Cardiovascular Drugs Flashcards

(190 cards)

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
Class III – K+ Channel blockers block what phase?
Phase 2 & 3
26
Class IV – Ca++ Channel blockers block what phase?
Phase 2
27
Aka Membrane stabilizing agent
Type I anti-arrhythmic drugs
28
Phase of action potential that can cause homeostasis
PHASE 2
29
Generally act by inhibiting fast sodium channels responsible for initial cardiac cell depolarization and impulse conduction.
Type I anti-arrhythmic drugs
30
In overdose, all Type I drugs have the potential to markedly depress
myocardial automaticity, conduction, and contractility
31
Class Ia
✓ Disopyramide ✓ Quinidine ✓ Procainamide
32
Class Ib
✓ Lidocaine ✓ Mexeletine ✓ Tocainide
33
Class Ic
✓ Moricizine ✓ Flecainide ✓ Propefanone
34
Depress the FAST sodium dependent channel, slowing phase zero of the cardiac action potential.
Class Ia agents
35
Prolong Action Potential Duration
Class Ia
36
Diastereoisomer of Quinine
Quinidine
37
Quinidine moa
● sodium channel blocker ● alpha receptor blocker ● anticholinergic action
38
Adr of Quinidine
Cinchonism
39
An N-metabolite, which is a highly reactive metabolite
Procainamide (Pronestyl®)
40
Procainamide moa
sodium channel blocker, neuromuscular blocker
41
Adr of Procainamide
GI upset, SLE-like symptoms
42
Disopyramide (Norpace®) is a vagolytic causing (CUD)
urinary retention, constipation, and dry mouth
43
Commonly used for suppression of acute and chronic supraventricular and ventricular arrhythmias
Quinidine and procainamide
44
has ganglionic-and neuromuscular-blocking activity
Procainamide
45
has alpha-adrenergic receptor blocking activity
Quinidine
46
Toxic dose of Quinidine
1 g
47
Toxic dose of Procainamide
5 g
48
Toxic dose of Disopyramide
1 g
49
Quinidine and disopyramide (both are anticholinergic) can cause:
Dry mouth Dilated pupils (Mydriasis) Delirium Flushed skin
50
All type Ia agents can produce
● Seizures ● Coma ● Respiratory arrest
51
Cinchonism
tinnitus, vertigo, deafness, visual disturbances
52
indicated for patients unresponsive to sodium bicarbonate therapy
Cardiac pacemaker
53
Active metabolite of procainamide
N-Acetylprocainamide (NAPA)
54
Weak sodium channel blocking ability
Class Ib
55
Analog of lidocaine
Tocainide
56
Adr of Tocainide
GIT upset, Paresthesia, Tremor, Ataxia
57
A congener of lidocaine that is resistant to first pass hepatic metabolism.
Mexiletine
58
Adr of Mexiletine
Ataxia, Blurry vision
59
an aminoacyl amide synthetic derivative of cocaine
Lidocaine
60
It is an antidysrhythmic and local anesthetic agent
Lidocaine
61
Lidocaine (Xylocaine) is metabolized to two active metabolites
monoethyl glycine xylidide (MEGX) and glycine xylidide (GX)
62
Strong sodium channel blocking ability but no effect on action potential
Class Ic
63
Both sodium and potassium channel blocking effect.
Flecainide
64
was withdrawn from US and Canadian markets in Dec of 1991 due to increased mortality in the cardiac dysrhythmia trial
Encainide
65
analogue of lysergic acid, is at least 10 times more potent than procainamide.
