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vasopressor and anti arrhythmics Flashcards

1
Q

Medications used to raise blood pressure in cases of hypotension
o Medications that constrict blood vessels, raising blood pressure
o Used primarily in shock and critical care settings to manage hypotension
o Increase systemic vascular resistance (SVR) and/or cardiac output to improve perfusion to vital organs

A

vasopressors

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2
Q

Drugs used to treat abnormal heart rhythms (arrhythmias)
o Aim to restore normal sinus rhythm, control heart rate, or prevent arrhythmia recurrence

A

anti-arrhythmics

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3
Q

ability or property of muscle to shorten, or become reduced
in size, or develop increased tension

A

contractility

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4
Q

influencing the contractility of muscular tissue (strength of
contraction)

A

inotropic

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5
Q

drug causing constriction of blood vessels

A

vasopressor

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6
Q

affecting the rate of rhythmic movements such as the
heartbeat (rate of contraction)

A

Chronotropic

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7
Q

process of sodium excretion in the urine through the action of the kidneys

A

natriuresis

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8
Q

amount of venous return to the ventricle

A

preload

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9
Q

exert effect through α-1, β-1, & β-2

A

catecholamines

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10
Q

enhanced myocardial contractility

A

B-1 stimulation

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11
Q

vasodilation in vascular smooth muscle cells through
increased intracellular Ca2+ uptake

A

B-2 stimulation

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12
Q

smooth muscle contraction and an increase in systemic
vascular resistance

A

α-1 Stimulation

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13
Q

renal vasodilation through dopaminergic receptors in the kidney

A

D-1 and D-2 Stimulation

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14
Q

First-line for septic shock

A

Norepinephrine (Levophed)

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15
Q

Used in anaphylaxis and advanced cardiac life support (ACLS)

A

Epinephrine:

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16
Q

Used for various shock states, with dose-dependent effects

A

dopamine

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17
Q

Often adjunct in septic shock

A

vasopressin

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18
Q

Pure α1 agonist, used in hypotension with a low heart rate

A

Phenylephrine

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19
Q

inotropes

A

Dobutamine
Milrinone

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20
Q

Preferred vasopressor in septic shock and ACLS post-ROSC

A

Norepinephrine (NE) (levophed)

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21
Q

MOA:
o Large ↑ vasoconstriction and modest ↑ in CO
o Potent α-1 agonist effect (vasoconstriction) with modest β-1 agonist effect (increase
HR and contractility)
o Reflex bradycardia usually occurs in response to the ↑ MAP

A

Norepinephrine (NE) (levophed)

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22
Q

ADR of Norepinephrine (NE) (levophed)

A

Prolonged NE infusion can cause direct cardiac toxicity

Arrhythmias, bradycardia, peripheral (digital) ischemia, HTN with non-selective BB

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23
Q

Indications:
* Treatment of anaphylaxis, ACLS (asystole/PEA, pulseless VT/VF)
* 2nd-line agent in septic shock (after NE), management of hypotension after coronary artery bypast graft surgery (CABG)

A

Epinephrine (Epi) (Adrenaline)

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24
Q

MOA:
* Potent β-1 agonist (cardiac stimulation) and moderate β-2 (bronchodilation) and α-1 agonists
o β effects > @ low doses
o α-1 effects > @ higher doses (vasoconstriction)

A

Epinephrine (Epi) (Adrenaline)

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25
Q

Effects:
* Low doses: ↑ CO and ↓ PVR
* β-1 inotropic and chronotropic effects
* β-2 and α-1 effects offset
* High doses: ↑ PVR and ↑ CO (alpha predominates at higher doses)

A

Epinephrine (Epi) (Adrenaline)

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26
Q

ADR of Epinephrine (Epi) (Adrenaline)

A

ADRs:
* Ventricular arrhythmias
* Severe HTN resulting in cerebrovascular hemorrhage
* Cardiac ischemia
* Sudden cardiac death

