Vasopressors used in shock

A vasopressor causes vasoconstriction and an inotrope increases the force of cardiac contraction.
The role of inotropes and vasopressors is very important in the resuscitation of a patient, prescribing these can best be done by an experienced physician. Every doctor has his or own method of starting the patient on these drugs. Most of the hospitals have there own protocol.
In this article we will discuss the role of the three most commonly given inotropes and vasopressors.

Clinical classification of a patient in shock -

CLASS I
CLASS II
CLASS III
CLASS IV
Blood loss (ml)
<750
750-1500
1500-2000
>2000
Blood loss (%)
<15
15-30
30-40
>40
CNS (Mental status)
Slightly anxious
Mildly anxious
Anxious and confused
Confused and lethargic
Pulse rate (bpm)
<100
>100
>120
>140
Blood pressure
Normal
Normal
Decreased
Decreased
Pulse pressure
Normal or increased
Decreased
Decreased
Decreased
Respiratory Rate
14-20
20-30
30-40
>35
Capillary blanch test
Normal
Positive
Positive
Positive
Urine Output
30 or more
20-30
5-15
Negligible

Different types of receptors on which these drugs work -
  1. Alpha Receptors:
    These are present in the heart. On stimulation these induces significant vasoconstriction and have some slight inotropic effect.
  2. Beta 1 Receptors:
    These are adrenergic receptors present in the heart. On stimulation they have an inotropic effect on the heart with minimal vasoconstriction.
  3. Beta 2 Receptors: These adrenergic receptors are present in the smooth muscle cells of the blood vessels. Their stimulation induces vasodilation; bronchodilation.
  4. Dopamine Receptors:
    These are present in the renal, splanchnic, coronary and cerebral vascular beds. Stimulation of these receptors leads to vasodilation.
Now let us discuss the most commonly used inotropes and vasopressors-

DOPAMINE
At low doses (1-4 mcg/kg/min) dopamine acts predominately o dopamine 1 receptors in the renal mesenteric, cerebral and coronary beds, resulting in selective vasodilatation.
At a dosage of 5-10 µg/kg/min, beta1-adrenergic effects induce an increase in cardiac contractility and heart rate.
At dosages of about 10 µg/kg/min, alpha-adrenergic effects lead to arterial vasoconstriction and elevation in blood pressure.
Common indications are -
Hypotension due to sepsis or cardiac failure.
As at low doses it increases the renal blood flow thus it can also be given in patients with acute renal failure and mesenteric ischemia.

DOBUTAMINE
Not actually a vasopressor, It has an inotropic effect and also causes vasodilatation. It predominantly acts on the beta 1 receptor there by improving the contractility of the heart and the ventricular filling. Due to the action on the beta 2 receptors and in response to the improved cardiac output,  there is overall vasodilatation which occurs.
It is usually given when inotropic support is necessary for the treatment of patients with hypo perfusion states in whom cardiac output is insufficient to meet the circulatory demands.
NORADRENALINE
It acts on both alpha 1 and beta 1 receptors and functions as a peripheral vasoconstrictor and as an inotropic stimulator of the heart and dilator of coronary arteries respectively.
*It should not be given to patients who are hypotensive from blood volume deficits except as an emergency measure to maintain coronary and cerebral artery perfusion until blood volume replacement therapy can be completed.
Many consider Noradrenaline to be the drug of choice in septic shock.

Interesting facts you would like to know about these Inotropes/Vasopressors –
  • Before starting inotropes fluid resuscitation (uptil 4 L) should be given in patients, here normal saline or ringer lactate are fluids of choice. But may be given directly in frank shock i.e. systolic blood pressure of less than 70 mmhg or signs of tissue hypo perfusion.
  • Vasopressor administration is required for persistent hypotension once adequate intravascular volume expansion has been achieved.
  • The recommended first-line agent for septic shock is either norepinephrine or dopamine.
  • Noradrenaline can increase blood pressure successfully in patients with sepsis who remain hypotensive after fluid resuscitation and dopamine. Recent studies have showed that a great proportion of patients were resuscitated successfully with noradrenaline as compared to dopamine.
  • Noradrenaline has shown to show less adverse effect. It is considered to be quite safer than other vasopressors.
  • Clinical trials have failed to prove any beneficial effects of low dose dopamine in patients of acute renal failure and mesenteric ischemia.
  • Dopamine at a dosage of 2-3 µg/kg/min is known to initiate diuresis by increasing renal blood flow in healthy animals and volunteers.
  • Considering the real side effects of dopamine infusion, the use of renal-dose dopamine should be abandoned.
  • Dobutamine can enhance tissue oxygen delivery in patients with septic shock who have received adequate fluid resuscitation and vasopressor support.
  • A trial of increasing oxygen delivery is recommended in patients who have evidence of tissue hypoxia.

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