Cardiac Medications Flashcards
(201 cards)
1
Q
What is an advantage and disadvantage to giving an increased dose of a selective adrenergic antagonist?
A
Advantage: increased bioavailability
Disadvantage: decreased selectivity
2
Q
Which drugs have the greatest affinity for alpha1 receptors compared to alpha2 receptors?
A
Prazosin
Terazosin
Doxazosin
3
Q
Why don’t we typically use a lot of alpha antagonists in anesthesia?
A
They cause vasodilation (like volatile agents) leading to hypotension, reflex tachycardia and increased cardiac O2 consumption
4
Q
What alpha antagonist has the same affinity for both alpha1 and alpha2 receptors?
A
Phentolamine
5
Q
What are alpha antagonists primarily used to treat?
A
HTN
Pathology
BP lability
6
Q
Which alpha antagonists have a higher affinity for the alpha2 receptor than the alpha1 receptor?
A
Rauwolscine
Yohimbine
Tolazoline
7
Q
What is the mechanism of action of Phentolamine?
A
Non-selective alpha antagonist that causes reflex mediated and alpha2 associated increases in HR and CO
8
Q
What intraoperative hypertensive emergencies can Phentolamine be used to treat?
A
Pheochromocytoma manipulation
Autonomic hyperreflexia
9
Q
What is the dose of Phentolamine used to treat hypertensive emergencies?
A
30-70mcg/kg
10
Q
Does a paralyzed patient require anesthesia?
A
Yes, for sympathetic response and visceral pain
11
Q
What alpha antagonist can be used to treat extravascular administration of sympathomimetic agents?
A
Phentolamine (2.5-5mg) give in combination with local anesthetics
12
Q
Which alpha antagonist is associated with decreased Hct after long term use?
A
Phenoxybenzamine, a non-selective alpha antagonist
13
Q
How does a pheochromocytoma affect Hct?
A
Causes vasoconstriction leading to a decreased intravascular volume leading to a relative increase in Hct. The Kidneys see increased Hct and decrease production of erythropoietin
14
Q
Why is Phenoxybenzamine less associated with tachycardia from decreased SVR?
A
Less alpha2 antagonism
15
Q
What dose of Phenoxybenzamine should be given for pheochromocytoma?
A
PO dose 0.5-1mg/kg given preoperatively
16
Q
Why is it important to check a current HH prior to administering Phenoxybenzamine?
A
It causes vasodilation which can decrease Hct and affect O2 carrying capacity
17
Q
What is the prototype alpha1 selective antagonist?
A
Prazosin
18
Q
What are common uses for Prazosin?
A
Pre-op preparation of pheochromocytoma
Essential HTN
Decrease afterload in patients with heart failure
Raynaud phenomenon
19
Q
What class of drugs can be combined with Prazosin use in treatment of essential HTN?
A
Thiazides
20
Q
Which alpha antagonists are safest to use in patients with heart failure?
A
Alpha1 antagonists, tachycardia is not typically seen in these agents
21
Q
Which alpha antagonist provides irreversible blockade?
A
Phenoxybenzamine
22
Q
What are some common side effects of alpha antagonists?
A
HoTN
Tachycardia
Stuffy nose
23
Q
What are some additional side effects of Phenoxybenzamine and why?
A
Nausea, fatigue and sedation, it crosses the BBB
24
Q
Why are non-selective alpha antagonists more likely to cause tachycardia?
A
Baroreflex causes SNS to be activated blocked alpha2 as well, cannot have negative feedback when too much NE
25
What three factors should help determine which beta blocker to use?
Selectivity
Elimination 1/2 life
Bioavailability
26
What is the prototype beta blocker?
Propanolol
27
What are the CV effects of propanolol?
Non-selective:Decreased HR and contractility --> B1Increased vascular resistance --> B2
28
Why is propanolol limited in anesthetic practice?
There are better, more selective drugs
29
What two drugs should be used with caution in patient who have been taking propanolol long term?
Fentanyl
Amide local anesthetics
There is a decreased clearance for both of these drugs
30
Why do some patient go on different medication to treat HTN instead of a beta blocker?
