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PHCT MIDTERMS > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

Any drug or agent that affects the function of the heart and circulatory system, specifically blood vessels.

A

Cardiovascular Drugs

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2
Q

Affects heart and blood vessels.

A

● Anti-arrhythmic Drugs
● Beta-adrenergic Blockers
● Vasodilators
● Clonidine and Related Drugs

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3
Q

occur once the atria are filled with blood

A

P wave

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4
Q

came from firing of signals from the SA node

A

P wave

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5
Q

Time peaks for the signal to travel from SA node to AV node.

A

PR interval

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6
Q

Firing of AV node.

A

QRS complex

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7
Q

Aka ventricular depolarization

A

QRS complex

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8
Q

aka Atrial depolarization

A

P wave

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9
Q

Last phase of ventricular depolarization

A

S wave

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10
Q

Aka Plateau (due to its flat area)

A

ST segment

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11
Q

aka ventricular repolarization

A

T wave

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12
Q

Opening of Na channel causing Na influx

A

PHASE 0

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13
Q

Aka Rapid depolarization phase

A

PHASE 0

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14
Q

Early fast repolarization

A

PHASE 1

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15
Q

Closure of Na channel; opening of K and Cl channel

A

PHASE 1

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16
Q

Sustained balance between inward movement of Ca (influx) and outward movement of potassium (efflux)

A

PHASE 2

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17
Q

Ca channel opens and K channel remain open

A

PHASE 2

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18
Q

Rapid repolarization

A

PHASE 3

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19
Q

Ca channel closes, but K channel continues to be opened.

A

PHASE 3

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20
Q

Diastole or resting state

A

PHASE 4

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21
Q

Plateau

A

PHASE 2

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22
Q

Interfere with Na channel (affect the Phase 0 by decreasing this)

A

Sodium channel blockers

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23
Q

All channels close

A

PHASE 4

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24
Q

Class I – Na+ Channel Blockers block what phase?

A

Phase 0

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25
Q

Class III – K+ Channel blockers block what phase?

A

Phase 2 & 3

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26
Q

Class IV – Ca++ Channel blockers block what phase?

A

Phase 2

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27
Q

Aka Membrane stabilizing agent

A

Type I anti-arrhythmic drugs

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28
Q

Phase of action potential that can cause homeostasis

A

PHASE 2

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29
Q

Generally act by inhibiting fast sodium channels responsible for initial cardiac cell depolarization and impulse conduction.

A

Type I anti-arrhythmic drugs

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30
Q

In overdose, all Type I drugs have the potential to markedly depress

A

myocardial automaticity, conduction, and contractility

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31
Q

Class Ia

A

✓ Disopyramide
✓ Quinidine
✓ Procainamide

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32
Q

Class Ib

A

✓ Lidocaine
✓ Mexeletine
✓ Tocainide

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33
Q

Class Ic

A

✓ Moricizine
✓ Flecainide
✓ Propefanone

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34
Q

Depress the FAST sodium dependent channel, slowing phase zero of the cardiac action potential.

A

Class Ia agents

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35
Q

Prolong Action Potential Duration

A

Class Ia

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36
Q

Diastereoisomer of Quinine

A

Quinidine

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37
Q

Quinidine moa

A

● sodium channel blocker
● alpha receptor blocker
● anticholinergic action

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38
Q

Adr of Quinidine

A

Cinchonism

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39
Q

An N-metabolite, which is a highly reactive metabolite

A

Procainamide (Pronestyl®)

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40
Q

Procainamide moa

A

sodium channel blocker, neuromuscular blocker

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41
Q

Adr of Procainamide

A

GI upset, SLE-like symptoms

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42
Q

Disopyramide (Norpace®) is a vagolytic causing (CUD)

A

urinary retention, constipation, and dry mouth

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43
Q

Commonly used for suppression of acute and chronic supraventricular and ventricular arrhythmias

A

Quinidine and procainamide

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44
Q

has ganglionic-and neuromuscular-blocking activity

A

Procainamide

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45
Q

has alpha-adrenergic receptor blocking activity

A

Quinidine

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46
Q

Toxic dose of Quinidine

A

1 g

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47
Q

Toxic dose of Procainamide

A

5 g

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48
Q

Toxic dose of Disopyramide

A

1 g

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49
Q

Quinidine and disopyramide (both are anticholinergic) can cause:

