Contents
- Understanding Shock
- Four Types of Shock
- Hemodynamic Profiles by Shock Type
- Vasopressor Medications
- Norepinephrine (Levophed)
- Epinephrine
- Vasopressin (ADH)
- Inotropic Agents
- Shock Treatment Algorithm
- Vasopressor Administration Safety
- Normal Hemodynamic Values Reference
- Cardiogenic Shock Hemodynamic Profile
- Distributive (Septic) Shock Hemodynamic Profile
- Hypovolemic Shock Hemodynamic Profile
- Shock Type Comparison Table
- Cardiogenic Shock Treatment Strategy
- Distributive (Septic) Shock Treatment Strategy
- Hypovolemic Shock Treatment Strategy
- Vasopressor Receptor Targets & Uses
- Vasopressin Unique Properties
- Matching Treatment to Hemodynamic Profile
Understanding Shock
- Shock is a state of inadequate tissue perfusion and oxygen delivery
- Results in cellular dysfunction and potential organ failure
- Early recognition and treatment is critical for survival
- Lactate elevation (>2 mmol/L) indicates tissue hypoperfusion
Four Types of Shock
- HYPOVOLEMIC: Loss of circulating volume (hemorrhage, dehydration, burns)
- CARDIOGENIC: Pump failure (MI, cardiomyopathy, arrhythmias)
- DISTRIBUTIVE: Vasodilation (sepsis, anaphylaxis, neurogenic)
- OBSTRUCTIVE: Physical obstruction (PE, tamponade, tension pneumothorax)
Hemodynamic Profiles by Shock Type
- Hypovolemic: ↓CO, ↓CVP, ↓PAOP, ↑SVR
- Cardiogenic: ↓CO, ↑CVP, ↑PAOP, ↑SVR
- Distributive (warm): ↑CO, ↓CVP, ↓PAOP, ↓SVR
- Distributive (cold/late): ↓CO, variable CVP, variable PAOP, ↑SVR
- Obstructive: ↓CO, ↑CVP, variable PAOP, ↑SVR
Test what you just learnedJump to CCRN-style practice questions on this topic — instant feedback with full rationales.
Start Free Practice →Vasopressor Medications
- NOREPINEPHRINE (Levophed): First-line for septic shock, α1 > β1 effects
- EPINEPHRINE: Second-line, potent α and β agonist, increases HR and contractility
- VASOPRESSIN: Non-catecholamine, V1 receptor agonist, adjunct to norepinephrine
- DOPAMINE: Dose-dependent effects, higher arrhythmia risk than norepinephrine
- PHENYLEPHRINE: Pure α1 agonist, may decrease CO, use in hyperdynamic states
Norepinephrine (Levophed)
- First-line vasopressor for septic shock per Surviving Sepsis Guidelines
- Mechanism: α1-adrenergic (vasoconstriction) > β1 (inotropy)
- Dose range: 0.01-3 mcg/kg/min, titrate to MAP ≥65 mmHg
- Advantages: Minimal tachycardia, maintains cardiac output
- Side effects: Peripheral vasoconstriction, tissue necrosis if extravasates
Epinephrine
- Mechanism: β1 and β2 at low doses, α1 predominates at high doses
- Uses: Anaphylaxis (IM 0.3-0.5mg), cardiac arrest, refractory shock
- Dose: 0.01-0.5 mcg/kg/min IV infusion for shock
- Increases HR, contractility, and BP
- Caution: Tachyarrhythmias, myocardial ischemia, hyperglycemia
Vasopressin (ADH)
- Mechanism: V1 receptor activation causes vasoconstriction
- Non-catecholamine - does not work through adrenergic receptors
- Fixed dose: 0.03-0.04 units/min (not titrated)
- Used as adjunct to norepinephrine in septic shock
- Advantages: Effective when catecholamine resistance develops
Inotropic Agents
- DOBUTAMINE: β1 agonist, increases contractility and CO, may cause hypotension
- MILRINONE: PDE-3 inhibitor, "inodilator" - increases inotropy and causes vasodilation
- Use inotropes when CO is low despite adequate preload
- Dobutamine: 2.5-20 mcg/kg/min, first-line for cardiogenic shock
- Milrinone: 0.375-0.75 mcg/kg/min, useful in RV failure and pulmonary HTN
Shock Treatment Algorithm
- 1. Identify shock type through history, exam, and hemodynamic data
- 2. Volume resuscitation: 30 mL/kg crystalloid for sepsis (unless cardiogenic)
- 3. Start vasopressors if MAP <65 after fluids or if profound hypotension
- 4. Target MAP ≥65 mmHg (may need higher in chronic hypertension)
- 5. Monitor lactate clearance as marker of resuscitation adequacy
- 6. Add inotropes if low cardiac output despite adequate preload and afterload
