Adjuncts 1: catecholamines, noncatecholamines, beta blockers, CCBs, alpha blockers, vasodilators, antiarrythmics Flashcards Preview

Anesthesia Pharm Oral Exam > Adjuncts 1: catecholamines, noncatecholamines, beta blockers, CCBs, alpha blockers, vasodilators, antiarrythmics > Flashcards

Flashcards in Adjuncts 1: catecholamines, noncatecholamines, beta blockers, CCBs, alpha blockers, vasodilators, antiarrythmics Deck (179):
1

Epinephrine: class

Endogenous catecholamine and nonselective adrenergic agonist at a1, a2, b1, b2

2

Epinephrine: MoA

Binds to adrenergic receptors, stimulating G-coupled proteins, adenylate cyclase, and cAMP.

Low doses = stimulation of beta2 = vasodilation, bronchodilation, decreased histamine release

Higher doses = stimulation of alpha1 = peripheral, renal, splanchnic vasoconstriction and decrease in bronchial secretions

3

Epinephrine: PK

Onset 1-2 mins IV
DOA 5-10 mins
E 1/2t = 30 secs
Small Vd = poor lipid solubility

4

Epinephrine: AE

Tachycardia and severe HTN
Arrhythmias
Cerebral hemorrhage
Hyperglycemia
Hypokalemia
Increased IOP
Periph vascular insufficiency

Headache, nervousness, tremor

5

Epinephrine: CI

Non-anaphylactic shock
Cardiac arrhythmias
Severe hypertension
Pheochromocytoma
Active labor
Cerebral or coronary artherosclerosis
Glaucoma
Renal insufficiency

6

Epinephrine: dosing

2-8mcg IV for hypotension
10mcg/kg for resuscitation

Continuous infusion:
1-2mcg/min beta2
4-5mcg/min beta 1
10-20mcg/min alpha 1 + beta

7

Norepi class:

Endogenous catecholamine
Direct acting nonselective adrenergic agonist
Alpha and B1 >>>>> B2

8

Norepi MoA:

Binds to alpha and beta1 adrenergic receptors, stimulating C-coupled proteins, adenylate cyclase, and cAMP.

Low doses = increased CO (inotrophy and chronotrophy) and increased blood pressure.

High doses = potent alpha1 effects outweighs beta --> arterial constriction and decreased vital organ blood flow.

9

Epinephrine: metabolism

COMT and MAO in the blood, liver, kidneys; metabolites excreted in urine

10

Norepi: PK

Rapid onset
Limited DOA
E1/2t = 2.5 mins

11

Norepi: metabolism

COMT and MAO in the blood, liver, kidneys; metabolites excreted in urine

12

Norepi: AE

Usually a result of intense vasoconstriction...

HTN
Severe bradycardia
End organ ischemia
Hemorrhagic stroke or ischemia of cerebral vessels
Renal vasoconstriction + oliguria

Anxiety and headache

13

Norepi: CI

HTN
Extreme hypovolemia
Mesenteric or PVD

14

Norepi: dosing

0.01-0.1mcg/kg/min or 4-16mcg/min

15

Isoproterenol: class

Synthetic catecholamine
Selective beta adrenergic receptor agonist (beta1 >> beta 2)

16

Isoproterenol: MoA

Stimulates beta adrenergic receptors, stimulating g-coupled protein receptors, further stimulating adenylate cyclase and cAMP within the cell.

Beta 1 = increases inotropy and chronotropy of the heart

Beta 2 = Vascular, GI, pulmonary and uterine relaxation

17

Isoproterenol: PK

Immediate onset
DOA 5-10mins
E1/2t = 2.5-5mins

18

Isoproterenol: metabolism

COMT in liver and lungs
40-50% unchanged in urine

19

Isoproterenol: AE

Tachycardia, dysrhythmias
MI and increased O2 consumption
Decreased CBF
Peripheral vasodilation and hypotension

20

Isoproterenol: CI

HAT
Hypersensitivity
Angina/CAD
Tachycardia

21

Isoproterenol: dosing

0.5 - 10 mcg/min

22

Dobutamine: class

Synthetic catecholamine (analog of isoproterenol)
Direct acting selective beta 1 adrenergic receptor agonist with some beta 2 activity at clinical doses