A

Dry mouth
Dilated pupils (Mydriasis)
Delirium
Flushed skin

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50
Q

All type Ia agents can produce

A

● Seizures
● Coma
● Respiratory arrest

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51
Q

Cinchonism

A

tinnitus, vertigo, deafness, visual disturbances

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52
Q

indicated for patients unresponsive to sodium bicarbonate therapy

A

Cardiac pacemaker

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53
Q

Active metabolite of procainamide

A

N-Acetylprocainamide (NAPA)

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54
Q

Weak sodium channel blocking ability

A

Class Ib

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55
Q

Analog of lidocaine

A

Tocainide

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56
Q

Adr of Tocainide

A

GIT upset, Paresthesia, Tremor, Ataxia

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57
Q

A congener of lidocaine that is resistant to first pass hepatic metabolism.

A

Mexiletine

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58
Q

Adr of Mexiletine

A

Ataxia, Blurry vision

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59
Q

an aminoacyl amide synthetic derivative of cocaine

A

Lidocaine

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60
Q

It is an antidysrhythmic and local anesthetic agent

A

Lidocaine

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61
Q

Lidocaine (Xylocaine) is metabolized to two active metabolites

A

monoethyl glycine xylidide (MEGX) and glycine xylidide (GX)

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62
Q

Strong sodium channel blocking ability but no effect on action potential

A

Class Ic

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63
Q

Both sodium and potassium channel blocking effect.

A

Flecainide

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64
Q

was withdrawn from US and Canadian markets in Dec of 1991 due to increased mortality in the cardiac dysrhythmia trial

A

Encainide

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65
Q

analogue of lysergic acid, is at least 10 times more potent than procainamide.

A

Encainide

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66
Q

Fatal adr of Encainide

A

cardiac dysrhythmia

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67
Q

related to propranolol

A

Propafenone

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68
Q

Common adr of Class Ic drugs

A

● Dizziness
● Blurred vision
● Ventricular arrhythmias

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69
Q

Overdose of Class Ib may cause:

A

● sedation
● confusion
● coma
● seizures
● respiratory arrest
● cardiactoxicity

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70
Q

TOCAINIDE AND MEXILETINE Side effects may include:

A

● Dizziness
● Paresthesias
● Tremor
● Ataxia
● GIT disturbance

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71
Q

FLECAINIDE, ENCAINIDE, PROPAFENONE, MORICIZINE Side effects

A

● Dizziness
● Blurred vision
● Headache
● GIT upset
● Ventricular arrhythmias

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72
Q

Overdose of Class Ic causes:

A

● Hypotension
● Bradycardia
● AV block
● Asystole
● QRS and QT intervals are prolonged

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73
Q

Widely used for the treatment of hypertension, angina pectoris, migraine headaches, and glaucoma

A

Type II anti-arrhythmic drugs or Beta-adrenergic blockers

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74
Q

Repolarization is also delayed, resulting in a prolonged QT interval that may be associated with ______________

A

polymorphic ventricular tachycardia

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75
Q

Selective Beta-blockers (BEAM)

A

Betaxolol, Bisoprolol, Esmolol, Acebutolol, Atenolol, Metoprolol

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76
Q

Beta-blockers with Membrane Stabilizing Activity (anesthetic-like effect) (PALM)

A

Propranolol, Pindolol, Acebutolol, Labetalol, Metoprolol

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77
Q

Beta-blockers with ISA

A

Acebutolol, Bisoprolol, Carteolol, Pindolol, Penbutolol

78
Q

Beta-blockers with mixed alpha and beta blocking effect

A

Labetalol, Carvedilol

79
Q

NONSELECTIVE BETA-BLOCKERS

A

Nadolol, Propranolol, Pindolol, Sotalol, Timolol

80
Q

Further depresses myocardial contractility and conduction

A

Propranolol

81
Q

Because of its lipid solubility, it enhances brain penetration and can cause seizures and coma

A

Propranolol

82
Q

Other agents with beta-agonist activity that may cause hypertension

A

Pindolol

83
Q

Prolongs QT interval in a dose-dependent manner

A

Sotalol

84
Q

May cause torsades de pointes and ventricular fibrillation

A

Sotalol

85
Q

Common treatment of torsades de pointes

A

Isoproterenol, magnesium, overdrive pacing

86
Q

fatal polymorphic ventricular tachycardia

A

Torsades de pointes

87
Q

Effect of beta-blocker overdose most common in patients with preexisting asthma or chronic bronchospastic disease

A

Bronchospasm

88
Q

T/F: Beta-blockers may cause hypoglycemia and hyperkalemia

A

TRUE

89
Q

There are no clear guidelines, but beta-blocker ingestion of only _____ times the therapeutic dose should be considered potentially life-threatening in all patients.