Undesirable side effects such as feeling groggy or dizziness. Beta blockers cross BBB
31
What kind of patients would benefit from metoprolol use?
Asthmatics, smokers, patients with COPD since it is a beta1 specific antagonist
32
Which beta antagonist is most selective to beta1?
Atenolol
33
Why is Atenolol desirable in the outpatient setting?
Long acting, only needs to be taken once a day
34
Other than airway pathology, patients with what disease may also benefit from a beta1 selective antagonist?
Metabolic disease (Diabetes)
35
What beta antagonist is best to give in the OR if the patient is not naive to beta blockers?
Metoprolol
36
Which beta1 antagonist has the fastest onset and shortest duration of action?
Esmolol
Onset: 60 sec
Duration: 10 mins
37
Why is Esmolol so short acting?
Metabolized by plasma esterases
38
What conditions is Esmolol good for controlling intraoperatvely?
Pheochromocytoma
Thyrotoxicosis
Cocaine toxicity
Thyroid storm
39
How might Esmolol also be used by an anesthetist?
May give prior to intubation to prevent sympathetic stimulation (HTN and tachycardia) of laryngoscopy
40
Why doesn't Esmolol cross the BBB?
Poor lipid solubility
41
Which agent is considered a combined alpha-beta antagonist?
Labetalol
42
Which receptors does Labetalol antagonize?
Alpha1 and NON-selective beta receptor blockade
43
How does Labetalol's affinity compare to Phentolamine?
Labetalol has 1/10 affinity to alpha1
44
How does Labetalol's affinity compare to propanolol?
Labetalol has 1/3 affinity to beta receptors
45
What is the beta to alpha ratio of Labetalol?
7:1 beta to alpha
46
What is Labetalol used to treat?
Intraoperative HTN
| Hypertensive crisis
47
What is the mechanism of action of Labetalol?
Decreases BP (alpha1 and beta2 blockade) with attenuated reflex tachycardia (beta1)
48
What beta antagonist is best to give in the OR if the patient is naive to beta blockers?
Esmolol
49
What is the standard concentration of Labetalol?
5mg/mL
50
What is the standard concentration of Esmolol?
10mg/mL
51
What is the standard concentration of Metoprolol?
1mg/mL
52
What is the dose of Labetalol?
0.1-0.5mg/kg
53
What is the dose of Esmolol?
0.2-0.5mg/kg
54
What is the dose of Metoprolol?
0.05-0.1mg/kg
55
What is the mechanism of action of ACE inhibitors?
Prevents the conversion of angiotensin I to angiotensin II
56
What is the action of angiotensin II?
Vasoconstriction and increased Na from aldosterone release
57
What is the mechanism of action of beta blockers?
Antagonism of beta1 causes slowed AV conduction with and increased PR interval and vasculature opposes B2 vasodilation
58
What is the mechanism of action of angiotensin receptor blockers (ARBs)?
Prevent angiotensin II from from occupying the angiotensin I receptor (AT1 receptor)
59
What is thought to cause a chronic cough when taking ACE inhibitors?
ACE breaks down bradykinins, if you inhibit ACE you have an excess of bradykinins which are thought to cause the cough
60
Why are ACE inhibitors contraindicated in renal artery stenosis?
ACE inhibitors impede autoregulation of the arteries
61
What population is at a greater risk of developing angioedema?
African Americans have a 5x greater risk
62
What is thoughts to cause angioedema from ACE inhibitor use?
Bradykinins, associated with vasodilation and increased vascular permeability May also be a genetic component
63
What are the side effects associated with ACE inhibitor use?
```
Cough
Angioedema/agranulocytosis
Proteunuria/Potassium excess
Taste changes
Orthostatic HoTN
Pregnancy contraindication
Renal artery stenosis contraindication
Increased renin
Leukopenia/Liver tox
```
64
How are an individuals hemodynamics typically controlled with normal physiologic function?
SNS
RAAS
Vasopressin
65
If a patient is taking an ACE inhibitor, what is the only function left to control hemodynamics?
