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Pharm II Final > Cardiac Medications > Flashcards

Cardiac Medications Flashcards

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

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2
Q

Which drugs have the greatest affinity for alpha1 receptors compared to alpha2 receptors?

A

Prazosin
Terazosin
Doxazosin

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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

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4
Q

What alpha antagonist has the same affinity for both alpha1 and alpha2 receptors?

A

Phentolamine

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5
Q

What are alpha antagonists primarily used to treat?

A

HTN
Pathology
BP lability

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6
Q

Which alpha antagonists have a higher affinity for the alpha2 receptor than the alpha1 receptor?

A

Rauwolscine
Yohimbine
Tolazoline

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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

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8
Q

What intraoperative hypertensive emergencies can Phentolamine be used to treat?

A

Pheochromocytoma manipulation

Autonomic hyperreflexia

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9
Q

What is the dose of Phentolamine used to treat hypertensive emergencies?

A

30-70mcg/kg

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10
Q

Does a paralyzed patient require anesthesia?

A

Yes, for sympathetic response and visceral pain

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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

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12
Q

Which alpha antagonist is associated with decreased Hct after long term use?

A

Phenoxybenzamine, a non-selective alpha antagonist

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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

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14
Q

Why is Phenoxybenzamine less associated with tachycardia from decreased SVR?

A

Less alpha2 antagonism

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15
Q

What dose of Phenoxybenzamine should be given for pheochromocytoma?

A

PO dose 0.5-1mg/kg given preoperatively

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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

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17
Q

What is the prototype alpha1 selective antagonist?

A

Prazosin

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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

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19
Q

What class of drugs can be combined with Prazosin use in treatment of essential HTN?

A

Thiazides

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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

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21
Q

Which alpha antagonist provides irreversible blockade?

A

Phenoxybenzamine

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22
Q

What are some common side effects of alpha antagonists?

A

HoTN
Tachycardia
Stuffy nose

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23
Q

What are some additional side effects of Phenoxybenzamine and why?

A

Nausea, fatigue and sedation, it crosses the BBB

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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

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25
Q

What three factors should help determine which beta blocker to use?

A

Selectivity
Elimination 1/2 life
Bioavailability

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26
Q

What is the prototype beta blocker?

A

Propanolol

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27
Q

What are the CV effects of propanolol?

A

Non-selective:Decreased HR and contractility –> B1Increased vascular resistance –> B2

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28
Q

Why is propanolol limited in anesthetic practice?

A

There are better, more selective drugs

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29
Q

What two drugs should be used with caution in patient who have been taking propanolol long term?

A

Fentanyl
Amide local anesthetics
There is a decreased clearance for both of these drugs

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30
Q

Why do some patient go on different medication to treat HTN instead of a beta blocker?

A

Undesirable side effects such as feeling groggy or dizziness. Beta blockers cross BBB

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31
Q

What kind of patients would benefit from metoprolol use?

A

Asthmatics, smokers, patients with COPD since it is a beta1 specific antagonist

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32
Q

Which beta antagonist is most selective to beta1?

A

Atenolol

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33
Q

Why is Atenolol desirable in the outpatient setting?

A

Long acting, only needs to be taken once a day

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34
Q

Other than airway pathology, patients with what disease may also benefit from a beta1 selective antagonist?

A

Metabolic disease (Diabetes)

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35
Q

What beta antagonist is best to give in the OR if the patient is not naive to beta blockers?

A

Metoprolol

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36
Q

Which beta1 antagonist has the fastest onset and shortest duration of action?

A

Esmolol
Onset: 60 sec
Duration: 10 mins

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37
Q

Why is Esmolol so short acting?

A

Metabolized by plasma esterases

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38
Q

What conditions is Esmolol good for controlling intraoperatvely?

A

Pheochromocytoma
Thyrotoxicosis
Cocaine toxicity
Thyroid storm

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39
Q

How might Esmolol also be used by an anesthetist?

A

May give prior to intubation to prevent sympathetic stimulation (HTN and tachycardia) of laryngoscopy

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40
Q

Why doesn’t Esmolol cross the BBB?

A

Poor lipid solubility

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41
Q

Which agent is considered a combined alpha-beta antagonist?

A

Labetalol

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42
Q

Which receptors does Labetalol antagonize?

A

Alpha1 and NON-selective beta receptor blockade

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43
Q

How does Labetalol’s affinity compare to Phentolamine?

A

Labetalol has 1/10 affinity to alpha1

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44
Q

How does Labetalol’s affinity compare to propanolol?

