 22 mmHg, PA 35/22 (mean 26) mmHg.

Device parameters: Speed 5200 RPM, Power 4.5 W, Flow 3.2 L/min, PI 1.2.

TEE: Well-positioned inflow cannula, no LV thrombus, severely dilated RV with reduced function, moderate-severe TR, septum bowing leftward, AV not opening.

Questions:

(a) What is the diagnosis? Explain the pathophysiology of this complication following LVAD implantation. (5 marks)

Model Answer:

Diagnosis: Right ventricular failure post-LVAD implantation (1 mark)

Pathophysiology (1 mark each, max 4):

1. Increased venous return to RV: LVAD unloads LV, removing "dam" effect; increased cardiac output delivered to RV, which was previously protected by low LV output

2. Leftward interventricular septal shift: LV unloading causes leftward septal bowing (seen on echo); reduces RV septal contribution to systolic function (normally 20-40% of RV output)

3. Reduced RV coronary perfusion: Low aortic diastolic pressure reduces RV coronary perfusion; RV coronary flow occurs in systole and diastole (unlike LV)

4. Pre-existing RV dysfunction unmasked: This patient had pre-operative moderate RV dysfunction and moderate-severe TR - high-risk features

5. Perioperative factors: Cardiopulmonary bypass causes inflammation, myocardial stunning; transfusion-related lung injury increases PVR; volume loading increases RV preload

6. Geometry changes: Acute geometry changes impair RV function; pericardiotomy removes pericardial constraint

(b) Outline your management strategy for this patient. (8 marks)

Model Answer:

Optimize RV Preload (2 marks):

• CVP 22 mmHg suggests RV volume overload
• Gentle diuresis (furosemide infusion) to reduce CVP to 12-15 mmHg
• Avoid over-diuresis (need adequate LV filling for LVAD)
• Consider ultrafiltration if oliguric
• Avoid further volume loading

Reduce RV Afterload (2 marks):

• Initiate inhaled nitric oxide (iNO) 20-40 ppm
  • Selective pulmonary vasodilator
  • No systemic hypotension
  • Reduces PA pressures, improves RV output
• Alternative: Inhaled epoprostenol (10-50 ng/kg/min)
• Later: Oral sildenafil when tolerating enterals

Inotropic Support (2 marks):

• Continue milrinone (inotrope + pulmonary vasodilator) - ideal for RV failure
• Consider increasing to 0.5-0.75 mcg/kg/min
• Dobutamine can be added (β1 agonism)
• Epinephrine provides inotropy but may increase PVR at higher doses
• Wean catecholamines as possible (high doses increase PVR)

Systemic Perfusion and RV Coronary Perfusion (1 mark):

• Maintain MAP >65 mmHg with norepinephrine
• RV coronary perfusion depends on systemic pressure
• Vasopressin may be helpful (avoids pulmonary vasoconstriction)

Rhythm Optimization (1 mark):

• Maintain sinus rhythm (atrial kick important for RV filling)
• If AF develops: Cardioversion, amiodarone
• Ensure appropriate AV synchrony

(c) Despite 12 hours of maximal medical therapy, the patient remains in refractory RV failure. What are your options? (4 marks)

Model Answer (1 mark each, max 4):

1. Temporary RVAD implantation:

   • Impella RP (percutaneous, RA→PA, 4 L/min support)
   • CentriMag (surgical, requires central cannulation, up to 10 L/min)
   • Provides RV support while assessing for recovery
   • 50-70% of temporary RVADs successfully weaned

2. Biventricular support (BiVAD):

   • If durable RV support anticipated
   • Higher mortality than isolated LVAD
   • May use second durable LVAD (rare) or TAH

3. VA-ECMO:

   • Provides biventricular support plus oxygenation
   • Bridge to decision/recovery
   • Limited by LV distension (may need LV venting)

4. Urgent heart transplant listing:

   • If patient already listed as BTT
   • Upgrade to Status 1 (emergency) if available
   • May need MCS bridge to transplant

5. Goals of care discussion:

   • If no further escalation appropriate
   • Patient/family discussion about prognosis
   • Consider withdrawal of support if futile

(d) What pre-operative factors predict the need for RVAD support? (3 marks)

Model Answer (1 mark each, max 3):

---

Hot Case Scenarios

Hot Case 1: Post-LVAD Implantation Day 2

Scenario:

You are asked to review a 58-year-old male on Day 2 post-HeartMate 3 LVAD implantation. He is intubated and sedated. The nursing staff are concerned about persistent hypotension despite escalating vasopressors.

Candidate Approach:

Initial Observations:

• Monitoring: HR 115 bpm sinus tachycardia, invasive arterial waveform flat (continuous-flow expected), CVP 24 mmHg, PAP 42/24 (mean 30), SpO2 signal intermittent
• Device: Speed 5400 RPM, Power 4.8 W, Flow 3.0 L/min, PI 0.8 (low)
• Infusions: Norepinephrine 0.3 mcg/kg/min, milrinone 0.5 mcg/kg/min, vasopressin 0.04 units/min
• Chest drains: 300 mL over last 4 hours (within acceptable range)

Systematic Assessment:

"I note this patient is Day 2 post-HeartMate 3 LVAD implantation with persistent hypotension requiring high-dose vasoactive support. The key finding is elevated CVP (24 mmHg) with low pulsatility index (0.8), which together suggest right ventricular failure with inadequate left ventricular filling for the LVAD. I would approach this systematically..."