High and prolonged doses can cause direct cardiac toxicity

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27
Q

Indications: hemodynamic support and inotropic support in advanced heart failure

A

dopamine

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28
Q

MOA:
* Variety of effects depending on the dose
* Low dose (dopamine receptors)
* Moderate dose (beta-1)
* High dose (alpha-1)
* Most often used as a 2nd-line alternative to NE in patients with
absolute or relative bradycardia and a low risk of tachyarrhythmias
* Severe hypotension cardiogenic shock

A

dopamine

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29
Q

Low-dose: (1-5 mcg/kg/minute): Dopaminergic (D1 and D2
stimulation) dopamine

A

↑ renal blood flow and urine output (direct effects on renal tubules)

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30
Q

Intermediate-dose: (5-10 mcg/kg/minute): β-1 stimulation dopamine

A

↑ HR, cardiac contractility, and CO (positive inotropic + chronotropic
effects)

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31
Q

High-dose: (>10 mcg/kg/minute) α-1 activity dominates + some β-1 activity dopamine

A

Vasoconstriction, ↑ BP + ↑ HR,
cardiac contractility, and CO

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32
Q

Dopamine
ADRs

A
  • Severe hypertension (especially in pts on nonselective β-blockers)
  • Ventricular arrhythmias
  • Cardiac ischemia
  • Tissue ischemia/gangrene (high doses or due to tissue extravasation)
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33
Q

Indications: diabetes insipidus, esophageal variceal bleeding, and vasodilatory shock
* Precise role in vasodilatory shock not fully defined
* Primarily used as a 2nd-line agent in refractory vasodilatory shock (usually septic shock )
* Also used to reduce dose of 1st-line agent

A

Vasopressin (ADH = antidiuretic hormone)

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34
Q

MOA:
* Stimulates V1 (agonist = constriction of vascular smooth muscle) and V2
receptors (water reabsorption in renal collecting duct)
* Causes less direct coronary and cerebral vasoconstriction than
catecholamines
* Increased systemic vascular resistance and mean arterial blood pressure— may see HR and CO decrease in response (PNS engages and increases vagal tone = less ADH

A

Vasopressin (ADH = antidiuretic hormone)

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35
Q

Vasopressin (ADH = antidiuretic hormone)
ADRs:

A
  • Arrhythmias
  • Hypertension
  • Decreased CO
  • Cardiac ischemia
  • Severe peripheral vasoconstriction causing ischemia (especially skin)
  • Rebound hypotension following withdrawal
  • Hyponatremia
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36
Q

Indications: (FYI): hyperdynamic sepsis, anesthesia-induced
hypotension

A

phenylephrine

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37
Q

MOA:
* Vasoconstriction with minimal cardiac inotropy or chronotropy (alpha-1 selective agonist)
* Potential disadvantage: may ↓ stroke volume, so reserved for pts in whom NE is contraindicated due to arrhythmias or who have failed other therapies

Not recommended for septic shock except in the following circumstances: 1) when
norepinephrine (preferred first-line agent) is associated with serious arrhythmias; 2)
when cardiac output is known to be high and BP persistently low; or 3) used as salvage therapy when the combination of vasopressor/inotropic agents and low-dose vasopressin fail to achieve target mean arterial pressure (MAP)

A

phenylephrine

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38
Q

Clinical use:
* Septic shock (NE)
* Cardiogenic shock (NE + dopamine)
* Anaphylaxis (Epi)
* HOTN with bradycardia

A

vasopressor summary

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39
Q

vasopressor ADR

A
  • Tachycardia, arrhythmias
  • Peripheral ischemia
  • HTN
    Monitoring: continuous BP monitoring, urine output, titrate based on clinical
    response
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40
Q

Indications:
* Medically refractory heart failure and cardiogenic shock (low cardiac output)
* Can be given for palliative measures for end-stage HF, cardiogenic shock, short-term bridge to
transplant
* Also used in ACLS (post-ROSC) and cardiac stress echo

A

dobutamine

41
Q

MOA:
* Primarily β-1 agonist, some β-2 and α-1 agonism
* Potent inotrope: ↑ Contractility, HR, and CO
* NOT a vasopressor, but an inotrope that causes vasodilation (↓SVR)
* Vasodilation at normal doses
* Vasoconstriction progressively dominates at higher infusion rates
* Significantly ↑ myocardial oxygen consumption (stress test)
* Tolerance can develop after just a few days of therapy
* Adrenergic receptors become desensitized and downregulated