23

Dobutamine: MoA

Binds with beta1 adrenergic receptors, stimulating G-coupled proteins, adenylate cyclase, and cAMP within the cell causing influx of Ca+ and promoting cardiac muscle contractility

24

Dobutamine: PK

Onset 1-2mins
Peak effect in 10 mins

25

Dobutamine: metabolism

COMT and MAO in blood, liver, kidneys, GI tract
Metabolites excreted in urine

26

Dobutamine: AE

Dyspnea
Tachycardia, SVT
Thrombocytopenia and platelet inhibition
Phlebitis
Down regulation of beta receptors after 3 days of tx = tolerance

Fever, headache, nausea
Paresthesia

TOXICITY = anorexia, NV, tremor, head, SOB, angina, chest pain, anxiety

27

Dobutamine: CI

Hypersensitivity
Hypovolemia
CAD without CHF
Caution in pregnancy

28

Dobutamine: dosing

Start at 0.5-1mcg/kg/min; titrate every few minutes to 2-20mcg/kg/min

Max dose 40mcg/kg/min

29

Dopamine: class

Endogenous catecholamine
Alpha, beta adrenergic, and dopaminergic receptor agonist

30

Dopamine: MoA

Low doses – agonize dopaminergic 1 receptors in coronary, renal, and mesenteric vascular smooth muscle cells to stimulate G-CP, AC, cAMP

Medium doses – agonize beta 1 adrenergic receptors in cardiac myocytes to increase contractility = +inotrope = ↑CO and HR

High doses – agonize alpha1 in GU, GI, heart, liver and vascular smooth muscle

31

Dopamine: PK

Rapid onset

32

Dopamine: metabolism

MAO and COMT
Beta hydroxylated to norepinephrine, then methylated to epinephrine in liver and plasma
Eliminated in urine

33

Dopamine: AE

Limb ischemia if extravasated
Tachycardia, angina, palpitations
Dyspnea
Increased IOP
Hyperglycemia

Headache, N/V

34

Dopamine: CI

Right heart failure d/t increase pulm art pressure
MAOIs
Sulfa allergy
V-fib
Pheochromocytoma
Cocaine use (exaggerated response)

35

Dopamine: dosing

0.5 to 2mcg/kg/min low dose
2-5mcg/kg/min medium dose
>10mcg/kg/min large dose

36

Vasopressin: class

Exogenous antidiuretic peptide and vasopressor

37

Vasopressin: MoA

Stimulates V1 receptors on vascular smooth muscle, glomerular mesangial cells, and vasa recta causing potent vasoconstriction

Stimulates V2 receptors on basolateral cell membrane of renal collecting ducts to ↑ water reabsorption and constricts glomerular efferent arteriole to maintain GFR

38

Vasopressin: PK

Onset = nasal 1hr
DOA = nasal 3-8hrs

39

Vasopressin: metabolism

Metabolized by tissue peptidases
Rapid oral inactivation by trypsin
E1/2t 10-20min

40

Vasopressin AE:

Coronary artery vasospasm, angina, MI
Vasoconstriction and HTN
Increased peristalsis, N/V, and abd pain
Decreased PLTs
Tremor, headache, fever, diaphoresis

41

Vasopressin: CI

Hypersensitivity
Caution w/ NSAIDs, carbamazepine (inc AVP effect)

42

Vasopressin: dosing

Refractory cardiac arrest: 40 units IV push
Esophageal varicies: 20 units over 5 mins
Hemorrhagic/septic shock: 0.04 units/min
DI: 100-200mU/hr IV

43

Ephedrine: class

Synthetic non-catecholamine
Indirect alpha 1 and beta 2 agonist
Direct beta 1 agonist

44

Ephedrine: MoA

Indirectly: increases NE release from post ganglionic SNS nerve, activating receptors
Directly: binds to receptors and activates G protein, activates or intracellular enzyme adenylate cyclase to cAMP and phospholipase C