Examiner Questions and Model Answers:

Q: How would you confirm your suspected diagnosis?

A: "I would request urgent bedside transthoracic or transesophageal echocardiography looking for:

• RV size and function (expect dilated, reduced function)
• Interventricular septal position (expect leftward bowing)
• Tricuspid regurgitation severity
• LV cavity size (may be small if underfilled)
• Inflow cannula position (ensure no obstruction)
• Pericardial effusion or tamponade

I would also assess end-organ function with lactate, renal function, and hepatic function markers."

Q: The echo confirms severe RV dysfunction with leftward septal bowing. How would you manage this?

A: "This confirms RV failure post-LVAD. My management would focus on:

1. Optimize RV preload: CVP 24 mmHg suggests volume overload. I would commence diuretic infusion (furosemide) aiming for CVP 12-15 mmHg, being careful not to under-fill the LV.

2. Reduce RV afterload: I would initiate inhaled nitric oxide at 20 ppm, titrating to effect on PA pressures. This provides selective pulmonary vasodilation without systemic hypotension.

3. Support RV contractility: Continue milrinone as it has both inotropic and pulmonary vasodilator effects. Consider adding dobutamine if further inotropy needed.

4. Maintain systemic perfusion: Continue norepinephrine to support coronary perfusion to the RV. May need to accept higher vasopressor doses temporarily.

5. Optimize rhythm: Ensure sinus rhythm; if AF develops, consider cardioversion.

6. Ventilator optimization: Minimize PEEP to reduce RV afterload while maintaining oxygenation.

I would involve the VAD coordinator and cardiac surgical team to discuss the threshold for mechanical RV support."

Q: Despite maximal therapy, the patient continues to deteriorate. What are your options?

A: "If refractory to maximal medical therapy, options for mechanical RV support include:

1. Impella RP: Percutaneous microaxial pump providing 4 L/min RV support. Inserted via femoral vein, positioned RA to PA.

2. CentriMag RVAD: Surgical centrifugal pump requiring central cannulation. Provides up to 10 L/min support.

3. VA-ECMO: Provides biventricular support plus oxygenation. May need LV venting to prevent distension.

I would also ensure the patient's transplant status is reviewed - if listed as BTT, they may be prioritized for urgent transplant.

If no further escalation is appropriate, I would discuss goals of care with the family."

---

Hot Case 2: LVAD Patient with Altered Consciousness

Scenario:

You are called to review a 65-year-old female with HeartMate 3 LVAD (destination therapy, implanted 2 years ago) who presented via ambulance with acute confusion and left-sided weakness for 2 hours. She was stable on warfarin (INR 2.3 three days ago) and aspirin 81mg.

Candidate Approach:

Initial Assessment: "I would approach this as a potential acute stroke in a VAD patient, which is a time-critical emergency. I would assess airway, breathing, and circulation while gathering information about the neurological deficit."

Primary Survey:

• A: Airway patent, patient confused but responding
• B: RR 18, SpO2 adequate on room air
• C: Doppler BP 78 mmHg, no palpable pulse (expected), device functioning (controller shows normal parameters)
• D: GCS 13 (E3V4M6), left facial droop, left arm weakness 2/5, left leg 3/5
• E: Temperature 36.8°C

Device Check:

• Speed 5600 RPM, Power 5.2 W, Flow 5.5 L/min, PI 3.5 - all normal

Examiner Questions and Model Answers:

Q: What is your differential diagnosis?

A: "Given the acute focal neurological deficit with left hemiparesis in this VAD patient on anticoagulation, my differential includes:

1. Ischemic stroke (most likely given acute onset, focal deficit)

   • Cardioembolic from device
   • Pump thrombosis with embolization
   • Paradoxical embolism

2. Hemorrhagic stroke

   • Warfarin-related (despite therapeutic INR)
   • Underlying AVM or aneurysm

3. Non-stroke diagnoses (less likely with focal findings):

   • Hypoglycemia (check glucose immediately)
   • Metabolic encephalopathy
   • Seizure with Todd's paralysis
   • Subdural hematoma"

Q: What investigations would you order urgently?

A: "I would order:

1. Urgent CT head non-contrast: Differentiate ischemic from hemorrhagic stroke - time-critical

2. CT angiography (if ischemic): Identify large vessel occlusion amenable to thrombectomy

3. Bloods: BSL (immediately), coagulation (INR, aPTT), FBC, renal function, LDH and plasma-free Hb (rule out pump thrombosis)

4. ECG: Check rhythm (AF increases embolic risk)

5. Echocardiography: Once stabilized, assess for intracardiac thrombus

6. Device interrogation: VAD coordinator to download device data, assess for alarms or parameter changes"

Q: The CT shows a large right MCA territory ischemic stroke with no hemorrhage. CT angiography confirms M1 occlusion. What is your management?

A: "This patient has a large vessel occlusion ischemic stroke requiring urgent intervention.

Immediate Management:

1. Acute stroke team activation: Neurology and interventional neuroradiology

2. Mechanical thrombectomy: This is the treatment of choice for LVO

   • IV thrombolysis (t-PA) is generally avoided in LVAD patients due to bleeding risk and anticoagulation, though some centers consider it
   • Mechanical thrombectomy can be performed without thrombolysis

3. Maintain BP: Target Doppler BP 70-80 mmHg (usual target); avoid hypotension

4. Continue anticoagulation: Do not reverse unless hemorrhagic transformation or need for emergency surgery

5. ICU admission: For post-procedure monitoring, neurological assessment

6. VAD team involvement: Coordinate care with VAD coordinator

Secondary Prevention:

• Review anticoagulation compliance and targets
• Assess for pump thrombosis (LDH, power trends)
• AF screening if not already known
• Optimize BP control long-term"

Q: What if the CT had shown intracerebral hemorrhage?

