We return to our 48-year-old patient: jaundiced, hypotensive, drowsy, and bleeding. In decompensated cirrhosis, every treatment targets a disrupted system — splanchnic vasodilation, portal hypertension, toxin accumulation, and renal hypoperfusion.

Although these patients look fluid overloaded, they are effectively hypovolaemic. Start with small aliquots of balanced crystalloid, avoiding 0.9% saline. In hepatorenal syndrome or tense ascites, 20% albumin is key — not just for volume expansion, but for circulatory and anti-inflammatory support.

Once volume is optimised, flow must be redirected. Terlipressin reverses splanchnic vasodilation, reduces portal pressure, and improves renal perfusion. If contraindicated, noradrenaline targeting a MAP ≥65 mmHg is an effective alternative.

Variceal bleeding reflects portal hypertension, not missing clotting factors. Use restrictive transfusion, correct platelets and fibrinogen selectively, start antibiotics early, and proceed to endoscopic banding once haemodynamically stable. Avoid blanket correction of INR — treat bleeding, not numbers.

Hepatic encephalopathy management focuses on reversing precipitants and reducing ammonia with lactulose and rifaximin, while protecting the airway in advanced grades. Infection screening is essential — SBP and sepsis worsen vasodilation and renal failure, with albumin improving outcomes.

Renal dysfunction is functional, not structural. Albumin plus vasoconstrictors can restore perfusion. Nutrition is critical: early enteral feeding with adequate protein supports recovery and ammonia clearance.

Bottom line: cirrhosis care works when physiology drives every decision.

In this episode, I walk through the real-world critical care management of acute decompensated alcohol-related liver disease, using a high-risk ICU case to anchor the discussion. The focus is on understanding the underlying physiology—portal hypertension, rebalanced haemostasis, hepatic encephalopathy, infection, and hepatorenal syndrome—and translating that physiology into clear first-hour priorities at the bedside.

Listeners are guided through airway and circulatory decision-making, rational use of albumin, vasopressors, antibiotics, lactulose and rifaximin, and careful blood product transfusion, while avoiding common pitfalls such as reflexive FFP or over-resuscitation.

The episode emphasises early recognition of red flags, the central role of infection as a precipitant, and the interconnected nature of multi-organ failure in acute-on-chronic liver disease, all framed within pragmatic UK ICU practice.

This episode offers a structured, bedside-focused exploration of Non-Invasive Ventilation (NIV) for acute hypercapnic respiratory failure in COPD, aligned with NICE NG115 and BTS/ICS 2016 guidance. Aimed at early-career critical care nurses, it breaks the topic down into physiology, practical setup, monitoring, and escalation.

Key Topics Covered

• Mechanisms behind acute-on-chronic hypercapnic respiratory failure in COPD.

• How NIV improves ventilation, reduces CO₂, and decreases work of breathing.

• Evidence-based indications for NIV initiation.

• Practical bedside steps for the first hour of therapy.

• How to titrate settings, troubleshoot problems, and recognise failure.

• Common complications and when to escalate to invasive ventilation.

Case-Based Learning
The episode follows Mr. Harris, a 68-year-old man with severe COPD presenting with type 2 respiratory failure. His clinical deterioration, ABG results (pH 7.25, pCO₂ 9.8 kPa), and work of breathing set the scene for understanding when and why NIV is beneficial.

Physiology Essentials
Listeners are guided through the impact of airway obstruction, air trapping, hyperinflation, respiratory muscle fatigue, and CO₂ narcosis. NIV's core actions—improving tidal volume with IPAP and splinting airways with EPAP—are linked directly to these mechanisms.

Practical Bedside Framework

• Start with IPAP 12 cmH₂O / EPAP 4 cmH₂O and FiO₂ around 28%, aiming for SpO₂ 88–92%.

• Reassure the patient, optimise positioning, secure a comfortable mask seal, and monitor synchrony.

• Repeat ABG at 1 hour; look for rising pH and falling CO₂.

• Adjust pressures in small increments if needed while monitoring for leaks, agitation, hypotension, or gastric distension.

Monitoring and Escalation
Success indicators include reduced respiratory rate, improved alertness, and trending normalisation of pH. Red flags include worsening acidosis, declining consciousness, mask intolerance, or inability to maintain the airway—prompting urgent senior review.

Common Complications
Facial pressure sores, gastric distension, aspiration risk, anxiety, and haemodynamic compromise are highlighted with practical prevention strategies.

Five Golden Rules

1. Recognise early and initiate NIV promptly.

2. Start simple with standard pressures and controlled oxygen.

3. Reassess rapidly with a 1-hour ABG.

4. Escalate quickly if failure criteria develop.

5. Protect the patient with meticulous care and communication.

Outcome
After an hour of NIV, Mr. Harris' pH rises to 7.32 and pCO₂ falls to 8.2 kPa, with clear clinical improvement—illustrating the value of timely, well-managed NIV in COPD.

Closing
The episode reinforces the importance of physiological understanding in delivering confident, effective NIV care at the bedside.