Cardiac Drugs Flashcards
(192 cards)
1
Q
What is the mechanism of action of Digoxin?
A
Inhibits sodium-potassium ATP pump in cardiac muscle cells, results in increased intracellular calcium
2
Q
What are some of the cardiac effects of Digoxin?
A
Increased inotropy Decreased left ventricular preload, afterload, wall tension, and oxygen consumption Increased stroke volume Decreased heart size Increases automaticity Decreases AV conduction
3
Q
What happens to the Frank-Starling curve in a patient taking Digoxin?
A
Shifts to the left
4
Q
How is Digoxin eliminated?
A
Primarily by kidneys with 35% excreted daily
5
Q
Where is a tissue reservoir site for Digoxin?
A
Skeletal muscles - elderly have increased likelihood of elevated plasma levels due to decreased muscle mass
6
Q
What is the MOA of Theophyline?
A
Nonselective PDE inhibitor that inhibits all fractions of PDE isoenzymes
7
Q
How is Theophyline metabolized and excreted?
A
Metabolized by liver and excreted by kidneys
8
Q
What is the MOA of milrinone?
A
Inhibition of PDEIII (phosphodiesterase enzyme III) that leads to increased intracellular concentrations of cAMP and cGMP that ultimately cause inward movement of calcium ions
9
Q
What are the primary effects of milrinone?
A
Positive inotropy with vascular and airway smooth muscle relaxation
10
Q
What are some clinical signs of digitalis toxicity?
A
Anorexia Nausea Vomiting Transitory amblyopia and scotomata Pain simulating trigeminal neuralgia Extremity pain
11
Q
What is the normal plasma concentration for Digoxin?
A
0.5-2.5 ng/mL, >3 ng/mL indicates toxicity
12
Q
How does hyperkalemia affect Digoxin?
A
reduces enzyme-inhibiting actions of glycosides and reduces the effects of Digoxin
13
Q
What is the mechanism of action of class 1 antirhythmics?
A
sodium channel blockers, prolongs phase 0
14
Q
What is the mechanism of action of class 2 antirhythmics?
A
beta blockers, decreases phase 4 slope
15
Q
What is the mechanism of action of class 3 antirhythmics?
A
potassium channel blockers, elongates phase 3 and increases effective refractory period
16
Q
What is the mechanism of action of class 4 antirhythmics?
A
calcium channel blockers, prolongs phase 0
17
Q
What class of antirhythmic is Procainamide?
A
Class 1A
18
Q
What is the mechanism of action of Procainamide?
A
blocks sodium channels and prolongs upstroke of the action potential, slows conduction, and prolongs the WRS duration on ECG
also prolongs APD by nonspecific blockade of potassium channels
19
Q
What property of Procainamide causes hypotension?
A
Ganglion-blocking properties that reduces peripheral vascular resistance
20
Q
What are Procainamide’s toxic effects?
A
excessive action potential prolongation, QT-interval prolongation, and induction of Torsades and syncope
21
Q
What are some side effects of Procainamide?
A
Lupus-like symptoms Hypotension Nausea Diarrhea Rash Rarely - pleuritis, pericarditis, agranulocytosis, hepatitis
22
Q
How is Procainamide metabolized?
A
metabolite metabolized hepatically
23
Q
What is a metabolite of Procainamide and what is its significance?
A
NAPA, can cause Torsades if accumulated
24
Q
How is Procainamide eliminated and what is its half-life?
A
Kidneys, half life of 3-4 hours
25
What are the clinical indications of using peripheral vasodilators
treat hypertensive crises, produce controlled hypotension, and facilitate LV forward stroke volume
26
Does SNP dilate veins, arteries, or both?
Both; decreases preload and after load
27
What is a molecule of SNP made of?
1 nitro group and 5 cyanide molecules
28
How is SNP metabolized
hemoglobin
29
How are the cyanide molecules generally eliminated?