A: "If hemorrhagic stroke was identified, my management would differ significantly:

1. Urgent reversal of anticoagulation:

   • Stop warfarin immediately
   • Prothrombin Complex Concentrate (PCC) - 4-factor preferred, dose based on INR
   • IV Vitamin K 10mg for sustained reversal
   • Target INR less than 1.5

2. Blood pressure management: Avoid hypertension (target Doppler BP 70-80 or lower if symptomatic)

3. Neurosurgical consultation: For consideration of hematoma evacuation depending on size, location, clinical status

4. ICU admission: Close neurological monitoring, ICP management if needed

5. VAD implications: Reversal of anticoagulation increases pump thrombosis risk

   • Close device monitoring (LDH, power, flow)
   • Restart anticoagulation when safe (usually 7-14 days, individualized)
   • Balance thrombosis risk against re-bleeding risk"

---

Viva Scenarios

Viva 1: LVAD Indications and Patient Selection

Opening Statement: "A 54-year-old male with ischemic cardiomyopathy is referred for consideration of LVAD implantation. He has LVEF 15%, NYHA Class IIIB symptoms despite optimal medical therapy, and is not a transplant candidate due to obesity (BMI 38)."

Expected Discussion Points:

Q: What are the indications for LVAD implantation?

A: "LVAD indications are based on the treatment strategy:

1. Bridge to Transplant (BTT): ~25% of implants

   • Patient listed for heart transplant
   • LVAD maintains end-organ function while awaiting donor

2. Bridge to Candidacy/Decision (BTC): ~45% of implants

   • Not currently transplant eligible
   • VAD allows time to reassess eligibility

3. Destination Therapy (DT): ~25% of implants

   • Not transplant candidate
   • LVAD as definitive long-term therapy
   • This patient would fall into this category

4. Bridge to Recovery (BTR): less than 5%

   • Goal is myocardial recovery
   • Most common in myocarditis, peripartum cardiomyopathy

The hemodynamic indications include:

• LVEF ≤25%
• Peak VO2 less than 14 mL/kg/min
• NYHA III-IV despite optimal medical therapy
• Inotrope dependence
• Recurrent HF hospitalizations"

Q: How would you classify this patient's severity using INTERMACS?

A: "INTERMACS (Interagency Registry for Mechanically Assisted Circulatory Support) profiles classify disease severity:

• Profile 1 (Crash and Burn): Critical cardiogenic shock
• Profile 2 (Sliding Fast): Progressive decline on inotropes
• Profile 3: Stable on inotropes
• Profile 4: Resting symptoms on oral therapy
• Profile 5: Exertion intolerant
• Profile 6: Exertion limited
• Profile 7: Advanced NYHA III

This patient with NYHA IIIB symptoms on optimal oral therapy would be Profile 4 or 5. Profile 4-5 patients have lower operative mortality but also less absolute benefit compared to medical therapy than Profile 1-3 patients. The decision to implant in Profile 4-5 considers trajectory, quality of life, and patient preferences."

Q: What contraindications should be assessed?

A: "I would assess for both absolute and relative contraindications:

Absolute Contraindications:

• Irreversible multi-organ failure
• Active uncontrolled sepsis
• Severe irreversible cognitive impairment
• Active malignancy with less than 2 year prognosis
• Inadequate social support/compliance concerns

Relative Contraindications (for this patient):

• Obesity (BMI 38): Associated with higher infection, bleeding, mortality; many programs have BMI cutoff 35-40
• Significant RV dysfunction (needs assessment)
• Severe aortic insufficiency
• Renal dysfunction
• Hepatic dysfunction
• Coagulopathy
• Pulmonary disease

For this patient, his BMI would need discussion with the VAD team. Many would require weight loss before implantation, or accept higher perioperative risk."

Q: What RV assessment would you perform?

A: "RV failure post-LVAD occurs in 20-40% of patients, and 5-10% require RVAD. I would assess:

Echocardiographic Assessment:

• RV size (dilated suggests failure)
• RV function (TAPSE, RV FAC, S' wave)
• Tricuspid regurgitation severity
• Tricuspid annular dilation

Hemodynamic Assessment (right heart catheterization):

• CVP/PCWP ratio (>0.63 predicts RV failure)
• RV stroke work index
• Pulmonary vascular resistance
• Transpulmonary gradient

Clinical Predictors:

• Need for inotropes/IABP pre-operatively
• Elevated creatinine
• Elevated bilirubin
• Mechanical ventilation

Risk scores (CRITT, EUROMACS RV risk score) help quantify the probability of needing RVAD support."

---

Viva 2: Continuous-Flow Hemodynamics

Opening Statement: "Tell me about the hemodynamic principles of continuous-flow LVADs and how this affects patient assessment in ICU."

Expected Discussion Points:

Q: How does a continuous-flow LVAD generate flow?

