Positive Inotropes Flashcards

1
Q

Shock definition

A
  • peripheral circulatory failure resulting in underperfusion of tissues
  • increase in anaerobic metabolism
  • more acidic pH
  • increased lactate
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2
Q

septic shock

A
  • increased CI
  • decreased PCWP, SVR
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3
Q

hypovolemic shock

A
  • decrease CI, PCWP
  • increase in SVR
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4
Q

cardiogenic shock

A
  • decrease in CI
  • increase PCWP, SVR
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5
Q

CHF effects on the body

A
  • decreased intracellular cAMP
  • downregulation of beta receptors
  • impaired coupling between beta receptors and adenylate cyclase
  • responds to preload reduction, afterload reduction and improved contractility
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6
Q

low cardiac output syndrome effects to the body

A
  • pts coming of CPB
  • have inadequate O2 delivery, hemodilution, hypocalcemia, hypomagnesemia, kaliuresis, variable levels of SVR
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7
Q

low cardiac output syndrome pathophysiology

A
  • stunned myocardium
  • hypocontractile myocardium in response to ischemia and reperfusion
  • beta receptor down regulation
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8
Q

treatment of LCOS

A
  • positive inotropes to increase the contractility
  • hypotension, unlike CHF responds poorly to vasodilators alone
  • goal to increase SvO2 > 70%, increase O2 consumption, lactate <2
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9
Q

cAMP dependent positive inotropes

A
  • beta agonists
  • dopaminergic agonists
  • phosphodiesterase inhibitors
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10
Q

cAMP independent positive inotropes

A
  • cardiac glycosides
  • Ca++
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11
Q

pure beta-1 agonists

A
  • dobutamine
  • isoproterenol
  • inodilators
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12
Q

hemodynamic effects of pure beta-1 agonists

A
  • increased HR
  • increased A-V conduction
  • decreased SVR and PVR (beta-2)
  • variable effect on myocardial O2 consumption
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13
Q

mixed alpha and beta inotropes

A
  • NE, epi, dopamine
  • inoconstrictors
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14
Q

mixed alpha and beta agonists hemodynamic effects

A
  • increased vascular resistance
  • increased myocardial O2 consumption
  • increased HR
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15
Q

arrhythmogenic potential (in order)

A
  • doubutamine < DA < epi < isoproterenol
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16
Q

how cAMP dependent positive inotropes work in the body

A
  • catecholamines bind to beta receptors and activate a membrane-bound guanine nucleotide bonding protein
  • this activates adenyl cyclase and generates cAMP
  • cAMP increases Ca influx via slow channels and increases Ca sensitivity
  • = increased force of contraction and velocity of relaxation
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17
Q

low dose epi effects

A
  • stimulates beta-2
  • decreases SVR and essentially vasodilates
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18
Q

intermediate dose epi effects

A
  • stimulates beta 1
  • inotrope (increase HR, contractility, CO)
  • increased automaticity
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19
Q

high dose epi effects

A
  • stimulate alpha 1
  • increased aortic DBP
  • reflex brady
  • vasoconstrictor
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20
Q

norepinephrine effects on the body

A
  • primarily alpha 1
  • beta 1 overshadowed by alpha 1
  • beta 2 effects are minimal
  • CO may increase at low doses but decrease at higher doses b/c of reflex brady and increased afterload
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21
Q

epi and NE compared

A
  • comparable increase in MAP
  • EPI produces a greater CO
22
Q

isoproterenol effects on the body

A
  • beta1, beta 2, (no alpha 1)
  • increase HR, contractility, cardiac automaticity
  • decreased SVR and DBP
  • net effect = increase CO and decreased MAP
  • bronchodilator
23
Q

isoproterenol side effects

A
  • tachycardia (increased myocardial O2 consumption)
  • diastolic hypotension
  • increased incidence of arrythmias
  • avoid in cardiogenic shock and ischemic heart disease
24
Q

isoproterenol uses

A
  • chemical pacemaker (after heart transplant or complete HB)
  • bronchospasm management after anesthesia
  • decrease PVR w/ pulm HTN and RV failure
25
Q

Dobutamine effects on the body

A
  • acts primarily on beta 1 with small beta 2 and alpha 1
  • dilates coronary vasculature
  • no dopaminergic receptor activity
  • increase renal blood flow by increase CO
  • can be inactivated in NSS (alkaline solutions) prepare in D5W
26
Q

D1 receptors - (like 1 & 5)

A
  • g couple - stimulate adenylate cyclase - activate cAMP
  • causes smooth muscle vasodilation
  • naturesis and diuresis
27
Q

