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Clinical Pharmacology 2 > Vasopressors + antirrhythmics > Flashcards

Vasopressors + antirrhythmics Flashcards

1
Q

CABG

A

coronary artery bypass grafting

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2
Q

APD

A

action potential duration

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3
Q

NSR

A

normal sinus rhythm

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4
Q

ERP

A

effective refractory period

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5
Q

What are medications that raise BP in cases of hypotension?

A

vasopressors –> constrict blood vessels, used in shock and critical care, increase SVR and CO

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6
Q

What are medications that treat abnormal heart rhythms?

A

anti-arrhythmics

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7
Q

catecholamiens vs D1 and D2

A

catecholamines - SNS w/ adrenergic receptors

D1 and D2 = renal vasodilation w/ dopaminergic receptors in kidney

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8
Q

What is first line for septic shock

A

vasopressor - norepinephrine (levophed)

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9
Q

What is used in anaphylaxis and ACLS?

A

vasopressor - epinephrine

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10
Q

What is used for various shock states w/ dose dependent effects?

A

vasopressor - dopamine

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11
Q

What is used in adjunt in septic shock?

A

vasopressor - vasopressin

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12
Q

What is used in hypotension w/ low HR?

A

, vasopressor - phenylephrine, pure a1 agonist

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13
Q

What are ex of inotropes?

A

dobutamine and milrinone

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14
Q

What’s the MOA of norepinephrine (levophed)

A

large increase of vasoconstriction and modest increase of CO
potent a-1 effect, modest B-1 effect
reflex bradychardia occurs w/ increase of MAP

prolonged infusion = direct cardiac toxicity

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15
Q

What are ADRs of norepinephrine (levophed)?

A

arrhythmias, bradycardia, peripheral (digital) ischemia, HTN w/ non-selective BB?

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16
Q

What are indications of epinephrine (adrenaline)?

A

treatment of anaphylaxis, ACLS (asystole/PEA, pulseless VT/VF), 2nd line in septic shock, management of HOTN after CABG

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17
Q

What’s the MOA of epinephrine?

A

potent B-1 agonist (cardiac stimulant) and moderate B-2 agonist (bronchodilation) and alpha 1 agonist

B effects > @ low doses
a effects > @ higher doses (vasoconstriction)

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18
Q

What are some effects of epinephrine (adrenaline)

A

low: high CO and low PVR
b-1 inotropic + chronotropic effects
B-2 and a-1 can offset
high: high CO and high PVR

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19
Q

What are ADRs of epinephrine?

A

ventricular arrythmias, severe HTN resulting in hemorrhage, cardiac ischemia, sudden death

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20
Q

What are indications for dopamine?

A

hemodynamic support + inotropic support in advanced HF

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21
Q

What’s the MOA of dopamine?

A

low - dopamine receptors
moderate - beta 1
high - alpha 1

often used as 2nd line to NE in patients w/ bradycardia and low risk of tachyarrythmias

severe hypotension cardiogenic shock

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22
Q

What are effects of dopamine?

A

low dose - dopaminergic (D1/D2 stimulation) to increase renal blood flow + urine output

intermediate - B-1 stimulation, high HR, CO, contractility (both ino and chrono)

high - vasoconstriction, high BP + HR, CO, contractility (a1 dominates)

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23
Q

What are ADRs of dopamine?

A

severe HTN (esp w/ nonselective beta blockers)
ventricular arrythmias
cardiac ischemia
tissue ischemia/gangrene in high doses

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24
Q

What are indications for ADH (vasopressin)?

A

diabetes inspidus, esophageal variceal bleeding, vasodilatory shock (2nd line), also can reduce dose of 1st line agent

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25
Q

What’s the MOA of ADH?

A

stimulates V1 and V2 receptors, less coronary cerebral vasoconstriction, increases systemic resistance and mean ABP, which could lower HR and CO

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26
Q

What are ADRs of ADH?

