Positive Inotropes Flashcards
Cardiogenic shock causes
MI
Myocarditis
Arrhythmias
Valvular disease
CMP
Obstructive shock
Tamponade
Tension pneumo
PE
Distributive shock
Sepsis
Anaphylaxis
What does CHF respond to?
preload reduction
afterload reduction
Improved contraction
Low cardiac output syndrome (LCOS) causes
in patients coming off CPB
A combo of:
Inadequate DO2
Hemoilution
Hypocalcemia, hypomagnesemia
Kaliuresis
Tissue thermal gradients
Variable SVR
LCOS risk factors
DM
Old age
Female
Pre op decreased EF
Long duration CPB
LCOS patho & treatment
Stunned hypocontractile myocardium in response to ischemia and reperfusion
Positive inotropes
Increase DO2 (SvO2 >70%)
Increase VO2 (arterial lactate <2mmol/L)
cAMP dependent vs independent drugs
Beta agonists, dopaminergic agonists, PDE inhibitors
Cardiac glycosides
Calcium
Inodilator drugs and effects
Isoproterinol
Dobutamine
–
Increase HR
Increased AV conduction
Decreased SVR/PVR
Variable myocardial o2 consumption
Inoconstrictor drugs and effects
NE, Epi, Dopamine
Increased SVR
Increased O2 consumption
Increased HR
When not to use inodilators?
Tachyarrhythmias
When not to use levo/NE?
Low CO
this will decrease perfusion and cause renal failure
When not to use Dig?
Hypokalemia, renal failure, bradycardia, drug interactions
Arrhythmogenic potenital
1- isoproterinol
Epi
DA
Dobutamine
How does cAMP work in the heart
Drug bind Gs receptor on cell membrane
Gs actives adenylyl cyclase
Adenylyl cyclase converts ATP to cAMP
cAMP cause contraction via influx of CA from slow channels and causes ca sensitivity of CA regulatory proteins
cAMP broken down by PDDE3 to AMP
EPI receptors per dose
low- B2 1-2mcg/min vasodilation decreases SVR, though map stays same from mild increase in CO
Medium- B1 4mcg/min increase HR , inotropy, automaticity (PVCs)
high- A1 >4mcg/min