D2 receptors (like 2,3,4)

A
  • g coupled - inhibits AC - inhibits cAMP
  • presynaptic: inhibit NE and promote vasodilation
  • attenuate the beneficial effects of DA on renal blood flow
28
Q

low dose dopamine effects

A
  • stimulates D1 (vasodilation in renal, mesentery, coronary, cerebral arteries)
  • inhibits aldosterone
  • increases RBF, GFR, Na excretion and UO)
29
Q

renal dose dopamine

A
  • not renal protective
  • tolerance develops after 2-48 hrs
  • blunts resp drive
  • impairs GI function
  • increases renin (counters effects)
  • immunosuppression and endocrine suppression
30
Q

intermediate dopamine effects (beta receptor effects)

A
  • increased myocardial contractility and CO without change in HR and BP
  • releases endogenous NE (arrythmias)
31
Q

high dose dopamine

A
  • alpha effects take over
32
Q

uses of dopamine

A
  • treatment of decreased CO, systemic BP
  • treatment of increased LVEDP
33
Q

dopamine side effects

A
  • interferes with ventilatory response to hypoxia
  • high doses inhibit insulin
34
Q

fenoldopam (corlopam)

A
  • selective D1 agonist, moderate alpha 2
  • decreases SVR and renal vasculature resistance resulting in decrease BP and increase LVEF and RBF
  • reserved for sever HTN
  • 10-100 x more potent than dopamine
35
Q

Fenoldopam uses

A
  • for severe HTN
  • do not bolus
  • not renal protective
  • can be given peripherally
36
Q

phosphodiesterase III inhibitors

A
  • cAMP dependent, slow the metabolism of cAMP to 5AMP, increasing cAMP concentrations, increase Ca sensitivity and influx of contractile proteins
  • peripherally, arterial and venous vasodilation
  • increase CO
37
Q

Inamrinone

A
  • dose-dependent increase in SV and CI
  • decreases SVR and PVR after CABG
  • more effective than dobutamine coming off CPB
  • with poor LV function , as effective as epi but combined are superior
38
Q

adverse reactions with inamrinone

A
  • thrombocytopenia
  • do not give with AS
  • arrythmias
39
Q

milrinone

A
  • inotropic similar to inamrinone but 10-20 x more potent without risk of thrombocytopenia
40
Q

glucagon

A
  • acts at a receptor other than beta to increase cAMP
  • increase CI, HR, BP
  • decreases SVR and LVEDP
  • increases coronary and pulm vascular resistance
41
Q

glucagon drug interactions

A
  • anticholinergic medications
  • vitamin K antagonists (increases INR)
  • 3-10 mg bolus for beta blocker toxicity
42
Q

digoxin

A
  • positive inotrope
  • negative dromotrope
  • negative chronotrope
  • made from foxglove plant
  • should only be used in pts with CHF and a-fib together
43
Q

How digoxin works

A
  • inhibits Na/K ATPase which causes reduced Ca removal
  • more Ca = stronger beat and less Na and K = slower conduction
44
Q

swooping ST segment with digoxin

A
  • does not mean anything other than the pt is on digoxin
45
Q

digoxin toxicity

A
  • plasma levels > 3ng/ ml
  • with CHF keep less than toxic, a-fib treat to results
  • associated with decrease in intracellular K
46
Q

predisposing causes of digoxin toxicity

A
  • hypokalemia
  • hypomagnesemia
  • hypoxemia
  • hypercalcemia
  • hypothyroid
47
Q

presentation of digoxin toxicity

A
  • early = anorexia (often complain of sick stomach)
  • PVCs
  • paroxysmal a-tach with block
  • mobitz type II A-V block
  • v fib
48
Q

treatment of digoxin toxicity

A
  • correcting predisposing causes (K, Mag, hypoxemia)
  • phenytoin and lido to suppress ventricular arrythmias
  • atropine to increase HR
  • beta blocker to increase automaticity
49
Q

Digibind

A
  • Fab (antibody fragments) bind to drug and decrease plasma concentrations and cardiac glycosides
  • fab- digitalis is eliminated by kidney
  • do not check levels (will be elevated but effects of toxicity will be gone)
50
Q

giapreza (angiotensin II)

A
  • for hypotension with septic shock or other disruptive shock
  • vasoconstriction and increases in aldosterone
  • metabolized by ACE and aminopeptidases
  • drug interaction with ACE inhibitor and ARBs
51
Q

side effects of giapreza

A
  • DVT and arterial thrombosis
  • should be on prophylactic treatment for blood clots