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Inotropes and Vasoactive Meds Flashcards

1
Q

what is inotrope?

A

medication that affects the strength of the hearts contraction (squeeze), positive or negative

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2
Q

what is a chronotrope?

A

medication that affects the hearts rate by impacting the neuronal stimulation of the heart, either increases or decreases

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3
Q

4 vasoactive gtts we primarily use for inotrope purposes

A

Epi, Dobutamine, Dopamine and Milrinone (primacor)

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4
Q

3 vasoactive gtts we primarily use as pressors

A

Norepi (Levo), Vasopressin (Vaso), Neosynephrine (NEO or phenylephrine)

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5
Q

what is an inodilator? what are the two main ones we use?

A

is an inotrope BUT vasodilates blood vessels instead of constricts (dobutamine and milrinone)

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6
Q

what do inodilators often need to be paired with?

A

a vasopressor!

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7
Q

what two vasopressors have no inotropic effects?

A

vasopressin and phenylephrine/Neo

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8
Q

what three meds are used for vasodilation but have no inotropic effect?

A

Nitroglycerin, nitroprusside, and nesintide

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9
Q

what are two arterial vasodilator gtts we use?

A

nitroprusside (nipride) and nicardipine (cardene)

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10
Q

what is the venous vasodilator gtt we use?

A

nitroglycerin

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11
Q

where are alpha 1, alpha 2, beta 1 and beta 2 receptors located? what happens with receptor activation?

A

alpha 1- vascular smooth muscle (action: vasconstriction of blood vessel walls, increases arterial pressure, causes sphincter contraction in GI and bladder)
alpha 2- brain and periphery (action: may lower BP/HR and alter NT function)
beta 1- primarily SA node, AV node and ventricular muscle in the heart (action: increase inotrope and chronotrope, and therefore CO)
beta 2- primarily in airway smooth muscle, some vascular smooth muscle (action: bronchodilatation of lungs and vasodilation of blood vessel walls)

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12
Q

MOA of epi

A

sympathomimetic catecholamine (produced by adrenal medulla in response to stress) that is nonselective alpha and beta

  • lower doses (under 5) primarily act on beta 1 receptors to increase contractility, thus increasing CO and myocardial oxygen consumption (alpha 1 and beta 2 cancel eachother out) and decrease SVR
  • At higher doses (>5), alpha 1 predominates meaning you increase CO but also increase SVR (primarily in splanchnic, renal, skin circulations)
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13
Q

7 ADRs/Contraindications of epi

A

tachycardia, arrhythmias, increases myocardial oxygen consumption, hyperglycemia (alpha effect- inhibits insulin secretion), splanchnic ischemia (alpha effect), lactic acidosis (beta- promotes lipolysis and glycolysis), necrosis with long term use

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14
Q

dosing and titration of epi

A 
CVICU: 1-10 mcg/min
start at 1 mcg/min, titrate up by 1 mcg 
usually 1-5 mcg/min for inotropic effect
5-10 more pressor effect
max 10-35 depending on refractory shock
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15
Q

3 indications for epi

A
  • 1ST LINE for borderline CO/CI after CPB in ABSENCE of tachycardia or ventricular ectopy
  • Stimulation of sinus node when intrinsic heart rate is low
  • resusciation during cardiac arrest or anaphylatic shock
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16
Q

onset of action for dobutamine

A

1-10 mins

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17
Q

dosing/titration of dobutamine

A

initial 0.5-2.5 mcg/kg/min, usual maintenance range 2-20 mcg/kg/hr, increase 1-4 mcg/kg/hr q 10 mins

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18
Q

onset of action for dopamine

A

5 minutes

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19
Q

dosing/titration of dopamine

A

range 1-10 mcg/kg/min
increase by 2.5 mcg/kg/min
*3-10 most optimal for CO, >10 to raise BP

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20
Q

onset of action for milrinone

A

5-15 minutes

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21
Q

dosing/titration for milrinone

A

usually given with a bolus of 50 mcg/kg over 10 mins along with gtt
range 0.125-0.5 mcg/kg/min
titrate by 0.25
(titrate every 4-6 hours, half life is 2-3 hrs)

