Shock and vasopressor agents. Which one?

Shock and when to use vasopressor agents

Shock is the term used to describe the physiologic state when there is tissue hypoperfusion throughout multiple organs.

Decreased tissue perfusion leads to decreased tissue oxygen delivery. Early recognition of shock is essential because sustained decreases in oxygen delivery will lead to end-organ failure and, possibly, death.

Shock can have multiple causes. Shock is generally classified into 3 well-accepted categories^[2]:

• Hypovolemic shock. In this form of shock, decreased cardiac preload leads to decreased cardiac output. Hypovolemia may occur as a result of numerous etiologies, including gastrointestinal bleeding, pancreatitis, trauma, or diarrhea.
  
  
• Cardiogenic shock. In cardiogenic shock, pump failure leads to decreased cardiac output. Pump failure may be a result of a myocardial infarction or cardiomyopathy. Other cardiac causes include valvular defects, arrhythmias, or pericardial tamponade.
  
  
• Distributive shock. In this category, the primary defect is a decrease in the systemic vascular resistance (SVR). Sepsis is the primary form of distributive shock, but other etiologies include drug/toxin reactions and anaphylaxis.
  
  

The initial management, regardless of etiology, involves the support of the airway, respiration, and perfusion.

Vasopressors are used to support tissue perfusion in patients who remain hypotensive despite adequate repletion with intravenous fluids. However, there are no large clinical trials comparing outcomes with different vasopressors. But, as noted previously, the primary initial defect in septic shock is a drop in the systemic vascular resistance. Thus, if treatment with a vasopressor is indicated, using a medication with vasoconstrictive activities is usually preferred.

Dopamine is a drug which, depending on the dose, has variable physiologic effects.

At doses < 2 mcg/kg/min, dopamine stimulates dopamine receptors, resulting in vasodilatation.

At doses between 5 and 10 mcg/kg/min, dopamine also stimulates beta-1 adrenergic receptors, resulting in increased cardiac output.

At doses > 10 mcg/kg/min, dopamine stimulates alpha-adrenergic receptors, leading to vasoconstriction, which increases the systemic vascular resistance. So, depending on the dose of dopamine, it is possible to achieve different physiologic effects. Dopamine is typically used in the treatment of septic shock or cardiogenic shock.

Dobutamine is a drug that primarily stimulates beta-1 receptors, leading to increased inotropic and chronotropic effects.^[6] to al lesser extent, dobutamine also stimulates beta-2 adrenergic receptors, leading to vasodilatation. This combination of effects contributes to increased cardiac output with decreased systemic vascular resistance. Dobutamine is typically used for patients with cardiogenic shock. It is not routinely used in septic shock because it can lower systemic vascular resistance, thus leading to a risk of hypotension.

Noradrenaline acts on both alpha-1 and alpha-2 adrenergic receptors to cause vasoconstriction