Approach to non traumatic shock
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Infographic
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Slide deck
Tight, illustrated review.
MCQs
20 questions available
Easy · 5
Medium · 11
Hard · 4
Case simulations
Learn this topic by working through ED cases step-by-step.
medium
~15 min
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72M with Crushing Chest Pain and Hypotension
A 72-year-old male presents with severe crushing substernal chest pain, diaphoresis, and profound hypotension indicative of cardiogenic shock.
medium
~15 min
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48M with Hematemesis and Shock
A 48-year-old male with a history of alcohol abuse presents with severe hematemesis and tachycardia, requiring massive hemorrhage protocol initiation.
hard
~15 min
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84F with Tearing Epigastric Pain
An 84-year-old female presents with acute tearing epigastric pain radiating to the back, severe hypertension, and vomiting.
medium
~15 min
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50M with Hypotension, Bradycardia, and Weakness
A 50-year-old male presents with profound weakness, diminished reflexes, and the classic triad of neurogenic shock.
Mind map
Summary
1. THE 2-MINUTE PHYSIOLOGY (Rapid Pathophysiology)
- The Core Breakdown: Shock is a life-threatening state defined by the persistent, inadequate delivery of oxygen and nutrients necessary to meet cellular metabolic demands. This systemic supply/demand mismatch forces cells into anaerobic metabolism, leading to the accumulation of toxic byproducts (like lactate) and rapidly progressing to multiple organ dysfunction syndrome (MODS) and death if uncorrected.
- The Four Hemodynamic Pillars: The mechanical or cellular breakdown driving this hypoperfusion is classically categorized into four distinct mechanisms:
- Hypovolemic: An absolute loss of intravascular volume (loss of "tank" fluid) due to dehydration or hemorrhage, leading to severely decreased preload and subsequent drop in cardiac output.
- Cardiogenic: A primary "pump" failure (e.g., massive myocardial infarction, lethal dysrhythmias) where the heart cannot generate adequate stroke volume despite adequate or elevated preload.
- Distributive: A pathological loss of systemic vascular resistance (leaky or dilated "pipes") driven by cytokine cascades (sepsis), histamine release (anaphylaxis), or loss of sympathetic tone (neurogenic), leading to relative hypovolemia.
- Obstructive: A physical, mechanical barrier to cardiac output or venous return (e.g., massive pulmonary embolism, tension pneumothorax, or cardiac tamponade).
2. THE BEDSIDE ACTION PLAN (Rapid ER Management)
- Immediate Stabilization: Approach all patients systematically (Airway, Breathing, Circulation). Establish large-bore IV access, place the patient on continuous cardiac monitoring, and obtain a 12-lead ECG. Stabilization and diagnostic investigation must occur simultaneously.
- Fluid Resuscitation: Optimal early treatment centers on aggressive resuscitation with intravenous crystalloid fluids to increase perfusion to vital organs. Caveat: If hemorrhagic shock is suspected, transition volume expansion from crystalloids to blood products as soon as blood is available.
- First-Line Vasoactive Agents & Titrations:
- Target Goal: Titrate vasoactive agents every 2-5 minutes to a strict mean arterial pressure (MAP) goal of (\ge) 60 mm Hg.
- Norepinephrine: The standard first-line vasopressor for undifferentiated and distributive/septic shock.
- Epinephrine: Administer 0.01–0.5 mcg/kg/minute as a continuous IV infusion as a potent alternative to norepinephrine. For anaphylactic shock, administer 0.3–0.5 mg intramuscularly early.
- Vasopressin: Administer 0.03–0.04 units/minute continuous IV infusion to augment norepinephrine in refractory septic shock.
- Dobutamine: Add at 2–20 mcg/kg/minute continuous infusion if low cardiac output (cardiogenic shock) is suspected via bedside echocardiography.
3. THE DIAGNOSTIC GRID (Differential Diagnosis & Workup)
- Top "Can't-Miss" Etiologies (By Category):
- Cardiogenic Mimics: Acute coronary syndrome (ACS), congestive heart failure, or lethal dysrhythmias.
- Hypovolemic Mimics: Occult gastrointestinal hemorrhage (melena, hematemesis), ruptured abdominal aortic aneurysm (AAA), or profound dehydration.
- Distributive Mimics: Septic shock (occult infection), Anaphylaxis (diffuse hives, airway compromise), Neurogenic shock (spinal cord injury).
- Obstructive Mimics: Massive Pulmonary Embolism (PE) or Cardiac Tamponade.
- Prioritized Diagnostic Workup:
- Tier 1 (Bedside): Point-of-Care Ultrasound (POCUS) to expedite the categorization of shock and guide resuscitation. 12-lead ECG to rule out arrhythmias or ACS.