Rodinase enzyme causes the cyanide to be attached to Vit B12 ( thiocyanate) which is then excreted by the kidneys
30
What is the onset of SNP?
immediate
31
What is the DOA of SNP?
3-5 minutes
32
What is the standard dose of SNP?
0.3-10mcg/kg/min
33
What could be a detrimental effect of SNP?
reflex tachycardia, leading to increased O2 demand and potentially cause myocardial ischemia
34
SNP molecule is what percent cyanide?
44%
35
What is the purpose of controlled hypotension
operations that require a bloodless field and reduced blood loss
36
Why is SNP good to use for hypertensive emergencies?
ease of titration, rapid onset, short DOA, and efficacy
37
Which drug has a risk of causing cyanide toxicity
SNP
38
What are the effects of cyanide toxicity?
tissue hypoxia, anaerobic metabolism, and eventually death
39
What is the treatment for cyanide toxicity?
3% sodium nitrate, sodium thiosulfate, Vit B12, discontinue infusion, treat acidosis, administer 100% O2
40
Does hydralazine dilate veins, arteries, or both?
arteries; decreases after load
41
What is the standard dose of hydralazine?
2.5-10mg IV
42
What is the onset of hydralazine?
10-20 minutes
43
Metabolism/excretion of hydralazine?
liver/renal
44
Does hydralazine decrease SBP or DBP more?
DPB
45
What is the DOA of hydralazine?
unpredictable
46
Does nitroglycerin dilate veins, arteries, or both?
veins primarily; decreases preload; can cause arterial dilation at higher doses
47
Which vasodilator is most commonly used for angina
nitroglycerin
48
What is the MOA of nitroglycerin?
contains a nitro group which contributes to NO mediated vasodilation
49
What is the onset of nitroglycerin?
2-5 minutes
50
What is the DOA of nitroglycerin?
5-10 minutes
51
Which drug to people develop rapid tolerance to?
nitroglycerin
52
What can be done to reverse nitroglycerin tolerance?
a drug free interval of 12-14 hours
53
T/F: Nitroglycerin reduces myocardial ischemia primarily by dilating coronary arteries and increasing blood supply to the myocardium?
F: reduces ischemia primarily by reducing preload and therefore reducing myocardial oxygen consumption
54
What are SE of nitroglycerin?
Headache, flushing, decreased sensitivity to heparin
55
Which vasodilator is effective in reducing sphincter of Oddi spasm?
nitroglycerin
56
Is tachycardia more marked with A1 or A2 antagonists?
A2 because they increase NE release increasing B1 stimulation at the heart
57
Phentolamine has what effect at A1 and A2 receptors
A1=A2 antagonist
58
What are some adverse effects related to Phentolamine administration
cardiac stimulation, tachycardia, arrhythmias, myocardial ischemia
59
What are clinical uses of phentolamine
pheochromocytoma excision, HTN crisis, extravascular administration of sympathomimetic agents
60
What is dose of phentolamine?
30-70mcg/kg IV
61
What effect does prazosin have on a1 vs. a2 receptors?
a1>>>>>>a2 antagonist
62
Why is prazosin's reduced a2 activity beneficial
results in relative absence of tachycardia
63
What are the clinical uses of Prazosin?
preop prep for patients with pheo, essential HTN, decreasing after load in patients with heart failure, raynaud phenomenon
64
What are some EKG changes associated with Digoxin?
Scooped ST
Biphasic T wave
Shortened QT
Long PR
65
How long does it take to see effects of Digoxin administered IV?
5-30 minutes
66
If a patient has kidney disease, should the Digoxin dose be decreased? And if so, by how much?
Eliminated via kidneys so dose needs to be decreased by 75%
67
Does Digoxin have any effects on someone with normal cardiac function?
No
68
How can Digoxin be used in anesthesia?
Can be administered prophylactically to someone with limited cardiac reserve or in patients with CAD recovering from anesthesia (administered day before surgery and 0.25 mg given before induction)
69
What are the dosing recommendations for Digoxin?
