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Pharm 2 > Positive Inotropes > Flashcards

Positive Inotropes Flashcards

(51 cards)

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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

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

isoproterenol effects on the body

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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

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

isoproterenol uses

Study These Flashcards
A
  • chemical pacemaker (after heart transplant or complete HB)
  • bronchospasm management after anesthesia
  • decrease PVR w/ pulm HTN and RV failure
25
Dobutamine effects on the body
- 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
D1 receptors - (like 1 & 5)
- g couple - stimulate adenylate cyclase - activate cAMP - causes smooth muscle vasodilation - naturesis and diuresis
27
D2 receptors (like 2,3,4)
- g coupled - inhibits AC - inhibits cAMP - presynaptic: inhibit NE and promote vasodilation - attenuate the beneficial effects of DA on renal blood flow
28
low dose dopamine effects
- stimulates D1 (vasodilation in renal, mesentery, coronary, cerebral arteries) - inhibits aldosterone - increases RBF, GFR, Na excretion and UO)
29
renal dose dopamine
- not renal protective - tolerance develops after 2-48 hrs - blunts resp drive - impairs GI function - increases renin (counters effects) - immunosuppression and endocrine suppression
30
intermediate dopamine effects (beta receptor effects)
- increased myocardial contractility and CO without change in HR and BP - releases endogenous NE (arrythmias)
31
high dose dopamine
- alpha effects take over
32
uses of dopamine
- treatment of decreased CO, systemic BP - treatment of increased LVEDP
33
dopamine side effects
- interferes with ventilatory response to hypoxia - high doses inhibit insulin
34
fenoldopam (corlopam)
- 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
Fenoldopam uses
- for severe HTN - do not bolus - not renal protective - can be given peripherally
36
phosphodiesterase III inhibitors
- 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
Inamrinone
- 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
adverse reactions with inamrinone
- thrombocytopenia - do not give with AS - arrythmias
39
milrinone
- inotropic similar to inamrinone but 10-20 x more potent without risk of thrombocytopenia
40
glucagon
- 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
glucagon drug interactions
- anticholinergic medications - vitamin K antagonists (increases INR) - 3-10 mg bolus for beta blocker toxicity
42
digoxin
- positive inotrope - negative dromotrope - negative chronotrope - made from foxglove plant - should only be used in pts with CHF and a-fib together
43
How digoxin works
- inhibits Na/K ATPase which causes reduced Ca removal - more Ca = stronger beat and less Na and K = slower conduction
44
swooping ST segment with digoxin
- does not mean anything other than the pt is on digoxin
45
digoxin toxicity
- plasma levels > 3ng/ ml - with CHF keep less than toxic, a-fib treat to results - associated with decrease in intracellular K
46
predisposing causes of digoxin toxicity
- hypokalemia - hypomagnesemia - hypoxemia - hypercalcemia - hypothyroid
47
presentation of digoxin toxicity
- early = anorexia (often complain of sick stomach) - PVCs - paroxysmal a-tach with block - mobitz type II A-V block - v fib
48
treatment of digoxin toxicity
- correcting predisposing causes (K, Mag, hypoxemia) - phenytoin and lido to suppress ventricular arrythmias - atropine to increase HR - beta blocker to increase automaticity
49
Digibind
- 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
giapreza (angiotensin II)
- 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
side effects of giapreza
- DVT and arterial thrombosis - should be on prophylactic treatment for blood clots

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