A

2-3

90
Q

Bradycardia and hypotension resistant should be treated with _________________

A

Glucagon, 0.1-0.3 mg/kg IV bolus

91
Q

Dose of glucagon given in patients with bradycardia and hypotension caused by beta-blockers overdose

A

0.1-0.3 mg/kg

92
Q

Wide complex conduction defects caused by membrane-depressant poisoning may respond to ____________

A

Hypertonic sodium bicarbonate 1-2 meq/kg

93
Q

Torsades de pointes, polymorphous ventricular tachycardia associated with QT prolongation resulting from sotalol poisoning can be treated with _______________

A

Isoproterenol infusion, magnesium, or overdrive pacing

94
Q

Blocks potassium channels to prolong the duration of the action potential and the effective refractive period.

A

Type III anti-arrhythmic drugs or Potassium channel Blockers

95
Q

A quaternary benzylammoniumcompound for treating lidocaine-refractory arrhythmias

A

Bretylium

96
Q

Major toxic side effect of Bretylium is _____________ caused by inhibition of catecholamine release

A

hypotension

97
Q

Rapid intravenous injection of Bretylium may cause

A

transient hypertension, nausea, and vomiting

98
Q

A non-competitive beta-adrenergic blocker, which may explain its tendency to cause bradyarrhythmias.

A

Amiodarone

99
Q

may release iodine and chronic use has resulted in altered thyroid function

A

Amiodarone

100
Q

Amiodarone may release

A

Iodine

101
Q

An iodinated benzofuran with similar structure to thyroxine an iodinated benzofuran with similar structure to thyroxine

A

Amiodarone

102
Q

Amiodarone has side effects of

A

● Photosensitivity
● Hyperthyroidism (up to 16%)
● Pulmonary fibrosis
● Skin pigmentation (blue nail coloration)
● Corneal deposits

103
Q

Amiodarone has a very long half-life of ______

A

40-50 days

104
Q

Chronic use of Amiodarone may cause:

A

– Ventricular arrhythmias
– Bradyarrhythmias (sinus arrest, AV block)
– May aggravate cardiac failure
– Pneumonitis
– Pulmonary fibrosis
– Photosensitivity dermatitis
–Corneal deposits

105
Q

Dilate peripheral arterioles to lower blood pressure

A

VASODILATORS

106
Q

Alpha-adrenergic blocking agents

A

VASODILATORS

107
Q

Reflex sympathetic response results in tachycardia and occasionally cardiac arrhythmias

A

VASODILATORS

108
Q

Vasodilators that have been in clinical practice since the 1940’s

A

phenoxybenzamine, phentolamine, tolazaline

109
Q

1st selective α1 inhibitor was introduced in the early 1970’s

A

Prazosin

110
Q

newer α1 selective agents (DITUT)

A

Doxazosin, indoramin, terazosin, trimazosin, and urapidil

111
Q

Prazosin and other newer α1 specific agents are associated with ___________

A

little or no reflex tachycardia

112
Q

Acute overdose of Vasodilators may cause:

A

● Headache
● Nausea
● Dizziness
● Weakness
● Syncope
● Orthostatic hypotension
● Warm flushed skin
● Palpitations
● Lethargy and ataxia in children
● Cerebral and myocardial ischemia
● Acute renal failure

113
Q

long-acting vasodilators (TD)

A

Terazosin and doxazosin

114
Q

Terazosin and doxazosin are long-acting and eliminated 60% in feces; thus, repeat-dose __________________ may enhance their elimination.

A

activated charcoal

115
Q

Type IV drugs or calcium channels (type IV) uses

A

● Anti-hypertensive
● Anti-arrythmic
● Anti-angina

116
Q

Non- dihydropyridine CCB

A

Verapamil, Diltiazem

117
Q

Dihydropyridine CCB (-dipine)

A

amlodipine, felodipine, isradipine, nicardipine, nifedipine, nisoldipine

118
Q

4 CARDIOVASCULAR EFFECTS OF CCB

A

● Peripheral vasodilatation
● Negative chronotropy (decreased heart rate)
● Negative inotropy (decreased cardiac contractility)
● Negative dromotropy (decreased cardiac conduction)

119
Q

decreased free fatty acid utilization by the myocardium produce

A

hyperglycemia, lactic acidosis, and depressed cardiac contractility

120
Q

may be helpful to determine heart size and presence or absence of congestive heart failure or ALI

A

chest radiograph

121
Q

If bowel obstruction is suspected, ______________ is recommended.