Encainide
66
Fatal adr of Encainide
cardiac dysrhythmia
67
related to propranolol
Propafenone
68
Common adr of Class Ic drugs
● Dizziness ● Blurred vision ● Ventricular arrhythmias
69
Overdose of Class Ib may cause:
● sedation ● confusion ● coma ● seizures ● respiratory arrest ● cardiactoxicity
70
TOCAINIDE AND MEXILETINE Side effects may include:
● Dizziness ● Paresthesias ● Tremor ● Ataxia ● GIT disturbance
71
FLECAINIDE, ENCAINIDE, PROPAFENONE, MORICIZINE Side effects
● Dizziness ● Blurred vision ● Headache ● GIT upset ● Ventricular arrhythmias
72
Overdose of Class Ic causes:
● Hypotension ● Bradycardia ● AV block ● Asystole ● QRS and QT intervals are prolonged
73
Widely used for the treatment of hypertension, angina pectoris, migraine headaches, and glaucoma
Type II anti-arrhythmic drugs or Beta-adrenergic blockers
74
Repolarization is also delayed, resulting in a prolonged QT interval that may be associated with ______________
polymorphic ventricular tachycardia
75
Selective Beta-blockers (BEAM)
Betaxolol, Bisoprolol, Esmolol, Acebutolol, Atenolol, Metoprolol
76
Beta-blockers with Membrane Stabilizing Activity (anesthetic-like effect) (PALM)
Propranolol, Pindolol, Acebutolol, Labetalol, Metoprolol
77
Beta-blockers with ISA
Acebutolol, Bisoprolol, Carteolol, Pindolol, Penbutolol
78
Beta-blockers with mixed alpha and beta blocking effect
Labetalol, Carvedilol
79
NONSELECTIVE BETA-BLOCKERS
Nadolol, Propranolol, Pindolol, Sotalol, Timolol
80
Further depresses myocardial contractility and conduction
Propranolol
81
Because of its lipid solubility, it enhances brain penetration and can cause seizures and coma
Propranolol
82
Other agents with beta-agonist activity that may cause hypertension
Pindolol
83
Prolongs QT interval in a dose-dependent manner
Sotalol
84
May cause torsades de pointes and ventricular fibrillation
Sotalol
85
Common treatment of torsades de pointes
Isoproterenol, magnesium, overdrive pacing
86
fatal polymorphic ventricular tachycardia
Torsades de pointes
87
Effect of beta-blocker overdose most common in patients with preexisting asthma or chronic bronchospastic disease
Bronchospasm
88
T/F: Beta-blockers may cause hypoglycemia and hyperkalemia
TRUE
89
There are no clear guidelines, but beta-blocker ingestion of only _____ times the therapeutic dose should be considered potentially life-threatening in all patients.
2-3
90
Bradycardia and hypotension resistant should be treated with _________________
Glucagon, 0.1-0.3 mg/kg IV bolus
91
Dose of glucagon given in patients with bradycardia and hypotension caused by beta-blockers overdose
0.1-0.3 mg/kg
92
Wide complex conduction defects caused by membrane-depressant poisoning may respond to ____________
Hypertonic sodium bicarbonate 1-2 meq/kg
93
Torsades de pointes, polymorphous ventricular tachycardia associated with QT prolongation resulting from sotalol poisoning can be treated with _______________
Isoproterenol infusion, magnesium, or overdrive pacing
94
Blocks potassium channels to prolong the duration of the action potential and the effective refractive period.
Type III anti-arrhythmic drugs or Potassium channel Blockers
95
A quaternary benzylammoniumcompound for treating lidocaine-refractory arrhythmias
Bretylium
96
Major toxic side effect of Bretylium is _____________ caused by inhibition of catecholamine release
hypotension
97
Rapid intravenous injection of Bretylium may cause
transient hypertension, nausea, and vomiting
98
A non-competitive beta-adrenergic blocker, which may explain its tendency to cause bradyarrhythmias.
Amiodarone
99
may release iodine and chronic use has resulted in altered thyroid function
Amiodarone
100
Amiodarone may release
Iodine
101
An iodinated benzofuran with similar structure to thyroxine an iodinated benzofuran with similar structure to thyroxine
Amiodarone
102
Amiodarone has side effects of
● Photosensitivity ● Hyperthyroidism (up to 16%) ● Pulmonary fibrosis ● Skin pigmentation (blue nail coloration) ● Corneal deposits
103
Amiodarone has a very long half-life of ______
40-50 days
104
Chronic use of Amiodarone may cause:
– Ventricular arrhythmias – Bradyarrhythmias (sinus arrest, AV block) – May aggravate cardiac failure – Pneumonitis – Pulmonary fibrosis – Photosensitivity dermatitis –Corneal deposits
105
Dilate peripheral arterioles to lower blood pressure
VASODILATORS
106
Alpha-adrenergic blocking agents
VASODILATORS
107
Reflex sympathetic response results in tachycardia and occasionally cardiac arrhythmias
VASODILATORS
108
Vasodilators that have been in clinical practice since the 1940’s
phenoxybenzamine, phentolamine, tolazaline
109
1st selective α1 inhibitor was introduced in the early 1970’s
Prazosin
110
newer α1 selective agents (DITUT)
Doxazosin, indoramin, terazosin, trimazosin, and urapidil
111
Prazosin and other newer α1 specific agents are associated with ___________
little or no reflex tachycardia
112
Acute overdose of Vasodilators may cause:
● Headache ● Nausea ● Dizziness ● Weakness ● Syncope ● Orthostatic hypotension ● Warm flushed skin ● Palpitations ● Lethargy and ataxia in children ● Cerebral and myocardial ischemia ● Acute renal failure
113
long-acting vasodilators (TD)
Terazosin and doxazosin
114
Terazosin and doxazosin are long-acting and eliminated 60% in feces; thus, repeat-dose __________________ may enhance their elimination.
