Vasopressor Therapy

Basics

Shock

  • A life-threatening manifestation of circulatory failure leading to:
    • Cellular and tissue hypoxia
    • Cell death and vital organ dysfunction
    • Manifests as hypotension
  • Often need vasopressors to increase blood pressure (BP) to combat shock, after attempting adequate volume resuscitation

Types Of Shock

  • Distributive: Peripheral vasodilation:
    • Septic: Organ dysfunction from dysregulated host response to infection
    • Anaphylactic: Severe hypersensitivity reaction mediated by IgE
    • Neurogenic: Disruption of autonomic pathway due to trauma to the spinal cord
    • Endocrine: Endocrine imbalance (ie, adrenal failure, myxedema coma)
  • Hypovolemic: Decreased intravascular volume:
    • Hemorrhagic (ie, GI bleed, trauma)
    • Nonhemorrhagic:
      • Renal losses (ie, hyperaldosteronism)
      • GI losses (ie, vomiting, diarrhea)
      • Skin/insensible losses (ie, burns)
      • 3rd spacing
  • Cardiogenic: Intracardiac processes leading to decreased cardiac output (CO) (ie, cardiomyopathy, structural defect)
  • Obstructive: Extracardiac processes leading to decreased left ventricular CO (ie, pulmonary embolism, tension pneumothorax)

Pharmacology

  • Vasopressors: Increase mean arterial pressure (MAP):
    • Increase systemic vascular resistance (SVR) via peripheral vasoconstriction
    • Mediated by multiple receptors:
      • α1-Adrenergic receptor
      • Vasopressin-1a receptor
      • Angiotensin receptor-1
  • Inotropes: Increase CO:
    • Increase myocardial contraction
    • Increase CO by increasing heart rate and/or stroke volume (SV)
    • Mediated by cardiac α-adrenergic receptor

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