A

dobutamine

42
Q

Dobutamine
ADRs:

A

Tachycardia
* Cardiac ischemia
* Proarrhythmic (Atrial Fibrillation, Ventricular Tachycardia)
* can occur at any dose

43
Q

Phosphodiesterase-3 Enzyme (PDE) inhibitor

Indications: Inotropic support in heart failure or in heart transplant recipients
* VERY useful if adrenergic receptors are downregulated or
desensitized (usually in chronic HF or after chronic β-agonist
administration)
* Recommended inotrope if patient is not on a beta blocker and not
hypotensive

A

Milrinone

44
Q

MOA:
* Potent inotrope and vasodilator: ↑ Contractility and vasodilation
* Effects similar to those of dobutamine but with a lower incidence of dysrhythmias
* Vasodilatory effects limit use in hypotensive pts

A

Milrinone

45
Q

Depolarization: voltage gated Na channels open

A

phase 0

46
Q

initial repolarization:
- voltage gated Na channels close
- voltage gated K channels begin to open

A

phase 1

47
Q

Plateu:
- voltage gated Ca channels open
- K efflux continues
- myocytes contraction

A

Phase 2

48
Q

Rapid repolarization:
- voltage gated Ca channels close
- slow voltage gated K channels open

A

phase 3

49
Q

resting permeability
- High K permeability

A

phase 4

50
Q

what medication is used at phase 0

A

Class 1: Na channel blocker

51
Q

what medication is used at phase 2

A

class 4: Ca channel blocker

52
Q

what medication is used at phase 3

A

class 3: K channel blocker

53
Q

what medication is used at phase 4

A

class 2: beta blocker

54
Q

the relative refractory period coincides with what wave

A

T wave

55
Q
  • Ia = Disopyramide (Norpace), Quinidine, Procainamide (Pronestyl)
  • Ib = Lidocaine (Xylocaine), Mexiletine (Mexitil, fast dissociation)
  • Ic = Flecainide (Tambocor), Propafenone (Rhythmol, slow
    dissociation)
A

Class I: Na+ channel blockers

56
Q

Metoprolol (Toprol), Atenolol (slow HR and
conduction)

A

Class II: β-blockers

57
Q

Amiodarone (Cordarone, Pacerone),
Dofetilide (Tikosyn, prolong action potential), Ibutilide (Corvert), Sotalol
(Betapace

A

Class III: K+ channel blockers

58
Q

Diltiazem
(Cardizem), Verapamil (Calan) (slow AV conduction

A

Class IV: non-dihydropyridine calcium channel blocker

59
Q
  • Drugs are characterized by ability to block sodium entry into
    the cell during depolarization
  • This decreases the rate of rise of phase 0 of the action potential
  • These drugs also suppress automaticity of the Purkinje fibers
    and bundle of His
A

Sodium Channel Blockers
Class I drugs are sodium channel blocker

60
Q
  • Drugs: Quinidine, Procainamide,
    Disopyramide
  • MOA: Slow the rate of rise of phase 0 by
    prolonging duration of action potential and
    increases the effective refractory period of
    the ventricle
  • Large block of both open Na & K Channels at
    normal heart rates, hence both QRS & QT
    affected
A

Class Ia Drugs

61
Q

Indications: Treatment of ventricular and atrial arrhythmias in patients without a history
of ischemic heart disease
ADRs:
* Increased arrhythmias including torsades
* Hypotension
* Tinnitus, headache
* lupus-like syndrome***
Quinidine: used primarily for malaria, but not arrhythmias due to ADRs, proarrhythmic &
better drug options available
Procainamide: Hypotension common with IV

A

Class Ia Drugs

62
Q

Drugs: Lidocaine (IV), Mexiletine (PO)
MOA: shorten action potential duration (APD) and refractory period of the Purkinje fibers
* These drugs decrease the duration of action potential during phase 0 depolarization in the Purkinje fibers (conducting fibers in the heart) and ventricular muscles**
* High affinity for open & inactivated Na channels