45

Ephedrine: PK

Rapid onset
DOA 1 hr
E1/2 t 3hrs

46

Ephedrine: metabolism

COMT, though inefficiently; 40% unchanged in the urine

47

Ephedrine: AE

Tachyphylaxis
Arrhythmias
HTN
MI
CNS stim

48

Ephedrine: CI

Hypersensitivity
Severe HTN
Arrhythmias
CHF
Glaucoma
MAOIs
Cocaine use (be cautious)

49

Ephedrine: dosing

5-25 mg IV

50

Phenylephrine: class

Synthetic non-catecholamine
Selective alpha 1 adrenergic agonist

51

Phenylephrine: MoA

Binding to alpha1 receptor causes direct stimulation of g-protein coupled receptor, increases adenylate cyclase, and cAMP, leading to an influx of calcium on systemic VENOUS vascular smooth muscle and vasoconstriction

52

Phenylephrine: PK

Onset

53

Phenylephrine: AE

Reflex bradycardia
Hypertension and decreased CO d/t increased afterload
Decreased renal, splanchnic, cutaneous blood flow
Decreased UO
Metabolic acidosis

Anxiety, HA, nervousness, weakness, paresthesia
Rebound nasal congestion

54

Phenylephrine: CI

Hypersensitivity
Glaucoma
Severe HTN and tachycardia
Arrythmias
Caution in elderly, heart blocks, HTN, bradycardia

55

Phenylephrine: dosing

50-200mcg IV bolus Q5mins

20-180mcg/min to start with maintenance at 10-60mcg/min

56

Esmolol: class

Selective beta 1 adrenergic antagonist

57

Esmolol: MoA

Reversibly binds to beta 1 adrenergic receptor antagonists to inhibit the binding of NE, EPI, and other beta agonist, preventing the stimulation of G-coupled protein receptors, adenylate cyclase, and cAMP

Slows SA rate and conduction through the AV node and decreases contractility, reducing cardiac O2 demand

58

Esmolol: PK

Onset: 30-60 sec
DOA = 10-15mins
E1/2t = 9 mins
High Vd
55% PB

59

Esmolol: metabolism

Plasma esterases and excretion in the urine

60

Esmolol: AE

Severe bradycardia
Hypotension
Heart block
CHF and pulmonary edema
POI d/t propylene glycol

Syncope/dizziness
Headache

61

Esmolol: CI

Hypersensitivity
CHF
Concurrent CCB (= complete heart block)
Sick sinus syndrome
Severe hypotension
HR dependent
Asthma and COPD (in high doses)
Pregnancy

62

Esmolol: dosing

5-10mg IV Q3-5mins to total dose of 80mg
300-500mcg/kg/min

63

Labetalol: class

Beta 1, beta 2, alpha1 adrenergic antagonist

64

Labetalol: MoA

Reversibly binds to beta1, beta2, alpha1 adrenergic receptor antagonists to inhibit the binding of NE, EPI, and other beta agonist, preventing the stimulation of G-coupled protein receptors, adenylate cyclase, cAMP.

Slows SA node rate (beta 1), slows conduction through the AV node (beta 1), decreases contractility (beta 1), and causes peripheral, cerebral, and coronary vasodilation (alpha 1)

65

Labetalol: PK

Onset = 3-5 mins
Peak effect 5-10mins (redose 5-10mins)
E1/2t = 5-8hrs
Vd 7L/kg
50% PB

66

Labetalol: metabolism

Hepatic microsomal enzymes
Eliminated in urine 50% - fecal 50%

67

Labetalol: AE

Bronchospasm*
Fluid retention*
Hypoglycemia*
Severe bradycardia
Hypotension
Heart block

Syncope/dizziness
Headache

68

Labetalol: CI

Hypersensitivity
Asthma/COPD
Severe CHF
Concurrent CCB use (= complete heart block)
Severe hypotension or bradycardia
Sick sinus syndrome

69

Labetalol: dosing

5-10mg IV Q5-10mins up to 300mg total

70

Metoprolol: class

Selective beta 1 adrenergic antagonist

71

Metoprolol: MoA

Reversibly binds to beta 1 adrenergic receptor antagonists to inhibit the binding of NE, EPI, and other beta agonist, preventing the stimulation of G-coupled protein receptors, adenylate cyclase, and cAMP

Slows SA rate and conduction through the AV node and decreases contractility, reducing cardiac O2 demand