0.125 - 0.25 mg/day
70
What can speed the metabolism of Theophylline?
Cigarettes
71
What is the loading/maintenance dose of Theophylline?
Loading dose of 5 mg/kg IV followed by infusion of 0.5 - 1 mg/kg/hr
72
What are some of the cardiac effects of Calcium?
Intense positive inotropy (lasts 10-20 minutes)
Increased stroke volume
Decreased left ventricular end-diastolic pressure
Decreased heart rate
Decreased systemic vascular resistance
73
When would it be ideal to administer Calcium during anesthesia?
At the end of cardiopulmonary bypass to improve contractility and stroke volume--patients usually hypocalcemic from cardioplegic solutions and citrated blood
74
Which contains more calcium: 10% calcium chloride or 10% calcium gluconate?
10% Calcium chloride (should only be administered via central line)
75
What are the dosing recommendations for calcium?
5 to 10 mg/kg IV (Stoelting)
76
What is the mechanism behind hypotension caused by Milrinone?
Inhibits PDEIII --> Increased cAMP --> EFFLUX of calcium from smooth muscle cells --> vasodilatation
(cAMP acts opposite in smooth muscle cells than cardiac muscle cells)
77
What are the dosing recommendations for Milrinone?
50 mcg/kg IV bolus followed by 0.5 mcg/kg/min
| Stoelting and Nagelhout
78
What is the treatment for Digitalis toxicity?
Correction of predisposing cause
Drugs to treat arrhythmias (Lidocaine or Atropine)
Insertion of temporary pacemaker if complete heart block present
Supplemental potassium (decreases binding of Digoxin)
Fab-fragments (antibodies to Digoxin)
79
What drugs decrease GI absorption of cardiac glycosides?
Oral antacids
80
What drugs can increase the likelihood of arrhythmias with Digoxin?
Sympathomimetics
| Pancuronium
81
What is the most common arrhythmia with Digitalis toxicity?
Atrial tachycardia (Stoelting)
82
In patients with normal renal function, which drugs frequently cause Digitalis toxicity?
Diruetics that cause potassium depletion
83
What effect does Phenoxybenzamine have on a1 vs. a2 receptors?
a1>a2; irreversible antagonist
84
Method of action for ARB's?
Produce antihypertensive effects by blocking vasoconstrictive effects of angiotensin-2 without affecting ACE activity
85
What are the side effects of ACE Inhibitors?
C - Cough
A - Angioedema/ Agranulocytosis
P - Proteinurea/ Potassium excess
T - Taste change
O - Orthostatic hypotension - controversial
P - Pregnancy contraindication (fetal renal damage)
R - Renal artery stenosis contraindication
I - Increases renin
L - Leukopenia / liver toxicity
86
What is the dose for phenoxybenzamine?
0.5-1.0mg/kg
87
What is the pathophysiology behind angioedema?
Bradykinins associated with vasodilation and increased vascular permeability. Can be hereditary.
88
When are alpha antagonist most beneficial in treating a hypertensive crisis
when it is due to excess circulating alpha agonists (pheo, overdose on sympathomimetic drugs, or clonidine withdrawal
89
Method of action for ACE Inhibitors?
Prevent the conversion of angiotensin-1 to angiotensin-2
90
Method of action for ARB's?
Produce antihypertensive effects by blocking vasoconstrictive effects of angiotensin-2 without affecting ACE activity
91
What complication may present when treating with vasopressin?
It can cause coronary vasospasm, which can induce MI.
92
Which population has a greater risk of angioedema?
African American - 5 times greater
93
What is the pathophysiology behind angioedema?
Bradykinins associated with vasodilation and increased vascular permeability. Can be hereditary
94
What is responsible for the cough caused by ACE-I?
The accumulation of excess bradykinin, which is usually broken down by angiotensin converting enzyme (ACE).
95
What intrinsic mechanisms are responsible for hemodynamic maintenance?