A

arrythmias, HTN, low CO, cardiac ischemia, severe peripheral vasoconstriction, rebound HOTN, hyponatremia

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27
Q

What’s the MOA of phenylephrine?

A

vasoconstriction w/ minimal inotrophy or chronotrophy
may lower stroke volume, so reserved for pts in who norepinephrine is contraindicated due to arrythmias or failed other therapies

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28
Q

When is phenylephrine recommended?

A

Not recommended septic shock UNLESS
1) when NE is associated w/ serious arrythmias
2) when CO is known to be high and BP low
3) salvage therapy when combo fail to achieve target MAP

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29
Q

what are ADRs of phenylephrine?

A

reflex bradycardia, HTN (nonselective BB), severe peripheral and visceral vasoconstriction tissue necrosis w/ extravasation (central line preferred)

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30
Q

In summary what are the clinical uses of vasopressors?

A

septic shock (NE)
cardiogenic shock (NE + dopamine)
anaphylaxis (epi)
HOTN w/ bradycardia

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31
Q

What are ADRs of vasopressors

A

tachycardia, arrythmias, peripheral ischemia, HTN
continuous BP monitoring, UO, titrate based on response

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32
Q

What are the indications for dobutamine?

A

medically refractory heart and failure and cardiogenic shock (Low CO), also pallative for end stage HF, cardiogenic shock, shor-term bridge to transplant
ACLS and echo

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33
Q

What’s the MOA of dobutamine?

A

primarily B-1 agonist, potent inotrope with high contractility, HR, CO

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34
Q

What are ADRs of dobutamine?

A

tachycardia, cardiac ischemia, proarrythmic that can occur at any dose

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35
Q

What does milrinone do?

A

phosphodieterase-3 enzyme inhibitor

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36
Q

What’s the recommended inotrope if patient is not on a beta blocker or not hypotensive?

A

milrinone

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37
Q

What’s milrinone’s MOA?

A

potent inotrope and vasodilator; increasing contractility and vasodilation

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38
Q

What are ADRS of milrinone?

A

proarrythmic (torsades de points), hypotension, cardiac ischemia

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39
Q

What are class I antiarrhythmics?

A

Na+ channel blockers

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40
Q

What are class I a antiarrhythmics?

A

disopyramide (norpace), quinidine, procainamide (pronestyl)

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41
Q

What are class Ib antiarrhythmics?

A

lidocaine (xylocaine), mexiletine (mexitil, fast dissociation)

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42
Q

What are class Ic antiarrhythmics?

A

flecainide (tambocor), propafenone (rhythmol, slow dissociation)

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43
Q

What are class II antiarrhythmics?

A

beta blockers

44
Q

What are examples of beta blockers?

A

metoprolol (toprol), atenolol (slow HR and conduction)

45
Q

What are class III antiarrhythmics?

A

K+ channel blockers

46
Q

What are examples of K+ channel blockers?

A

amiodarone (cordarone, pacerone), dofetilide (tikosyn, prolong action potential), ibutilide (corvert), sotalol (betapace)

47
Q

What are class IV antiarrhythmics?

A

non-dihydropyridine CCBs

48
Q

What are examples of class IV antiarrhythmics?

A

Diltiazem (cardizem), verapamil (Calan, slow AV conduction)

49
Q

What are class V antiarrhythmics?

A

adenosine (adenocard), digoxin (digitalis, lanoxin) paroxysmal SVT

50
Q

What’s the general MOA of class I antiarrhythmics?

A

block sodium entry into cell during depolarization – decreases rate of rise of phase 0 of action potential, also suppressing automaticity of Purkinje fibers + bundle of His

51
Q

What’s the MOA of class Ia drugs?

A

slow rate of rise of phase 0 by prolonging duration of AP and increasing effective refractory period – QRS and QT are affected, whole shift

52
Q

What class are these drugs: quinidine, procainamide, disopyramide?

