Case — 70-year-old man in cardiac failure with hypotension and tachypnoea: pathophysiology, differentials, investigations, and management in the ED, ward and after discharge

Underlying pathophysiology. A primary fall in cardiac output (from pump failure, arrhythmia, valve failure or mechanical complication) causes systemic hypoperfusion. Compensatory sympathetic activation and renin– angiotensin–aldosterone activation raise heart rate and systemic vascular resistance, which further increases afterload and myocardial oxygen demand while reducing coronary perfusion — a vicious spiral of ischaemia → worsening contractility → lower output → more ischaemia. Simultaneously, raised left ventricular filling pressure is transmitted to the pulmonary capillaries, causing interstitial and alveolar oedema; this reduces compliance and impairs gas exchange, and the resulting hypoxaemia and metabolic (lactic) acidosis drive the tachypnoea. Systemic hypoperfusion causes acute kidney injury, hepatic dysfunction, delirium and a systemic inflammatory response with inappropriate vasodilatation.

Haemodynamic profiling at the bedside. Classify immediately by congestion ("wet or dry") and perfusion ("warm or cold"):

Differential diagnosis — cardiac causes to consider. Acute myocardial infarction with pump failure (the commonest cause); mechanical complications of MI — acute mitral regurgitation from papillary muscle rupture, ventricular septal rupture, free wall rupture with tamponade; tachyarrhythmia or bradyarrhythmia including complete heart block; critical aortic stenosis; acute severe valvular regurgitation from infective endocarditis; myocarditis; Takotsubo cardiomyopathy; cardiac tamponade; and decompensation of known heart failure.

Differential diagnosis — non-cardiac mimics that must be excluded. Sepsis and septic shock with myocardial depression (fever, warm periphery, high lactate, source of infection); massive pulmonary embolism (right ventricular failure with clear lungs, raised JVP, hypoxia with hypocapnia); hypovolaemia and gastrointestinal bleeding; tension pneumothorax; aortic dissection with tamponade or acute aortic regurgitation; anaphylaxis; drug toxicity — beta-blocker, calcium channel blocker or digoxin overdose; adrenal crisis and severe hypothyroidism (myxoedema); and severe anaemia or thyrotoxicosis causing high-output failure.

Investigations that discriminate between them.

Emergency Department management — immediate stabilisation. ABCDE, monitored bed, two cannulae, arterial line if shocked, urinary catheter for hourly output. Sit the patient up and give oxygen to target SpO 94–98%; 2 escalate to CPAP or non-invasive ventilation, which reduces preload and afterload, improves oxygenation and reduces intubation; intubate if exhausted, obtunded or acidotic despite NIV. Do NOT give nitrates or high-dose diuretic first in a hypotensive patient — nitrates are contraindicated at systolic BP < 90 mmHg. Instead: give a cautious 250 mL fluid challenge only if the IVC is collapsed and there is no pulmonary oedema; otherwise start noradrenaline to restore a mean arterial pressure ≥ 65 mmHg, then add an inotrope (dobutamine or levosimendan) to restore perfusion. Once perfused, give intravenous furosemide for congestion. Correct arrhythmia (urgent DC cardioversion for haemodynamically unstable tachyarrhythmia; pacing for complete heart block), and if ACS is the cause arrange immediate primary PCI.

Ward or coronary care management. Continue continuous monitoring of rhythm, blood pressure, saturation, hourly urine output, daily weight and strict fluid balance, with daily renal function and electrolytes. Wean vasopressors and inotropes as perfusion recovers, then titrate diuretics to a negative fluid balance, adding a thiazide or acetazolamide for diuretic resistance. Treat the precipitant — revascularisation, antibiotics, rate or rhythm control, correction of anaemia and thyroid dysfunction. Reintroduce and uptitrate disease-modifying therapy as soon as the patient is off inotropes and euvolaemic: ACE inhibitor or ARNI, beta-blocker, MRA and SGLT2 inhibitor. Provide VTE prophylaxis, early mobilisation, pressure-area care, delirium prevention, nutrition and dietitian input. Refer for device therapy (ICD/CRT) assessment once the ejection fraction has been reassessed at 3 months on optimal therapy.

Geriatric considerations throughout. A 70-year-old may have reduced β-adrenergic responsiveness, arterial stiffening, diastolic dysfunction and limited renal reserve, so he is exquisitely preload-sensitive and tolerates neither over-filling nor over-diuresis. Give fluid in 250 mL aliquots with reassessment. Actively look for and prevent acute kidney injury, delirium, falls, hospital-acquired infection, pressure sores, constipation and deconditioning. Review the whole drug chart — stop NSAIDs and other precipitants; review anticholinergic and sedative burden. Undertake a comprehensive geriatric assessment, and discuss ceilings of care, escalation and resuscitation status early with the patient and family.

Discharge planning. Discharge only when the patient is euvolaemic, on stable oral therapy for at least 24 hours, with stable renal function. Provide: a written management plan with daily weights and an action plan for a weight gain of more than 2 kg in three days; education on salt and fluid moderation, medication purpose and side effects; a reconciled and simplified drug list; enrolment in cardiac rehabilitation; influenza, pneumococcal and COVID-19 vaccination; and social and functional support with an occupational therapy home assessment. Arrange heart failure nurse follow-up within 7 days and clinic review within 2 weeks, with early uptitration of the four pillars — multidisciplinary nurse-led follow-up is the intervention that most reliably reduces readmission.

Longer-term follow-up and prognosis. Repeat echocardiography at 3 months on optimal therapy to guide ICD/CRT referral. Monitor renal function and potassium after each dose change. Screen and treat iron deficiency (intravenous iron), anaemia, atrial fibrillation, sleep apnoea, depression and frailty. Secondary prevention if ischaemic — antiplatelet therapy, statin, blood pressure and glycaemic control, smoking cessation. Counsel on driving restrictions and vaccination. Prognosis after cardiogenic shock remains poor, so advance care planning should be revisited, and the caregiver's physical and emotional health should be assessed as part of ongoing review.

DanGer Shock (NEJM 2024) — the first adequately powered randomised trial of mechanical circulatory support in cardiogenic shock. In STEMI-related cardiogenic shock, a microaxial flow pump (Impella CP) reduced 180-day all-cause mortality compared with standard care, though at the cost of significantly more bleeding, limb ischaemia, haemolysis and renal replacement therapy. This is the first positive mortality trial in this field (intra-aortic balloon counterpulsation was neutral in IABP-SHOCK II), and it supports early referral of selected patients to a shock team at a centre with mechanical circulatory support — while the complication profile makes patient selection critical in the frail older patient.

Culprit-lesion-only revascularisation and rapid post-discharge uptitration. CULPRIT-SHOCK established that in shock complicating multivessel disease, culprit-lesion-only PCI is superior to immediate multivessel PCI (less death and renal replacement therapy) — staged treatment of remaining lesions is the correct approach. After stabilisation, STRONG-HF showed that high-intensity uptitration of guideline-directed therapy to full dose within 2 weeks of discharge, with four follow-up visits in 2 months, significantly reduced death and heart failure readmission at 180 days, and this benefit was preserved in older patients — making the first two weeks after discharge the highest-value period of the whole admission.