- Tier 2 (The Shock Panel): Draw a complete blood count (CBC), comprehensive metabolic panel, bedside glucose, coagulation profile, and urinalysis.
- Tier 3 (Biomarkers & Typing): Serum lactate (marker of tissue perfusion), Troponin, Arterial/Venous blood gas, and an immediate Type and Screen.
4. THE VISUAL BOARD (ECG / POCUS / Imaging)
- The RUSH Exam (Rapid Ultrasound in SHock): This is the definitive visual checklist for undifferentiated hypotension, evaluating the "Pump" (Heart), "Tank" (Intravascular volume/fluid), and "Pipes" (Aorta/Deep veins).
- Hypovolemic Shock: Hyperdynamic, hypercontractile heart (Pump), with a flat, collapsed inferior vena cava (IVC) and absence of B-lines (Tank).
- Cardiogenic Shock: Hypodynamic, poorly contracting left ventricle or dilated heart (Pump), with a plump, distended IVC and diffuse B-lines in the lungs indicating pulmonary edema (Tank).
- Distributive Shock: Hyperdynamic heart (Pump) with a collapsed IVC (Tank).
- Obstructive Shock: Hyperdynamic heart with right ventricular strain/thrombus or pericardial effusion (Pump), and a distended IVC (Tank).
5. THE SCORING MATRIX (Risk Stratification & Guidelines)
- Sustained Hypotension Criteria: Clinical instability in shock is formally defined as sustained hypotension with a systolic blood pressure (SBP) < 90 mm Hg, or a drop of > 40 mm Hg from baseline lasting for > 15 minutes, or the explicit requirement for vasopressors to maintain perfusion.
- Transfusion Thresholds: In patients with concurrent acute coronary syndrome (ACS) or stable cardiovascular disease who are bleeding, transfuse packed red blood cells (PRBCs) to maintain a hemoglobin (\ge) 7 g/dL to 8 g/dL.
6. THE DANGER ZONE (Pitfalls & Critical Actions)
- Pitfall - The Intubation Hemodynamic Crash: Reflexively performing rapid sequence intubation (RSI) on a patient with obstructive shock (e.g., massive pulmonary embolism) before optimizing hemodynamics. Critical Action: Avoid intubation and positive pressure ventilation if possible in obstructive shock, as the increased intrathoracic pressure will severely decrease venous return and cardiac output, precipitating cardiac arrest.
- Pitfall - Delayed Source Control: Pushing endless fluids in septic or hemorrhagic shock without addressing the root cause. Critical Action: Early detection and intervention are critical; administer broad-spectrum antibiotics and secure source control immediately for sepsis, and transition rapidly to hemorrhage control and blood products for bleeding.
- Pitfall - Ignoring Anaphylaxis Triggers: Treating the hypotension of anaphylaxis with fluids alone. Critical Action: Administer early IM epinephrine; if the patient is refractory and on a beta-blocker, you must consider administering glucagon.
7. MCQ MASTERCLASS (Written Exam Tips)
- Buzzwords: A patient presents in shock with a "hyperdynamic left ventricle, distended IVC, and absent lung sliding on ultrasound." Diagnosis: Obstructive shock secondary to a tension pneumothorax.
- High-Yield Fact: The definitive initial test to rapidly narrow the differential diagnosis of undifferentiated shock at the bedside is Point-of-Care Ultrasound (POCUS) utilizing the RUSH protocol.
- Common Distractor: A patient in profound shock with a massive pulmonary embolism requires airway support. An option suggests "Immediate endotracheal intubation." Differentiate: This is a lethal trap. Positive pressure ventilation worsens right ventricular failure and drops cardiac output in PE. The correct answer focuses on volume optimization, inotropes, or thrombolysis before/instead of intubation.
8. THE BOARDROOM SCRIPT (OSCE & Oral Board Tips)
- The Opening Salvo: "This patient is presenting in undifferentiated shock. My immediate priorities are to stabilize the ABCs, place the patient on a cardiac monitor, establish dual large-bore IV access, and order a stat 12-lead ECG. I will hold off on positive pressure ventilation until I can rule out an obstructive etiology."
- Articulating the Workup: "To rapidly differentiate the etiology, I am performing a bedside RUSH ultrasound exam to evaluate the pump, tank, and pipes. Simultaneously, I want a comprehensive shock lab panel drawn, including a serum lactate, troponin, CBC, CMP, and an immediate type and screen."
- Formulating the Resuscitation: "The ultrasound reveals a hyperdynamic heart with a collapsed IVC, consistent with hypovolemic or distributive shock. I will immediately initiate an aggressive crystalloid fluid bolus. If the MAP does not rapidly improve to my target of 65 mm Hg, I will start a continuous norepinephrine infusion and evaluate for occult bleeding or sepsis."