72

Metoprolol: PK

Onset Rapid
E1/2 life = 3-7hrs
12% PB

73

Metoprolol: metabolism

Hepatic metabolism
Renal excretion

74

Metoprolol: AE

Bradycardia
Cardiac failure/asystole
Dyspnea
Heart block
Peripheral edema
Arterial insufficiency

75

Metoprolol: CI

Hypersensitivity
Sick sinus syndrome
Concurrent CCB use (= complete heart block)
Asthma and COPD (in high doses)
HR dependent pts

76

Metoprolol: dosing

1.25-5mg IV Q2-5mins to max of 15mg

77

Propranolol: class

Beta 1 and beta 2 adrenergic antagonist

78

Propranolol: MoA

Reversibly binds to beta 1 adrenergic receptor antagonists to inhibit the binding of NE, EPI, and other beta agonist, preventing the stimulation of G-coupled protein receptors, adenylate cyclase, and cAMP.

Slows SA rate and conduction through the AV node and decreases contractility, reducing cardiac O2 demand.

Causes peripheral, cerebral, and coronary vasodilation.

79

Propranolol: PK

Vd 4L/kg
90%PB
E1/2t = 4hrs

80

Propranolol: metabolism

1st pass effect & pulmonary uptake
Active metabolite: hydroxypropanolol
Excreted in the urine

81

Propranolol: AE

Bronchospasm*
Hypoglycemia*
Severe bradycardia
Severe hypotension
Heart block
Rebound tachycardia with rapid withdrawal

Syncope/dizziness

82

Propranolol: CI

Hypersensitivity
Asthma/COPD
Heart block
Concurrent CCB (= complete heart block)
PVD
DM
Pregnancy

83

Propranolol: dosing

0.25-0.5mg IV titrate to 1mg/min IV

84

Nifedipine: class

Dihydropyridine calcium channel antagonist

85

Nifedipine: MoA

Competitive binds to calcium channels in vascular smooth muscle to maintain them in the INACTIVATED CLOSED STATE, preventing the influx of calcium through slow L-type voltage gated Ca++ channels , preventing the contraction of vascular smooth muscle cells

86

Nifedipine: PK

Onset 1-3 mins
Peak 1-3 hrs
E1/2t = 3-7 hrs
90% PB

87

Nifedipine: metabolism

Hepatic CYP450 metabolism
Renal excretion

88

Nifedipine: AE

Reflex tachycardia
Hypotension
MI d/t decreased afterload
Skeletal muscle weakness

Flushing
Vertigo
HA

89

Nifedipine: CI

Hypersensitivity
Heart failure
Hypotension
Concomitant with grapefruit juice

90

Nifedipine: dosign

5-15mcg/kg

91

Verapamil: class

Non-dihydropyridine calcium channel antagonist
Class IV antiarrythmic

92

Verapamil: MoA

Competitively binds to calcium channels in cardiac muscle tissues to maintain them in the INACTIVATED CLOSED STATE, preventing the influx of calcium through slow L-type voltage gated Ca++ channels in cardiac muscle cells.

Primarily inotropic/chronotropic effects, not blood pressure.

93

Verapamil: PK

Onset

94

Verapamil: metabolism

CYP 450 enzymes
Active metabolite: norverapamil
70% unchanged in urine

95

Verapamil: AE

Heart failure
Peripheral edema
Increased K+ with blood products

Gingival hyperplasia
Dizziness

96

Verapamil: CI

Hypersensitivity
Renal failure
Wide QRS V-tach
Heart failure
WPW, SSS, bradycardia, or heart block (conduction abnormalities)

97

Verapamil: dosing

2.5-5mg IV over 2 mins

Then 5-10mg in 15 to 30 mins as needed

Max 20mg

98

Diltiazem: class

Benzothiazipine antiarrythmic

99

Diltiazem: MoA

Competitively binds to calcium channels in cardiac muscle tissues, and ARTERIOLAR vascular smooth muscle tissue maintaining them in INACTIVATE CLOSED STATE, preventing the influx of calcium through slow L-type voltage gated Ca++ channels and preventing the contraction of both vascular smooth muscle and cardiac muscle cells.