ADH (Vasopressin), RAAS, SNS
96
When a patient, who took their ACE Inhibitor the morning of surgery, exhibits hypotension that does not respond to Phenylephrine or ephedrine, what is the next line drug?
Vasopressin
97
What complication may present when treating with vasopressin?
It can cause coronary vasospasm, which can induce MI.
98
Why is Procainamdie typically given as a 2nd or 3rd choice for atrial or ventricular arrhythmias?
Lupus symptoms and frequent dosing required
99
What classification of antirhythmic is Lidocaine?
Class 1B
100
What is the mechanism of action of Lidocaine?
Blocks activated and inactivated sodium channels
101
How is Lidocaine administered?
Only IV, significant first pass effect taken PO
102
Is Lidocaine the least or most toxic of the sodium channel blockers?
Least toxic
103
What is a common side effect of Lidocaine?
Hypotension caused by suppression of myocardial contractility
104
What are the dosing recommendations for Lidocaine?
150-200 mg over 15 minutes followed by infusion of 2-4 mg/min
105
What is the mechanism of action of Verapamil?
Blocks inactivated and activated L-type calcium channels
106
What are some side effects of Verapamil?
Constipation
Lassitude
Nervousness
Peripheral edema
107
How is Verapamil metabolized?
Extensively by liver
108
What is Verapamil used to treat?
SVT
Tachydysrhythmias
Premature uterine contractions
109
What happens if you give someone Verapamil that's in Vtach?
Causes Vfib and circulatory collapse
110
Why would you not want to give Verapamil to someone who has AV nodal disease?
Can induce AV block, causes pronounced depression of AV nodal transmission
111
What is the mechanism of action of Diltiazem?
Blocks calcium channels in the AV node
112
In which classification of antirhythmic is Amiodarone?
Class 3, but blocks all other channels in other classes
113
What is the mechanism of action of Amiodarone?
Prolongs action potential duration on QT interval by blockade of potassium channels in heart; also blocks sodium, calcium, and adrenergic receptors
114
How is Amiodarone metabolized?
Hepatic metabolism
115
How is Amiodarone eliminated?
Elimination complex with rapid component of 3-10 days and slower component of several weeks. Effects are maintained for 1-3 months after discontinuation
116
What enzyme does Amiodarone interact with?
CYP3A4
117
What are some side effects of Amiodarone?
Hypotension
Symptomatic bradycardia or heart block in patients with preexisting sinus or AV node disease
Dose-dependent pulmonary toxicity
Abnormal liver function tests and hypersenstivity hepatitis
Skin deposits resulting in photodermatitis and gray-blue skin discoloration in sun-exposed areas
Asymptomatic corneal deposits
Halos in peripheral visual fields
118
How does Amiodarone affect T3 and T4?
Blocks peripheral conversion of T3 to T4 which can be a source of an accumulation of inorganic iodine or hyper/hypothyroidism
119
What is the mechanism of action of Adenosine?
A1 adenosine receptor agonist, ionic mechanisms in AV node are unknown, activates adenosine-sensitive K+ channels in SA and atrial myocytes
Causes inward current of potassium to hyperpolarize cell and inhibits outward calcium current
120
What is the half-life of Adenosine?
<10 seconds in the blood
121
What are some side effects of Adenosine?
```
Flushing
Shortness of breath
Chest burning
Afib
Headache
Hypotension
Nausea
Paresthesias
```
122
What are the dosing recommendations for Adenosine?
6 mg followed by 12 mg dose if needed
123
What does phase 0 of the cardio myocyte action potential consist of?
Rapid influx of sodium
124
What does phase 1 of the cardiomyocyte action potential consist of?
Sodium gates close and potassium leaves cell
125
What does phase 2 of the cardiomyocyte action potential consist of?
Calcium channels open while potassium channels are still open, equal balance of calcium coming into cell and potassium leaving the cell
126
What does phase 3 of the cardiomyocyte action potential consist of?
