On This Page (4 sections)
HR/SBP > 0.8–1.0 indicates occult shock and impending cardiovascular collapse
Target MAP >= 65 mmHg to maintain vital organ and renal capillary perfusion
Norepinephrine 0.05–0.5 mcg/kg/min (titrate q2–5min to MAP >= 65)
Perform immediate bedside POCUS: Pump (heart), Tank (IVC/eFAST), Pipes (aorta/DVT)
Safely infuse Norepinephrine via antecubital peripheral IV while preparing line
Bottom-Line Clinical Pearl
Shock is circulatory failure resulting in cellular dysoxia, NOT simply low blood pressure. Mean Arterial Pressure (MAP) < 65 mmHg or Shock Index (HR/SBP) > 0.8 warrants immediate bedside ultrasound (RUSH exam) to categorize the shock state into Distributive, Hypovolemic, Cardiogenic, or Obstructive. Start peripheral Norepinephrine early to maintain coronary perfusion; never administer large fluid boluses blindly in cardiogenic or obstructive shock.
Shock is defined as an imbalance between systemic oxygen delivery (DO2) and cellular oxygen consumption (VO2), leading to tissue hypoperfusion, cellular dysoxia, anaerobic glycolysis, and lactic acid production. Tachycardia and narrowed pulse pressure are early compensatory mechanisms; overt hypotension (MAP < 65 mmHg, SBP < 90 mmHg) is a late manifestation of cardiovascular collapse.
| Shock Category | Primary Etiology | Preload (CVP/Wedge) | Cardiac Output (CO) | Afterload (SVR) | ScvO2 (Mixed Venous O2) |
|---|---|---|---|---|---|
| Hypovolemic | Hemorrhage, severe dehydration, 3rd spacing, burns | DECREASED | DECREASED | INCREASED (compensatory vasoconstriction) | DECREASED (< 65%) |
| Cardiogenic | Acute MI, myocarditis, acute valvular rupture, severe dysrhythmia | INCREASED | DECREASED | INCREASED | DECREASED (< 60%) |
| Distributive | Septic shock, anaphylaxis, neurogenic shock, adrenal crisis | DECREASED or Normal | INCREASED (early hyperdynamic) | DECREASED (profound vasodilation) | INCREASED (> 75–80%) |
| Obstructive | Tension pneumothorax, cardiac tamponade, massive PE | INCREASED (JVD present) | DECREASED | INCREASED | DECREASED (< 65%) |
The RUSH protocol (Rapid Ultrasound in Shock and Hypotension) provides a structured 3-part bedside ultrasound exam that categorizes undifferentiated shock within 3 to 5 minutes at the bedside: The Pump, The Tank, and The Pipes.
| RUSH Component | Sonographic Target | Normal Findings | Pathologic Findings & Diagnostic Match |
|---|---|---|---|
| The PUMP: Contractility | Parasternal long/short, apical 4-chamber | Hyperdynamic LV ejection (EF 55–70%) | Hypokinetic/Akinetic LV -> Cardiogenic Shock; Hyperdynamic LV -> Septic/Hypovolemic Shock. |
| The PUMP: Pericardial Space | Subxiphoid 4-chamber view | No anechoic fluid strip around heart | Anechoic pericardial effusion with RV diastolic collapse -> Cardiac Tamponade. |
| The PUMP: Right Ventricle | Apical 4-chamber view | RV is 2/3 diameter of LV; no septal flattening | RV dilation (RV > LV) + McConnell sign + D-shaped septum -> Massive Pulmonary Embolism. |
| The TANK: Fullness (Preload) | IVC longitudinal view (subxiphoid) | IVC diameter 1.5–2.0 cm with > 50% inspiratory collapse | Flat/Collapsing IVC (< 1.0 cm) -> Hypovolemic/Distributive shock; Plethoric IVC (> 2.1 cm with < 50% collapse) -> Cardiogenic/Obstructive shock. |
| The TANK: Leak (eFAST) | Morison pouch, splenorenal, suprapubic | Sharp tissue interfaces, no free fluid | Anechoic free fluid strip in RUQ/LUQ/pelvis -> Internal Hemorrhage/Ruptured Ectopic. |
| The TANK: Compromise (Thorax) | Anterior 2nd–4th ICS bilateral lung zones | Lung sliding present; seashore sign on M-mode | Absence of lung sliding + stratosphere/barcode sign -> Tension Pneumothorax. |
| The PIPES: Arterial System | Suprarenal and infrarenal abdominal aorta | Aortic diameter < 3.0 cm from outer wall to outer wall | Abdominal aortic aneurysm (AAA >= 3.0 cm) or intimal flap -> Ruptured AAA/Aortic Dissection. |
| The PIPES: Venous System | Common femoral and popliteal veins | Vein lumen completely compresses under transducer pressure | Non-compressible vein lumen with hyperechoic intraluminal thrombus -> Deep Venous Thrombosis (DVT/PE). |
Vasoactive infusions are initiated when fluid resuscitation fails to restore MAP >= 65 mmHg, or immediately in cardiogenic/distributive shock to prevent fatal organ ischemia. Titrate every 2–5 minutes to objective endpoints (MAP >= 65 mmHg, urine output > 0.5 mL/kg/h, lactate clearance).