100

Diltiazem: PK

Onset

101

Diltiazem: metabolism

1st pass effect
CYP450 and 30% unchanged in the urine

102

Diltiazem: AE

Bradycardia
AV block
Heart failure
Edema

HA, flushing
Dizziness/syncope

103

Diltiazem: CI

Hypersensitivity

104

Diltiazem: dosing

SVT 0.25mg/kg over 2 mins + 0.35mg/kg prn

Pheo 3-10mcg/kg/min

105

Nifedipine: drug interactions

Potentiates NMB
Decreases anesthetic reqs
Use w/ BBs can cause heart block

106

Verapamil: drug interactions

Decreases anesthetic reqs
Use w/ BBs can cause heart block

107

Diltiazem: drug interactions

Potentiates NMB
Use w/ BBs can cause heart block

108

Phenoxybenzamine: class

Long acting, non-selective alpha adrenergic receptor antagonist

109

Phenoxybenzamine: MoA

Irreversibly binds to the alpha 1 and alpha 2 adrenergic receptors preventing the binding of NE, Epi, and other alpha agonists, preventing the stimulation of G-coupled proteins, adenylate cyclase, and cAMP.

Blocks alpha mediated vasoconstriction.

It also antagonizes Ach, Histamine, 5HT

110

Phenoxybenzamine: PK

Slow onset – Prodrug
60mins to peak
E1/2t 24 hrs

111

Phenoxybenzamine: metabolism

Hepatic metabolism
Renal and biliary excretion

112

Phenoxybenzamine: AE

Reflex tachycardia
Hypotension
Seizures
Palpitations
Sedation with chronic use (alpha 2)
Hypoglycemia

Flushing/syncope
Impotence
Nasal stuffiness
Dry mouth

113

Phenoxybenzamine: CI

Hypersensitivity
Hypotension
Hypovolemia

114

Phenoxybenzamine: dosing

10mg BID up to total 120mg/day oral – started 2-3 weeks pre op

115

Phentolamine: class

Short acting, non-selective alpha adrenergic receptor antagonist

116

Phentolamine: MoA

Competitively but REVERSIBLY binds to alpha 1 and alpha 2 adrenergic receptors, preventing the binding of NE, Epi, and other alpha agonists, preventing the stimulation of G-coupled proteins, adenylate cyclase, and cAMP.

Blocks alpha mediated vasoconstriction.

117

Phentolamine: PK

Onset =2-5 mins
DOA = 10-15 mins
E1/2L = 19 mins

118

Phentolamine: metabolism

Hepatic metabolism
10% excreted unchanged in urine

119

Phentolamine: AE

Tachycardia – reflexive
Severe hypotension
Arrhythmias
MI
Hypoglycemia

Dizziness
Flushing
Impotence
Nasal stuffiness
Abd cramps

120

Phentolamine: CI

Hypersensitivity
CAD, MI
Pregnant moms
Renal impairment
PUD

121

Phentolamine: dosing

30-70 mcg/kg IV to decrease BP from transient stimulation

Max 20mg

Extravasation = 10mg injected into affected site.

122

Prazosin: class

Selective alpha 1 adrenergic antagonist

123

Prazosin: MoA

Competitively binds to alpha 1 adrenergic receptors preventing the stimulation of G-coupled proteins, adenylate cyclase, and cAMP causing vasodilation of arterial and venous vasculature.

Leaves the inhibiting effect of alpha 2 activity on NE release intact = less likely to have reflex tachycardia

124

Prazosin: PK

Peak 3 hrs
E1/2 t = 3-4 hrs

125

Prazosin: metabolism

Hepatic metabolism, elimination via bile and feces NON RENALLY!!

126

Prazosin: AE

Hypotension
Fluid retention
Anticholinergic effects
N/V
Palpitations
Drug-induced lupus
Hepatotoxicty

Flushing/dizziness
Syncope
HA
Dry mouth
Nasal congestion

127

Prazosin: CI

Hypersensitivity
BB use (refractory hypotension)
Pregnant

128

Prazosin: drug interactions

Additive effects with diuretics/other BP meds

129

Prazosin: dosing

1mg PO at bedtime (max daily 20mg in divided doses)

130

Clonidine: class

Selective alpha 2 adrenergic antagonist

131

Clonidine: MoA

Inhibits sympathetic outflow from the medulla = decreased HR and contractility and vasomotor tone.