activated charcoal
115
Type IV drugs or calcium channels (type IV) uses
● Anti-hypertensive ● Anti-arrythmic ● Anti-angina
116
Non- dihydropyridine CCB
Verapamil, Diltiazem
117
Dihydropyridine CCB (-dipine)
amlodipine, felodipine, isradipine, nicardipine, nifedipine, nisoldipine
118
4 CARDIOVASCULAR EFFECTS OF CCB
● Peripheral vasodilatation ● Negative chronotropy (decreased heart rate) ● Negative inotropy (decreased cardiac contractility) ● Negative dromotropy (decreased cardiac conduction)
119
decreased free fatty acid utilization by the myocardium produce
hyperglycemia, lactic acidosis, and depressed cardiac contractility
120
may be helpful to determine heart size and presence or absence of congestive heart failure or ALI
chest radiograph
121
If bowel obstruction is suspected, ______________ is recommended.
abdominal radiography
122
Cardiac biomarkers, such as ___________, may help differentiate drug-induced bradycardia from ischemic causes.
troponin I
123
Empiric use of glucagon in adults may be warranted for patients with an unknown CCB overdose presenting with bradycardia or hypotension.
5-15 mg IV
124
T/F: Consider using calcium only if a witness confirms a calcium channel blocker overdose
TRUE
125
Calcium may induce _______________ in digoxin overdose, which can present with similar findings
fatal arrhythmias
126
If profound hypotension fails to respond to fluid resuscitation, administer a _______________
dopamine or norepinephrine drip
127
If the patient deteriorates to cardiac arrest from a calcium channel blocker overdose, perform _________
prolonged cardiopulmonary resuscitation (CPR)
128
may be tried if hemodynamically significant bradycardia occurs
Atropine
129
Mid-dose dopamine (_______ mcg/kg/min) may improve heart rate and contractility.
5-10
130
T/F: Administer IV calcium gluconate (up to 4 g) or IV calcium chloride (1g) and/or glucagon (5-10 mg) if hypotension persists.
TRUE
131
may be useful in early presentations (<12 h post-ingestion), especially in cases of extended-or delayed-release tablet ingestion
Gastric lavage
132
Activated charcoal (________ PO) should be administered after gastric lavage.
50-100 g
133
may be useful in extended-release preparations
Whole-bowel irrigation with polyethylene glycol solution
134
Administer ____________ followed by an infusion after fluid resuscitation is performed for persistent hypotension.
glucagon (5-10 mg IV bolus up to 15 mg)
135
Recommended pediatric dose of glucagon for CCB overdose is
50 mcg/kg IV over 5 minutes
136
can be administered for hypotension or heart block
Calcium chloride (1-4 g IV; preferably via central line, slowly)
137
Recommended pediatric dose of 10% Calcium Gluconate for CCB overdose is
60 mg/kg (max: 1g)
138
In the hypotensive patient, administer ____________ initially at medium-to-high doses early for cardiac contractility for heart rate support.
dopamine
139
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
Verapamil
140
has the greatest depressant effect on the heart and may decrease heart rate and cardiac output
Verapamil
141
phosphodiesterase inhibitor with inotropic activity, may be of additional benefit in profound cardiac contractile failure
Inamrinone
142
In multiple case reports, high-dose _________________ to maintain normal serum glucose levels have been successful for stabilizing cardiac output.
insulin infusion (0.1-1 U/kg/h) with dextrose infusion (usually D10W-D25W)
143
When using this technique, frequent monitoring of glucose and potassium every ___________ is necessary
20-30 minutes
144
Acts via cAMP to increase cardiac contractility and also may decrease heart block.
Glucagon
145
Moderates nerve and muscle performance, and facilitates normal cardiac function.
Calcium gluconate
146
1 g calcium gluconate = ___________ of elemental Ca
93 mg or 4.65 mEq
147
Adult dose of calcium gluconate
3-12 g slow IV push (10% solution [100 mg/mL])
148
Pediatric dose of calcium gluconate
100 mg (1 mL)/kg slow IV push)
149
Phosphodiesterase inhibitor that acts by inhibiting breakdown of cAMP, thus prolonging effect on the release of calcium into the cytosol.
