What are the different types of shock in an adult patient with a history of cardiovascular disease?

Types of Shock

Shock is classified into four major types based on underlying pathophysiology: cardiogenic, hypovolemic, distributive (including neurogenic and septic), and obstructive—each distinguished by characteristic hemodynamic patterns that guide diagnosis and treatment. 1

Cardiogenic Shock

Primary cardiac pump failure resulting in inadequate cardiac output and tissue hypoperfusion. 2

Hemodynamic Profile

• Cardiac index <2.2 L/min/m² with inadequate tissue perfusion 1
• Elevated systemic vascular resistance (SVR) as compensatory vasoconstriction attempts to maintain blood pressure 1
• Elevated pulmonary capillary wedge pressure (PCWP) >15 mmHg reflecting left ventricular failure and volume overload 1
• Elevated central venous pressure (CVP) >15 mmHg from right-sided filling pressures and backward failure 1
• Cardiac power output <0.6 W represents the most critical threshold for refractory shock 1

Clinical Presentation

• Systolic blood pressure <90 mmHg for ≥30 minutes or requiring vasopressors/inotropes to maintain adequate pressure 1
• Signs of end-organ hypoperfusion: decreased urine output (<0.5 mL/kg/h), altered mental status, cool extremities, elevated lactate (>2 mmol/L), acute liver or kidney injury 1
• Pulmonary congestion, jugular venous distension distinguishing it from hypovolemic shock 1

Common Causes

• Acute myocardial infarction (most common) occurring in 7-10% of AMI cases 1
• Other cardiac insults including acute decompensated heart failure, myocarditis, or mechanical complications 3, 4

Mortality

• 30-50% short-term mortality despite contemporary advances 2, 1

Hypovolemic Shock

Inadequate circulating volume resulting in decreased cardiac preload and output. 1

Hemodynamic Profile

• Decreased cardiac index due to insufficient preload 1
• Elevated SVR as compensatory vasoconstriction attempts to maintain perfusion pressure 1
• Decreased PCWP reflecting volume depletion 1
• Decreased CVP distinguishing it from cardiogenic shock 1
• Decreased SvO2 (<70%) indicating inadequate oxygen delivery with increased tissue extraction 1

Clinical Presentation

• Tachycardia as the body attempts to maintain cardiac output when stroke volume is reduced 1
• Decreased pulse pressure reflecting reduced stroke volume and increased arterial stiffness from vasoconstriction 1
• Absence of jugular venous distension (unlike cardiogenic shock) 1
• Cool, clammy extremities from peripheral vasoconstriction 1

Management Distinction

• Immediate fluid resuscitation with balanced crystalloids is the cornerstone of treatment with frequent reassessment of volume status 1
• Vasopressors should only be used transiently for life-threatening hypotension during active resuscitation, not as primary therapy 1

Distributive Shock

Pathological vasodilation resulting in decreased SVR despite normal or increased cardiac output. 1

Hemodynamic Profile

• Decreased SVR (the defining characteristic, opposite of cardiogenic shock) 1
• Normal or increased cardiac index in early stages 1
• Normal or decreased PCWP 1
• Normal or decreased CVP 1

Clinical Presentation

• Hypotension with warm extremities (unlike cardiogenic or hypovolemic shock) 1
• Increased lactate despite adequate cardiac output 1
• Tachycardia as compensatory mechanism 1

Subtypes

Septic Shock

• Most common form of distributive shock with systemic inflammatory response 1
• Late-stage septic shock can develop myocardial depression but primary hemodynamic pattern remains distributive with decreased SVR 1

Neurogenic Shock

• Results from spinal cord injury causing loss of sympathetic tone 5
• Norepinephrine is the preferred first-line vasopressor when mean arterial pressure requires pharmacologic support 5
• Fluid challenge with normal saline or Ringer's lactate should be administered first if no signs of overt fluid overload 5
• Rapid transfer to tertiary trauma center with neurosurgical capabilities is essential 5

Obstructive Shock

Mechanical obstruction to cardiac filling or outflow resulting in inadequate cardiac output. 6

Hemodynamic Profile

• Elevated CVP from impaired venous return or right heart filling 1
• Variable cardiac index depending on degree of obstruction 1
• The problem is mechanical compression preventing cardiac filling rather than primary myocardial pump failure 6

Common Causes and Management

Cardiac Tamponade

• Pericardial fluid compromising cardiac function with systemic hypotension 6
• Pulsus paradoxus may be present but can be absent in atrial septal defect, severe aortic regurgitation, or regional tamponade 6
• Urgent pericardiocentesis is the primary treatment, preferably with echocardiographic guidance, without delay in unstable patients 6
• Vasodilators and diuretics are absolutely contraindicated as they worsen obstructive physiology 6
• In trauma patients with tamponade and cardiac arrest, surgical drainage via thoracotomy is indicated rather than pericardiocentesis 6

Other Obstructive Causes

• Massive pulmonary embolism, tension pneumothorax, severe pulmonary hypertension 1

Practical Differentiation Approach

Physical Examination

• Look for jugular venous distension (elevated in cardiogenic/obstructive, absent in hypovolemic) 1
• Assess peripheral perfusion (cool in cardiogenic/hypovolemic, warm in distributive) 1
• Evaluate for pulmonary edema (present in cardiogenic, absent in others) 1

Point-of-Care Ultrasound

• Provides rapid differentiation between shock types 1
• Cardiogenic: decreased left ventricular contractility, dilated ventricles, B-lines indicating pulmonary edema 1
• Hypovolemic: collapsed inferior vena cava, hyperdynamic ventricles 1
• Obstructive (tamponade): pericardial effusion with right atrial/ventricular collapse 6

Invasive Hemodynamic Monitoring

• Pulmonary artery catheterization provides definitive measurements in refractory or unclear cases, including cardiac index, SVR, PCWP, and CVP 1
• Invasive arterial line monitoring is essential to guide vasopressor titration and assess response to therapy 5

Critical Pitfalls

• Do not confuse late-stage septic shock with cardiogenic shock—septic shock can develop myocardial depression but the primary hemodynamic pattern remains distributive with decreased SVR 1
• Dynamic changes in hemodynamic parameters occur rapidly as shock progresses or responds to treatment, emphasizing the need for continuous monitoring 1
• Severe tricuspid regurgitation causes underestimation of cardiac index by thermodilution method, necessitating the Fick method instead 1
• Age alone should not guide management decisions in cardiogenic shock; comprehensive interdisciplinary risk assessment is essential 2