Shock: Overview and Classification

Introduction

• Shock is characterized by inadequate tissue perfusion and oxygen delivery to meet cellular metabolic demands, resulting in cellular and possibly organ dysfunction.¹
• Shock is typically classified into four main types: hypovolemic, distributive, cardiogenic, and obstructive.²

Hypovolemic Shock^2-4

• Hypovolemic shock results from a significant loss of intravascular volume, leading to decreased preload, reduced cardiac output, and insufficient oxygen delivery.

Etiology

• Hemorrhagic shock is a form of hypovolemic shock in which severe blood loss leads to inadequate oxygen delivery at the cellular level. The causes of hemorrhage resulting in shock vary widely and include trauma, maternal hemorrhage, gastrointestinal hemorrhage, perioperative hemorrhage, and rupture of an aneurysm.
• Nonhemorrhagic causes (e.g., dehydration from vomiting, diarrhea, burns, or excessive fluid leakage into extravascular space).

Pathophysiology

• Decreased preload: Loss of intravascular volume reduces venous return to the heart, decreasing end-diastolic volume.
• Reduced stroke volume and cardiac output: According to the Frank-Starling mechanism, lower preload decreases myocardial fiber stretch, reducing stroke volume.
• Compensatory mechanisms: The body activates the sympathetic nervous system, leading to tachycardia and systemic vasoconstriction. Additionally, the renin-angiotensin-aldosterone system (RAAS) is stimulated to promote fluid retention.
• Progression: Prolonged hypoperfusion leads to anaerobic metabolism, lactic acidosis, and cellular injury.
• At the cellular level, hemorrhagic shock results when oxygen delivery is insufficient to meet the oxygen demand for aerobic metabolism. Cells subsequently transition to anaerobic metabolism. As a result of the mounting oxygen debt, lactic acid, inorganic phosphates, and oxygen free radicals start to accumulate. As adenosine triphosphate supplies dwindle, cellular homeostasis ultimately fails, and cell death ensues.
• At the tissue level, hypovolemia and vasoconstriction cause hypoperfusion and end-organ damage in the kidneys, liver, intestine, and skeletal muscle, which can lead to multiorgan failure in survivors.
• At the site of hemorrhage, the clotting cascade and platelets are activated, forming a hemostatic plug. Away from the site of hemorrhage, fibrinolytic activity increases to prevent microvascular thrombosis. Additionally, depleted platelet numbers, decreased platelet margination due to anemia, and reduced platelet activity contribute to coagulopathy and increased mortality.

Distributive Shock^5,6

• Distributive shock is characterized by an inappropriate distribution of blood flow and oxygen delivery secondary to decreased systemic vascular resistance (SVR) despite preserved or elevated cardiac output.

Etiology

• Septic shock (most common cause)
• Anaphylactic shock
• Neurogenic shock
• Endocrine causes
  • Adrenal crisis: Secondary to adrenal insufficiency (e.g., Addison’s disease, critical illness)
  • Thyroid storm: Excess thyroid hormone increases metabolic demand and vasodilation.
• Pancreatitis, burns, trauma-induced systemic inflammation, or drug-induced vasodilation (e.g., anesthetics or nitroprusside overdose)

Pathophysiology

• Endothelial dysfunction and vasodilation
  • Sepsis: Activation of endothelial cells via TLR (Toll-like receptor) signaling promotes the release of nitric oxide (NO) through inducible nitric oxide synthase.
  • Anaphylaxis: Mast cell degranulation releases histamine, causing profound vasodilation.
• Capillary leak and plasma extravasation
  • Endothelial barrier disruption increases vascular permeability.
  • Loss of oncotic pressure drives plasma into interstitial spaces, exacerbating hypovolemia.
• Impaired vascular tone regulation
  • Loss of sympathetic vasoconstrictive activity (e.g., neurogenic shock)
  • Excessive vasodilatory mediators (e.g., NO, prostaglandins, tumor necrosis factor-alpha [TNF-α]).
• Microcirculatory dysfunction
  • Impaired autoregulation causes maldistribution of blood flow.
• Mitochondrial dysfunction and oxygen utilization
  • Cytokines (TNF-α, IL-1β) and reactive oxygen species (ROS) impair mitochondrial respiration.
• Myocardial dysfunction
  • In late stages, circulating myocardial depressant factors (e.g., IL-1β, TNF-α) reduce myocardial contractility.

Cardiogenic Shock^7,8

• Cardiogenic shock is a life-threatening condition characterized by severely reduced cardiac output due to primary cardiac dysfunction, resulting in inadequate tissue perfusion and oxygen delivery despite normal or elevated intravascular volume.