A: "Continuous-flow LVADs use rotodynamic pumps that generate flow by imparting kinetic energy to blood:

Axial-flow pumps (e.g., HeartMate II):

• Use an Archimedes screw mechanism
• Blood flows along the axis of rotation
• Operate at 8,000-15,000 RPM
• Have mechanical bearings (contact points)

Centrifugal-flow pumps (e.g., HeartMate 3):

• Blood enters centrally and exits peripherally
• Centrifugal force propels blood outward
• Operate at 3,000-9,000 RPM
• HeartMate 3 is fully magnetically levitated (no contact)

Both generate continuous, non-pulsatile flow. The HeartMate 3 has an 'artificial pulse' - speed modulation of ±2000 RPM every 2 seconds - which creates some pulsatility and reduces stasis."

Q: Why is there no palpable pulse?

A: "The continuous-flow pump maintains relatively constant flow throughout the cardiac cycle. Although the native heart still contracts, contributing some additional stroke volume, this adds only 5-15 mmHg of pulse pressure.

The result is:

• Minimal or absent radial/carotid pulse
• Flattened arterial waveform
• Pulse pressure often less than 15 mmHg
• No Korotkoff sounds on auscultation

This has practical implications:

• Cannot assess circulation by pulse palpation
• Standard BP cuff measurement fails
• Pulse oximetry may be unreliable
• Must use alternative assessment methods"

Q: How do you measure blood pressure in these patients?

A: "Blood pressure is measured using Doppler technique:

1. Apply standard BP cuff to arm
2. Place Doppler probe over brachial or radial artery
3. Inflate cuff until Doppler signal disappears
4. Slowly deflate cuff
5. Record pressure when Doppler signal first returns

This 'Doppler opening pressure' approximates MAP in most continuous-flow patients. The target is typically 70-80 mmHg.

Arterial line monitoring shows a flattened waveform with minimal oscillation. The mean pressure remains interpretable."

Q: What is pulsatility index and how is it used?

A: "Pulsatility Index (PI) = (Maximum Flow - Minimum Flow) / Mean Flow

It reflects the contribution of native heart contraction to total flow. Normal range is 2.5-4.5.

Low PI (less than 1.5) suggests:

• Hypovolemia (reduced LV filling)
• RV failure (inadequate delivery to LV)
• Suction events (LV too empty)
• Inflow cannula obstruction

High PI (>6) suggests:

• Aortic insufficiency (blood returning to LV)
• Cardiac tamponade
• Severe arrhythmias
• Recovering LV function

PI is monitored continuously and trends are more important than absolute values. A falling PI may indicate worsening volume status or RV function."

---

Viva 3: Pump Thrombosis

Opening Statement: "A patient with HeartMate II LVAD is admitted with rising LDH and dark urine. Discuss your approach."

Expected Discussion Points:

Q: What is pump thrombosis and why does it occur?

A: "Pump thrombosis is the formation of thrombus within or around the mechanical components of the VAD, leading to impaired pump function and hemolysis.

Causes/Risk Factors:

• Subtherapeutic anticoagulation
• Infection (activates coagulation cascade)
• Suction events (endothelial damage)
• Low pump speeds (stasis)
• Device factors (HeartMate II higher risk than HeartMate 3)
• Patient factors (hypercoagulable states)

Pathophysiology:

• Thrombus forms on pump surfaces
• Impedes rotor movement
• Increases power consumption
• Causes mechanical hemolysis
• May embolize causing stroke
• Reduces pump output causing heart failure symptoms"

Q: What are the diagnostic markers?

A: "The classic triad is: Heart failure symptoms + Hemolysis + Device parameter changes

Laboratory Markers:

• LDH >2.5× upper limit of normal (most sensitive)
• Plasma-free hemoglobin >40 mg/dL
• Decreased haptoglobin
• Elevated indirect bilirubin
• Reticulocytosis
• Hemoglobinuria

Device Parameters:

• Increased power consumption (HeartMate: >10W)
• Decreasing estimated flow
• Power fluctuations
• Alarms for high power or low flow

Clinical Features:

• Recurrent heart failure symptoms
• Dark urine (hemoglobinuria)
• Jaundice
• Fatigue, dyspnea, edema

Imaging:

• Echo: Increased LV size, reduced decompression
• CT: May show pump thrombus (limited sensitivity)"

Q: How would you manage confirmed pump thrombosis?

A: "Management depends on severity and patient stability:

Medical Management (mild-moderate thrombosis, stable patient):

1. IV heparin infusion, target aPTT 60-80 seconds
2. Optimize volume status
3. Serial LDH monitoring (q6-12h)
4. If improving: Transition to warfarin with higher target

Thrombolytic Therapy (if medical management fails, not surgical candidate):

• t-PA 50mg over 4-6 hours, or
• t-PA 25mg bolus, may repeat
• High risk: Intracranial hemorrhage 5-10%
• Success rate 50-70%

Surgical Pump Exchange (preferred definitive treatment):

• Redo sternotomy, cardiopulmonary bypass
• Remove thrombosed pump, inspect cannulae
• Implant new pump
• Operative mortality 5-15%
• Reserved for: Refractory cases, hemodynamic instability, recurrent thrombosis

ECMO Bridge:

• If hemodynamically unstable
• Bridge to surgery or decision

I would involve the VAD coordinator and cardiac surgery team early in all cases."

Q: How has HeartMate 3 changed pump thrombosis rates?