A

class Ia drugs

53
Q

What class of drugs are indicated by: treatment of ventricular and atrial arrhythmias in patients w/o hx of ischemic heart disease?

A

class Ia drugs

54
Q

What are ADRs of Class Ia drugs?

A

increased arrhythmias including torsades, hypotension, tinnitus, headache, vision changes, thrombocytopenia, lupus-like syndrome**

55
Q

Is quinidine used in arrhythmias?

A

no - only for malaria bc of ADRs

56
Q

What’s common with procainamide IV?

A

hypotension

57
Q

What class are these drugs: lidocaine (IV), mexiletine (PO)?

A

class Ib drugs

58
Q

What’s the MOA of class 1b drugs?

A

shorten action potential duration and refractory period of Purkinje fibers – decrease duration of AP during phase 0 depolarization AND ventricular muscles

59
Q

What are the indications of class 1b drugs?

A

tx of ventricular arrhythmias (ventricular tachycardia, ventricular fibrillation, ventricular ectopy)

60
Q

What is lidocaine 2nd line to?

A

terminate v tach and vfib after defribillation (amiodarone is better) and only used in hospital/EMS setting and ineffective against atrial arrythmias

61
Q

What are ADRS of class 1b drugs?

A

CNS: confusion, vision change, drowsiness

62
Q

What class are these drugs: propafenone, flecainide

A

class 1c drugs

63
Q

What’s the MOA of class 1c drugs?

A

greatest effect on early depolarization and less on refractory period – blocks open Na channels + slow unbinding during diastole, QRS markedly prolonged during NSR

64
Q

What is this indicative of: supraventricular arrhythmias in patients WITHOUT structural heart disease, chronic suppression of ventricular arrhythmias?

A

class 1c drugs

65
Q

What are ADRs of class 1c?

A

better tolerated, increased arrythmias, CNS, increased mortality in patients w/ MI, CHF

66
Q

class 1a

A

complete shift

67
Q

class 1b

A

shorten AP

68
Q

class 1c

A

normal durations, longer depolarization, earliest and greatest effect on early depolarization

69
Q

What are these types of drugs: propanolol, atenolol, esmolol, metoprolol?

A

beta blockers

70
Q

What’s the MOA of beta blockers?

A

step 4 of conduction

cardiac B-1 receptor blockade + reduction in cAMP – results in modest reduction of Na and Ca currents + suppression of abnormal pacemakers –> cardiac membrane stabilization

conduction through SA and AV nodes = slowed –> refractory period is increased

PR interval is increased

71
Q

What are these indications of:
- prevent re-infarction + sudden death in patients w/ HF or MI
- treat exercise-induced arrythmias
- prevent occurence of AV node reentry
- control ventricular rate in patients w/ supraventricular tachyarrythmias by increasing AV node refractory period

A

beta blockers

72
Q

What are ADRs of beta blockers?

A

bronchospasm, cardiac depression, AV block, hypotension

73
Q

What type of drug are these; amiodarone, sotalol, dofetilide, ibutilide?

A

potassium channel blockers

74
Q

What’s the MOA of class 3 drugs, potassium channel blockers?

A

step 3 of cardiac depolarization

Prolong/delay repolarization

can prolong QT, and solatol is also a BB!

75
Q

What are indications for amiodarone?

A

DOC for acute treatment of ACLSVT and VF, slow ventricular rate + convert AF

76
Q

What PCB class 3 drugs are safe in concomitant HF?

A

amiodarone and dofetilide

77
Q

What are ADRs of PCB/class 3 drugs?

A

QT prolongation, torsades de points

78
Q

What two antiarrhythmics are shown to not increase mortality w/ long term use in patients w/ structural heart damage?

A

amiodarone and dofetalide

79
Q

What are adverse effects of amiodarone?

A

N/V, pulmonary fibrosis, hyper/hypothyroidism, corneal microdeposits, hepatotoxicity

80
Q

Can reactions be delayed in amiodarone?