Etiology

• Myocardial infarction: The most common cause of cardiogenic shock is extensive acute myocardial infarction.
• Cardiogenic shock can also be caused by mechanical complications—such as acute mitral regurgitation, rupture of the interventricular septum, or rupture of the free wall.
• Acute decompensated heart failure: Patients with chronic heart failure may decompensate acutely, leading to cardiogenic shock.
• Severe valvular heart disease: Valvular pathologies may lead to cardiogenic shock if severe or acute.
  • Aortic stenosis: Critical stenosis (<0.8 cm² valve area) results in a fixed cardiac output state.
  • Acute aortic regurgitation: Sudden regurgitant volume overload leads to LV dilation, reduced effective forward flow, and cardiogenic shock.
  • Acute mitral regurgitation: Often due to papillary muscle rupture or chordae tendineae rupture.
• Arrhythmias: Both tachyarrhythmias and bradyarrhythmias can impair cardiac output and precipitate cardiogenic shock.
• Right ventricular (RV) failure: Isolated RV failure or RV dysfunction secondary to pulmonary pathology can cause cardiogenic shock.
• Myocarditis: Inflammatory damage to the myocardium (e.g., viral myocarditis, autoimmune myocarditis) can lead to global systolic dysfunction and cardiogenic shock.
• Cardiomyopathies: Both acute and chronic cardiomyopathies, including dilated cardiomyopathy, hypertrophic cardiomyopathy, and stress-induced cardiomyopathy (Takotsubo), can precipitate cardiogenic shock.

Pathophysiology

• Decreased contractility: Myocardial ischemia or damage reduces stroke volume and cardiac output.
• Increased afterload: Compensatory vasoconstriction raises SVR, further impairing cardiac function.
• Elevated preload: Impaired ventricular emptying increases filling pressures, leading to pulmonary congestion and hypoxia.
• Vicious cycle: Reduced cardiac output perpetuates tissue hypoperfusion, exacerbating myocardial ischemia.

Obstructive Shock^9,10

• Obstructive shock arises from mechanical barriers to cardiac filling or output, leading to reduced cardiac output and systemic hypoperfusion.

Etiology and Pathophysiology

• Cardiac tamponade: Fluid accumulation in the pericardial sac compresses the heart, reducing diastolic filling and stroke volume. Common causes are malignancy, uremia, postcardiac surgery, trauma, or infections.

Pathophysiology:

Pericardial pressure exceeds intracardiac pressures, especially during diastole.
Right-sided heart chambers are more susceptible due to thinner walls, leading to impaired venous return and systemic congestion.

• Massive pulmonary embolism: A sudden increase in pulmonary vascular resistance (PVR) causes RV dilation and reduced contractility (acute cor pulmonale).

Pathophysiology:

Decreased left ventricular (LV) preload results in systemic hypoperfusion.

• Tension pneumothorax: Air trapped in the pleural space under positive pressure compresses the lungs and mediastinal structures, reducing venous return and cardiac output.

Pathophysiology:

Increased intrathoracic pressure causes mediastinal shift and collapses the inferior vena cava.
Reduced preload leads to systemic hypoperfusion. Compromised ventilation exacerbates hypoxemia.

• Severe pulmonary hypertension: Critical elevations in PVR lead to RV failure, impairing pulmonary blood flow and LV filling.

Pathophysiology:

Chronic pressure overload causes progressive RV dilation and systolic dysfunction.
Systemic venous congestion and reduced LV output lead to hypotension and hypoperfusion.

• Constrictive pericarditis: Chronic pericardial fibrosis or calcification restricts diastolic filling, mimicking features of cardiac tamponade. Common causes are postcardiac surgery, radiation therapy, tuberculosis, or idiopathic fibrosis.

Pathophysiology:

Impaired diastolic relaxation leads to equalization of pressures across all heart chambers.
Elevated venous pressures cause systemic congestion, while reduced stroke volume leads to low cardiac output.

• Aortic dissection: Acute dissection of the aortic wall creates a false lumen, which can obstruct blood flow or rupture into the pericardium, causing tamponade.

Pathophysiology:

Involvement of the ascending aorta (Stanford type A) can obstruct coronary flow, leading to ischemia or tamponade. Dissection of the descending aorta (Stanford type B) may impair perfusion to visceral organs and lower extremities.

Common Pathophysiological Features Across Shock States

• Cellular hypoxia: Decreased oxygen delivery leads to anaerobic metabolism, lactic acid production, and metabolic acidosis.
• Inflammatory cascade: Systemic inflammation can exacerbate tissue injury and organ dysfunction.
• Endothelial dysfunction: Altered endothelial barrier function promotes vascular permeability and edema.
• Microcirculatory impairment: Reduced perfusion at the capillary level disrupts oxygen extraction.

Clinical Anesthetic Implications

• Preoperative optimization: Patients at risk of shock should be identified and intravascular volume and cardiovascular function should be optimized.
• Intraoperative monitoring: Invasive and noninvasive monitoring (e.g., arterial lines, central venous pressure, cardiac output monitors) should be utilized to guide management.
• Fluid resuscitation: Fluid administration should be tailored based on the type of shock and hemodynamic goals.
• Vasoactive medications: Vasopressors (e.g., norepinephrine, vasopressin) and inotropes (e.g., dobutamine) should be used as indicated by the underlying etiology.
• Postoperative care: Signs of ongoing shock or organ dysfunction should be monitored in the postoperative period.