Vasopressin, SNS ablated by anesthesia and RAAS inhibited with ACE use
66
When might vasoplegic syndrome occur and what can be used to treat it?
Occurs when a patient has taken an ACE inhibitor day of surgery, induction induces massive hypotension that is refractory to traditional medications, vasopressin and methylene blue can be used to treat profound hypotension
67
What is a risk of using vasopressin in vasoplegic syndrome?
Causes constriction of the coronary arteries and places the patient at risk for MI
68
If a patient experiences angioedema with an ACE inhibitor can they use a ARB?
Yes, cross reactivity is only about 2.5%
69
What is the prototype carbonic anhydrase inhibitor?
Acetazolamide
70
What is the mechanism of action of carbonic anhydrase inhibitors?
Blocks carbonic anhydrase from converting H2CO3 to H and HCO3, thus Na doesn't have a negative charge to be reabsorbed into the blood (Na/HCO3 transporter)
71
What type of metabolic disturbance can occur with the use of carbonic anhydrase inhibitors?
Hyperchloremic metabolic acidosis
72
What portion of the renal tubule does carbonic anhydrase inhibitors act?
Proxima convoluted tubule
73
What is the mechanism of action of Loop diuretics?
Inhibits the Na/K/Cl transporter on the luminal side in the thick ascending loop of Henle (water follows)
74
What are the prototype Loop diuretics?
Furosemide and Ethacrynic acid
75
What commonly used drug class can interfere with Loop diuretics?
NSAIDs, COX increases renal blood flow
76
What drug allergy can occur with the use of loop diuretics?
Sulfa allergy
77
What is the mechanism of action of Thiazide diuretics?
Inhibits the NaCl transporter on the luminal side of epithelial cells in the distal convoluted tubule
78
What is the prototype Thiazide diuretic?
Hydrochlorothiazide
79
What drug allergy is associated with thiazide diuretic use?
Sulfonamides share cross reactivity
80
What metabolic disturbance is associated with thiazide diuretic use?
Hypokalemic metabolic alkalosis
81
What are the two classes of potassium sparing diuretics?
Aldosterone antagonists
| Na channel blockers
82
What is the mechanism of action of osmotic diuretics?
Osmotically active agent that is filtered by the glomerulus but not reabsorbed causes water to be retained in the segments promoting water diuresis
83
What is the prototype osmotic diuretic?
Mannitol
84
Where do potassium sparing diuretics work?
Collecting tubules and ducts
85
Where are the effects of an osmotic diuretic seen?
Proximal convoluted tubule and descending limb of the loop of Henle
86
What is the mechanism of action of ADH antagonists?
Inhibit the effect of ADH in the collecting tubule
87
What three drugs are considered direct vasodilators?
HydralazineSodium NitroprussideNitroglycerine
88
What type of derivative is Hydralazine?
Pthalazine derivative
89
What type of vessels does Hydralazine predominately work on?
Arterial bed thus causing decreased SVR
90
Why isn't Hydralazine typically used in the OR?
Slow onset (10-15 mins) and unpredictable
91
What is the dose of Hydralazine?
2.5-10mg IV
92
What causes the tachycardia seen with Hydralazine use?
Baroreflex and Unknown mechanism
93
What two agents should be used with Hydralazine to gain optimal antihypertensive effects?
Beta blocker and Diuretic
94
How is Hydralazine metabolized?
Acetylation (occurs in bowel or liver)
95
What is a rare but undesirable side effect of Hydralazine?
Drug induced lupus syndrome
96
Which vessels does Sodium Nitroprusside work on?
Arterial and Venous vascular smooth muscle
97
What percentage of Sodium Nitroprusside is cyanide?
44% by weight
98
What dose of Sodium Nitroprusside is associated with cyanide accumulation?
>2mcg/kg/min
99
What is the typical dose of Sodium Nitroprusside?
0.3mcg/kg/min
| MAX of 10mcg/kg/min (no more than 10 mins)
100
What is the composition of Sodium Nitroprusside?
Five cyanide molecules and a Nitro group
101
How does Sodium Nitroprusside interact with oxyhemoglobin?