A

Labetalol has 1/3 affinity to beta receptors

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45
Q

What is the beta to alpha ratio of Labetalol?

A

7:1 beta to alpha

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46
Q

What is Labetalol used to treat?

A

Intraoperative HTN

Hypertensive crisis

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47
Q

What is the mechanism of action of Labetalol?

A

Decreases BP (alpha1 and beta2 blockade) with attenuated reflex tachycardia (beta1)

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48
Q

What beta antagonist is best to give in the OR if the patient is naive to beta blockers?

A

Esmolol

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49
Q

What is the standard concentration of Labetalol?

A

5mg/mL

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50
Q

What is the standard concentration of Esmolol?

A

10mg/mL

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51
Q

What is the standard concentration of Metoprolol?

A

1mg/mL

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52
Q

What is the dose of Labetalol?

A

0.1-0.5mg/kg

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53
Q

What is the dose of Esmolol?

A

0.2-0.5mg/kg

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54
Q

What is the dose of Metoprolol?

A

0.05-0.1mg/kg

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55
Q

What is the mechanism of action of ACE inhibitors?

A

Prevents the conversion of angiotensin I to angiotensin II

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56
Q

What is the action of angiotensin II?

A

Vasoconstriction and increased Na from aldosterone release

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57
Q

What is the mechanism of action of beta blockers?

A

Antagonism of beta1 causes slowed AV conduction with and increased PR interval and vasculature opposes B2 vasodilation

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58
Q

What is the mechanism of action of angiotensin receptor blockers (ARBs)?

A

Prevent angiotensin II from from occupying the angiotensin I receptor (AT1 receptor)

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59
Q

What is thought to cause a chronic cough when taking ACE inhibitors?

A

ACE breaks down bradykinins, if you inhibit ACE you have an excess of bradykinins which are thought to cause the cough

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60
Q

Why are ACE inhibitors contraindicated in renal artery stenosis?

A

ACE inhibitors impede autoregulation of the arteries

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61
Q

What population is at a greater risk of developing angioedema?

A

African Americans have a 5x greater risk

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62
Q

What is thoughts to cause angioedema from ACE inhibitor use?

A

Bradykinins, associated with vasodilation and increased vascular permeability May also be a genetic component

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63
Q

What are the side effects associated with ACE inhibitor use?

A 
Cough
Angioedema/agranulocytosis
Proteunuria/Potassium excess
Taste changes
Orthostatic HoTN
Pregnancy contraindication
Renal artery stenosis contraindication
Increased renin
Leukopenia/Liver tox
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64
Q

How are an individuals hemodynamics typically controlled with normal physiologic function?

A

SNS
RAAS
Vasopressin

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65
Q

If a patient is taking an ACE inhibitor, what is the only function left to control hemodynamics?

A

Vasopressin, SNS ablated by anesthesia and RAAS inhibited with ACE use

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66
Q

When might vasoplegic syndrome occur and what can be used to treat it?

A

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

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67
Q

What is a risk of using vasopressin in vasoplegic syndrome?

A

Causes constriction of the coronary arteries and places the patient at risk for MI

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68
Q

If a patient experiences angioedema with an ACE inhibitor can they use a ARB?

A

Yes, cross reactivity is only about 2.5%

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69
Q

What is the prototype carbonic anhydrase inhibitor?

A

Acetazolamide

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70
Q

What is the mechanism of action of carbonic anhydrase inhibitors?

A

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)

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71
Q

What type of metabolic disturbance can occur with the use of carbonic anhydrase inhibitors?

A

Hyperchloremic metabolic acidosis

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72
Q

What portion of the renal tubule does carbonic anhydrase inhibitors act?

A

Proxima convoluted tubule

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73
Q

What is the mechanism of action of Loop diuretics?

A

Inhibits the Na/K/Cl transporter on the luminal side in the thick ascending loop of Henle (water follows)

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74
Q

What are the prototype Loop diuretics?

A

Furosemide and Ethacrynic acid

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75
Q

What commonly used drug class can interfere with Loop diuretics?

A

NSAIDs, COX increases renal blood flow

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76
Q

What drug allergy can occur with the use of loop diuretics?

A

Sulfa allergy

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77
Q

What is the mechanism of action of Thiazide diuretics?

A

Inhibits the NaCl transporter on the luminal side of epithelial cells in the distal convoluted tubule

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78
Q

What is the prototype Thiazide diuretic?

A

Hydrochlorothiazide

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79
Q

What drug allergy is associated with thiazide diuretic use?

A

Sulfonamides share cross reactivity

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80
Q

What metabolic disturbance is associated with thiazide diuretic use?