Inamrinone (Inocor)
150
Increases cardiac contractility outside the alpha and beta-adrenergic system through nonspecific stimulation of cAMP.
Inamrinone (Inocor)
151
Use with severely depressed cardiac output.
Inamrinone (Inocor)
152
Excessive inhibition of calcium influx can cause serious
cardiac depression, including cardiac arrest, bradycardia, atrioventricular block, and heart failure
153
Minor toxicity of CCB (troublesome but not usually requiring discontinuance of therapy) includes
flushing, dizziness, nausea, constipation, and peripheral edema
154
mainstay of therapy for the immediate relief of angina
Organic nitrates
155
These agents are simple nitric and nitrous acid esters of polyalcohols
Nitrates & Nitrites
156
may be considered the prototype of the Nitrates & Nitrites.
Nitroglycerin
157
used in the manufacture of dynamite
Nitroglycerin
158
Oral bioavailability of the traditional organic nitrates is very low, typically
< 10–20%
159
both absorbed efficiently by sublingual route and reach therapeutic blood levels within a few minutes.
Nitroglycerin and isosorbide dinitrate
160
highly volatile liquids
Amyl nitrite and related nitrites
161
Because of its unpleasant odor and short duration of action, ___________ is now obsolete for angina.
amyl nitrite
162
Once absorbed, the unchanged nitrate compounds have half-lives of only ___________.
2–8 minutes
163
results from complexing of cytochrome iron by the CN-ion
Cyanide poisoning
164
Administration of ______________ soon after cyanide exposure will regenerate active cytochrome.
sodium nitrite (NaNO2)
165
The cyanomethemoglobin produced can be further detoxified by __________
IV administration of sodium thiosulfate (Na2S2O3)
166
Nitrates are contraindicated if
intracranial pressure is elevated
167
major acute toxicities of organic nitrates are direct extensions of therapeutic vasodilation:
orthostatic hypotension, tachycardia, throbbing headache, glaucoma
168
T/F: nitrates can be used safely in the presence of increased intraocular pressure.
TRUE
169
Toxity in nitrates is often referred to as
Monday sickness
170
centrally acting adrenergic inhibitors and are commonly used for the treatment of hypertension
Clonidine, guanebenz, and methyldopa
171
has also been used to alleviate opioid and nicotine withdrawal symptoms
Clonidine
172
nasal decongestants that may cause toxicity identical to that of clonidine
Oxymetazoline and tetrahydrozoline
173
Decrease central sympathetic outflow by stimulating α2-adrenergic (inhibitory) receptors in the brain
Clonidine and related drugs MOT
174
Stimulate peripheral α1-receptors, resulting in vasoconstriction and transient hypertension (COT)
Clonidine, oxymetazoline, and tetrahydrozoline
175
Structurally similar to guanethidine, a ganglionic blocker, and has some neuronblocking action
Guanabenz
176
Further decrease sympathetic outflow by metabolism to a false neurotransmitter (alpha-methylnorepinephrine) or by decreasing plasma rennin activity
Methyldopa
177
Toxic dose of clonidine in children
0.1 mg
178
Toxic dose of clonidine in adults (Acute ingestion)
18.8 mg
179
Guanabenz mild toxicity developed in children who ingested
12 mg
180
Guanabenz mild toxicity developed in adults who ingested
120-320 mg
181
Guanabenz severe toxicity developed in a 19-month-old who ingested
28 mg
182
A 3-year-old child had moderate symptoms of Guanabenz toxicity after ingesting
480 mg
183
Toxic dose of methyldopa
> 2 g
184
Death was reported in an adult after a Methyldopa ingestion of
25 g
185
Generalized sympathetic depression and include:
● Papillary constriction ● Lethargy ● Coma ● Apnea ● Bradycardia ● Hypotension ● Hypothermia ● Paradoxic hypertension
186
Adr of Methyldopa
severe hemolytic anemia
187
Diagnosis should be suspected in patients with
pinpoint pupils, respiratory depression, hypotension, and bradycardia.
188
may mimic opioid overdose but does not usually respond to administration of naloxone
Clonidine overdose
189
caused by stimulation of peripheral α1-receptors
Paradoxic hypertension
190
Color flow vascular ultrasonography of the intra-abdominal arterial supply may confirm ___________.
bowel infarction