Cardiac - Inotropes & Pressors Flashcards
Adrenoreceptors and functions
(From LITFL)
A1 present in smooth muscle.
Causes vasoconstriction, relaxation of GI, contraction of GU
A2 present in CNS, arterioles, pancreas. Causes sedation, analgesia, vasodilation and inhibition of insulin release
B1 present in cardiac muscle and juxtaglomerular apparatus (JGA)
Causes ino/chrono/dromotropy (cAMP increases intracellular Ca2+) and in the JGA increases renin release.
B2 present in skeletal vascular and bronchial smooth muscle, liver and on cell membranes.
Causes vasodilation and bronchodilation, hepatic glycogenolysis, increases na+/k+ ATPase pump to increase intracellular K+
B3 present in fat, causes lipolyses and thermogenesis
MOA Epinephrine
B1- increased chrono/dromo/inotropy
B2- bronchodilation
Low doses B1&2>a1 decreased SVR
Higher doses A1>B1&2 increased SVR
Epinephrine dosages (adult)
Bradycardia/shock 2-20mcg/min
- UTD 1-40mcg
Anaphylaxis/bronchospasm 0.5mg IM, 50-100mcg IV/IO
Periarrest 10mcg IV/IO q2-3min
Intraarrest 1mg q3-5min
Epinephrine Formulary
CCP: 1mg/250mL= 4mcg/mL
OR
VCH: 3mg/250mL= 12mcg/mL
5mg/250mL= 20 mcg/mL
30mg/500mL= 60mcg/mL
Compatible with D5W, NS, LR, Ringer’s
Administer through central line or PIV for short-term
Pharmacokinetics of epinephrine
Onset: 30-90sec IM, 30sec IV
Peak: 4-10min IM, 3-5min IV
Duration: 5-10min
MOA of norepinephrine
“balanced inopressor”
A1: arteroconstriction (afterload/SVR), venoconstriction (SV/CO), and coronary artery constriction
A1>B1 and B2 effects
B1 increased contractility (and HR, but cancelled out by baroreflex-induced bradycardia)
B2 smooth vaso
Norepinephrine dosages (adult)
2-20mcg/min
*around 15mcg/min, consider layering in Vasopressin or other pressor
0.1mcg/kg/min up to 1mcg/kg/min
Norepinephrine indications
- Shock with hypotension refractory to fluid resuscitation (*vasodilatory)
- Cardiogenic shock with refractory hypotension
- Symptomatic bradycardia (? handbook)
Norepinephrine pharmacokinetics
Onset and peak immediate
Duration 1-2min
Norepinephrine infusions
4mg/250mL =16mcg/mL (single strength)
8mg/250mL = 32mcg/mL (double strength)
16mg/250mL= 64mcg/mL (quad strength)
central line access is preferred, can use peripheral IV for single strength through large bore
Compatible with NS, D5W, NS-D5W
Dobutamine MOA
Inodilator
(From AHA)
3:1 B1 to B2 affinity. Potent inotrope, with weaker chronotropy. Both A1 agonism and antagonism, with B2 stimulation, cause net effect of mild vasodilation. Higher doses cause vasoconstriction
Dobutamine indications
- Low cardiac index and low BP, but without hypotension (decompensated HF, cardiogenic shock, sepsis-induced myocardial dysfunction)
- Short-term management of patients with cardiogenic decompensation
MANY DRUG INTERACTIONS
Concomitant use with MAO inhibitors May cause prolonged HTN
Dobutamine dosages
2-20mcg/kg/min (max)
Dobutamine infusions
250mg/250mL= 1mg/mL (May appear pink due to oxidation, does not effect potency)
Compatible with N/S, D5W, NS-Dex combos, Ringer’s
Dobutamine pharmacokinetics
Onset: 1-10min
Peak: 10-20mins
Half-life: 2min
Dopamine MOA
Dose dependent:
Low: D1/D2 causes decreased SVR
Medium: additionally stimulates B1 (chrono and inotropy)
High: B1 and A1 increased SVR
Dopamine indications
- Symptomatic hypotension in the absence of hypovolemia (exp. Cardiogenic shock, bradycardia, sepsis, renal failure)
- post-arrest hypotension
- absence of more suitable agents