A: "The MOMENTUM 3 trial demonstrated dramatically lower pump thrombosis rates with HeartMate 3:

• HeartMate 3: 1.4% at 2 years
• HeartMate II: 10.6% at 2 years
• Freedom from pump thrombosis: 98.6% vs 89.4%

The reasons for lower thrombosis include:

1. Fully magnetically levitated rotor: No mechanical contact points
2. Wide blood flow gaps (0.5mm): Reduced shear stress
3. Artificial pulse feature: Speed modulation reduces stasis
4. Improved biocompatibility

HeartMate 3 is now the dominant device (>95% of new implants in USA) largely due to this safety advantage."

---

Viva 4: GI Bleeding in VAD Patients

Opening Statement: "A 62-year-old with LVAD presents with melena and hemoglobin drop from 110 to 78 g/L. Discuss your approach."

Expected Discussion Points:

Q: Why are VAD patients prone to GI bleeding?

A: "GI bleeding occurs in 15-30% of LVAD patients due to a 'perfect storm' of factors:

1. Acquired von Willebrand Disease (nearly universal):

   • High shear stress in pump (>5000 dynes/cm²)
   • Causes unfolding of vWF multimers
   • Exposes ADAMTS13 cleavage sites
   • Loss of high-molecular-weight vWF multimers
   • HMW-vWF essential for primary hemostasis

2. Angiodysplasia/AVM Formation:

   • Loss of pulsatility alters angiogenesis
   • Mucosal hypoxia → VEGF upregulation
   • Increased AVM formation, especially in GI tract

3. Anticoagulation Therapy:

   • Warfarin + aspirin for device
   • Increases bleeding risk

4. Altered hemostasis:

   • Platelet dysfunction
   • Uremia if renal impairment"

Q: How would you manage this acute presentation?

A: "I would manage this as a major GI bleed with additional VAD considerations:

Resuscitation:

• Large-bore IV access, crystalloid resuscitation
• Crossmatch and transfuse PRBCs (target Hb 70-80 g/L, may accept higher in VAD)
• Check and correct coagulopathy (FFP, vitamin K)
• PPI infusion (pantoprazole 8mg/hr)
• ICU admission

Anticoagulation Management:

• Hold warfarin
• Check INR urgently
• If supratherapeutic: Vitamin K, PCC for life-threatening bleeding
• Decision to reverse must balance bleeding vs thrombosis risk
• Contact VAD coordinator

Localization:

• Urgent gastroscopy (after resuscitation)
• Colonoscopy if upper GI negative
• Capsule endoscopy or push enteroscopy for small bowel (AVMs often in jejunum/ileum)
• CT angiography if active bleeding and endoscopy not possible

Endoscopic Therapy:

• Argon plasma coagulation for AVMs
• Clips, thermal therapy
• May require multiple procedures"

Q: What if the bleeding is recurrent or refractory?

A: "For recurrent or refractory GI bleeding, consider:

Medical Therapies (limited evidence):

• Octreotide: 100-200 mcg SC TDS or LAR 20-30mg monthly
• Thalidomide: 50-100mg daily (anti-angiogenic)
• Danazol: Anabolic steroid, may improve vWF
• Doxycycline: Anti-angiogenic properties (case reports)

Device Modification:

• Reduce pump speed (increases pulsatility, may improve vWF)
• Must balance with adequate hemodynamic support

Anticoagulation Modification (controversial):

• Lower INR target (2.0-2.5)
• Some patients managed on aspirin alone (higher thrombosis risk)
• Case-by-case decision with VAD team

Surgical/Interventional:

• Interventional radiology embolization
• Surgical resection (last resort)

Last Resort:

• Pump exchange to pulsatile device (rarely done)
• Heart transplant if eligible

These patients require ongoing multidisciplinary management."

---

Viva 5: Driveline Infection

Opening Statement: "A patient with HeartMate 3 LVAD presents with redness and purulent discharge from the driveline exit site. Discuss your management."

Expected Discussion Points:

Q: What is driveline infection and how is it classified?

A: "Driveline infection is the most common infection in LVAD patients (10-30% incidence) and the most common late complication.

Classification:

• Superficial/Exit site: Limited to exit site skin, no systemic signs
• Deep/Tunnel infection: Involves subcutaneous tunnel, may have abscess
• Pocket infection: Involves pump pocket (more common in HeartMate II with pre-peritoneal pocket)
• Endovascular: Bacteremia, possible endocarditis

Common Organisms:

• Staphylococcus aureus (40%): MSSA and MRSA
• Coagulase-negative staphylococci (20%)
• Pseudomonas aeruginosa (15%)
• Enterobacteriaceae (10%)
• Candida species (5%)
• Polymicrobial (10%)"

Q: What investigations would you perform?

A: "I would perform:

1. Wound cultures: Deep swab or aspirate (surface swabs less reliable)
2. Blood cultures: At least 2 sets (rule out bacteremia)
3. Inflammatory markers: CRP, procalcitonin, WBC
4. CT scan with contrast: Assess for:
   • Tunnel involvement
   • Abscess formation
   • Pocket involvement
   • Mediastinal extension
5. Echocardiography: If bacteremia (rule out endocarditis)
6. Device interrogation: Baseline function"

Q: How would you manage a superficial vs deep infection?