A

Hypokalemic metabolic alkalosis

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81
Q

What are the two classes of potassium sparing diuretics?

A

Aldosterone antagonists

Na channel blockers

82
Q

What is the mechanism of action of osmotic diuretics?

A

Osmotically active agent that is filtered by the glomerulus but not reabsorbed causes water to be retained in the segments promoting water diuresis

83
Q

What is the prototype osmotic diuretic?

A

Mannitol

84
Q

Where do potassium sparing diuretics work?

A

Collecting tubules and ducts

85
Q

Where are the effects of an osmotic diuretic seen?

A

Proximal convoluted tubule and descending limb of the loop of Henle

86
Q

What is the mechanism of action of ADH antagonists?

A

Inhibit the effect of ADH in the collecting tubule

87
Q

What three drugs are considered direct vasodilators?

A

HydralazineSodium NitroprussideNitroglycerine

88
Q

What type of derivative is Hydralazine?

A

Pthalazine derivative

89
Q

What type of vessels does Hydralazine predominately work on?

A

Arterial bed thus causing decreased SVR

90
Q

Why isn’t Hydralazine typically used in the OR?

A

Slow onset (10-15 mins) and unpredictable

91
Q

What is the dose of Hydralazine?

A

2.5-10mg IV

92
Q

What causes the tachycardia seen with Hydralazine use?

A

Baroreflex and Unknown mechanism

93
Q

What two agents should be used with Hydralazine to gain optimal antihypertensive effects?

A

Beta blocker and Diuretic

94
Q

How is Hydralazine metabolized?

A

Acetylation (occurs in bowel or liver)

95
Q

What is a rare but undesirable side effect of Hydralazine?

A

Drug induced lupus syndrome

96
Q

Which vessels does Sodium Nitroprusside work on?

A

Arterial and Venous vascular smooth muscle

97
Q

What percentage of Sodium Nitroprusside is cyanide?

A

44% by weight

98
Q

What dose of Sodium Nitroprusside is associated with cyanide accumulation?

A

> 2mcg/kg/min

99
Q

What is the typical dose of Sodium Nitroprusside?

A

0.3mcg/kg/min

MAX of 10mcg/kg/min (no more than 10 mins)

100
Q

What is the composition of Sodium Nitroprusside?

A

Five cyanide molecules and a Nitro group

101
Q

How does Sodium Nitroprusside interact with oxyhemoglobin?

A

Dissociated and forms methemoglobin while releasing NO and cyanide

102
Q

What enzyme breaks down cyanide and how is it metabolized?

A

Rhodanese enzyme located in the liver, combine vitamin b12 and creates thiocyanide which is excreted by the kidneys

103
Q

Which type of patients would you not want to use Sodium Nitroprusside and why?

A

Patients with preexisting cardiac disease, can cause rebound HTN and myocardial ischemia

104
Q

What causes the rebound HTN with used of Sodium Nitroprusside?

A

Transient release of renin from the kidneys

105
Q

What is a major indicator of cyanide toxicity?

A

Pink patient and decreased AVO2 difference (the difference between arterial and venous blood)

106
Q

How should you treat cyanide toxicity?

A

Stop the infusion, give 100% O2 correct acidosis Sodium thiosulfate & 3% Sodium nitrate

107
Q

What is the mechanism of action of cyanide?

A

Travels into the cell and prevents cellular respiration, the patient becomes hypoxic from the inside because the cells cannot used the oxygen

108
Q

What is the treatment of methemoglobinemia?

A

Methylene blue

109
Q

What type of vessels does Nitroglycerine work on?

A

Predominately the venous system (arterial at higher doses)

110
Q

What can’t Nitroglycerine be used for long periods of time?

A

Tolerance

111
Q

Why are Nitroglycerine and Sodium Nitroprusside predominately used in anesthesia?

A

Fast onset and titratable

112
Q

What is the metabolite of Nitroglycerine capable of producing?

A

Methemoglobin

113
Q

What medication would you want available if you needed tight BP control during a case?

A

Treat HTN: Nipride or NTGTreat HoTN: Phenylephrine and Levophed

114
Q

At what level of the spinal cord and below will the SNS be ablated if spinal is high?

A

T4 SNS chain takes out cardiac fibers

115
Q

What is the mechanism of action of calcium channel blockers?

A

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
Q

What receptor do calcium channel blockers work on?

A

L-type calcium channels located in the cardiac, skeletal and smooth muscle tissue

117
Q

What class of antiarrhythmics are calcium channel blockers and what action potential do they work on?