Repolarization, calcium channels close and potassium continues to leave cell
127
What does phase 4 of the cardiomyocyte action potential consist of?
Baseline or resting membrane potential
128
What phases make up the effective refractory period?
Phases 0-3
129
Which phases are involved in the nodal cell action potential?
Phase 0, 3, and 4
130
What antiarrhythmic classification does Diltiazem fall into?
Class 4
131
What are the electrophysiological effects of Adenosine?
Decreases phase 4 depolarization of SA node pacemaker cells
| Hyperpolarizes and suppression of calcium dependent myocytes
132
What are the prototype osmotic diuretics?
Mannitol and urea
133
What is the mechanism of action of osmotic diuretics?
Alter the osmolarity of the plasma, glomerular filtrate, and renal tubular fluid resulting in osmotic diuresis--water is absorbed from the proximal renal tubules and the loops of Henle
134
What are some clinical uses for osmotic diuretics?
Prophylaxis against acute renal failure
Differential diagnosis of acute oliguria
Treatment of increases in ICP, mannitol may also decrease formation of ICP
Decreasing IOP
135
Do osmotic diuretics alter the elimination rate of long-acting nondepolarizing neuromuscular blocking drugs?
No, glomerular filtration is not altered by Mannitol
136
What is the mechanism of action of potassium-sparing diuretics?
Acts in the distal convoluted tubules independent of aldosterone to produce diuresis, they cause an increase in the urinary excretion of sodium, chloride, and bicarb
137
What is the mechanism of action of thiazide diuretics?
Inhibits sodium reabsorption of sodium and chloride ions in the cortical portions of the ascending loops of Henle and to a lesser extent in the proximal renal tubules and distal renal tubules
138
What is the primary reason for Thiazide use?
Essential hypertension when diuresis, natriuresis, and vasodilation are synergistic
139
Are the Thiazide diuretic effects independent or dependent of acid-base balance?
Independent
140
What are common side effects of Thiazide diuretics?
Hypokalemia, hypochloremia, and metabolic alkalosis
| Can also cause hyperglycemia and aggravate diabetes mellitus
141
What is the prototype loop diuretic?
Furosemide
142
What is the mechanism of action of loop diuretics?
Inhibits reabsorption of sodium and chloride primarily in medullary portions of the ascending limb of loop of Henle
143
How does Furosemide affect renal physiology?
Evokes renal production of prostaglandins resulting in renal vasodilation and increased renal blood flow
144
What drug can attenuate the diuretic effect of Furosemide?
NSAIDS
145
What are some clinical uses of Furosemide?
Mobilization of edema fluid due to renal, hepatic, or cardiac dysfunction
Treatment of increased intracranial pressure
Inhibition of cellular uptake of calcium for hypercalcemia
Differential diagnosis of acute oliguria
Little use in the chronic treatment of essential hypertension
146
What is the most common side effect of Furosemide?
Electrolyte abnormalities
147
What is the prototype carbonic anhydrase inhibitor?
Acetazolamide
148
What is the primary site of action of carbonic anhydrase inhibitors in the kidney?
proximal renal tubules
149
What is the mechanism of action of carbonic anhydrase inhibitors?
Inhibits enzyme, carbonic anhydrase, activity that diminishes secretion of H+ ions and increases
150
What is the prototype for beta blockers?
Propanolol
151
What is the mechanism of action of Propanolol?
Beta 1 and Beta 2 antagonist
152
What is the mechanism of action of Metropolol?
Beta 1 selective antagonist
153
Which patient population would benefit from Metropolol or Atenolol?
Asthmatics or diabetics because of the little antagonism of beta 2 receptors
154
What is the mechanism of action of Atenolol?
Selective beta 1 antagonist
155
What is the mechanism of action of Labetalol?
Beta and alpha 1 antagonist
156
What is the mechanism of action of Esmolol?
Ultra short-acting beta 1 antagonist
157
What are some clinical applications for Propanolol?
