Acute Mesenteric Ischemia
Acute mesenteric ischemia occurs when intestinal blood flow becomes inadequate. Delayed recognition can allow reversible ischemia to progress to bowel necrosis, sepsis, and multiorgan failure.
Read previewResuscitation Review Blog
Emergency and critical care posts for repeated learning.
Public previews from the WBM Emergency & Critical Care medical education series. Continue each post through the Core Medical Education collection on Patreon.
Read More on PatreonPatient–Ventilator Dyssynchrony
Patient–ventilator dyssynchrony occurs when mechanical assistance does not match the patient's respiratory effort. The mismatch may involve starting a breath, delivering enough flow, or ending inspiration at the appropriate time.
Read previewDisseminated Intravascular Coagulation
Disseminated intravascular coagulation, or DIC, is systemic activation and disruption of coagulation caused by an underlying illness. It can produce both microvascular thrombosis and bleeding.
Read previewSalicylate Toxicity
Salicylate toxicity can produce tachypnea, nausea, tinnitus, confusion, and progressive organ dysfunction. Exposure may involve aspirin, bismuth subsalicylate, or other salicylate-containing products.
Read previewRefeeding Syndrome in Critically Ill Patients
Refeeding syndrome can develop when nutrition is restarted after significant undernutrition. The resulting electrolyte and metabolic shifts can impair cardiac, respiratory, and neurologic function.
Read previewSedation and Delirium in Mechanically Ventilated Patients
Sedation should have a defined purpose and target. Increasing an infusion may suppress visible agitation without correcting pain, dyspnea, withdrawal, or another underlying problem.
Read previewAbdominal Compartment Syndrome
Rising abdominal pressure can cause kidney, respiratory, and circulatory dysfunction at the same time. Consider it when oliguria, increasing ventilator pressures, and worsening hemodynamics develop alongside abdominal distention.
Read previewMyasthenic Crisis and Neuromuscular Respiratory Failure
Myasthenia gravis impairs neuromuscular transmission. Respiratory muscle weakness can reduce ventilation, while bulbar weakness compromises swallowing, cough, and airway protection.
Read previewTransfusion Reactions in the Critically Ill Patient
New fever, hypotension, or hypoxemia during transfusion requires assessment for a transfusion reaction. Preexisting sepsis or heart failure does not explain away a change that occurs while blood is being administered.
Read previewAcute Cholangitis and Biliary Sepsis
Acute cholangitis commonly develops when infection occurs in an obstructed biliary system. Stones, malignancy, strictures, and occluded stents are common causes.
Read previewMetabolic Alkalosis During Mechanical Ventilation
Metabolic alkalosis commonly develops during ICU treatment, particularly with diuresis or gastric losses. Management starts with identifying why bicarbonate is elevated and what is preventing the kidneys from excreting it.
Read previewBrain Death and Death by Neurologic Criteria
An unresponsive patient with devastating brain injury has not automatically met criteria for brain death. Poor prognosis and death by neurologic criteria are separate determinations.
Read previewSevere Asthma and Dynamic Hyperinflation
Severe asthma becomes dangerous when airflow obstruction turns ventilation into a mechanical trap. The immediate concern is often oxygen saturation, but the physiology that kills many intubated asthma patients is dynamic hyperinflation.
Read previewPulmonary Hypertension and Right Ventricular Failure in Critical Illness
Pulmonary hypertension turns the right ventricle into a high-risk chamber. The right ventricle is designed to eject blood into a low-pressure pulmonary circulation. When pulmonary vascular resistance rises, the RV may dilate, lose contractile efficiency, and fail.
Read previewA Physiologic Approach to Undifferentiated Shock
Shock is not a blood pressure diagnosis. Shock is inadequate tissue perfusion. The blood pressure may be low, normal, or temporarily supported by compensatory physiology. The key bedside task is identifying what is limiting oxygen delivery.
Read previewSympathomimetic Toxicity in Emergency Critical Care
Sympathomimetic toxicity is catecholamine excess. Patients may present with agitation, hypertension, tachycardia, diaphoresis, hyperthermia, mydriasis, seizures, myocardial ischemia, rhabdomyolysis, or acidosis. Common causes include cocaine, amphetamines, synthetic stimulants, and medication interactions.
Read previewRhabdomyolysis and Acute Kidney Injury
Rhabdomyolysis is muscle breakdown with systemic consequences. The kidney is one of the major organs at risk. When skeletal muscle cells are injured, they release intracellular contents including creatine kinase, potassium, phosphate, uric acid, and myoglobin.