A

abdominal radiography

122
Q

Cardiac biomarkers, such as ___________, may help differentiate drug-induced bradycardia from ischemic causes.

A

troponin I

123
Q

Empiric use of glucagon in adults may be warranted for patients with an unknown CCB overdose presenting with bradycardia or hypotension.

A

5-15 mg IV

124
Q

T/F: Consider using calcium only if a witness confirms a calcium channel blocker overdose

A

TRUE

125
Q

Calcium may induce _______________ in digoxin overdose, which can present with similar findings

A

fatal arrhythmias

126
Q

If profound hypotension fails to respond to fluid resuscitation, administer a _______________

A

dopamine or norepinephrine drip

127
Q

If the patient deteriorates to cardiac arrest from a calcium channel blocker overdose, perform _________

A

prolonged cardiopulmonary resuscitation (CPR)

128
Q

may be tried if hemodynamically significant bradycardia occurs

A

Atropine

129
Q

Mid-dose dopamine (_______ mcg/kg/min) may improve heart rate and contractility.

A

5-10

130
Q

T/F: Administer IV calcium gluconate (up to 4 g) or IV calcium chloride (1g) and/or glucagon (5-10 mg) if hypotension persists.

A

TRUE

131
Q

may be useful in early presentations (<12 h post-ingestion), especially in cases of extended-or delayed-release tablet ingestion

A

Gastric lavage

132
Q

Activated charcoal (________ PO) should be administered after gastric lavage.

A

50-100 g

133
Q

may be useful in extended-release preparations

A

Whole-bowel irrigation with polyethylene glycol solution

134
Q

Administer ____________ followed by an infusion after fluid resuscitation is performed for persistent hypotension.

A

glucagon (5-10 mg IV bolus up to 15 mg)

135
Q

Recommended pediatric dose of glucagon for CCB overdose is

A

50 mcg/kg IV over 5 minutes

136
Q

can be administered for hypotension or heart block

A

Calcium chloride (1-4 g IV; preferably via central line, slowly)

137
Q

Recommended pediatric dose of 10% Calcium Gluconate for CCB overdose is

A

60 mg/kg (max: 1g)

138
Q

In the hypotensive patient, administer ____________ initially at medium-to-high doses early for cardiac contractility for heart rate support.

A

dopamine

139
Q

first clinically useful member of CCB was the result of attempts to synthesize more active analogues of papaverine, a vasodilator alkaloid found in the opium poppy

A

Verapamil

140
Q

has the greatest depressant effect on the heart and may decrease heart rate and cardiac output

A

Verapamil

141
Q

phosphodiesterase inhibitor with inotropic activity, may be of additional benefit in profound cardiac contractile failure

A

Inamrinone

142
Q

In multiple case reports, high-dose _________________ to maintain normal serum glucose levels have been successful for stabilizing cardiac output.

A

insulin infusion (0.1-1 U/kg/h) with dextrose infusion (usually D10W-D25W)

143
Q

When using this technique, frequent monitoring of glucose and potassium every ___________ is necessary

A

20-30 minutes

144
Q

Acts via cAMP to increase cardiac contractility and also may decrease heart block.

A

Glucagon

145
Q

Moderates nerve and muscle performance, and facilitates normal cardiac function.

A

Calcium gluconate

146
Q

1 g calcium gluconate = ___________ of elemental Ca

A

93 mg or 4.65 mEq

147
Q

Adult dose of calcium gluconate

A

3-12 g slow IV push (10% solution [100 mg/mL])

148
Q

Pediatric dose of calcium gluconate

A

100 mg (1 mL)/kg slow IV push)

149
Q

Phosphodiesterase inhibitor that acts by inhibiting breakdown of cAMP, thus prolonging effect on the release of calcium into the cytosol.

A

Inamrinone (Inocor)

150
Q

Increases cardiac contractility outside the alpha and beta-adrenergic system through nonspecific stimulation of cAMP.

A

Inamrinone (Inocor)

151
Q

Use with severely depressed cardiac output.