```
HTN
Angina
Arrhythmias
Migraines
Hyperthyroidism
```
158
What effects does Propanolol have on HR and BP?
lowers HR and BP
159
What effects does Metropolol and Atenolol have on HR and BP?
Lowers HR and BP
160
What effects does Labetalol have on HR and BP?
Lowers BP with limited HR increase
161
What is a clinical application to use Labetalol?
HTN
162
What are some clinical applications for Metropolol and Atenolol?
Angina
HTN
Arrhythmias
163
What is a clinical application for Carvedilol?
Heart failure
164
What are clinical applications for Esmolol?
```
Rapid control of BP and arrhythmias
Pheochromocytoma
Cocaine toxicity?
Thyrotoxicosis
Myocardial ischemia intraoperatively
```
165
What is withdrawal hypersenstivity?
Acute discontinuation of beta antagonist therapy that results in excess SNS activity due to upregulation of beta receptors that manifests in 24-48 hours
166
What is the most common adverse effect of beta blockers?
bradycardia
167
What are some effects of beta blocker toxicity?
Bradycardia
Airway obstruction/constriction
Cardiac decompensation in patients with compensated heart failure because their cardiac output is dependent on sympathetic drive
168
Which beta blocker is only available IV?
Esmolol
169
What is the onset of action and duration of Esmolol?
Full effect evident within 5 minutes and action ceases within 10-30 minutes
170
What does long-term use of Phenoxybenzamine cause?
Decrease in hematocrit. It constricts peripheral vessels and shunts blood to vital organs and overly perfuses kidneys
171
What route can you administer Phenoxybenzamine?
PO
172
Which has a longer half-life, Labetalol or Metropolol?
Labetalol - 1/2 life 5 hrs (Metropolol 3-4 hours), need to keep this in mind when administering beta blocker to patient that is going home
173
What is the 1/2 life of Esmolol?
10 minutes
174
What are some concerns with patients who have been treated chronically with Propanolol?
Decreased clearance of local anesthetics
Decreased pulmonary clearance of fentanyl
(both are basic lipophilic amines)
175
Which beta blocker is the most selective to beta 1?
Atenolol
176
In whom would it be advantageous to give Atenolol?
Those who need beta 2 receptor activity: COPD/asthma, and severe CAD
177
What is the half-life of Atenolol?
6-9 hours (long-lasting anti-hypertensive drug therefore only given once a day PO)
178
How is Esmolol metabolized?
plasma esterases
179
Does Esmolol cross the BBB or placenta?
No, poor lipid solubility
180
Which beta blocker is the "go to" for someone that's never had a beta blocker?
Esmolol
181
What is the beta to alpha ratio of Labetalol?
7:1
182
What is Labetalol's affinity for alpha 1 receptors in comparison to phentolamine?
1/10th affinity
183
What is Labetalol's affinity for beta receptors in comparison to Propanolol?
1/3rd affinity
184
What is the dose of Verapamil?
75-150 mcg/kg IV
185
What are some of the pharmacokinetic properties of Verapamil?
Highly protein bound
Active metabolites
Elimination 1/2 time 3-7 hours
186
What drug has greater coronary and peripheral vasodilatory effects than Verapamil?
Nifedipine
187
What are some effects of Nifedipine?
Decreased BP - used PO to treat HTN
Baroreceptor-mediated increase in HR
Little to no effect on SA and AV node activity
Little effect on myocardial contractility
188
At what dose do you start a Nicardipine gtt?
5 mg/hr
189
How much can you increase a Nicardipine gtt every 5 minutes if needed?
2.5 mg/hr
190
What is the maximum dose of a Nicardipine gtt?
15 mg/hr
191
What is Diltiazem useful to treat?
HTN
SVTs
A-fib
Migraine headaches
192
What are some of the effects of Nicardipine?
Lacks SA and AV nodal effects
Has little effect on myocardial contractility
Has the greatest vasodilation effects
Very useful in short-term treatment of HTN