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22
Q

onset of action for levo

A

seconds

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23
Q

dosing/titration for levo

A

range is 1-20 mcg/min

titrate by 1 mcg/min (can be 2-3)

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24
Q

dosing/titration for cardene

A

range 2-15 mg/hr
titrate up by 1 mg/hr
**once BP controlled try to decrease to 3 mg/hr

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25
onset of action for vaso
minutes
26
dosing/titration for vaso
range 0.01-0.06 units/min | titrate up by 0.01 unit
27
onset of action for neo
seconds
28
dosing/titration for neo
range is 25-200 mcg/min
29
onset of action for cardene
10 minutes
30
onset of action for nitroprusside
less than 2 minutes
31
dosing/titration for nitroprusside
range 0.5-3 mcg/kg/min, increase rate 0.5 mcg/kg/minq 3-5 mins
32
dosing/titration for NTG
10-300 mcg/min | titrate by 25
33
MOA for Levo
sympathomimetic catecholamine that acts on primarily alpha 1 receptors to INCREASE SVR/BP, with some beta 1 action to help contractility/HR * some increase in CO * tachycardia less of an issue bc reflex brady offsets beta 1 effects
34
onset of epi
minutes
35
MOA of dobutamine
synthetic catecholamine- INODILATOR - Beta 1 effect for inotropic/chronotropic effect primarily - beta 2 vasodilates - dose dependent increase in CO (inc stroke volume more than HR) but decrease in SVR and ventricular filling pressures - BP might not change d/t inc SV but lower SVR
36
3 Indications for dobutamine, indication from american heart association
- MOST useful when CO is marginal and there is a mild elevation in SVR - moderate pulmonary vasodilator (can improve RV function by lowering RV afterload - synergestic effect in improving CO by when used with milrinone (common in txp pts) - AHA: severe systolic dysfunction that is almost or has progressed to cardiogenic shock
37
3 ADRs of dobutamine
caution if pt already hypotensive, tachycardia, dysrhythmias
38
6 ADRs of dopamine
tachycardia, arrhythmias, accelerates AV conduction in a-fib, V/Q mismatch (inhibits peripheral chemoreceptors which depress ventilation), may worsen renal function (esp low dose), alters CNS neurotransmitters
39
indication for dopamine, consider it in what type of clinical situation
may be considered in low CO state esp when SVR low and BP marginal, but other inotropes usually preferred d/t ADRs -maybe considered in cardiogenic shock d/t beta and alpha effects can raise BP while providing inotrope support
40
MOA of dopamine
endogenous catecholamine, NT and precursor for NE synthesis dose 1-3: vasodilates renal, mesenteric, cerebral, and coronary vessels *no longer recommended for acute renal failure in low doses dose 3-10: cardiac beta 1 stimulation (inotropic/chronotropic effect) and beta 2 (similar to dobutamine) dose >10: alpha 1 activation to vasoconstrict caused by NE release (raises SVR, BP, and filling pressures)
41
MOA of milrinone
phosphodiesterase III inhibitor that improves CO by reducing SVR/PVR and coronary vascular resistance along with an inotropic effect (inc contract, decrease BP) **alpha agent might be required to maintain BP
42
2 indications for milrinone
- 2nd med class used for low CO state (if catecholamine isnt working enough or ADRs/tachy interfering) - pts with RV dysfunction esp with PVR (from pulm HTN from mitral valve disease or awaiting txp)
43
4 ADRs for milrinone
hypotension, ventricular arrhythmia, headache, dizziness
44
2 indications for levo
- marginally low CO state with LOW BP caused by LOW SVR (pt warms and vasodilates) * if CI is above 2.2-2.5, then pure alpha agent might be better - pressor of choice in septic shock
45
3 ADRs for Levo
over vasoconstriction can cause end organ ischemia/peripheral ischemia, reflex bradycardia, hyperglycemia
46
MOA for vaso
acts on vasomotor V1 and V2 receptors to INCREASE SVR (synthetic anti-diuretic hormone) * improvement in cardiac fxn is related to improvement in PERFUSION pressure * if CI is marginal, may induce mesenteric ischemia with use (inc intestinal and gastric vasoconstriction) * does NOT alter PA pressures much
47
4 ADRs for vaso
-may induce vasospasm of arterial grafts/IMA, cardiac/mesenteric ischemia, hyponatremia, inability to clear free water
48
2 indications for vaso