A

Inamrinone (Inocor)

152
Q

Excessive inhibition of calcium influx can cause serious

A

cardiac depression, including cardiac arrest, bradycardia, atrioventricular block, and heart failure

153
Q

Minor toxicity of CCB (troublesome but not usually requiring discontinuance of therapy) includes

A

flushing, dizziness, nausea, constipation, and peripheral edema

154
Q

mainstay of therapy for the immediate relief of angina

A

Organic nitrates

155
Q

These agents are simple nitric and nitrous acid esters of polyalcohols

A

Nitrates & Nitrites

156
Q

may be considered the prototype of the Nitrates & Nitrites.

A

Nitroglycerin

157
Q

used in the manufacture of dynamite

A

Nitroglycerin

158
Q

Oral bioavailability of the traditional organic nitrates is very low, typically

A

< 10–20%

159
Q

both absorbed efficiently by sublingual route and reach therapeutic blood levels within a few minutes.

A

Nitroglycerin and isosorbide dinitrate

160
Q

highly volatile liquids

A

Amyl nitrite and related nitrites

161
Q

Because of its unpleasant odor and short duration of action, ___________ is now obsolete for angina.

A

amyl nitrite

162
Q

Once absorbed, the unchanged nitrate compounds have half-lives of only ___________.

A

2–8 minutes

163
Q

results from complexing of cytochrome iron by the CN-ion

A

Cyanide poisoning

164
Q

Administration of ______________ soon after cyanide exposure will regenerate active cytochrome.

A

sodium nitrite (NaNO2)

165
Q

The cyanomethemoglobin produced can be further detoxified by __________

A

IV administration of sodium thiosulfate (Na2S2O3)

166
Q

Nitrates are contraindicated if

A

intracranial pressure is elevated

167
Q

major acute toxicities of organic nitrates are direct extensions of therapeutic vasodilation:

A

orthostatic hypotension, tachycardia, throbbing headache, glaucoma

168
Q

T/F: nitrates can be used safely in the presence of increased intraocular pressure.

A

TRUE

169
Q

Toxity in nitrates is often referred to as

A

Monday sickness

170
Q

centrally acting adrenergic inhibitors and are commonly used for the treatment of hypertension

A

Clonidine, guanebenz, and methyldopa

171
Q

has also been used to alleviate opioid and nicotine withdrawal symptoms

A

Clonidine

172
Q

nasal decongestants that may cause toxicity identical to that of clonidine

A

Oxymetazoline and tetrahydrozoline

173
Q

Decrease central sympathetic outflow by stimulating α2-adrenergic (inhibitory) receptors in the brain

A

Clonidine and related drugs MOT

174
Q

Stimulate peripheral α1-receptors, resulting in vasoconstriction and transient hypertension (COT)

A

Clonidine, oxymetazoline, and tetrahydrozoline

175
Q

Structurally similar to guanethidine, a ganglionic blocker, and has some neuronblocking action

A

Guanabenz

176
Q

Further decrease sympathetic outflow by metabolism to a false neurotransmitter (alpha-methylnorepinephrine) or by decreasing plasma rennin activity

A

Methyldopa

177
Q

Toxic dose of clonidine in children

A

0.1 mg

178
Q

Toxic dose of clonidine in adults (Acute ingestion)

A

18.8 mg

179
Q

Guanabenz mild toxicity developed in children who ingested

A

12 mg

180
Q

Guanabenz mild toxicity developed in adults who ingested

A

120-320 mg

181
Q

Guanabenz severe toxicity developed in a 19-month-old who ingested

A

28 mg

182
Q

A 3-year-old child had moderate symptoms of Guanabenz toxicity after ingesting

A

480 mg

183
Q

Toxic dose of methyldopa

A

> 2 g

184
Q

Death was reported in an adult after a Methyldopa ingestion of

A

25 g

185
Q

Generalized sympathetic depression and include:

A

● Papillary constriction
● Lethargy
● Coma
● Apnea
● Bradycardia
● Hypotension
● Hypothermia
● Paradoxic hypertension

186
Q

Adr of Methyldopa

A

severe hemolytic anemia

187
Q

Diagnosis should be suspected in patients with

A

pinpoint pupils, respiratory depression, hypotension, and bradycardia.

188
Q

may mimic opioid overdose but does not usually respond to administration of naloxone

A

Clonidine overdose

189
Q

caused by stimulation of peripheral α1-receptors

A

Paradoxic hypertension

190
Q

Color flow vascular ultrasonography of the intra-abdominal arterial supply may confirm ___________.

A

bowel infarction

PHCT MIDTERMS (4 decks)

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