What are the changes in cardiac output, peripheral vascular resistance, and pulmonary capillary wedge pressure during anaphylactic shock?

Hemodynamic Changes During Anaphylactic Shock

During anaphylactic shock, cardiac output is decreased, peripheral vascular resistance is markedly reduced, and pulmonary capillary wedge pressure is typically low due to severe vasodilation and increased capillary permeability causing relative hypovolemia of up to 37% of circulating blood volume. 1

Pathophysiological Changes

Cardiac Output

• Initially decreases significantly due to:
  • Reduced venous return from peripheral vasodilation
  • Decreased coronary artery perfusion pressure
  • Impaired myocardial contractility
  • Relative hypovolemia from fluid extravasation 1
• Can decrease by 30-40% during severe anaphylactic shock
• May be further compromised by myocardial ischemia with ECG changes within minutes of severe shock 1

Peripheral Vascular Resistance

• Markedly reduced due to:
  • Massive systemic vasodilation (primary mechanism)
  • Release of mediators (histamine, tryptase, leukotrienes, PAF) causing direct vasodilation 2
  • Increased capillary permeability leading to fluid extravasation
• Results in profound reduction in venous tone 3
• Creates a mixed hypovolemic-distributive shock picture 3

Pulmonary Capillary Wedge Pressure (PCWP)

• Typically low due to:
  • Decreased venous return
  • Relative hypovolemia from fluid shifts
  • Reduced preload 1
• May be further affected by right ventricular dysfunction from pulmonary vasoconstriction
• Studies show that fluid loading can modestly increase cardiac index from 1.6 to 2.0 l·min⁻¹·m⁻² in normotensive patients with acute PE and low cardiac index 1

Clinical Implications

Cardiovascular Collapse Mechanism

• Vasodilation and increased capillary permeability can cause decreased preload and relative hypovolemia of up to 37% of circulating blood volume 1
• Myocardial damage may occur due to:
  • Coronary hypoperfusion from systemic vasodilation
  • Direct coronary vasoconstriction from released mediators 2
  • Potential for Kounis syndrome (allergic acute coronary syndrome) 2

Hemodynamic Monitoring Findings

• Decreased blood pressure (systolic often <90 mmHg)
• Tachycardia (compensatory mechanism)
• Decreased central venous pressure
• Low PCWP readings
• Reduced cardiac index
• Markedly decreased systemic vascular resistance

Treatment Considerations Based on Hemodynamics

Fluid Resuscitation

• Aggressive fluid resuscitation is essential to counteract hypovolemic-distributive shock 3
• Bolus doses of isotonic crystalloid (e.g., normal saline) titrated to systolic blood pressure above 90 mmHg 1
• May require large volumes due to ongoing capillary leak

Vasopressors

• Epinephrine is first-line treatment:
  • IV epinephrine 0.05 to 0.1 mg (5% to 10% of cardiac arrest dose) for patients not in arrest 1
  • Continuous infusion (5-15 mcg/min) may be more effective than bolus dosing 1
  • Increases vascular tone, myocardial contractility, and cardiac output 3
• Norepinephrine may be considered for persistent hypotension:
  • Potent vasopressor that promotes peripheral vasoconstriction 1
  • Particularly useful in shock with low systemic vascular resistance 1

Monitoring

• Close hemodynamic monitoring is essential due to risk of fatal epinephrine overdose 1
• Monitor for improvement in cardiac output, blood pressure, and peripheral perfusion
• Be alert for signs of myocardial ischemia, which may occur rapidly in severe shock 1

Pitfalls and Caveats

• Do not delay epinephrine administration while waiting for IV access - use IM route if IV not immediately available 4
• Avoid excessive fluid resuscitation in patients with signs of heart failure or pulmonary edema
• Be cautious with epinephrine in patients >35 years with cardiovascular disease due to risk of adverse effects 4
• Recognize that anaphylactic shock may not respond to standard anti-allergic treatment alone if coronary vasoconstriction is present 2
• Consider selective vasoconstrictors if initial treatment fails 3

Understanding these hemodynamic changes is crucial for effective management of anaphylactic shock and preventing progression to cardiac arrest and death.