A

yes - half life is 52 days

81
Q

What baseline do you need to chec for amiodarone?

A

PFT, CXR, thyroid panel, lipid profile, EKG, eye exam, CBC, BMP, neuro, derm
BMP - watching K+ and Mg2+ when on antiarrhythmic to avoid QT prolongation!

82
Q

What is your goal for K and Mg in amiodarone monitoring?

A

4 for K, 2 for Mg

83
Q

What are the two big drugs that interact with amidarone?

A

warfarin and digoxin, cyclosporine, phenytoin, statins– amiodarone inhibits 3A4, 1A2, 2D6, p-glycoprotein

84
Q

What class of antiarrhythmics are diltiazem and verapamil?

A

calcium channel blockers in group 4

85
Q

What’s the MOA of group 4 CCBs?

A

slow conduction through AV node and increase effective refractory period in AV node, blocking calcium in phase 0 and 2 of cardiac cycle, slowing conduction + prolong refractory period

prolongs PR interval

86
Q

What does this indicate: more effective against atrial than ventricular arrythmias, rate control in atrial fibrillation?

A

class IV - CCBs

87
Q

what are ADRs of CCBs/class 4?

A

cardiac - negative inotrope, AV node block, sinus arrest
non-cardiac - peripheral vasodilation, constipation

88
Q

REVIEW: What’s the MOA of class I antiarrhythmics?

A

block sodium channels to slow depolarization during aP

89
Q

REVIEW: What’s the MOA of class II antiarrhythmics?

A

block beta-adrenergic receptors to reduce HR and conduction velocity

90
Q

REVIEW: What’s the MOA of class III antiarrhythmics?

A

block potassium channels, prolong repolarization, increase refractory period

91
Q

REVIEW: What’s the MOA of class IV antiarrhythmics?

A

block calcium channels, slow AV node conduction, decrease HR

92
Q

REVIEW: What’s the use of class I antiarrhythmics?

A

ventricular arrythmias and atrial fibrillation (1a, 1c)

93
Q

REVIEW: What’s the use of class II antiarrhythmics?

A

afib, ventricular arrythmias, post-MI

94
Q

REVIEW: What’s the use of class III antiarrhythmics?

A

atrial and ventricular arrythmias, especially when others fail

95
Q

REVIEW: What’s the use of class IV antiarrhythmics?

A

afib and atrial flutter

96
Q

What must be corrected before initiation of antiarrhythmics?

A

K, Mg, Ca

97
Q

Can antiarrhythmics make some worse?

A

yes

98
Q

Do antiarrhythmics interact with other drugs?

A

yes

99
Q

What’s the MOA of adenosine?

A

stimulates adenosine receptors (a1) and decreases automaticity and AV node conduction – restoring normal sinus rhythm

100
Q

What are indications of adenosine?

A

paroxysmal SVT (acute)

101
Q

What are ADRs of adenosine?

A

flushing, dyspnea, AV nodal block, arrhythmia (PAC, PVC, afib)

102
Q

What’s the MOA of digoxin?

A

inhibits Na/K ATPase pump, increasing contraction, slowing conduction

Does not control HR in exercise

103
Q

Digoxin is ___ for AF or HF

A

2nd-3rd line

104
Q

What are ADRs of digoxin?

A

N/V, visual disturbances, AV block (drug level monitoring is required)! narrow therapeutic index

105
Q

What do these drugs work on:
- BBs
-CCBs
- adenosine
- digoxin
-antiarrhythmics (all except 1b)

A

AV nodal blocking drugs

106
Q

What do these drugs do:
- antiarrhtmics 1A, III
- tricyclic antidepressants
- quinolones
- phenothiazines
-haloperidol (haldol)
- ondansteron (zofran)

A

QT prolonging drugs

Clinical Pharmacology 2 (3 decks)

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