Dissociated and forms methemoglobin while releasing NO and cyanide
102
What enzyme breaks down cyanide and how is it metabolized?
Rhodanese enzyme located in the liver, combine vitamin b12 and creates thiocyanide which is excreted by the kidneys
103
Which type of patients would you not want to use Sodium Nitroprusside and why?
Patients with preexisting cardiac disease, can cause rebound HTN and myocardial ischemia
104
What causes the rebound HTN with used of Sodium Nitroprusside?
Transient release of renin from the kidneys
105
What is a major indicator of cyanide toxicity?
Pink patient and decreased AVO2 difference (the difference between arterial and venous blood)
106
How should you treat cyanide toxicity?
Stop the infusion, give 100% O2 correct acidosis Sodium thiosulfate & 3% Sodium nitrate
107
What is the mechanism of action of cyanide?
Travels into the cell and prevents cellular respiration, the patient becomes hypoxic from the inside because the cells cannot used the oxygen
108
What is the treatment of methemoglobinemia?
Methylene blue
109
What type of vessels does Nitroglycerine work on?
Predominately the venous system (arterial at higher doses)
110
What can't Nitroglycerine be used for long periods of time?
Tolerance
111
Why are Nitroglycerine and Sodium Nitroprusside predominately used in anesthesia?
Fast onset and titratable
112
What is the metabolite of Nitroglycerine capable of producing?
Methemoglobin
113
What medication would you want available if you needed tight BP control during a case?
Treat HTN: Nipride or NTGTreat HoTN: Phenylephrine and Levophed
114
At what level of the spinal cord and below will the SNS be ablated if spinal is high?
T4 SNS chain takes out cardiac fibers
115
What is the mechanism of action of calcium channel blockers?
Prevents the influx of calcium into the cell necessary for the contraction of smooth and cardiac muscle (AV nodal conduction time and effective refractory period are prolonged)
116
What receptor do calcium channel blockers work on?
L-type calcium channels located in the cardiac, skeletal and smooth muscle tissue
117
What class of antiarrhythmics are calcium channel blockers and what action potential do they work on?
Class 4, work on the cardiac nodal action potential
118
Where does dihydropyridine exert its action?
Blood vessels, causing relaxation and vasodilation
119
Where does non- dihydropyridine exert its action?
SA and AV node
120
What is the prototype calcium channel blocker?
Verapamil, synthetic derivative of pepavarine
121
What is the dose of Verapamil?
75-150mcg/kg IV
122
What is the significance of Verapamil's active metabolite?
It is shown to prolong the duration of action
123
What is the elimination half life of Verapamil?
3-7hrs
124
Why shouldn't you us IV verapamil with ventricular dysfunction, SA or AV nodal conduction disturbances or in the presence of β blockade?
If patient is having an MI & you decrease pressure & then get reflex tachy (increase demand, decrease supply)→patient gets worse
125
What type of calcium channel blocker is Nifedipine?
Dihydroperidine derivative (more vasodilatory effects than nodal)
126
What is the primary use of Nifedipine?
Treatment of HTN (coronary and peripheral vasodilation) reflex tachycardia from baroreflex
127
Why might a patient be taking Nifedipine for HTN?
Unable to tolerate ACE inhibitors and beta blockers
128
Which calcium channel blocker has the greatest vasodilating effects?
Nicardipine
129
What is the major use of Nicardipine?
Short term treatment of HTN by reducing afterload, can be used in OR
130
What is the initiating, titrating and max dose of Nicardipine?
Initiating: 5mg/hr
Titrate by 2.5mg/hr
Max: 15mg/hr
131
What is the only calcium channel blocker that improves exercise tolerance?
Nicardipine, it appears to reduce left ventricular dysfunction
132
Where is Diltiazem primary mechanism of action?
In the AV node for tachyarrhythmias (SVT, Afib)
133
What other pathology can Diltiazem be used to treat?
Migraine headaches
134
Which two CCB cause vasodilation?
Nicardipine and Nifedipine
135
Which two CCB affect the SA and AV nodal cells?
