What is the most likely diagnosis and guideline-directed management for an 80‑plus-year-old woman with acute decompensated heart failure in cardiogenic shock, on nasal bilevel positive airway pressure (BiPAP), receiving three inotropes, and a markedly elevated pro‑brain natriuretic peptide (pro‑BNP)?

Acute Decompensated Heart Failure with Cardiogenic Shock

This patient has acute decompensated heart failure (ADHF) in cardiogenic shock with a markedly elevated pro-BNP of 35,000 pg/mL, requiring triple inotropic support and non-invasive ventilation—the diagnosis is established and the immediate priority is hemodynamic stabilization, urgent echocardiography to identify mechanical complications, and transfer to a tertiary center with mechanical circulatory support capability. 1, 2

Diagnosis Confirmation

Pro-BNP of 35,000 pg/mL confirms severe cardiac dysfunction. In acute heart failure, pro-BNP values >300 pg/mL support the diagnosis, but levels this markedly elevated (>10,000 pg/mL) indicate severe decompensation and carry important prognostic information for high mortality risk. 1 The combination of triple inotropic requirement, non-invasive ventilation, and extreme natriuretic peptide elevation defines cardiogenic shock with respiratory failure. 1, 2

Cardiogenic shock is defined by: 1, 2, 3

• Systolic blood pressure <90 mmHg for >30 minutes despite adequate filling
• Signs of end-organ hypoperfusion (oliguria <0.5 mL/kg/h, cold extremities, altered mental status, lactate >2 mmol/L, metabolic acidosis)
• Cardiac index <2.2 L/min/m² with pulmonary capillary wedge pressure >15 mmHg

Immediate Diagnostic Actions

Perform urgent bedside echocardiography within minutes to assess left and right ventricular function, identify mechanical complications (ventricular septal rupture, acute mitral regurgitation, free-wall rupture), evaluate valvular function, and determine the hemodynamic phenotype. 1, 2, 3

Insert an invasive arterial line immediately for continuous accurate blood pressure monitoring—this is a Class I recommendation for all cardiogenic shock patients. 1, 2, 3

Obtain 12-lead ECG to identify acute coronary syndrome as the precipitating cause, which would mandate emergent coronary angiography within 2 hours. 1, 2, 3

Measure arterial blood gas with pH, PaCO₂, PaO₂, and lactate to assess oxygenation, ventilation adequacy, acid-base balance, and tissue perfusion. 1, 4 Serial lactate measurements track adequacy of resuscitation. 2, 3

Laboratory assessment should include: 1, 2

• Cardiac troponin (elevated in most cardiogenic shock cases)
• Creatinine and blood urea nitrogen (assess renal hypoperfusion)
• Electrolytes (sodium, potassium)
• Liver function tests (hepatic congestion from elevated venous pressure)
• Complete blood count

Consider early pulmonary artery catheterization when the shock phenotype is unclear or the patient fails initial therapy, as observational data suggest complete hemodynamic profiling improves outcomes. 2, 3 This allows measurement of cardiac output, pulmonary capillary wedge pressure, and mixed venous oxygen saturation to guide therapy. 1, 2

Hemodynamic Management Algorithm

Current Inotropic Support Assessment

The patient is already on triple inotropes—this represents refractory cardiogenic shock. 2, 3 Refractory shock is defined by persistent tissue hypoperfusion despite adequate doses of two vasoactive agents and treatment of the underlying cause. 2, 3

Verify the inotropic regimen includes: 1, 2, 3

• Norepinephrine as first-line vasopressor (to maintain mean arterial pressure ≥65 mmHg)—it is associated with lower mortality and fewer arrhythmias (~12% vs 24% with dopamine)
• Dobutamine as first-line inotrope (2-20 µg/kg/min) to increase cardiac output when low output persists
• Avoid dopamine as it carries higher arrhythmia and mortality risk; reserve only for bradycardic patients

If the third inotrope is dopamine, switch to norepinephrine immediately. 2, 3 If the third agent is milrinone or levosimendan, this is appropriate for refractory shock, especially if the patient has been on chronic beta-blockers. 1, 2

Respiratory Support Optimization

The patient is on nasal BiPAP—this is appropriate initial respiratory support. 1, 4 Non-invasive positive pressure ventilation (CPAP or BiPAP) should be started as soon as respiratory distress is present (respiratory rate >25 breaths/min, SpO₂ <90%) to decrease work of breathing and reduce intubation rates. 1, 4

Critical caveat: Use BiPAP with extreme caution in hypotensive patients, as positive pressure ventilation reduces venous return and can worsen blood pressure—monitor blood pressure closely and frequently. 4

Proceed to endotracheal intubation if: 1, 4

• PaO₂ <60 mmHg (8.0 kPa) despite BiPAP
• PaCO₂ >50 mmHg (6.65 kPa) with pH <7.35
• Inability to protect airway
• Severe altered mental status
• Hemodynamic collapse requiring immediate resuscitation

