What are the differences between cardiogenic, hypovolemic, and obstructive shock?

Differentiating Cardiogenic, Hypovolemic, and Obstructive Shock

Hemodynamic Profiles: The Key to Differentiation

The critical distinction between these three shock types lies in their hemodynamic patterns: cardiogenic shock presents with decreased cardiac output, elevated filling pressures (PCWP >15 mmHg), and increased systemic vascular resistance; hypovolemic shock shows decreased cardiac output, decreased filling pressures, and increased SVR; while obstructive shock demonstrates decreased cardiac output with elevated central venous pressure but variable PCWP depending on the obstruction site. 1

Cardiogenic Shock Hemodynamics

Primary cardiac dysfunction drives the hemodynamic collapse:

• Cardiac Index: <2.2 L/min/m² (often <1.8 L/min/m² in severe cases) due to impaired myocardial contractility 1, 2
• Cardiac Power Output: <0.6 W represents the most critical threshold for identifying refractory shock 1
• Pulmonary Capillary Wedge Pressure (PCWP): Elevated >15 mmHg, reflecting left ventricular failure and backward congestion 3, 1
• Central Venous Pressure (CVP): Elevated >15 mmHg from right-sided failure 1
• Systemic Vascular Resistance (SVR): Increased as compensatory vasoconstriction attempts to maintain blood pressure despite falling cardiac output 3, 1

Clinical presentation includes: Hypotension (SBP <90 mmHg for >30 minutes), pulmonary edema, jugular venous distension, cool extremities, altered mental status, oliguria (<0.5 mL/kg/h), and elevated lactate >2 mmol/L 3, 1

Hypovolemic Shock Hemodynamics

Intravascular volume depletion creates a distinct pattern:

• Cardiac Index: Decreased <2.2 L/min/m² due to inadequate preload, not myocardial dysfunction 1
• PCWP: Decreased <15 mmHg, distinguishing it from cardiogenic shock 1
• CVP: Decreased, reflecting low right-sided filling pressures 1
• SVR: Increased through compensatory vasoconstriction 1
• Mixed Venous Oxygen Saturation (SvO2): <70%, indicating inadequate oxygen delivery with increased tissue extraction 1

Clinical presentation includes: Tachycardia, decreased pulse pressure, flat neck veins, dry mucous membranes, poor skin turgor, and signs of hypoperfusion without pulmonary congestion 1, 4

Obstructive Shock Hemodynamics

Mechanical obstruction to blood flow creates unique patterns:

• Cardiac Index: Decreased due to mechanical impediment to cardiac filling or outflow 5, 6
• CVP: Elevated from impaired venous return or right heart obstruction 1
• PCWP: Variable depending on obstruction location—elevated in cardiac tamponade, decreased in massive pulmonary embolism 1
• SVR: Increased as compensatory response 5

Common causes include: Massive pulmonary embolism, tension pneumothorax, cardiac tamponade, and constrictive pericarditis 5, 6

Practical Diagnostic Algorithm

Step 1: Confirm Shock State

All three types share: Hypotension (SBP <90 mmHg or MAP <60 mmHg) and signs of end-organ hypoperfusion (altered mental status, oliguria, cool extremities, lactate >2 mmol/L) 3, 4

Step 2: Assess Volume Status and Cardiac Function

Physical examination findings:

• Jugular venous distension present: Suggests cardiogenic or obstructive shock (elevated CVP) 1
• Flat neck veins: Suggests hypovolemic shock (low CVP) 1
• Pulmonary congestion (rales, orthopnea): Specific for cardiogenic shock 3

Point-of-care ultrasound provides rapid differentiation:

• Cardiogenic: Decreased left ventricular contractility, dilated ventricles, B-lines indicating pulmonary edema 3
• Hypovolemic: Hyperdynamic but small left ventricle, collapsible inferior vena cava 3
• Obstructive: Specific findings depending on cause (right ventricular strain in PE, pericardial effusion in tamponade) 3

Step 3: Invasive Hemodynamic Monitoring When Diagnosis Unclear

Pulmonary artery catheter provides definitive measurements in refractory or unclear cases: 3, 1

• Measure cardiac index, SVR, PCWP, and CVP simultaneously
• Calculate cardiac power output in suspected cardiogenic shock
• Obtain measurements in triplicate for reliability 1

Critical pitfall: Severe tricuspid regurgitation causes underestimation of cardiac index by thermodilution; use Fick method instead 1

Management Implications Based on Shock Type

Cardiogenic Shock Treatment

Immediate revascularization for AMI-related shock is the standard of care 2

Pharmacologic support:

• Norepinephrine as first-line vasopressor when persistent hypotension with tachycardia exists 3
• Dobutamine as first-line inotrope to increase cardiac output, though associated with arrhythmias and hypotension 3, 2
• Avoid excessive fluid administration—worsens pulmonary edema and right ventricular failure 4

Mechanical circulatory support should be considered early in refractory shock (CPO <0.6 W despite maximal medical therapy) rather than prolonged medical optimization 1

Hypovolemic Shock Treatment

Immediate fluid resuscitation with balanced crystalloids is the cornerstone 4, 5

• Administer 30 mL/kg crystalloid rapidly
• Reassess volume status frequently
• Blood products for hemorrhagic shock with definitive hemorrhage control 3

Critical pitfall: Vasopressors should only be used transiently for life-threatening hypotension during active resuscitation, not as primary therapy 3

Obstructive Shock Treatment

Immediate life-saving intervention to relieve obstruction is required 5

• Needle decompression for tension pneumothorax
• Pericardiocentesis for cardiac tamponade
• Thrombolysis or embolectomy for massive pulmonary embolism

Fluid challenge may be beneficial in obstructive shock to optimize preload before definitive intervention 3

Common Diagnostic Pitfalls

Late-stage septic shock can mimic cardiogenic shock when myocardial depression develops, but the primary hemodynamic pattern remains distributive with decreased SVR 1

Dynamic changes occur rapidly as shock progresses or responds to treatment—continuous monitoring is essential rather than single measurements 1

Mixed shock states exist—a patient may have both hypovolemic and cardiogenic components (e.g., inferior MI with right ventricular infarction) requiring nuanced fluid management 3