Vasopressors and Inotropes in the Critically Ill Patient
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
- 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
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.
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
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
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
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
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