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
2
Q
septic shock
A
- increased CI
- decreased PCWP, SVR
3
Q
hypovolemic shock
A
- decrease CI, PCWP
- increase in SVR
4
Q
cardiogenic shock
A
- decrease in CI
- increase PCWP, SVR
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
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
7
Q
low cardiac output syndrome pathophysiology
A
- stunned myocardium
- hypocontractile myocardium in response to ischemia and reperfusion
- beta receptor down regulation
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
9
Q
cAMP dependent positive inotropes
A
- beta agonists
- dopaminergic agonists
- phosphodiesterase inhibitors
10
Q
cAMP independent positive inotropes
A
- cardiac glycosides
- Ca++
11
Q
pure beta-1 agonists
A
- dobutamine
- isoproterenol
- inodilators
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
13
Q
mixed alpha and beta inotropes
A
- NE, epi, dopamine
- inoconstrictors
14
Q
mixed alpha and beta agonists hemodynamic effects
A
- increased vascular resistance
- increased myocardial O2 consumption
- increased HR
15
Q
arrhythmogenic potential (in order)
A
- doubutamine < DA < epi < isoproterenol
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
17
Q
low dose epi effects
A
- stimulates beta-2
- decreases SVR and essentially vasodilates
18
Q
intermediate dose epi effects
A
- stimulates beta 1
- inotrope (increase HR, contractility, CO)
- increased automaticity
19
Q
high dose epi effects
A
- stimulate alpha 1
- increased aortic DBP
- reflex brady
- vasoconstrictor
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
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