Verapamil and Diltiazem
136
What are the phases of a cardiac myocyte?
```
0-Na channels open
1-K begins to leave
2-Ca channels open, K still leaving
3-Ca channels close, K still open (depolarization)
4-RMP
```
137
What are the phases of a cardiac nodal cell?
4-Slow rise in Na funny channels & T-type Ca channels0-Ca L-type channels open3-K channels open (repolarization) and L-type Ca channels become inactivated
138
What type of drugs are Class I antiarrhythmics?
Na Channel Blockers
139
What is the prototype Class 1A Na channel blocker?
Procanamide
140
What is the mechanism of action of Na channel blockers?
Work on cardiac myocytes by prolonging phase 0 resulting in an increased effective refractory period
141
What is a major disadvantage to using a Na channel blocker?
Causes QT prolongation and can lead to Torsades (caused by metabolite)
142
What is an undesirable side effect of Procanamide?
Has been known to cause Lupus like effects
143
What is a Class 1B Na channel blocker and what is its mechanism of action?
Lidocaine, works on activated and inactivated sodium channels (inside the cell)
144
What is a major concern when using a local anesthetic as an antiarrhythmic?
LAST, know the toxic dose prior to giving and consider if the surgeon has used any prior to administration
145
What is the dose of Lidocaine when using as an antiarrhythmic?
150-200mg IV over 15mins2-4mg/min infusion
146
Why type of antiarrhythmics are Class II?
Beta blockers
147
What is the mechanism of action of Beta blockers antiarrhythmic effects?
They decrease phase 4 slope on the cardiac nodal cells causing the cells to reach threshold at a slower rate
148
What type of arrhythmias are beta blockers useful in treating?
Treat SVT
A fib/flutter
Ventricular tachycardia (V tach)
149
What type of antiarrhythmics are class III?
Potassium channel blockers
150
What is the prototype potassium channel blocker?
Amiodarone
151
What is the mechanism of action of Potassium channel blockers?
They prolong phase three on the myocyte resulting in an It increased effective refractory period
152
What other ion channels does Amiodarone block?
Blocks inactivated sodium channels, adrenergic receptors and calcium channels --> peripheral dilation
153
What is a disadvantage to using Class III antiarrhythmic drugs?
Prolonged QT interval leading to Torsades and Vfib
154
How does Amiodarone affect thyroid function?
Prevents the conversion of T4 --> T3 which can lead to thyroid dysfunction
155
What type of antiarrhythmics are Class Iv?
Calcium channel blockers
156
What is the mechanism of action of Calcium channel blockers?
It takes longer to get through phase 0 at the SA node, therefore decrease firing at the SA node. Also slow conduction at the AV node
157
What are the three mechanisms causing cardiac arrhythmias?
Entrance automaticityTriggered automaticityReentry
158
How do we classify antiarrhythmic drugs?
Vaughan-Williams drug classification
159
True or False, only non-nodal cells have a true resting membrane potential?
True, RMP very negative at rest during phase four of the non-nodal cells
160
What two calcium channel blockers are non-dihydropyridines and where are they most effective?
Verapamil and Diltiazem prolong phase 0 of the cardiac nodal cells
161
What is the mechanism of action of Adenosine
A1 adenosine receptor agonist, activates adenosine sensitive K channel in SA and atrial myocytes, decreases phase 4
162
What type of patients is adenosine contraindicated in?
Not implicated in asthmatics due to mast cell release
163
What is the typical dose of adenosine?
6mg followed by 12mg if necessary
164
What two drugs block the effect of Adenosine?
Caffeine and Theophylline
165
What is the half life of Adenosine?
< 10 seconds
166
What is the mechanism of action of digoxin?
Reversibly inhibits Na/K ion transport system, interferes with outward transport of NA ions and decreased extrusion of Ca ions (increased Ca thought to cause increase in inotropy)
167
What mechanism slows the HR with Digoxin use?
Parasympathetic nervous system activity from sensitization of arterial baroreceptors and activation of the vagal nuclei/ nodose ganglion in CNS
168
What is the primary mechanism of clearance of Digoxin?