Vasopressor Administration Safety
- Central line preferred but peripheral OK for short-term low-dose infusions
- Continuous monitoring: arterial line for BP, telemetry for arrhythmias
- Never abruptly discontinue - wean gradually to prevent rebound hypotension
- Extravasation treatment: Phentolamine injection around site
- Document response to dose changes and reassess hemodynamic goals
Normal Hemodynamic Values Reference
- Cardiac Index (CI): 2.5-4.3 L/min/m² - measures heart pump efficiency adjusted for body size
- Central Venous Pressure (CVP): 2-6 mmHg - reflects right heart preload
- Pulmonary Artery Occlusion Pressure (PAOP): 6-12 mmHg - reflects left heart preload
- Systemic Vascular Resistance (SVR): 900-1400 dynes - measures afterload/vessel tone
- Mixed Venous O2 Saturation (SvO2): 60-80% - reflects oxygen supply vs demand balance
Cardiogenic Shock Hemodynamic Profile
- CARDIAC INDEX: Severely decreased (<2.0 L/min/m²) - heart muscle too weak to pump effectively
- PRELOAD (CVP/PAOP): Elevated (>15 mmHg) - blood backs up into heart and lungs since it cannot be ejected
- AFTERLOAD (SVR): Increased (>1600 dynes) - compensatory peripheral vasoconstriction to maintain BP
- SvO2: Decreased (<60%) - slow-moving blood allows tissues to extract nearly all available oxygen
- Clinical picture: Pump failure with congestion - cold extremities, pulmonary edema, hypotension
Distributive (Septic) Shock Hemodynamic Profile
- CARDIAC INDEX: Often elevated in early "warm" phase - heart compensates for widespread vasodilation
- PRELOAD (CVP/PAOP): Decreased or normal - relative hypovolemia from vasodilation
- AFTERLOAD (SVR): HALLMARK FINDING - very low (<800 dynes) - vessels lost tone and are "wide open"
- SvO2: Paradoxically HIGH (>80%) - blood moves too fast for tissue extraction OR cells too sick to use O2
- Clinical picture: Vasodilation with maldistribution - warm extremities initially, bounding pulses
Hypovolemic Shock Hemodynamic Profile
- CARDIAC INDEX: Decreased - insufficient fluid/blood volume to pump
- PRELOAD (CVP/PAOP): Low - the "tank is empty"
- AFTERLOAD (SVR): Increased - body clamps down on vessels to maintain pressure with remaining volume
- SvO2: Decreased (<60%) - reduced oxygen delivery with maintained tissue extraction
- Clinical picture: Volume depletion - tachycardia, flat neck veins, poor skin turgor, concentrated urine
Shock Type Comparison Table
- CARDIOGENIC: ↓CI, ↑CVP, ↑PAOP, ↑SVR, ↓SvO2 → Pump failure with backup
- SEPTIC (Early): ↑CI, ↓CVP, ↓PAOP, ↓↓SVR, ↑SvO2 → Vasodilation with hyperdynamic state
- HYPOVOLEMIC: ↓CI, ↓CVP, ↓PAOP, ↑SVR, ↓SvO2 → Empty tank with compensation
- KEY DIFFERENTIATOR: SVR is LOW only in distributive shock; HIGH in cardiogenic and hypovolemic
- SvO2 is paradoxically HIGH only in septic shock due to oxygen extraction/utilization defect
Cardiogenic Shock Treatment Strategy
- PRIMARY GOAL: Improve pump function while reducing cardiac workload
- POSITIVE INOTROPES: Dobutamine or low-dose Dopamine (<10 mcg/kg/min) to increase contractility
- AFTERLOAD REDUCTION: Nitroglycerin or Nitroprusside to decrease resistance heart pumps against
- AVOID excessive fluids - will worsen pulmonary congestion
- MECHANICAL SUPPORT: Consider IABP to improve coronary flow and decrease myocardial oxygen demand
Distributive (Septic) Shock Treatment Strategy
- PRIMARY GOAL: Restore vascular tone and fill the dilated vascular bed
- FLUID RESUSCITATION: First priority - 30 mL/kg crystalloid to fill dilated vessels
- VASOPRESSORS: Norepinephrine first-line to constrict vessels and increase SVR
- Phenylephrine (pure alpha) or high-dose Dopamine (>10 mcg/kg/min) as alternatives
- Vasopressin added to norepinephrine for refractory hypotension
Hypovolemic Shock Treatment Strategy
- PRIMARY GOAL: Replace lost volume - "fill the tank"
- VOLUME REPLACEMENT: Isotonic crystalloids (Normal Saline, Lactated Ringers) or blood products
