Vasopressors and Inotropes in the Critically Ill Patient

 RECEPTORS:

 Alpha-1 adrenergic receptors are located in vascular walls, induces significant vasoconstriction

 Beta-1 adrenergic receptors are most common in the heart and mediate ionotropy and chronotropy  

 Beta-2 adrenergic receptors in blood vessels induces vasodilatation

 Dopamine receptors are present in the renal, splanchnic, coronary, and cerebral vascular beds- stimulation of which leads to vasodilatation.  A second subtype of dopamine receptors causes vasoconstriction by inducing norepinephrine release 

  1. Norepinephrine aka LEVOPHED

FIRST LINE AGENT FOR SEPTIC SHOCK

Action– acts on alpha -=1 and beta-1 adrenergic receptors thus producing vasoconstriction as well as modest increase in cardiac output

Pros– Rapid BP control

Cons–  Need a central line

            Pt’s limbs can turn purple with prolonged usage

  1. Vasopressin

NOT TO BE USED AS A SINGLE PRESSOR. CONSIDER IN REFRACTORY SEPTIC SHOCK ONCE LEVOPHED REQUIREMENTS ARE MAXED.

Action – Increases vascular tone via stimulating V1 receptor including potentiation of catecholamine pressor agents.

Pros:   Well tolerated

            Can decrease dose of other pressors

Cons:  Contraindicated theoretically in patients with CAD or mesenteric ischemia.

 

  1. Epinephrine 

FIRST LINE IN ANAPHYLAXIS. CONSIDER IN EXTREME HEMODYNAMIC COLLAPSE

Action– Potent beta-1 adrenergic, moderate beta 2 and alpha-1 receptor effects. This results in an increased CO, with decreased SV and variable effect on the MAP. However at higher doses the alpha-adrenergic receptor effect predominates, producing increased SVR leading o increased CO.

Push dose courtesy of EMCrit: Take a 10 ml syringe with 9 ml of normal saline. Into this syringe, draw up 1 ml of epinephrine from the cardiac amp (amp contains Epinephrine 100 mcg/ml)Now you have 10 mls of Epinephrine 10 mcg/ml.

Dose: 0.5-2 ml every 2-5 minutes (5-20 mcg)

Onset: 1 minute

Duration: 5-10 minutes

Pros: should be push dose pressure of choice

Cons: Dysrhythmias, splanchnic vasoconstriction

 

  1. Phenylephrine

MOST FREQUENTLY UTILIZED IN ANESTHESIA INDUCED HYPOTENSION  

Action-            Potent purely alpha adrenergic agonist resulting in vasoconstriction

Push dose courtesy of EMCrit: Take a 3 ml syringe and draw up 1 ml of phenylephrine from the vial (vial contains phenylephrine 10 mg/ml). Inject this into a 100 ml bag of NS. Now you have 100 mls of phenylephrine 100 mcg/ml. Draw up some into a syringe; each ml in the syringe is 100 mcg

Dose: 0.5-2 ml every 2-5 minutes (50-200 mcg)

Onset: 1 minute

Duration: 20 minutes

Pros: can be used as push dose pressure

Cons: may decrease SV, so is reserved for patients in whom

                      norephinephrine is contraindicated due to arrhythmia 

  1. Dopamine

WITH ALL OF THE DRUGS WITHIN OUR ARMAMENTERIUM, THERE IS NO GOOD REASON TO NEED TO RESORT TO DOPAMINE

Action– It is the immediate precursor of norepinephrine and epinephrine. 

Different receptors for different doses

0-5ug           dopaminergic receptors leading to vasodilatation of renal and mesenteric vascular beds. This “renal dose” is ineffective as a pressure agent

5-10ug         B-adrenergic receptors lead to positive inotropic and chronotropic effects- you achieve increase in MAP through increase in SV and CO

10-20ug/kg/min           alpha-adrenergic receptors lead to systemic vasoconstriction- this is your pressor effect

 

Pros:               Can be given via peripheral line

                        It can be an effective pressor at higher doses.

                        Good if someone is bradycardic and hypotensive

Cons:              Tachycardia (in 15% of patients who receive it)

                        May impair splanchnic blood flow at higher doses

                        Ineffective in acidosis

                        You’ll never need to use it

 

INOTROPES

1.  Dobutamine

Action- Beta 1 activity (major), Beta 2 and alpha (minor). This results with

increased CO with decreased SVR (+/- small reduction in blood pressure)

 Pros: used frequently in heart failure and cardiogenic shock

Cons: not routinely used in sepsis because of risk of hypotension

 

            2. Milrinone    

Action– A phosphodiasterase 3- inhibitor in cardiac and vascular muscle.  This inhibitory action is consistent with cAMP mediated increases in intracellular ionized calcium and contractile force in cardiac muscle, as well as with cAMP dependent contractile protein phosphorylation and relaxation in vascular muscle. Thus having inotropic and vasodiliatary properties.

Pros: lower incidence of dysrhythmias

Cons: Not to be used in the hypotensive patient

 

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