Positive Inotropes Flashcards

1
Q

Shock

A
  • peripheral circulatory failure resulting in underperfusion of tissues
  • decreased oxygen delivery to tissues
  • increased anaerobic metab (more acidic ph, increased lactate)
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2
Q

Septic Shock

A

Increased CI
Decreased PCWP
Decreased SVR

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3
Q

Hypovolemic Shock

A

Decreased CI
Decreased PCWP
Increased SVR

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4
Q

Cardiogenic Shock

A

Decreased CI
Increased PCWP
Increased SVR

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5
Q

CHF

A

end result of many conditions
(ischemic heart disease, HTN)
-decreased intracellular cAMP, downreg of beta receptors - impaired coupling of beta recept and AC

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6
Q

CHF responds to….

A

preload reduction, afterload reduction, improved contraction

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7
Q

LCOS: Risk Factors

A

Low cardiac output syndrome

risk factors: DM, increasing age, female, preop decreased LVEF, increased duration of CPB

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8
Q

Pts coming off CPB…

A

inadequate o2 delivery to tissue, hemodilution, mild hypocalcemia, hypomagnesemia, kaliuresis, tissue thermal gradients, variable levels of SVR

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9
Q

LCOS Patho

A
  • stunned myocardium (hypocontractile myocardium in response to ischemia and reperfusion)
  • Beta receptor down-regulation has been reported
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10
Q

LCOS Tx

A
  • positive inotropes to increase contractility of normal and stunned myocardium
  • HoTN, unlike CHF, responds poorly to vasodilators alone
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11
Q

LCOS Goal

A

in critically ill.. increase O2 delivery (keep SVO2 > 70%), increase O2 consumption (arterial blood lactate = 2 mmol/L)

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12
Q

Positive Inotropes: cAMP Dependent

A

Beta Agonists
Dopaminergic Agonists
Phosphodiesterase Inhibitors

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13
Q

Positive Inotropes: cAMP Independent

A

Cardiac Glycosides

Calcium

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14
Q

Positive Inotropes: Hemodynamic Effects

A

increased contractility with increased SV and often decreased LVEDP and V

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15
Q

Positive Inotropes: “Pure” Beta 1 Agonists

A

dobutamine, isoproterenol, inodilators

  • increased HR, AV conduction -decreased SVR and PVR (B2)
  • variable effect on MVO2
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16
Q

Positive Inotropes: Mixed Alpha and Beta Agonists

A

NE, Epi, dopamine - inoconstrictors

  • increased vascular resistance
  • increased MVO2
  • increased HR
17
Q

Positive Inotropes: Arrhythmogenic potential

A

Isoproterenol > Epi > DA > Dobutamine

18
Q

Phosphodiesterase III Inhibitors

A
  • slow metabolism of cAMP to 5’AMP –> increaseing intracellular cAMP concentration
  • increase Ca sensitivity of contractile proteins
  • Increase Ca influx
  • peripherally, arterial and venous vasodilation
  • increased CO
19
Q

Epinephrine - Low Dose

A

B2
B2 in skeletal muscle/peripheral –> decreased SVR, no change in MAP

Alpha 1 at skin, mucosa and hepatorenal

20
Q

Epi - Mid Dose

A

B1 increased HR, contractility, CO, automaticity

21
Q

Epi - High Dose

A

Alpha 1 tx dose, vasoconstrict all over but no significant effect on cerbral arterioles

*maintains myocardial and cerebral perfusion

22
Q

Digoxin toxicity

A

associated with decreased intracellular K
early s/s: NV, anorexia,

PVCs, mobitz 2 block

V-fib - most frequent cause of death

23
Q

Predisposing causes of dig tox

A
hypokalemia
hypomag
hypoxemia
hypercalcemia
hypothyroid
24
Q

Most common arrhythmia with dog tox…

A

paroxysmal atrial tachy with block

25
Q

1st step to treat dig tox

A

correct cause - give K, mag supplement, correct hypoxemia

26
Q

Drugs for dig tox

A

lidocaine/phenytoin for arrhythmia
atropine to increase HR
beta blocker- effect may be limited by pos inotropic effect
may need to pace

27
Q

Digibind

A

bind and decrease plasma concentrations of drug
eliminated by kidneys
do not check levels!