- Low BP that is poorly responsive to Levo or Neo - Vasoplegia (vasodilatory shock) after CPB associated with good CI that is NOT responsive to Levo/Neo * Levo PREFERRED when CI marginal
49
what type of pt do you NOT want to use dobutamine in?
heart failure caused by impaired ventricular filling (DIASTOLIC dysfunction, NEED MORE FILLING) *i think bc increased HR and decreasing afterload
50
MOA for cardene
CCB that acts as antihypertensive - inhibits calcium influx into vascular smooth muscle cells, which leads to non uniform vasodilation (greatested in cerebral circulation) - negative inotropic effect (does NOT effect sinus or AV node) - may inc CO a bit due to main decrease on SVR/some PVR
51
2 Indications for cardene
- acute control of HTN (postop or HTN emergencies | - acute ischemic stroke that require acute BP decrease for thrombolytic therapy
52
4 adrs for cardene and which condition is it contraindicated in?
reflex tachycardia, hypotension, facial flushing, headache | -contraindicated in aortic stenosis bc profound hypotension can occur
53
MOA for neo
PURE alpha receptor that produces widespread vasoconstriction (INC SVR) -constriction usually produces reflex bradycardia and dec in CO
54
2 Indications for neo
- increase SVR when pt is HYPOtensive with a GOOD CO | - reversal of hypotension from spinal anesthesia (but still need to be cautious due to further dec CO)
55
3 ADRs for neo
generalized hypoperfusion of vital organs, reflex braycardia, low CO
56
MOA and dose differences for NTG
organic nitrate with vasodilator, antiplatelet, and antianginal effects * converts to nitric oxide which promotes vascular smooth muscle relaxation and lower BP the more the dose is increased * Lower doses: venodilator more (under 50) and decreases cardiac filling pressures, doesnt change CO much * higher doses: arterial dilator, which then leads to increased CO
57
3 Indications for NTG
- augmenting CO in pts with acute decompensated HF - relieving CP with unstable angina - treating hypertensive emergencies
58
ADRs for NTG
hypotension bad for RHF pts, further BP dec in pts who have taken PDE5 inhibitor recently, inc intracranial pressure (inc cerebral blood flow), inc pulm shunting in ARDs pt
59
MOA for nitroprusside (NTP)
similar to NTG: converts to nitric oxide to promote vascular smooth muscle dilation (MORE arterial dilator than venous) *has potential to promote cyanide accumulation
60
2 indications for NTP
- ST management of acute decompensated HF - need rapid reduction in BP (HTN emergencies, acute aortic dissection) * not used much anymore due to cyanide toxicity
61
what should be given with NTP?
thiosulfate to limit cyanide toxicity
62
what is a vasopressor?
an agent that causes vasoconstriction, either venous or arterial (aka vasoconstrictors)
63
what is a common postop medication class that is a negative inotrope?
Beta blockers
64
what is a dromotropic agent?
increases the conduction speed through the heart and AV node
65
what is a lusitropic agent and an example?
an agent that increases diastolic relaxation often through a calcium mediated process, aka catecolamines
66
what is bathmotropy?
the principle of myocardial excitability, positive bathmotropy means the agent makes the myocardium easier to depolarize by bringing the resting membrane potential and depolarization threshold closer together negative bathmotropy means greater distance between the resting membrane potential and depol threshold
67
where are dopamine receptors located? what are its vasoactive effects when stimulated?
Primarily located in the brain to affect NT functions but can also affect vasculature to promote vasodilation and diuresis (dilation of renal arteries)
68
where is vasopressin 1 (V1) receptors located and what happens when activated?
located in vascular smooth muscle and platelets, promotes vasoconstriction (increase in SBP) WITHOUT impacting pulmonary vasculature **may promote thrombosis
69
where are V2 receptors located and what happens when you activate them?
located in renal collecting ducts and epithelial cells, activation leads to an antidiuretic effect
70
where are V3 receptors located and what does activation lead to?
Located on anterior pituitary, activation leads to release of corticotropin which stimulates release of corticosteroids from adrenal glands

CT Surgery (6 decks)

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