The Critical Care Practitioner
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...
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HHS (Hyperosmolar Hyperglycaemic State) is the quiet counterpart to DKA. It develops slowly in older type 2 diabetics with residual insulin, leading to extreme hyperglycaemia and dehydration without ketosis. In this 2-hour deep dive, Jonathan explains why HHS kills through water loss and hyperviscosity rather than acid, and how to manage it safely. Key Learning Points: · Pathophysiology: Relative insulin deficiency → no ketones, but relentless osmotic diuresis → hyperosmolarity > 320 mOsm/kg. ...
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Diabetic ketoacidosis (DKA) is not just “high blood sugar” — it’s a hormonal storm caused by absolute insulin deficiency and a surge of counter-regulatory hormones. The result is a triad of hyperglycaemia, dehydration, and metabolic acidosis. We follow Sophie, a 23-year-old with type 1 diabetes who arrives with vomiting, Kussmaul breathing, glucose 28 mmol/L, ketones 5.6 mmol/L, and pH 7.08. 🔍 What’s Going Wrong? No insulin → cells can’t use glucose → liver produces more. Glucose spills into urine → osmotic diuresis → 6–8L fluid + electrolyte loss. Fat breakdown...
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Summary: In this episode, we spotlight a stealthy ICU disruptor — hypophosphataemia. Based on a 2024 narrative review in the Journal of Clinical Medicine, we explore why phosphate matters, how it goes missing in critically ill patients, and why you should care even when it’s just “a little low.” What’s Covered: The vital role of phosphate in energy, oxygen delivery, and muscle function Why hypophosphataemia affects 20–80% of ICU patients Clinical consequences, from muscle weakness to respiratory failure, arrhythmias, and delirium Common causes: refeeding, DKA, diuretics,...
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What is DKA? – The triad of hyperglycaemia, ketonaemia, and metabolic acidosis (JBDS 2023 definitions). Pathophysiology explained – Insulin deficiency, ketone production, and why potassium is so tricky. Clinical features – Polyuria, dehydration, Kussmaul breathing, acetone breath, and red flags for deterioration. Investigations – Capillary ketones, blood gases, electrolytes, ECG, and screening for precipitants. Management (UK guidelines) – Fluids first, fixed-rate insulin infusion, careful potassium replacement, and always treat the trigger. Pitfalls – Starting insulin...
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Mobilisation in the ICU raises two big questions: is it safe, and will staff embrace it? In this discussion, Jonathan explores both sides of the story: Safety first: Large prevalence studies show mobilisation is happening, though often inconsistently. A systematic review of 1,800+ sessions found serious adverse events in only 0.6% — most minor and short-lived. Even patients on CRRT can safely mobilise with planning, adequate staff, and the right equipment. Consensus guidelines outline clear safety screens, covering oxygen, ventilator settings, vasopressors, and line security. ...
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Summary For much of critical care history, immobility was the norm: patients were sedated, kept still, and “protected.” But decades of research have revealed the hidden costs — profound muscle wasting, delirium, and long-term disability. Jonathan explores how our understanding of mobilisation in ICU has evolved — from the recognition of harm caused by bedrest, to the first landmark studies proving that early movement is both feasible and beneficial. From Bedrest to Better: Why Mobilise in ICU? ICU-acquired weakness: Patients can lose 15–20% of muscle mass within the first week of...
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Sedation practices in the ICU have evolved dramatically over the past decade — but are we truly following the evidence? In this episode of The Critical Care Practitioner Podcast, Jonathan takes you through the key milestones in sedation guidance, the persistent gap between recommendations and real-world practice, and the emerging shift toward human-centered, wakeful care. What You’ll Learn in This Episode: PAD Guidelines (2013) & beyond: How Barr et al. and later ATS/CHEST summaries shaped modern sedation practice. Where we fall short: Why deep sedation is still common and...
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Overview In this episode we explore the three main sedatives used in critical care and how to choose the right agent for the right patient. Highlights Benzodiazepines: once the workhorse of ICU sedation, but now linked to more delirium and longer ventilation. Still useful in alcohol withdrawal and seizures. Propofol: rapid on/off, easy to titrate, helpful for daily sedation holds and neuro assessments. Watch for hypotension, lipid issues, and the rare risk of infusion syndrome. Dexmedetomidine: provides light, cooperative sedation with minimal respiratory depression and less delirium,...
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We’ve explored the history of sedation in ICU, the impact of daily awakening trials, and the risks of deep sedation. In this episode, we focus on how to embed that evidence into practice — through the use of structured sedation protocols. Protocols don’t just provide guidance; they transform everyday ICU culture, reduce variation in care, and improve outcomes. But implementing them isn’t always easy. This episode explores the why, what, and how of sedation protocols — and the cultural shift they demand. What You’ll Learn in This Episode 🏥 Why protocols were needed: how...
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For much of critical care history, immobility was the norm: patients were sedated, kept still, and “protected.” But decades of research have revealed the hidden costs — profound muscle wasting, delirium, and long-term disability.
Jonathan explores how our understanding of mobilisation in ICU has evolved — from the recognition of harm caused by bedrest, to the first landmark studies proving that early movement is both feasible and beneficial.
From Bedrest to Better: Why Mobilise in ICU?
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ICU-acquired weakness: Patients can lose 15–20% of muscle mass within the first week of critical illness.
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Long-term outcomes: ARDS survivors tracked for five years showed persistent disability and reduced independence.
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Sedation & delirium: Deep sedation increases delirium risk; mobilisation reduces both incidence and duration.
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Physiological rationale: Even minimal movement supports cardiovascular tone, respiratory function, circulation, and cognition.
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Core message: Bedrest is not neutral — it is actively harmful. Mobilisation offers protection for both brain and body.
Proof in Practice: The First Mobilisation Trials
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Feasibility (Morris et al., 2008): Protocol-led mobilisation cut time to first mobilisation (5 vs 11 days), with no increase in adverse events.
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Landmark RCT (Schweickert et al., 2009):
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Early PT/OT + daily sedation interruption vs SAT alone.
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59% vs 35% regained independence at discharge.
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Patients had less delirium and spent fewer days ventilated.
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Implementation (Needham et al.): Demonstrated how embedding mobilisation into daily ICU practice improves outcomes and serves as a model for quality improvement.
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Core message: Early mobilisation is not only possible — it improves patient-centred outcomes safely.
Key Takeaways
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Bedrest and heavy sedation accelerate weakness, delirium, and disability.
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Mobilisation is both biologically plausible and clinically effective.
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Early trials proved feasibility, safety, and functional benefits.
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Success requires:
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Lighter sedation targets and daily SATs.
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Interdisciplinary teamwork (nursing, PT/OT, medical).
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Structured protocols and safety screens.
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Overall message: Mobilisation should no longer be an afterthought in ICU. It is a therapeutic intervention — one that supports recovery, preserves dignity, and helps patients walk out of intensive care with more than just survival.