A

Class Ib Drugs

63
Q

Indications: treatment of ventricular arrhythmias (ventricular tachycardia,
ventricular fibrillation, and ventricular ectopy)
* Lidocaine: 2nd-line (vs Amiodarone) to terminate VTach and prevent VFib after defibrillation
* Used only in a hospital/EMS setting (IV only)
* Ineffective against atrial arrhythmias
ADRs: Central nervous system (CNS): confusion, change in vision,
drowsiness

A

Class Ib Drugs

64
Q

Drugs: Propafenone, Flecainide
MOA: greatest effect on the early
depolarization; less of an effect on the refractory period of the ventricle
* Blocks open Na channels & very slow unbinding during diastole, QRS markedly prolonged during NSR
- wide QRS

A

Class Ic Drugs

65
Q

Indications:
* Supraventricular arrhythmias in patients without structural heart
disease
* Also useful in chronic suppression of ventricular arrhythmias
ADRs: Better tolerated than Ia and Ib
* Increased arrhythmias
* CNS (dizziness, visual disturbances, headache) Increased mortality in patients with MI, can worsen H

A

Class Ic Drugs

66
Q

Drugs: Propranolol, Atenolol, Esmolol, Metoprolol
MOA: cardiac β-1 receptor blockade and reduction in cAMP
* Results in a modest reduction of both sodium and calcium currents
and suppression of abnormal pacemakers
* Rhythm stabilization MOA is unknown
* Results in cardiac membrane stabilization**
* Conduction through SA and AV nodes is slowed and the
refractory period is increased**

A

Class II Drugs: Beta Blocker

67
Q

Indications:
* Prevent re-infarction & sudden death in patients with heart failure or myocardial infarction
* Treat exercise-induced arrhythmias
* Prevent occurrence of AV node reentry (e.g. patients with paroxysmal supraventricular tachycardia)
* Control ventricular rate in patients with supraventricular tachyarrhythmias by
increasing the AV node effective refractory period
ADRs: Bronchospasm, cardiac depression, AV block**, hypotension

A

Class II Drugs

68
Q

Drugs: Amiodarone, Sotalol, Dofetilide, Ibutilide
MOA:
* Prolong/delay repolarization**
* Sometimes designated as potassium channel blockers, actually delay K efflux
* Drugs show complex pharmacological properties
* Classified together because all prolong APD without altering phase 0 depolarization or the resting membrane potential
Prolong QT (Amiodarone the least)
Sotalol also BB

A

Class III Drugs: Potassium Channel Blocker

69
Q

Indications:
* Amiodarone: Drug of choice for acute treatment of ACLS VT and VF; slow ventricular rate and convert AF
* Atrial Fibrillation
* Safe in concomitant heart failure***: amiodarone and dofetilide
ADRs:
* QT prolongation, Torsades de pointes **

Amiodarone and Dofetalide are the only two antiarrhythmics shown to not increase mortality with long term use in patients with structural heart damage
(post MI, HFrEF)

A

Class III Drugs

70
Q

toxicity of amiodarone (GI) adverse effects

A

nausea, vomiting

71
Q

toxicity of amiodarone (Pulmonary) adverse effects

A

pulmonary fibrosis

72
Q

toxicity of amiodarone (endocrine) adverse effects

A

hyperthyroidism, hypothyroidism

73
Q

toxicity of amiodarone (opthalmologic) adverse effects

A

corneal microdeposits

74
Q

toxicity of amiodarone (hepatic) adverse effects

A

hepatotoxicity

75
Q

half life of amiodarone

A

52 days

76
Q

what to check at baseline before amioderane

A
  • PFT, CXR, thyroid panel, lipid profile, EKG, eye exam, CBC, BMP,
    neuro and dermatologic exams
  • BMP watching for K+ and Mg++ when on an antiarrhythmic to avoid
    QT prolongation
    o K+ goal 4, Mg++ goal 2
77
Q

what does amiodarone inhibit

A

CYP3A4, 2C9, 1A2, 2D6, and p-glycoprotein

78
Q

Drug Interactions with Amiodarone

A

warfarin (reduce warfirn dose by 50%)

digoxin (reduce digoxin dose by 25-50%)