| Vasoactive Agent | Receptor Activity | Dosing Range | Primary Clinical Indications | Adverse Effects & Cautions |
|---|---|---|---|---|
| Norepinephrine (Levophed) | Alpha-1 ++++ Beta-1 ++ | 0.05–0.5 mcg/kg/min (titrate q2–5min) | FIRST-LINE agent in Septic Shock, Undifferentiated Shock, and Cardiogenic Shock. | Peripheral digital ischemia at extreme doses; tachycardia in hypovolemia. |
| Epinephrine (Adrenalin) | Alpha-1 ++++ Beta-1 ++++ Beta-2 ++ | 0.05–0.5 mcg/kg/min | FIRST-LINE in Anaphylactic Shock; second-line in Septic Shock or post-ROSC cardiogenic shock. | Marked tachycardia, tachydysrhythmias, transient hyperlactatemia via aerobic muscle glycolysis. |
| Vasopressin (Pitressin) | V1 receptor ++++ (vascular smooth muscle) | 0.03 units/min FIXED dose (do NOT titrate) | Second-line adjuvant in Septic Shock (add when Norepinephrine reaches 0.25 mcg/kg/min). | Coronary and mesenteric vasoconstriction; skin necrosis with extravasation. |
| Phenylephrine (Neo-Synephrine) | Alpha-1 pure +++++ | 0.5–5.0 mcg/kg/min (or push-dose 50–200 mcg) | Hypertrophic cardiomyopathy (HOCM), critical aortic stenosis, tachyarrhythmia-induced hypotension. | Reflex bradycardia from pure vasoconstriction; reduces stroke volume in failing hearts. |
| Dobutamine (Dobutrex) | Beta-1 ++++ Beta-2 ++ | 2.5–20 mcg/kg/min infusion | Cardiogenic shock with low cardiac output and elevated filling pressures (SBP must be > 90 mmHg). | Vasodilation from beta-2 stimulation (drops BP if given without vasopressor); ventricular dysrhythmias. |
Administering excess fluid to a patient whose heart is on the flat portion of the Frank-Starling curve causes pulmonary edema, right heart strain, and worsened mortality. Static measurements (CVP) have zero predictive value for fluid responsiveness. Use dynamic physiological maneuvers:
- Passive Leg Raise (PLR) Test: Transition patient from 45-degree semi-recumbent to supine with legs elevated 45 degrees for 60–90 seconds. Autotransfuses ~300 mL of blood from the lower extremities. A > 10% increase in stroke volume or cardiac output (measured via Doppler velocity-time integral VTI or arterial line pulse contour) confirms fluid responsiveness. Reversible upon lowering legs.
- End-Expiratory Occlusion Test (Ventilated Patients): Pause ventilation at end-expiration for 15 seconds. Interrupts cyclic decrease in venous return; an increase in pulse pressure or stroke volume > 5% predicts fluid responsiveness.
- Velocity-Time Integral (VTI) on POCUS: Apical 5-chamber view measuring pulsed-wave Doppler across the left ventricular outflow tract (LVOT). Normal VTI is 18–22 cm. VTI < 15 cm indicates low stroke volume; an increase >= 10–15% after fluid challenge confirms responsiveness.
- Balanced Crystalloids vs Normal Saline: Large randomized trials (SMART and SALT-ED) proved that balanced crystalloids (Lactated Ringer's or Plasma-Lyte) significantly reduce major adverse kidney events (MAKE) and mortality compared to 0.9% Normal Saline, which induces hyperchloremic metabolic acidosis and renal vasoconstriction.
Clinical Caution
The Push-Dose Pressor Bridge: In peri-arrest hypotension or acute post-induction collapse: Administer push-dose Phenylephrine (100 mcg IV: 1 mL of 100 mcg/mL solution q2–5min) or push-dose Epinephrine (10 mcg IV: 1 mL of 10 mcg/mL 'cardiac' dilute solution q2–5min) as an immediate temporizing bridge while the continuous infusion is being prepared.
Test Your Shock & Undifferentiated Hypotension Clinical Acumen
Directly launch an active-recall practice block from our validated question bank with comprehensive explanations and distractor analyses.
Distinguish primary life-threats from mimics. On board exams (COMLEX Level 1, 2-CE, 3 & USMLE), initial stabilizing interventions (airway, IV access, non-invasive ventilation, empiric reversal) always take precedence over diagnostic imaging.
Evaluate autonomic tone: Sympathetic viscerosomatics (T1–L2) cause acute paraspinal tissue texture changes (erythema, bogginess, hypertonicity). Suboccipital release (CN X Vagus) and rib raising normalize autonomic outflow and thoracic cage mechanics.
Related Emergency Protocols & Differentials
Sepsis & Septic Shock
Surviving Sepsis bundle, broad antibiotics, and resuscitation.
Open Protocol Related EM ProtocolCardiac Arrest & Resuscitation
ACLS protocols and peri-arrest management.
Open Protocol Related EM ProtocolAcute Pulmonary Embolism
Obstructive shock and RV failure management.
Open Protocol