Clearance primarily by kidneys
169
What is the primary inactive tissue reservoir for Digoxin?
Skeletal muscle (watch use in elderly)
170
What population has an increased tolerance to Digoxin?
Pediatrics
171
What anesthetic consideration is thought to increase the drug effect of Digoxin?
Hyperventilation, can cause hypokalemia (0.5mEq) and hypokalemia is thought to increase myocardial binding
172
What is considered a toxic blood lever of Digoxin in adults?
>3ng/mL is within toxic range
173
What is the most common cardiac dysrhythmia associated with Digoxin toxicity?
Atrial Tachycardia
174
What is the most frequent cause of death with Digoxin use?
Ventricular fibrillation
175
What is the mechanism of action of Theophylline?
non specific PDE inhibitor, Decreases the hydrolysis of cGMP and cAMP which increases intracellular levels resulting in stimulation of Ca into cardiac and vascular smooth muscle
176
How is theophylline metabolized and excreted?
Hepatic metabolism and excreted by the kidneys
177
What type of patients metabolize Theophylline faster?
Cigarette smokers
178
What is an undesirable side effect of Theophylline?
GERD, relaxes sphincters
179
What is an important anesthetic consideration when using Theophylline with volatiles?
Increases the chances of dysrhythmias
180
What are the effects of parenteral calcium?
Produces an intense positive inotropic effect, increase in stroke volume and decrease in left ventricular end diastolic pressure
181
What medication should not be given simultaneously with parenteral Ca and why?
Digoxin, cardiac dysrhythmias may occur (especially if pt is hypokalemic)
182
What type of drug is Milrinone?
PDE III inhibitor
183
What does PDE III specifically work on?
PDE3 is clinically significant because of its role in regulating heart muscle, vascular smooth muscle and platelet aggregation.
184
How is Milrinone excreted?
80% unchanged by Kidneys
185
How does acidosis affect Milrinone's effects?
Acidosis attenuates inotropic effects
186
What is an important dose dependent effect of Milrinone on the blood?
Thrombocytopenia
187
What are some common EKG changes seen with Digoxin use at therapeutic levels?
Scooped ST (Dali Mustache) Biphasic TShortened QT (could be hypercalcemia)Long PR
188
What EKG changes are seen with Digoxin toxicity?
PVCSinus BradyAV blockRegular A fibVtach (biphasic)
189
What is the antidote for Digoxin toxicity?
Digibind
190
Acceleration of pacemaker discharge is often brought on by increased phase 4 depolarization slope, what can cause this to occur?
HypokalemiaBeta adrenergic stimulationPositive chronotropic drugsFiber stretchAcidosisCurrents of Injury
191
What determines the diastolic interval?
Primarily by the slope of phase 4 (pacemaker potential)
192
Shortening of which two components results in an increase in pacemaker rate?
The duration of the action potentialDuration of the diastolic interval
193
What type of afterpolarizations interrupt phase 3 of the nodal action potential?
Early afterpolarizations (EADs)
194
What type of afterpolarizations interrupt phase 4 of the nodal action potential?
Delayed Afterpolarizations (DADs)
195
When are EADs usually exacerbated?
At slow heart rates and thought to contribute to the development of long QT arrhythmias
196
When are DADs usually exacerbated?
Often occur when intracellular Ca is increased, fast heart rates and thought to be related to arrhythmias associated with digitalis excess, catecholamines and myocardial ischemia
197
Wolff-Parkinson-White is an example of what type of conduction abnormality?
Reentry
198
What three things must be present for reentry to occur?
There must be an obstacle, establishing a circuitThere must be a unidirectional block, conduction must die at some pointConduction time around the circulation must be long enough
199
What are the oldest group of anti arrhythmic drugs?
Sodium channel blockers, Class I
200
Thiocyanate toxicity affects which organ system the most and what type of symptoms are seen?
Neurotoxicityhyperreflexia, confusion, psychosis and miosis, may progress to seizures and coma
201
How does thiocyanate toxicity affect the endocrine system?
Can cause hypothyroidism, inhibits the uptake and binding of iodine