Enhance antinociceptive state by inhibiting release of spinal substance P.

Inhibit central thermoregulatory control to decrease vasoconstriction and shivering.

Also affects the function of K+ channels in the CNS = making cell hyperpolarized = decreased anesthetic requirements

132

Clonidine: PK

Onset 30-60mins
Peak 60-9mins
DOA 8 hrs PO
E1/2t 9-12hrs
30% PB
2L/kg

133

Clonidine: metabolism

50% metabolized in liver, 50% excreted unchanged

134

Clonidine: AE

Bradycardia
Heart failure
Hepatotoxicity
Sedation
Postural hypotension
Rebound hypertension with abrupt withdrawal
Sodium and water retention

Dry mouth
Skin rash
Impotence

135

Clonidine: CI

Pregnant women
Prior to surgery
Hypersensitivity

136

Clonidine: dosing

0.2mg-0.3mg/day

Epidural and SAB = 150-450mcg

137

Hydralazine: class

Direct acting vasodilator

138

Hydralazine: MoA

Activates guanylate cyclase which leads to membrane hyperpolarization, K+ channel activation, inhibition of calcium release from SR in vascular smooth muscle.

Can trigger reflexive tachycardia.

139

Hydralazine: PK

IV onset 5-20mins
Peak 15-20mins
E1/2t = 4 hrs (4x in renal dz)
E1/2L = 100hrs d/t strong binding to smooth muscle
90% PB

140

Hydralazine: metabolism

Metabolized in the liver with extensive first pass effect

141

Hydralazine: AE

Anemias, hepatotoxicity

Increased ICP, head ache, fever, chills, anxiety, disorientation, depression and coma

RA, lupus like syndrome, cramps, weakness, tremors, neuritis

Tachycardia, angina, orthostatic hypotension, dizziness, palpitations,

Nasal congenstion, dyspnea

Anorexia, NV, diarrhea, constipation, ileus

Impotence, difficult micturition

142

Hydralazine: CI

Hypersensitivity
Dissecting aortic aneurysm
CAD
Mitral valve rheumatic heart disease

Prolonged onset should be considered before redosing

143

Hydralazine: dosing

2.5 - 20 mg IV Q4hrs

144

Nitroglycerin: class

Organic nitrate and venodilator

145

Nitroglycerin: MoA

Generates Nitric Oxide to stimulate production of cGMP to cause peripheral and smooth muscle vasodilation.

Increased venous capacitance decreases the preload to the right side of the heart = decreased right and left end diastolic pressure = decreased myocardial demand.

146

Nitroglycerin: PK

IV peak

147

Nitroglycerin: AE

Reflex tachycardia
Tachypnea
Increase in ICP with decreased intracranial compliance
Increased bleeding time
Dizziness, lightheadedness, syncope
N/V

148

Nitroglycerin: CI

Hypertrophic obstructive cardiomyopathy
Severe aortic stenosis
Hypotension, shock or MI with low left ventricular filling pressures
Increased ICP
Glaucoma
Severe anemaia
Cardiac tamponade
Restrictive cardiomyopathy or pericarditis

149

Nitroglycerin: metabolism

Metabolism results in nitrate metabolite capable of producing methemoglobin by oxidation of ferrous ion in hgb

150

Nitroglycerin: dosing

5-200mcg/min IV

151

Milrinone: class

Phosphodiesterase inhibitor vasodilator

152

Milrinone: MoA

Selectively inhibits phosphodiesterase III which is a heart specific enzyme responsible for degradation of cAMP, which increases calcium and thus increases contractility and inotropic effects. Increased cAMP also works in vascular smooth muscle to cause vasodilation and decrease peripheral vascular resistance. This all increases cardiac output.