A: "Management depends on depth and severity:

Superficial Exit Site Infection:

• Optimize driveline care (immobilization, cleaning)
• Oral antibiotics based on culture (2-4 weeks)
  • "Empiric: Fluoroquinolone + TMP-SMX or linezolid (covers MRSA)"
  • Adjust to culture results
• Daily dressing changes with antiseptic
• Close outpatient follow-up
• Most can be managed outpatient

Deep/Tunnel Infection:

• Hospital admission
• IV antibiotics (4-6 weeks minimum)
  • "Empiric: Vancomycin + anti-pseudomonal (piperacillin-tazobactam or cefepime)"
  • Adjust to culture results
• Surgical debridement (may require OR)
• Consider driveline relocation
• VAC therapy for wound
• Long-term suppressive oral antibiotics often required

Pocket Infection:

• Prolonged IV antibiotics (6+ weeks)
• Aggressive surgical debridement
• May require pump exchange if refractory

All infections require VAD coordinator and infectious diseases involvement."

Q: How can driveline infections be prevented?

A: "Prevention is critical as treatment is difficult:

1. Driveline immobilization: Abdominal binder or commercial anchor device to prevent movement/trauma

2. Patient education: Intensive pre-operative training on exit site care

3. Exit site care:

   • Daily inspection for signs of infection
   • Sterile dressing technique
   • Appropriate cleansing agents (chlorhexidine)
   • Keep site dry

4. Showering/bathing:

   • Only after complete healing (6-8 weeks)
   • Protective covers
   • Pat dry carefully
   • No swimming (pool, ocean)

5. Prompt treatment: Early recognition and treatment of minor exit site changes

6. Nutrition and glycemic control: Optimize wound healing

7. Avoid trauma: Careful positioning, loose clothing, avoid belt pressure"

---

Viva 6: Cardiac Arrest in VAD Patient

Opening Statement: "You are called to a cardiac arrest in a patient with a HeartMate 3 LVAD. The nursing staff report the patient collapsed and is unresponsive. Discuss your approach."

Expected Discussion Points:

Q: How does resuscitation differ in a VAD patient?

A: "Cardiac arrest in a VAD patient requires modified assessment and management:

Key Differences:

1. No palpable pulse at baseline: Cannot use pulse check to assess circulation
2. Device may be providing some output: Even in arrest, continuous-flow may maintain some perfusion
3. Chest compressions controversial: May dislodge cannulae, damage device
4. Standard ALS drugs still indicated: Epinephrine, amiodarone
5. Defibrillation is safe: External pads can be used

Assessment:

• Consciousness (primary indicator)
• Check device: Controller functioning? Alarms? Batteries connected?
• Doppler signal over peripheral artery
• End-tidal CO2 if intubated
• Capillary refill, skin temperature"

Q: What is the initial approach?

A: "My initial approach:

1. Call for help: Cardiac arrest team, VAD coordinator

2. Check device immediately:

   • Controller powered on?
   • Batteries connected?
   • Any alarms?
   • Check connections (driveline to controller)

3. Assess patient:

   • Responsiveness
   • Breathing
   • Doppler signal over brachial/radial artery
   • ETCO2 if ventilated

4. If device functioning (no alarms, power connected):

   • Likely arrhythmia or other cause
   • Attach defibrillator pads
   • Check rhythm - if VF/VT: Defibrillate
   • Consider other causes (hypovolemia, tamponade, tension pneumothorax)

5. If device NOT functioning (alarms, power disconnected):

   • Troubleshoot device urgently
   • Reconnect power sources
   • If truly device failure: Chest compressions may be considered"

Q: What about chest compressions?

A: "Chest compressions in VAD patients are controversial:

Arguments Against:

• May dislodge inflow/outflow cannulae
• May damage pump
• May cause hemothorax or tamponade
• If device is functioning, continuous flow already providing output
• Compressions may not add significant benefit

Arguments For:

• If device has truly failed, compressions may provide some output
• Standard resuscitation training is to compress
• Some survival reported with compressions

Current Recommendations:

• If device is functioning: Focus on arrhythmia management (defibrillation) and reversible causes
• If device has failed and cannot be restored: Compressions may be performed
• Compressions should not delay defibrillation or addressing device issues

The key is: Identify why the patient arrested and address that cause:

• VF/VT: Defibrillate
• Hypovolemia: IV fluids
• Tamponade: Drainage
• Device failure: Troubleshoot/replace power
• Severe RV failure: Inotropes, consider MCS"

Q: What are the common causes of cardiac arrest in VAD patients?

A: "Common causes include:

1. Arrhythmias (most common):

   • VF/VT from underlying cardiomyopathy
   • May have functioning device with VF
   • Treat with defibrillation, antiarrhythmics

2. Pump failure:

   • Controller malfunction
   • Driveline fracture
   • Pump thrombosis (gradual, rarely acute arrest)

3. Disconnection/Power failure:

   • Driveline disconnect from controller
   • Both batteries depleted
   • Check and reconnect power

4. Suction event:

   • Severe hypovolemia
   • RV failure
   • Inflow obstruction

5. Stroke (hemorrhagic):

   • Massive hemorrhage causing herniation

6. Tamponade:

   • Post-operative bleeding
   • Late complication

7. Sepsis:

   • Driveline infection progressing

Management involves rapidly identifying and treating the underlying cause while supporting the patient."