A

Class 4, work on the cardiac nodal action potential

118
Q

Where does dihydropyridine exert its action?

A

Blood vessels, causing relaxation and vasodilation

119
Q

Where does non- dihydropyridine exert its action?

A

SA and AV node

120
Q

What is the prototype calcium channel blocker?

A

Verapamil, synthetic derivative of pepavarine

121
Q

What is the dose of Verapamil?

A

75-150mcg/kg IV

122
Q

What is the significance of Verapamil’s active metabolite?

A

It is shown to prolong the duration of action

123
Q

What is the elimination half life of Verapamil?

A

3-7hrs

124
Q

Why shouldn’t you us IV verapamil with ventricular dysfunction, SA or AV nodal conduction disturbances or in the presence of β blockade?

A

If patient is having an MI & you decrease pressure & then get reflex tachy (increase demand, decrease supply)→patient gets worse

125
Q

What type of calcium channel blocker is Nifedipine?

A

Dihydroperidine derivative (more vasodilatory effects than nodal)

126
Q

What is the primary use of Nifedipine?

A

Treatment of HTN (coronary and peripheral vasodilation) reflex tachycardia from baroreflex

127
Q

Why might a patient be taking Nifedipine for HTN?

A

Unable to tolerate ACE inhibitors and beta blockers

128
Q

Which calcium channel blocker has the greatest vasodilating effects?

A

Nicardipine

129
Q

What is the major use of Nicardipine?

A

Short term treatment of HTN by reducing afterload, can be used in OR

130
Q

What is the initiating, titrating and max dose of Nicardipine?

A

Initiating: 5mg/hr
Titrate by 2.5mg/hr
Max: 15mg/hr

131
Q

What is the only calcium channel blocker that improves exercise tolerance?

A

Nicardipine, it appears to reduce left ventricular dysfunction

132
Q

Where is Diltiazem primary mechanism of action?

A

In the AV node for tachyarrhythmias (SVT, Afib)

133
Q

What other pathology can Diltiazem be used to treat?

A

Migraine headaches

134
Q

Which two CCB cause vasodilation?

A

Nicardipine and Nifedipine

135
Q

Which two CCB affect the SA and AV nodal cells?

A

Verapamil and Diltiazem

136
Q

What are the phases of a cardiac myocyte?

A 
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
Q

What are the phases of a cardiac nodal cell?

A

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
Q

What type of drugs are Class I antiarrhythmics?

A

Na Channel Blockers

139
Q

What is the prototype Class 1A Na channel blocker?

A

Procanamide

140
Q

What is the mechanism of action of Na channel blockers?

A

Work on cardiac myocytes by prolonging phase 0 resulting in an increased effective refractory period

141
Q

What is a major disadvantage to using a Na channel blocker?

A

Causes QT prolongation and can lead to Torsades (caused by metabolite)

142
Q

What is an undesirable side effect of Procanamide?

A

Has been known to cause Lupus like effects

143
Q

What is a Class 1B Na channel blocker and what is its mechanism of action?

A

Lidocaine, works on activated and inactivated sodium channels (inside the cell)

144
Q

What is a major concern when using a local anesthetic as an antiarrhythmic?

A

LAST, know the toxic dose prior to giving and consider if the surgeon has used any prior to administration

145
Q

What is the dose of Lidocaine when using as an antiarrhythmic?

A

150-200mg IV over 15mins2-4mg/min infusion

146
Q

Why type of antiarrhythmics are Class II?

A

Beta blockers

147
Q

What is the mechanism of action of Beta blockers antiarrhythmic effects?

A

They decrease phase 4 slope on the cardiac nodal cells causing the cells to reach threshold at a slower rate

148
Q

What type of arrhythmias are beta blockers useful in treating?

A

Treat SVT
A fib/flutter
Ventricular tachycardia (V tach)

149
Q

What type of antiarrhythmics are class III?

A

Potassium channel blockers

150
Q

What is the prototype potassium channel blocker?

A

Amiodarone

151
Q

What is the mechanism of action of Potassium channel blockers?

A

They prolong phase three on the myocyte resulting in an It increased effective refractory period

152
Q

What other ion channels does Amiodarone block?

A

Blocks inactivated sodium channels, adrenergic receptors and calcium channels –> peripheral dilation

153
Q

What is a disadvantage to using Class III antiarrhythmic drugs?

A

Prolonged QT interval leading to Torsades and Vfib

154
Q

How does Amiodarone affect thyroid function?