- For hemorrhage: Balanced transfusion with PRBCs, FFP, Platelets (1:1:1 ratio)
- VASOPRESSORS: Only as temporary bridge during/after volume replacement if BP dangerously low
- Address underlying cause: Stop bleeding, treat GI losses, manage burns
Vasopressor Receptor Targets & Uses
- NOREPINEPHRINE: Alpha (++++) & Beta-1 (++) → First-line septic shock, increases SVR and MAP
- PHENYLEPHRINE: Pure Alpha (++++) → Potent vasoconstriction for distributive shock, no cardiac stimulation
- DOBUTAMINE: Beta-1 (++++) & Beta-2 (++) → Increases contractility for cardiogenic shock, may cause vasodilation
- EPINEPHRINE: Alpha, Beta-1, Beta-2 (++++) → Cardiac arrest, severe shock, increases HR and BP
- DOPAMINE: Dose-dependent → Low dose: contractility; High dose (>10 mcg/kg/min): vasoconstriction
Vasopressin Unique Properties
- RECEPTOR: V1 receptors - NON-ADRENERGIC pathway (does not use alpha/beta receptors)
- MECHANISM: Direct smooth muscle contraction causing vasoconstriction
- ADVANTAGE: Effective when adrenergic receptors are downregulated (catecholamine resistance)
- DOSING: Fixed dose 0.03-0.04 units/min - NOT titrated like other vasopressors
- USE: Added to norepinephrine in septic shock to help raise SVR through alternative pathway
Matching Treatment to Hemodynamic Profile
- HIGH SVR + LOW CO → Think cardiogenic → Use inotropes (Dobutamine), reduce afterload
- LOW SVR + HIGH/NORMAL CO → Think distributive → Use vasopressors (Norepinephrine)
- HIGH SVR + LOW PRELOAD → Think hypovolemic → Give volume first, then pressors if needed
- Always reassess hemodynamics after each intervention
- Goal: Normalize CI, optimize preload, achieve MAP ≥65 mmHg, clear lactate
Can you answer these 3 CCRN questions?
Here are 3 questions from our premium bank. The full rationale explains exactly why the right answer is right — and why the 3 distractors trap most test-takers.
Premium Practice Question
A 71-year-old arrives with dyspnea and chest pressure. Skin is cool and clammy. VS: HR 118, BP 78/44, SpOâ‚‚ 92% on 4 L NC. Crackles present bilaterally. Hemodynamics: CI 1.7, CVP 18, PAOP 24, SVR 1750, SvOâ‚‚ 54%. Which shock type best fits?
- Hypovolemic
- Distributive (early septic)
- Cardiogenic
- Neurogenic
Rationale: Low CI + high CVP/PAOP + high SVR + low SvOâ‚‚ with pulmonary congestion is classic cardiogenic shock (pump failure with backup and compensatory vasoconstriction)....
Unlock full rationale + 692 more questions
Premium Practice Question
A patient on an IABP reports worsening chest pain. The arterial waveform shows balloon deflation occurring after the next systolic upstroke begins, and assisted systolic pressure appears higher than expected. What is the most likely problem/effect?
- Early inflation → decreased coronary perfusion
- Late inflation → decreased diastolic augmentation
- Late deflation → increased afterload and myocardial oxygen demand
- Early deflation → improved unloading
Rationale: Late deflation means the balloon is still inflated as systole starts, which increases afterload and myocardial O₂ demand—can worsen ischemia and hemodynamics....
Unlock full rationale + 692 more questions
Premium Practice Question
A 63-year-old is 24 hours post–inferior MI. Suddenly develops acute respiratory distress, frothy sputum, hypotension, and a new loud holosystolic murmur at the apex. SpO₂ 84% on NRB. What is the most likely cause?
- Acute pericarditis
- Papillary muscle rupture → acute severe mitral regurgitation
- Right ventricular infarct causing preload collapse
- Dressler syndrome
Rationale: Sudden pulmonary edema + shock + new holosystolic murmur post-MI strongly suggests papillary muscle rupture leading to acute severe MR (a surgical emergency)....
Unlock full rationale + 692 more questions
Want the full CCRN experience?
Practice with 695+ exam-style questions, adaptive flashcards, and AI-powered weak-area drilling inside the Zero Deficit app.
Start Free →