Read previewProne Positioning in ARDS
Prone positioning is not just a way to improve the oxygen saturation. In severe ARDS, proning changes the distribution of ventilation, perfusion, lung stress, and regional overdistension.
Read previewSudden Hypoxemia During Mechanical Ventilation
Sudden hypoxemia on the ventilator should trigger a structured bedside response. The differential is broad, but the first priority is identifying immediately reversible threats.
Read previewDKA, Osmolality, and Cerebral Edema
DKA treatment is more than closing the anion gap. It is controlled correction of a severe metabolic and osmotic disturbance.
Read previewMassive Gastrointestinal Bleeding Resuscitation
Massive GI bleeding is a resuscitation problem before it is an endoscopy problem. Endoscopy can be definitive, but the patient must survive long enough to get there.
Read previewStatus Epilepticus in Critical Care
Status epilepticus is a neurologic emergency and a systemic physiologic emergency. The longer seizures continue, the harder they become to stop and the more secondary injury accumulates.
Read previewBlood Pressure Management After Cardiac Arrest
Return of spontaneous circulation is not the end of resuscitation. After cardiac arrest, the brain and heart remain vulnerable to secondary injury. Blood pressure management is one piece of that post-arrest physiology.
Read previewAtrial Fibrillation with RVR in Critical Illness
Atrial fibrillation with rapid ventricular response is common in critical illness. It is often a sign of physiologic stress rather than an isolated rhythm problem.
Read previewARDS and Cardiogenic Pulmonary Edema
Bilateral infiltrates and hypoxemia do not automatically mean ARDS.
Read previewAcute Liver Failure in the ICU
Acute liver failure is a multisystem critical illness. It is defined by acute liver injury, coagulopathy, and encephalopathy in a patient without preexisting cirrhosis. The liver fails, but the brain, kidneys, circulation, lungs, and immune system are all affected.
Read previewBalanced Crystalloids and Normal Saline in Critical Illness
Intravenous fluids are drugs.
Read previewSeptic Cardiomyopathy: When Distributive Shock Also Becomes Pump Failure
Septic shock is often taught as distributive shock.
Read previewAnaphylactic Shock: Why Epinephrine Treats More Than Blood Pressure
Anaphylaxis is not just an allergic reaction.
Read previewWide Complex Tachycardia in Shock: Treat the Patient, Not the Rhythm Strip
Wide complex tachycardia can create diagnostic anxiety.
Read previewARISE FLUIDS: Early Vasopressors vs More Fluid in Septic Shock
Septic shock resuscitation continues to evolve.
Read previewThe Crashing COPD Patient: Why Oxygen, CO2, and Work of Breathing All Matter
The crashing COPD patient is not simply a patient with a high carbon dioxide level.
Read previewHyponatremic Seizures: Why Chronicity Matters More Than the Sodium Number
Hyponatremia is dangerous because the brain lives inside a fixed skull.
Read previewKetamine vs Etomidate for RSI: What the Newer Evidence Actually Shows
Induction drug choice during emergency intubation has always carried strong opinions.
Read previewCardiogenic Shock: Why Blood Pressure Can Look Better While Perfusion Gets Worse
Cardiogenic shock is not defined by blood pressure alone.
Read previewThe Case of the Rising Plateau Pressure: Compliance, Resistance, or Auto-PEEP?
A rising ventilator pressure is not a diagnosis.
Read previewPREOXI and the Physiology of Preoxygenation: Oxygen Alone vs Oxygen Plus Pressure
Preoxygenation is not just placing oxygen near the patient's face.
Read previewBeta-Blocker and Calcium Channel Blocker Overdose: Why Shock Becomes Metabolic
Beta-blocker and calcium channel blocker overdoses can both cause profound cardiovascular collapse.
Read previewSevere Pancreatitis in the ICU: Capillary Leak, Third Spacing, and Organ Failure
Severe pancreatitis is not just abdominal pain with an elevated lipase.
Read previewWhen the Ventilator Causes Shock: A Bedside Framework for Post-Intubation Collapse
When a patient crashes after intubation, the airway is often blamed.
Read previewHigh-Flow Nasal Cannula: Why Flow Matters, Not Just FiO2
High-flow nasal cannula is not simply a comfortable oxygen device.
Read previewStress Ulcer Prophylaxis After REVISE: Who Actually Needs a PPI in the ICU?
Stress ulcer prophylaxis has always involved a tradeoff.
Read previewHypotension After Intubation: Why the Airway Can Collapse the Circulation
Emergency intubation is not just an airway procedure. It is a major hemodynamic event.
Read previewPermissive 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.
Read preview