Hypotension After Intubation: Why the Airway Can Collapse the Circulation
Emergency intubation is not just an airway procedure. It is a major hemodynamic event.
Read previewResuscitation Review Blog
Emergency and critical care posts for repeated learning.
Public previews from the WhiteBoard Medicine medical education series. Continue each post through the Core Medical Education collection on Patreon.
Read More on PatreonPermissive Hypercapnia: When a High PaCO2 Protects the Lung
Hypercapnia usually makes clinicians uncomfortable.
Read previewVasopressin in Septic Shock: Restoring Vascular Tone Without More Catecholamine
Septic shock is often dominated by vasoplegia.
Read previewNorepinephrine vs Epinephrine: Different Pressors, Different Physiology
Not all vasopressors solve the same problem.
Read previewThe Lethal Triad in Trauma: Hypothermia, Acidosis, and Coagulopathy
Trauma resuscitation is not only about replacing lost blood.
Read previewLactate Clearance: Useful Signal, Dangerous Target When Misunderstood
Lactate is one of the most useful and most misunderstood markers in critical care.
Read previewPEEP and Hemodynamics: When Better Oxygenation Reduces Cardiac Output
PEEP can improve oxygenation.
Read previewDriving Pressure in ARDS: Why Plateau Minus PEEP Matters
ARDS makes the functional lung smaller.
Read previewHyperkalemia: Why the ECG Can Be Reassuring Until It Suddenly Is Not
Hyperkalemia is dangerous because it changes cardiac electrophysiology.
Read previewDKA Physiology: Why the Patient Is Breathing So Fast
The rapid breathing in DKA is not anxiety.
Read previewCardiac Tamponade: Why a Small Effusion Can Cause Big Shock
Cardiac tamponade is a pressure problem.
Read previewStress Ulcer Prophylaxis in the ICU: What REVISE Adds to the Pantoprazole Debate
Stress ulcer prophylaxis has always involved a tradeoff.
Read previewOxygen Targets in Mechanically Ventilated Patients: How Much Oxygen Is Too Much?
Oxygen is lifesaving.
Read previewEarly Neuromuscular Blockade in ARDS: What ACURASYS and ROSE Teach Us
Paralysis in ARDS is not primarily about making the ventilator screen look cleaner.
Read previewLow Tidal Volume Ventilation: Why the ARDSNet Trial Changed Critical Care
ARDS is not just a problem of oxygenation.
Read previewDynamic Hyperinflation and Auto-PEEP: The Hidden Cause of Hypotension After Intubation
Not all hypotension after intubation comes from sedation.
Read previewAcute Kidney Injury in Shock: Why Creatinine Lags Behind the Physiology
This is one of the most important concepts in critical care nephrology. A patient can have significant kidney injury before the creatinine looks impressive.
Read previewRight Ventricular Failure in the ICU: Why Fluids Can Make Shock Worse
The right ventricle is not just a smaller left ventricle. It is a thin-walled chamber designed to move blood through a low-pressure, low-resistance pulmonary circulation.
Read previewTargeted Temperature Management After Cardiac Arrest: Brain Injury, Fever, and the Evolution of Evidence
After cardiac arrest, the brain may remain injured by a complex cascade of ischemia-reperfusion physiology.
Read previewStress-Dose Steroids in Septic Shock: Vascular Responsiveness, Shock Reversal, and Where the Evidence Lands
Patients develop vasodilation, endothelial dysfunction, capillary leak, inflammatory dysregulation, impaired catecholamine responsiveness, and sometimes relative corticosteroid insufficiency. This is why corticosteroids remain part of the septic shock conversation.
Read previewCVP Is Not Preload: What Central Venous Pressure Can and Cannot Tell You
Central venous pressure is one of the most misunderstood numbers in critical care. It is often treated as a preload measurement.
Read previewDead Space Ventilation: Why PaCO2 Rises Despite a "Normal" Minute Ventilation
Carbon dioxide clearance is not determined by minute ventilation alone. It is determined by alveolar ventilation.
Read previewVV-ECMO in Severe ARDS: Oxygen Delivery, Lung Rest, and the EOLIA Trial
In severe ARDS, the functional lung is small, inflamed, heavy, and heterogeneously aerated.
Read previewMetabolic Acidosis in Critical Illness: When the pH Is a Marker and When It Becomes the Problem
Metabolic acidosis is common in critical illness. It can be caused by shock, renal failure, ketoacidosis, toxins, diarrhea, lactic acidosis, or impaired tissue oxygen utilization.
Read previewNoninvasive Preoxygenation Before Intubation: Why PREOXI Matters
Critically ill patients often have limited oxygen reserve, high shunt fraction, increased oxygen consumption, hemodynamic instability, and very little tolerance for apnea.
Read previewVideo Laryngoscopy in Critical Illness: First-Pass Success and the DEVICE Trial
Every additional intubation attempt increases the risk of hypoxemia, aspiration, airway trauma, esophageal intubation, hypotension, and cardiac arrest.
Read previewSodium Channel Blocker Toxicity: Why the ECG Becomes the Resuscitation Tool
In many toxicologic emergencies, the ECG is not just diagnostic. It is a resuscitation monitor.