79
Q

Drugs: Diltiazem and Verapamil
MOA: slow conduction through the AV node and increase the effective
refractory period in the AV node
* Block the slow inward calcium current during phases 0 and 2 of the
cardiac cycle
* Slowing the inward calcium current, slows conduction and prolongs effective refractory period
* Inhibits SA and AV nodes thus prolonging PR

A

Class IV: Calcium Channel Blockers

80
Q

Indications: more effective against atrial than ventricular arrhythmias
* Rate control in atrial fibrillation

ADRs:
* Cardiac: negative inotrope, AV node block, sinus arrest
* Non-cardiac: peripheral vasodilation, constipation

A

Class IV Drugs

81
Q

Block sodium channels to slow depolarization during action potentia

A

class 1

82
Q

Block beta-adrenergic receptors to reduce heart rate and conduction
velocity

A

class 2

83
Q

Block potassium channels, prolong repolarization, and increase the
refractory period

A

class 3

84
Q

Block calcium channels, slow AV node conduction, and decrease heart rate

A

class 4

85
Q

Used for ventricular arrhythmias (Ia, Ic) and atrial fibrillation (Ia, Ic)

A

class 1

86
Q

Indicated for atrial fibrillation, ventricular arrhythmias, and post-myocardial
infarction

A

Class II (Beta-blockers

87
Q

Used for atrial and ventricular arrhythmias, especially when
other drugs fail

A

Class III (Potassium channel blockers

88
Q

Effective for atrial fibrillation and atrial flutter

A

Class IV (Calcium channel blockers

89
Q

Class I:
Ia ADR

A

Quinidine (tinnitus, headache, vision changes, thrombocytopenia, lupus-like syndrome)

90
Q

Class I:
Ib ADR

A

Lidocaine (CNS effects, confusion, seizures)

91
Q

Class I:
Ic ADR

A

Flecainide (pro-arrhythmic, especially in structural heart disease)

92
Q

Class II (Beta-blockers) ADR

A

Bradycardia, hypotension, bronchospasm

93
Q

Class III (Potassium channel blockers) ADR

A

QT prolongation, Amiodarone: Pulmonary fibrosis,
thyroid abnormalities, hepatotoxicit

94
Q

Class IV (Calcium channel blockers) ADR

A

Bradycardia, AV block, hypotension

95
Q

special considerations for anti arrhythmics

A
  • Electrolyte Imbalances: Potassium, magnesium, and calcium levels must be
    corrected before initiation
  • Pro-arrhythmic Effects: Some anti-arrhythmic medications can worsen arrhythmias
    in certain patients
  • Drug Interactions: Many anti-arrhythmic drugs interact with other medications (e.g.,
    amiodarone with warfarin, statins)
96
Q

MOA: Stimulates adenosine receptors (A1) in
heart, decreases automaticity and AV node
conduction
* Slows conduction time through the AV node,
interrupting the re-entry pathways through the
AV node, restoring normal sinus rhythm
Indications: paroxysmal SVT (acute)
* Half-life <10 seconds
ADR: Flushing, dyspnea, AV nodal block,
arrhythmia (can develop PACs, PVCs, Afib)

A

adenosine

97
Q

MOA:
* Partially inhibits Na+/K+-ATPase pump, thus increases contraction
* Parasympathetic action in AV node = slows conduction
* Does not control heart rate during exercise
Indications: 2nd -3rd line for AF or heart failure
ADRs:
* Toxicity: N/V, visual disturbances (blurred vision/halos), AV block
(Drug level monitoring required!)
* Narrow Therapeutic Index

A

Digoxin

98
Q

AV Nodal Blocking Drugs

A
  • Beta-blockers
  • Calcium channel blockers = Verapamil & diltiazem
  • Adenosine
  • Digoxin
  • Antiarrhythmics
  • All but class IB (lidocaine & mexiletine
99
Q

QT-Prolonging Drugs

A
  • Antiarrhythmics: 1A, III
  • Tricyclic antidepressants
  • Quinolones
  • Phenothiazines
  • Haloperidol (Haldol)
  • Ondansetron (Zofran)

pharm (3 decks)

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