---

---

References

Landmark Trials

1. Rose EA, Gelijns AC, Moskowitz AJ, et al. Long-term use of a left ventricular assist device for end-stage heart failure. N Engl J Med. 2001;345(20):1435-1443. PMID: 11717165 (REMATCH)

2. Miller LW, Pagani FD, Russell SD, et al. Use of a continuous-flow device in patients awaiting heart transplantation. N Engl J Med. 2007;357(9):885-896. PMID: 17967141 (HeartMate II BTT)

3. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous-flow left ventricular assist device. N Engl J Med. 2009;361(23):2241-2251. PMID: 19920051 (HeartMate II DT)

4. Mehra MR, Naka Y, Uriel N, et al. A fully magnetically levitated circulatory pump for advanced heart failure. N Engl J Med. 2017;376(5):440-450. PMID: 28211672 (MOMENTUM 3)

5. Mehra MR, Uriel N, Naka Y, et al. A fully magnetically levitated left ventricular assist device - final report. N Engl J Med. 2019;380(17):1618-1627. PMID: 30571454 (MOMENTUM 3 Final)

6. Mehra MR, Goldstein DJ, Cleveland JC, et al. Five-year outcomes in patients with fully magnetically levitated vs axial-flow left ventricular assist devices in the MOMENTUM 3 randomized trial. JAMA. 2022;327(10):1266-1275. PMID: 35052322 (MOMENTUM 3 5-Year)

7. Rogers JG, Pagani FD, Tatooles AJ, et al. Intrapericardial left ventricular assist device for advanced heart failure. N Engl J Med. 2017;376(5):451-460. PMID: 28526653 (ENDURANCE)

Registry Data

8. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: Special focus on framing the impact of adverse events. J Heart Lung Transplant. 2017;36(10):1080-1086. PMID: 28942782

9. Molina EJ, Shah P, Kiernan MS, et al. The Society of Thoracic Surgeons Intermacs 2020 Annual Report. Ann Thorac Surg. 2021;111(3):778-792. PMID: 33385346

10. Shah P, Yuzefpolskaya M, Engelman DT, et al. Society of Thoracic Surgeons Intermacs 2022-2023 Annual Report. Ann Thorac Surg. 2024;117(1):51-70. PMID: 37148016

11. Kormos RL, Cowger J, Pagani FD, et al. The Society of Thoracic Surgeons Intermacs database annual report: Evolving indications, outcomes, and scientific partnerships. J Heart Lung Transplant. 2019;38(2):114-126. PMID: 30586764

Guidelines

12. Feldman D, Pamboukian SV, Teuteberg JJ, et al. The 2013 International Society for Heart and Lung Transplantation Guidelines for mechanical circulatory support. J Heart Lung Transplant. 2013;32(2):157-187. PMID: 23352391

13. Potapov EV, Antonides C, Crespo-Leiro MG, et al. 2019 EACTS Expert Consensus on long-term mechanical circulatory support. Eur J Cardiothorac Surg. 2019;56(2):230-270. PMID: 31100109

14. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure. J Am Coll Cardiol. 2013;62(16):e147-e239. PMID: 23747642

Physiology and Hemodynamics

15. Slaughter MS, Pagani FD, Rogers JG, et al. Clinical management of continuous-flow left ventricular assist devices in advanced heart failure. J Heart Lung Transplant. 2010;29(4 Suppl):S1-39. PMID: 20181499

16. Uriel N, Morrison KA, Garan AR, et al. Development of a novel echocardiography ramp test for speed optimization and diagnosis of device thrombosis in continuous-flow left ventricular assist devices. J Am Coll Cardiol. 2012;60(18):1764-1775. PMID: 23040584

17. Rao V, Slater JP, Edwards NM, et al. Surgical management of valvular disease in patients requiring left ventricular assist device support. Ann Thorac Surg. 2001;71(5):1448-1453. PMID: 11383782

18. Cowger JA, Aaronson KD, Romano MA, et al. Consequences of aortic insufficiency during long-term axial continuous-flow left ventricular assist device support. J Heart Lung Transplant. 2014;33(12):1233-1240. PMID: 25179757

Complications - Pump Thrombosis

19. Starling RC, Moazami N, Silvestry SC, et al. Unexpected abrupt increase in left ventricular assist device thrombosis. N Engl J Med. 2014;370(1):33-40. PMID: 24283197

20. Najjar SS, Slaughter MS, Pagani FD, et al. An analysis of pump thrombus events in patients in the HeartWare ADVANCE bridge to transplant and continued access protocol trial. J Heart Lung Transplant. 2014;33(1):23-34. PMID: 24418731

21. Kirklin JK, Naftel DC, Kormos RL, et al. Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) analysis of pump thrombosis in the HeartMate II left ventricular assist device. J Heart Lung Transplant. 2014;33(1):12-22. PMID: 24418730

22. Uriel N, Han J, Morrison KA, et al. Device thrombosis in HeartMate II continuous-flow left ventricular assist devices: a multifactorial phenomenon. J Heart Lung Transplant. 2014;33(1):51-59. PMID: 24290832

Complications - Bleeding

23. Suarez J, Patel CB, Felker GM, et al. Mechanisms of bleeding and approach to patients with axial-flow left ventricular assist devices. Circ Heart Fail. 2011;4(6):779-784. PMID: 22086832

24. Uriel N, Pak SW, Jorde UP, et al. Acquired von Willebrand syndrome after continuous-flow mechanical device support contributes to a high prevalence of bleeding during long-term support and at the time of transplantation. J Am Coll Cardiol. 2010;56(15):1207-1213. PMID: 20598466

25. Crow S, Chen D, Milano C, et al. Acquired von Willebrand syndrome in continuous-flow ventricular assist device recipients. Ann Thorac Surg. 2010;90(4):1263-1269. PMID: 20868825