Read previewMassive Pulmonary Embolism: Right Ventricular Afterload and Obstructive Shock
Pulmonary embolism becomes immediately life-threatening when the right ventricle fails.
Read previewRestrictive vs Liberal Fluids in Septic Shock: What Modern Trials Actually Teach Us
Septic shock resuscitation often begins with fluid. That makes physiologic sense. Sepsis causes vasodilation, capillary leak, relative hypovolemia, and impaired venous return. Fluids may increase stressed venous volume, improve preload, and augment cardiac output.
Read previewOxygen Delivery: Why Hemoglobin, Cardiac Output, and Saturation Matter More Than SpO2 Alone
A patient can have an SpO2 of 100% and still have inadequate oxygen delivery to tissues.
Read previewTranexamic Acid in Trauma: Timing, Fibrinolysis, and What the Modern Evidence Supports
Bleeding trauma patients do not die from blood loss alone. They die from a complex interaction of hemorrhage, shock, hypothermia, acidosis, coagulopathy, endothelial injury, and impaired clot stability.
Read previewVenous Congestion: The Physiology Behind VExUS
When discussing shock, critical illness, and organ dysfunction, we often focus heavily on arterial circulation. Mean arterial pressure, cardiac output, and systemic vascular resistance dominate many bedside conversations. Yet many patients in the ICU suffer not from inadequate arterial flow, but from excessive venous pressure.
Read previewThe Physiology of Septic Myocardial Dysfunction
Septic shock is often described as a distributive form of shock characterized by vasodilation and microcirculatory dysfunction. While these features are certainly important, they can distract from another common manifestation of severe sepsis: myocardial dysfunction.
Read previewANDROMEDA-SHOCK: Capillary Refill Versus Lactate-Guided Resuscitation
For decades, lactate has served as one of the primary markers used to guide resuscitation in septic shock. Elevated lactate levels are associated with worse outcomes and have become deeply embedded in sepsis protocols.
Read previewWhy Lactate Rises: Beyond Tissue Hypoperfusion
Few laboratory values receive as much attention in critical care as lactate. Elevated lactate levels often trigger aggressive resuscitation efforts, serial measurements, and heightened concern for impending circulatory collapse.
Read previewMechanical Ventilation and the Failing Right Ventricle
Most discussions regarding mechanical ventilation focus on oxygenation and carbon dioxide clearance. However, positive pressure ventilation exerts profound effects on cardiovascular physiology, particularly on the right ventricle.
Read previewSedation Strategy in Mechanically Ventilated Patients
Sedation is one of the most frequently administered therapies in the ICU, yet it is often approached as a matter of comfort alone. In reality, sedation influences nearly every aspect of critical care.
Read previewVasopressor Escalation in Septic Shock: When Norepinephrine Isn't Enough
Norepinephrine remains the first-line vasopressor for septic shock and is often highly effective at restoring arterial pressure. However, a subset of patients develop refractory vasodilatory shock despite escalating doses.
Read previewInterpreting ScvO2 and Central Venous Oxygen Saturation
Central venous oxygen saturation, or ScvO2, is one of the most misunderstood hemodynamic variables in critical care. Many clinicians recognize low values as concerning but are less comfortable interpreting normal or elevated measurements.
Read previewCLOVERS: Early Vasopressors Versus Liberal Fluids in Septic Shock
For years, septic shock management has emphasized aggressive fluid administration early in resuscitation. However, growing evidence suggested that excessive fluid accumulation may contribute to organ dysfunction, prolonged ventilation, and worse outcomes.
Read previewContinuous Renal Replacement Therapy: Diffusion, Convection, and Solute Clearance
Many clinicians become comfortable ordering CRRT long before they fully understand how it actually removes solutes. While modern CRRT machines automate much of the process, understanding the underlying physiology can improve prescription design and troubleshooting at the bedside.
Read previewFluid Removal During CRRT: The Physiology of De-resuscitation
One of the most challenging aspects of critical care is determining when fluid resuscitation should end and fluid removal should begin.
Read previewCLASSIC: Restrictive Versus Standard Fluid Therapy in Septic Shock
For decades, fluid administration has been considered a cornerstone of septic shock management. Yet increasing evidence suggested that excessive fluid accumulation may contribute to organ dysfunction, respiratory failure, and prolonged critical illness.
Read previewAPROCCHSS: Hydrocortisone and Fludrocortisone in Septic Shock
The role of corticosteroids in septic shock has been debated for decades. Some studies suggested benefit, others demonstrated little effect, and clinicians remained divided regarding when steroids should be used.
Read previewVA-ECMO Physiology: Native Cardiac Output, Afterload, and Differential Hypoxemia
VA-ECMO is often described as temporary cardiopulmonary support, but understanding how it interacts with the native circulation requires a much deeper appreciation of cardiovascular physiology.
Read previewLeft Ventricular Unloading During VA-ECMO
One of the most important physiologic concepts in mechanical circulatory support is that VA-ECMO can simultaneously save the heart and stress the heart.
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