Positive Inotropes Flashcards

1
Q

Cardiogenic shock

A

MI
Myocarditis
Arrhythmias
Valvular disease
CMP

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2
Q

Obstructive shock

A

Tamponade
Tension pneumo
PE

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3
Q

Distributive shock

A

Sepsis
Anaphylaxis

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4
Q

What does CHF respond to?

A

preload reduction
afterload reduction
Improved contraction

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5
Q

Low cardiac output syndrome (LCOS) causes

A

in patients coming off CPB
A combo of:
Inadequate DO2
Hemoilution
Hypocalcemia, hypomagnesemia
Kaliuresis
Tissue thermal gradients
Variable SVR

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6
Q

LCOS risk factors

A

DM
Old age
Female
Pre op decreased EF
Long duration CPB

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7
Q

LCOS patho & treatment

A

Stunned hypocontractile myocardium in response to ischemia and reperfusion
Positive inotropes
Increase DO2 (SvO2 >70%)
Increase VO2 (arterial lactate <2mmol/L)

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8
Q

cAMP dependent vs independent drugs

A

Beta agonists, dopaminergic agonists, PDE inhibitors
Cardiac glycosides
Calcium

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9
Q

Inodilator drugs and effects

A

Isoproterinol
Dobutamine

Increase HR
Increased AV conduction
Decreased SVR/PVR
Variable myocardial o2 consumption

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10
Q

Inoconstrictor drugs and effects

A

NE, Epi, Dopamine
Increased SVR
Increased O2 consumption
Increased HR

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11
Q

When not to use inodilators?

A

Tachyarrhythmias

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12
Q

When not to use levo/NE?

A

Low CO
this will decrease perfusion and cause renal failure

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13
Q

When not to use Dig?

A

Hypokalemia, renal failure, bradycardia, drug interactions

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14
Q

Arrhythmogenic potenital

A

1- isoproterinol
Epi
DA
Dobutamine

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15
Q

How does cAMP work in the heart

A

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

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16
Q

Levo doses

A

CO increases at low doses, but high doses increase afterload and cause reflex brady

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16
Q

EPI receptors per dose

A

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

17
Q

Catecholamine complications

A

Tissue ischemia
increased myocardial consumption and work
Inrease cardiac arrhythmias
Enhance lipolysis and gluconeogenesis
Activate coagulation

18
Q

Isoproterinol effects

A

B1 B2
Increase hr, inotropy
Decrease SVR and DBP
Increased CO and decreased map
Bronchodilator

19
Q

Isoproterinol SE

A

Tachycardia
DBP hypotension
Increased O2 consumption
Arrhythmias
Dont use in pt with ischemic heart diseases

20
Q

Indications for isoproterinol

A

3rd degree HB
Bronchospasm during anesthesia
Decrease PVR in PH
Torsades, short QT syndrome

21
Q

Dobutamine

A

B1 B2 small A1
Not as strong as isoproterinol
No DA
Increases renal blood flow by increasing CO
Increases CO and HR
High doses may cause arrhythmias
Not useful in low SVR/low BP patients

22
Q

Renal dose Dopamine

A

0.5-2mcg/kg/min
Increased RBF, GFR, NA secretion, urine out put, but NOT RENAL PROTECTIVE

22
Q

How must dobutamine be prepared?

A

D5W not NS which will inactivate it

23
Q

DA and glucose, oxygen

A

inhibits release of insulin, causing hyperglycemia
Blunts respiratory drive

24
Q

PDE3 inhibitors effects

A

Stop the breakdown for cAMP
Increase CA influx
Increase sensitivity of contractile proteins to CA
Increased CO, although decreased SVR and PVR

25
Q
A
26
Q

PDE3 inhibitor drugs

A

Milrinone- no risk of thrombocytopenia, stronger than inamrinone, shorter half life, decreased dose in RF.
Inamrinone- increases SC and CI after CABG, more effective than DA, but equal to epi causes thrombocytopenia,

27
Q

Glucagon effects

A

Increases CI, HR, BP, decreases SVR and LVEDP

28
Q

When to use glucagon, SE

A

Cardiac failure caused by beta blockers
NV, hyperglycemia, increased PVR/ coronary perfusion

29
Q

Dig class and effect

A

Cardiac glycoside
Positive inotrope
- chronotropy
- dromotropy

30
Q

Dig MOA electrolytes

A

Block (slows) NAKATPase, which holds NA in and keeps K out
This reduced NA doesnt allow NA/C pump to work, keeping more CA inside cell

31
Q

When to use dig

A

A fib RVR
HF
Often used with diuretic and ace inhibitor

32
Q

Dig toxicity effects

A

> 3ng/ml
Hyperkalemia bc it cant go back into cell
Risk factors: hypokalemia, hypomagnesemia, hypoxemia, hypercalcemia, hypothyroid

33
Q

DIG toxicity presentation

A

Anorexia, nv
PVC
Atrial tachy w block
V fib and death
2nd degree type 2 block

34
Q

Dig toxicity treatment

A

K, Mag, O2
Phenytoin/lidocaine for arrhythmias
Atropine for low hr
BB for automaticity
pacing if HB

35
Q

Digibind

A

binds to dig in dig toxicity
eliminated by kidneys
levels are useless for several days so dont check

36
Q

Dig interactions

A

Amio
Verapamil
PPI
Reglan
many more

37
Q

Giapreza effects / se

A

Vasoconstriction and aldosterone release
interaction with acei and arbs
se: DVT so give prophylaxis blood thinner
tachycardia, delirium, thrombocytopenia

38
Q

Plan for low CO

A

Real 1st- optimize HR
1st- optimize preload
2nd- optimize afterload
3rd- optimize inotropy
Last- IABP, LVAD if low CO and ischemia persists

39
Q

Dig normal sign

A

Swoop in QRS

40
Q

Dig normal sign

A

Swoop in QRS