153

Milrinone: PK

Onset 5-15mins
Peak after 5 mins
E1/2time = 2.5hrs
Vd = 0.4L/kg
70% PB

154

Milrinone: metabolism

80% unchanged in the urine

155

Milrinone: AE

Cardiac dysrhythmias, ventricular arrhythmias, and supraventricular arrhythmias
Hypotension
Angina
Headaches
Hypokalemia, tremor, thrombocytopenia

156

Milrinone: CI

Hypersensitivity
Acute MI

157

Milrinone: dosing

50mcg/kg IV over 10mins + 0.375mcg/kg/min maintenance infusion

158

Adenosine: class

Antiarrythmic, endogenous nucleoside consisting of adenine and pentose sugar

159

Adenosine: MoA

Adenosine acts on adenosine A1 receptors in the cardiac conduction system that are linked to acetylcholine activated G-coupled potassium channels (Kach). This leads to slowing of cardiac conduction tissue, slowing SA node conduction, and a delay in AV node conduction.

160

Adenosine: PK

E1/2 life = 10 sec; immediate onset, must be IV pushed very fast

161

Adenosine: metabolism

Intracellular enzyme metabolism. No hepatic/renal involvement.

162

Adenosine: AE

Headache, dizziness, parasthesia
Palpitations, chest pain
Hypotension
Dyspnea
Chest pressure
Numbness

163

Adenosine: CI

Hypersensitivity
2nd or 3rd degree heart block
SSS without pacer
Bronchospastic and restrictive lung disease
(not effective in afib, aflutter, VT)

164

Adenosine: dosing

SVT: 6mg IV, if not effective give 12mg, if not effective give 18mg

Controlled hypotension: 220mcg/kg/min

165

Amiodarone: class

Class III antiarrhythmic (with Class I, II, IV effects)
Benzofurane derivative containing iodine
Atrial and ventricular dysrhythmic

166

Amiodarone: MoA

Alters lipid membrane where ion channels are located, particularly the K+ channels responsible for repolarizations

Also blocks Na+ and Ca++ channels, as well as alpha/beta receptors

167

Amiodarone: PK

Onset – IV is rapid
Vd 66L/kg
96% PB
E1/2t = 29days
Duration after d/c therapy = 7-50days

168

Amiodarone: metabolism

CYP450 microsomal enzymes with biliary excretion
Active metabolite: DEA

169

Amiodarone: AE

Hypotension
Bradycardia
AV block, prolonged QTc and VT, torsades,
Decreased response to catecholamines
Pulm fibrosis, alveolar pneumonitis, ARDS (2% of pts)
Hyper/hypothyroidism, photosensitivity

170

Amiodarone: CI

Hypersensitivity
Cardiogenic shock, bradycardia, 2nd or 3rd degree heart block
Pregnancy

171

Amiodarone: drug interactions

Inhibits CYP450 enzymes = increased conc of warfarin, procainamide, digoxin

Fentanyl = cardiac arrest, bradycardia, hypotension

172

Amiodarone: dosing

A-flutter, Stable VT/SVT: 150mg IV over 10 mins, 1 mg/min over next 6 hrs, then 0.5 mg/min over next 18hrs

Pulseless VT/VF: 300mg IVP, then 150mg IVP, then gtt

173

Digoxin: class

Antiarrythmic
Cardiac glycoside

174

Digoxin: MoA

Directly inhibits Na+/K+/ATPase pump, which increases Na+ in cardiac myocytes, which decreases Ca++ outflow by Na+/Ca++ pump, which increases available calcium for cardiac muscle contractions.

Also decreases sympathetic tone and increases vagal tone to slow conduction through SA and AV nodes

175

Digoxin: PK

Onset = 5-30mins IV
Peak 1-5 hrs
E1/2life = 30-48hrs
Vd 7L/kg
25% PB

176

Digoxin: metabolism

Hepatic metabolism
50% excreted by kidneys unchanged.

177

Digoxin: AE

EKG changes: prolonged PR interval, ST depression, T wave changes
Dysrhythmias
Heart block

Blurred vision
NV, diarrhea, headache, fatigue

178

Digoxin: CI

Vfib, v-tach, heart block
IHSS
Renal impairment (decrease dose)
Hypokalemia, hypomagnesemia or hypercalcemia can lead to toxicity

179

Digoxin: dosing

Loading dose = 0.75-1.5mg PO or 0.5-1.0mg IV
Maint dose = 0.125-0.5mg PO or 0.25mg IV

Therapeutic level 0.5-2.0ng/mL