Cardiovascular · Hard
This case is fictional and exists for study. It describes no real patient.
68 years · male
A 68-year-old male presents to the emergency department with severe shortness of breath, orthopnoea, and worsening lower limb swelling over three days. He has a history of ischaemic cardiomyopathy with a reduced ejection fraction of 28% and hypertension. On examination, he appears distressed and is unable to complete full sentences. His peripheries are cold and clammy to touch with delayed capillary refill. Precordial palpation demonstrates a laterally displaced apex beat and an S3 gallop is audible. Auscultation reveals widespread bilateral coarse crackles in the mid-to-lower lung fields. Jugular venous pressure is elevated 6 cm above the sternal angle with marked bilateral pitting ankle oedema.
Vital signs
- HR
- 115 bpm
- BP
- 86/54 mmHg
- RR
- 32/min
- Temp
- 36.4 °C
- SpO₂
- 88%
Examination findings
- Cold, clammy extremities with capillary refill time of 4 seconds
- S3 gallop and laterally displaced apex beat
- Bilateral coarse crackles extending up to mid-lung zones
- JVP elevated 6 cm above sternal angle with positive hepatojugular reflux
Investigations
| NT-proBNP | 8400 pg/mL | reference: < 125 |
| Serum Creatinine | 185 µmol/L | reference: 60-110 |
| Serum Potassium | 5.1 mmol/L | reference: 3.5-5.0 |
| Troponin T | 42 ng/L | reference: < 14 |
Question 1 of 3
Which haemodynamic classification best describes this patient's current clinical presentation?
The patient demonstrates features of volume overload/congestion (elevated JVP, bilateral lung crackles, peripheral oedema, marked NT-proBNP elevation = 'wet') alongside signs of severe end-organ hypoperfusion (hypotension, tachycardia, cold clammy skin, capillary refill time of 4 seconds, worsening renal function = 'cold'). This 'cold and wet' profile represents acute decompensated heart failure with cardiogenic shock. 'Warm and wet' indicates congestion without hypoperfusion. 'Cold and dry' reflects hypoperfusion/hypovolaemia without congestion. 'Warm and dry' represents a compensated baseline state.
Teaching point: Acute heart failure is haemodynamically categorized by perfusion ('warm' vs 'cold') and congestion ('dry' vs 'wet'); 'cold and wet' indicates severe shock requiring inotropic or vasopressor support.
Question 2 of 3
In addition to oxygen therapy, which of the following is the most appropriate initial pharmacological strategy to restore haemodynamic stability?
In patients with acute decompensated heart failure accompanied by cardiogenic shock or symptomatic hypotension (systolic BP < 90 mmHg) and organ hypoperfusion ('cold and wet'), inotropic agents such as dobutamine are indicated to increase cardiac output and improve organ perfusion. Intravenous nitrates (Option D) are potent vasodilators and are strictly contraindicated when systolic BP is below 90 mmHg due to the risk of precipitating profound cardiac arrest. Sacubitril/valsartan (Option B) is used for chronic management in stable patients and should never be initiated during acute haemodynamically unstable states. Intravenous beta-blockers (Option A) are negative inotropes and would severely worsen heart failure and cardiogenic shock.
Teaching point: Intravenous vasodilators like nitrates are contraindicated in acute heart failure with a systolic blood pressure below 90 mmHg; inotropes are required when signs of low cardiac output and hypoperfusion are present.
Question 3 of 3
Regarding the patient's long-term disease-modifying oral heart failure therapy, which action is most appropriate during this acute initial management phase?
During acute heart failure decompensation with cardiogenic shock, hypotension, or acute kidney injury, disease-modifying therapy such as beta-blockers and ACE inhibitors/ARBs should be temporarily withheld or down-titrated. Beta-blockers exert negative inotropic effects that can exacerbate acute cardiogenic shock, while ACE inhibitors worsen renal hypoperfusion and hypotension. Once the patient is haemodynamically stable, euvolaemic, and weaned off inotropes, these medications should be re-introduced cautiously. Continuing full doses (Option A) or increasing beta-blockers (Option C) will deepen cardiogenic shock and exacerbate hypoperfusion. Loop diuretics (Option D) remain essential for managing fluid overload; withholding them permanently is incorrect.
Teaching point: Beta-blockers and ACE inhibitors should be temporarily held or reduced during acute heart failure decompensation presenting with hypotension, shock, or acute renal impairment.
Key learning points
- Acute heart failure haemodynamic profiles guide management: 'cold and wet' signifies hypoperfusion with fluid overload, carrying the highest mortality.
- Intravenous nitrates are contraindicated in acute decompensated heart failure when systolic blood pressure is below 90 mmHg; inotropes (e.g., dobutamine) are indicated for persistent hypoperfusion.
- Chronic disease-modifying heart failure medications (beta-blockers and ACE inhibitors) must be held or down-titrated during acute haemodynamic instability and cardiogenic shock.
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