Titrate FiO₂ to maintain SpO₂ >90%, but avoid hyperoxia as oxygen causes vasoconstriction and reduces cardiac output in non-hypoxemic patients. 4

Hemodynamic Targets

Aim for the following perfusion markers: 1, 2, 3

• Mean arterial pressure ≥65 mmHg
• Systolic blood pressure >90 mmHg
• Cardiac index >2.0-2.2 L/min/m²
• Urine output >0.5 mL/kg/h
• Progressive lactate clearance
• Improvement in mental status
• Mixed venous oxygen saturation (SvO₂) ≥65%
• Pulmonary capillary wedge pressure <20 mmHg

Escalation to Mechanical Circulatory Support

This patient meets criteria for mechanical circulatory support (MCS) consideration. 2, 3 Refractory shock with triple inotropic requirement and ongoing tissue hypoperfusion mandates evaluation for short-term MCS after assessing age, comorbidities, and neurological status. 2, 3

Do NOT use intra-aortic balloon pump (IABP) routinely—the IABP-SHOCK II trial showed no mortality benefit (Class III recommendation). 1, 2, 3 IABP may only be considered for mechanical complications such as ventricular septal rupture or acute mitral regurgitation as a bridge to surgery. 1, 2, 3

Consider Impella micro-axial pump or short-term ventricular assist device in selected patients with severe refractory shock, as these provide superior hemodynamic support compared to IABP. 2, 3 Device selection depends on hemodynamic phenotype determined by pulmonary artery catheter. 3

Veno-arterial ECMO is not recommended routinely as current data have not demonstrated survival benefit and it carries higher bleeding and vascular complication rates. 3

Transfer and Systems-Based Care

Transfer this patient urgently to a tertiary center with 24/7 cardiac catheterization capability, dedicated ICU/CCU, and short-term mechanical circulatory support availability—failure to transfer is associated with markedly higher mortality. 1, 2, 3

Activate a multidisciplinary shock team (interventional cardiology, cardiac surgery, heart failure specialists, intensivists) immediately, as team-based care is associated with 39% reduction in 30-day mortality (hazard ratio 0.61; 95% CI 0.41-0.93). 2, 3

Identification of Underlying Cause

If acute coronary syndrome is identified on ECG or troponin elevation, perform emergent coronary angiography within 2 hours with intent to revascularize the culprit lesion—this is the only therapy proven to reduce mortality in cardiogenic shock. 2, 3

If echocardiography reveals mechanical complications (ventricular septal rupture, acute mitral regurgitation, free-wall rupture), these require early surgical intervention after Heart Team discussion. 1, 3

If no acute coronary syndrome or mechanical complication is identified, consider other precipitants: 1

• Acute decompensation of chronic heart failure
• Myocarditis
• Takotsubo cardiomyopathy
• Tachycardia-induced cardiomyopathy
• Acute valvular dysfunction
• Pulmonary embolism (though less likely given the clinical picture)

Medication Adjustments

Suspend all oral heart failure medications (ACE inhibitors, ARBs, sacubitril/valsartan, beta-blockers) during the acute shock phase, as these can worsen hypotension and are contraindicated in cardiogenic shock. 1, 3 These can be cautiously reintroduced only after hemodynamic stability is achieved for ≥24 hours without vasopressors/inotropes. 3

Diuretics should be used cautiously in cardiogenic shock—while pulmonary congestion requires decongestion, aggressive diuresis can worsen cardiac output and renal perfusion. 1 Titrate diuretics to relieve congestion while maintaining adequate perfusion pressure. 1

Prognosis and Decision-Making

In-hospital mortality in cardiogenic shock remains 40-50% despite modern therapies. 3 The combination of advanced age (late 80s), triple inotropic requirement, and extreme pro-BNP elevation indicates very high mortality risk. 1, 5

Goals of care discussion should occur early with the patient (if able) and family, addressing realistic expectations, potential for meaningful recovery, and appropriateness of escalating to mechanical support or considering palliative measures. 2, 3

Contraindications to escalation of mechanical support include: 3

• Anoxic brain injury
• Irreversible end-organ failure
• Prohibitive vascular access
• Do-not-resuscitate order
• Severe frailty or limited functional status prior to admission

Critical Pitfalls to Avoid

Do not delay transfer to a tertiary center—every hour of delay increases mortality risk. 2, 3

Do not use routine IABP—randomized trials have definitively shown no benefit. 1, 2, 3

Do not use dopamine or epinephrine as first-line agents—they increase arrhythmia and mortality risk. 1, 2, 3

Do not perform multivessel PCI if acute MI is identified—treat only the culprit lesion, as multivessel intervention increases mortality and renal failure. 2, 3

Do not continue BiPAP if blood pressure deteriorates—positive pressure can precipitate hemodynamic collapse in hypotensive patients. 4

Do not delay intubation if respiratory failure worsens—early intubation with controlled ventilation is safer than prolonged BiPAP failure. 1, 4