22.3 Acute Cardiorespiratory Emergencies: Pulmonary Embolism, Acute Severe Asthma and COPD, Non-Invasive Support and Acute Heart Failure

22.3 Acute Cardiorespiratory Emergencies: Pulmonary Embolism, Acute Severe Asthma and COPD, Non-Invasive Support and Acute Heart Failure

Pulmonary Embolism (PE)

Clinical Probability and Diagnosis

Symptoms include dyspnoea, pleuritic pain, haemoptysis, syncope and tachycardia. Clinical probability is assessed with the Wells or revised Geneva scores. In low or intermediate probability, a normal D-dimer (age-adjusted after 50 years) excludes PE; otherwise CT pulmonary angiography is the main test. Bedside echocardiography showing right ventricular dysfunction supports the diagnosis in an unstable patient who cannot be moved.

Risk Stratification (ESC 2019)

• Anticoagulation: low molecular weight heparin or a DOAC in most patients; unfractionated heparin when thrombolysis or intervention may be needed or in severe renal impairment.
• Supportive care in shock: avoid large fluid boluses, which can worsen right ventricular dilation; use noradrenaline; avoid intubation where possible because induction and positive pressure can precipitate cardiovascular collapse. ECMO may be considered in refractory cases.

Acute Severe Asthma

Severity Assessment (Adults)

Treatment

• Oxygen to $S_p\text{O}_2$ of 94-98%.
• Nebulised salbutamol 5 mg (back-to-back or continuous if severe) and ipratropium 0.5 mg every 4-6 hours.
• Corticosteroids: prednisolone 40-50 mg orally or hydrocortisone 100 mg intravenously.
• Magnesium sulphate 1.2-2 g intravenously over 20 minutes for severe or life-threatening asthma.
• Intravenous aminophylline or salbutamol only on senior advice.
• Intubation and ventilation for exhaustion, deteriorating consciousness or respiratory arrest. Use ketamine or propofol for induction; ventilate with a low rate, small tidal volume and long expiratory time, accepting permissive hypercapnia, to avoid dynamic hyperinflation. If hypotension occurs after intubation, disconnect the ventilator briefly to allow gas trapping to empty and exclude tension pneumothorax.

Acute Exacerbation of COPD

• Controlled oxygen: target $S_p\text{O}_2$ 88-92% in patients at risk of hypercapnic respiratory failure (Venturi masks).
• Nebulised bronchodilators, oral prednisolone 30-40 mg for 5 days, and antibiotics when sputum is purulent or there are signs of pneumonia.
• Non-invasive ventilation for persistent hypercapnic acidosis despite optimal treatment (see below).

Non-Invasive Respiratory Support

Non-Invasive Ventilation (NIV)

Bilevel positive airway pressure (inspiratory positive airway pressure, IPAP, and expiratory positive airway pressure, EPAP) via a face or nasal mask.

Strongest indications:

• Acute hypercapnic respiratory failure in COPD with pH 7.25-7.35 and $P_a\text{CO}_2$ above 6.5 kPa despite medical therapy (reduces intubation and mortality); patients with pH below 7.25 can be trialled in a critical care setting with a low threshold for intubation.
• Cardiogenic pulmonary oedema (CPAP or NIV improves oxygenation and work of breathing).
• Obesity hypoventilation and neuromuscular or chest wall disease.
• Immunocompromised patients with hypoxaemic failure (selected).

Typical settings: start IPAP about 15 cmH2O and EPAP about 4-5 cmH2O, increasing IPAP towards 20-25 cmH2O as tolerated; reassess blood gases at 1-2 hours.

Contraindications: respiratory arrest, inability to protect the airway, severe agitation or reduced consciousness (except hypercapnic encephalopathy in COPD), facial trauma, recent upper gastrointestinal surgery, vomiting, untreated pneumothorax and haemodynamic instability. Failure to improve within 1-4 hours should prompt escalation to intubation if appropriate.

Continuous Positive Airway Pressure (CPAP)

Provides a constant pressure, recruits alveoli, increases FRC and reduces left ventricular afterload; used for cardiogenic pulmonary oedema, obstructive sleep apnoea and hypoxaemic respiratory failure.

High-Flow Nasal Oxygen (HFNO)

• Heated, humidified gas at up to about 60 L/min with a controlled $F_I\text{O}_2$ (21-100%).
• Effects: matches or exceeds patient inspiratory flow so the delivered $F_I\text{O}_2$ is reliable, washes out nasopharyngeal dead space, produces a small flow-dependent PEEP (about 1 cmH2O per 10 L/min with the mouth closed), and improves comfort and secretion clearance.
• Used for hypoxaemic respiratory failure (the FLORALI trial suggested benefit in severe hypoxaemia), post-extubation support and preoxygenation and apnoeic oxygenation.
• The ROX index ($S_p\text{O}_2/F_I\text{O}_2$ divided by respiratory rate) helps predict HFNO failure; a value below about 3.85 at 12 hours suggests a high risk of intubation.

Acute Heart Failure and Cardiogenic Shock

Assessment

Classify the patient by congestion ("wet" or "dry") and perfusion ("warm" or "cold"). Investigate with ECG, troponin, natriuretic peptides, echocardiography, chest radiograph and lactate, and look for precipitants (CHAMPIT: acute Coronary syndrome, Hypertensive emergency, Arrhythmia, Mechanical cause, Pulmonary embolism, Infection, Tamponade).

Treatment of Acute Pulmonary Oedema

• Sit the patient up, give oxygen to $S_p\text{O}_2$ above 90%, and use CPAP or NIV for respiratory distress.
• Intravenous loop diuretics for congestion.
• Vasodilators (nitrates) when systolic blood pressure is adequate (above about 110 mmHg), especially in hypertensive pulmonary oedema.
• Routine opioids are not recommended.

Cardiogenic Shock

Definition: systolic blood pressure below 90 mmHg (or vasopressors needed) with signs of hypoperfusion (cold peripheries, oliguria, confusion, raised lactate) despite adequate filling.

• Acute myocardial infarction is the commonest cause: emergency revascularisation of the culprit lesion improves survival.
• Noradrenaline is the preferred vasopressor; dobutamine or levosimendan as inotropes; milrinone is an inodilator.
• Mechanical circulatory support (intra-aortic balloon pump, microaxial flow pumps, venoarterial ECMO) in selected patients; routine intra-aortic balloon pumping did not improve survival in IABP-SHOCK II, and venoarterial ECMO did not reduce mortality in ECLS-SHOCK.
• Treat mechanical complications (acute mitral regurgitation, ventricular septal rupture, tamponade) surgically.

Right Ventricular Failure

Common in PE, pulmonary hypertension and inferior myocardial infarction. Principles: optimise preload (avoid overload), maintain systemic pressure to perfuse the right coronary artery (noradrenaline, vasopressin), reduce pulmonary vascular resistance (avoid hypoxaemia, hypercapnia and acidosis; consider inhaled nitric oxide), and support contractility (dobutamine, milrinone, levosimendan).