26. Demirozu ZT, Radovancevic R, Hochman LF, et al. Arteriovenous malformation and gastrointestinal bleeding in patients with the HeartMate II left ventricular assist device. J Heart Lung Transplant. 2011;30(8):849-853. PMID: 21561794

27. Draper KV, Huang RJ, Gerson LB. GI bleeding in patients with continuous-flow left ventricular assist devices: a systematic review and meta-analysis. Gastrointest Endosc. 2014;80(3):435-446.e1. PMID: 25042534

Complications - Infection

28. Topkara VK, Kondareddy S, Malik F, et al. Infectious complications in patients with left ventricular assist device: etiology and outcomes in the continuous-flow era. Ann Thorac Surg. 2010;90(4):1270-1277. PMID: 20868826

29. Goldstein DJ, Naftel D, Holman W, et al. Continuous-flow devices and percutaneous site infections: clinical outcomes. J Heart Lung Transplant. 2012;31(11):1151-1157. PMID: 22766020

30. Hannan MM, Husain S, Mattner F, et al. Working formulation for the standardization of definitions of infections in patients using ventricular assist devices. J Heart Lung Transplant. 2011;30(4):375-384. PMID: 21419995

31. Gordon RJ, Quagliarello B, Lowy FD. Ventricular assist device-related infections. Lancet Infect Dis. 2006;6(7):426-437. PMID: 16790383

Complications - Stroke

32. Acharya D, Loyaga-Rendon R, Morgan CJ, et al. INTERMACS analysis of stroke during support with continuous-flow left ventricular assist devices. JACC Heart Fail. 2017;5(10):703-711. PMID: 28958344

33. Frontera JA, Starling R, Engstrom S, et al. Neurologic complications after left ventricular assist device implantation. Stroke. 2014;45(9):2750-2757. PMID: 30638371

34. Kato TS, Schulze PC, Yang J, et al. Pre-operative and post-operative risk factors associated with neurologic complications in patients with advanced heart failure supported by a left ventricular assist device. J Heart Lung Transplant. 2012;31(1):1-8. PMID: 22055095

Complications - RV Failure

35. Kormos RL, Teuteberg JJ, Pagani FD, et al. Right ventricular failure in patients with the HeartMate II continuous-flow left ventricular assist device: incidence, risk factors, and effect on outcomes. J Thorac Cardiovasc Surg. 2010;139(5):1316-1324. PMID: 20132950

36. Dang NC, Topkara VK, Mercando M, et al. Right heart failure after left ventricular assist device implantation in patients with chronic congestive heart failure. J Heart Lung Transplant. 2006;25(1):1-6. PMID: 16399522

37. Matthews JC, Koelling TM, Pagani FD, Aaronson KD. The right ventricular failure risk score a pre-operative tool for assessing the risk of right ventricular failure in left ventricular assist device candidates. J Am Coll Cardiol. 2008;51(22):2163-2172. PMID: 18510965

38. Potapov E, Meyer D, Swaminathan M, et al. Inhaled nitric oxide after left ventricular assist device implantation: a prospective, randomized, double-blind, multicenter, placebo-controlled trial. J Heart Lung Transplant. 2011;30(8):870-878. PMID: 21530319

Cardiac Arrest and Resuscitation

39. Peberdy MA, Gluck JA, Ornato JP, et al. Cardiopulmonary resuscitation in adults and children with mechanical circulatory support. Circulation. 2017;135(24):e1115-e1134. PMID: 28584092

40. Shinar Z, Bellezzo J, Paradis N, et al. Emergency department management of patients with continuous-flow left ventricular assist devices. J Emerg Med. 2014;47(1):1-8. PMID: 24725823

41. Samuels LE, Holmes EC, Samuels FL. Selective use of cardiopulmonary resuscitation in patients with ventricular assist devices. Ann Thorac Surg. 1998;66(3):715-720. PMID: 9768921

Australian Context

42. Kure CE, Rosenfeldt FL, Merry CJ, et al. The Alfred Ventricular Assist Device Program: 15 years of experience. Heart Lung Circ. 2018;27(4):453-461. PMID: 29054619

43. Hayward CS, Salamonsen R, Keogh AM, et al. Effect of alteration in pump speed on pump output and left ventricular filling with continuous-flow left ventricular assist device. ASAIO J. 2011;57(6):495-500. PMID: 22016218

44. Jansz P, Merry C, Ross D, et al. The Australian experience with the HeartWare ventricular assist device. J Heart Lung Transplant. 2013;32(4S):S114. (Abstract)

45. Connellan M, Iyer A, Robson D, et al. Long-term outcomes of LVAD and heart transplantation in Australia. Heart Lung Circ. 2022;31(S2):S123-S124. PMID: 35587227

Device Technology

46. Mehra MR. The burden of haemocompatibility with left ventricular assist systems: a complex weave. Eur Heart J. 2019;40(8):673-677. PMID: 30452555

47. Netuka I, Sood P, Pya Y, et al. Fully magnetically levitated left ventricular assist system for treating advanced HF: A multicenter study. J Am Coll Cardiol. 2015;66(23):2579-2589. PMID: 26670056

48. Heatley G, Sood P, Goldstein D, et al. Clinical trial design and rationale of the Multicenter Study of MagLev Technology in Patients Undergoing Mechanical Circulatory Support Therapy With HeartMate 3 (MOMENTUM 3) investigational device exemption clinical study protocol. J Heart Lung Transplant. 2016;35(4):528-536. PMID: 26746933

---

Last Updated: January 2026 MedVellum CICM Team