A

Prevents the conversion of T4 –> T3 which can lead to thyroid dysfunction

155
Q

What type of antiarrhythmics are Class Iv?

A

Calcium channel blockers

156
Q

What is the mechanism of action of Calcium channel blockers?

A

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
Q

What are the three mechanisms causing cardiac arrhythmias?

A

Entrance automaticityTriggered automaticityReentry

158
Q

How do we classify antiarrhythmic drugs?

A

Vaughan-Williams drug classification

159
Q

True or False, only non-nodal cells have a true resting membrane potential?

A

True, RMP very negative at rest during phase four of the non-nodal cells

160
Q

What two calcium channel blockers are non-dihydropyridines and where are they most effective?

A

Verapamil and Diltiazem prolong phase 0 of the cardiac nodal cells

161
Q

What is the mechanism of action of Adenosine

A

A1 adenosine receptor agonist, activates adenosine sensitive K channel in SA and atrial myocytes, decreases phase 4

162
Q

What type of patients is adenosine contraindicated in?

A

Not implicated in asthmatics due to mast cell release

163
Q

What is the typical dose of adenosine?

A

6mg followed by 12mg if necessary

164
Q

What two drugs block the effect of Adenosine?

A

Caffeine and Theophylline

165
Q

What is the half life of Adenosine?

A

< 10 seconds

166
Q

What is the mechanism of action of digoxin?

A

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
Q

What mechanism slows the HR with Digoxin use?

A

Parasympathetic nervous system activity from sensitization of arterial baroreceptors and activation of the vagal nuclei/ nodose ganglion in CNS

168
Q

What is the primary mechanism of clearance of Digoxin?

A

Clearance primarily by kidneys

169
Q

What is the primary inactive tissue reservoir for Digoxin?

A

Skeletal muscle (watch use in elderly)

170
Q

What population has an increased tolerance to Digoxin?

A

Pediatrics

171
Q

What anesthetic consideration is thought to increase the drug effect of Digoxin?

A

Hyperventilation, can cause hypokalemia (0.5mEq) and hypokalemia is thought to increase myocardial binding

172
Q

What is considered a toxic blood lever of Digoxin in adults?

A

> 3ng/mL is within toxic range

173
Q

What is the most common cardiac dysrhythmia associated with Digoxin toxicity?

A

Atrial Tachycardia

174
Q

What is the most frequent cause of death with Digoxin use?

A

Ventricular fibrillation

175
Q

What is the mechanism of action of Theophylline?

A

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
Q

How is theophylline metabolized and excreted?

A

Hepatic metabolism and excreted by the kidneys

177
Q

What type of patients metabolize Theophylline faster?

A

Cigarette smokers

178
Q

What is an undesirable side effect of Theophylline?

A

GERD, relaxes sphincters

179
Q

What is an important anesthetic consideration when using Theophylline with volatiles?

A

Increases the chances of dysrhythmias

180
Q

What are the effects of parenteral calcium?

A

Produces an intense positive inotropic effect, increase in stroke volume and decrease in left ventricular end diastolic pressure

181
Q

What medication should not be given simultaneously with parenteral Ca and why?

A

Digoxin, cardiac dysrhythmias may occur (especially if pt is hypokalemic)

182
Q

What type of drug is Milrinone?

A

PDE III inhibitor

183
Q

What does PDE III specifically work on?

A

PDE3 is clinically significant because of its role in regulating heart muscle, vascular smooth muscle and platelet aggregation.

184
Q

How is Milrinone excreted?

A

80% unchanged by Kidneys

185
Q

How does acidosis affect Milrinone’s effects?

A

Acidosis attenuates inotropic effects

186
Q

What is an important dose dependent effect of Milrinone on the blood?

A

Thrombocytopenia

187
Q

What are some common EKG changes seen with Digoxin use at therapeutic levels?

A

Scooped ST (Dali Mustache) Biphasic TShortened QT (could be hypercalcemia)Long PR

188
Q

What EKG changes are seen with Digoxin toxicity?

A

PVCSinus BradyAV blockRegular A fibVtach (biphasic)

189
Q

What is the antidote for Digoxin toxicity?

A

Digibind

190
Q

Acceleration of pacemaker discharge is often brought on by increased phase 4 depolarization slope, what can cause this to occur?

A

HypokalemiaBeta adrenergic stimulationPositive chronotropic drugsFiber stretchAcidosisCurrents of Injury

191
Q

What determines the diastolic interval?

A

Primarily by the slope of phase 4 (pacemaker potential)

192
Q

Shortening of which two components results in an increase in pacemaker rate?

A

The duration of the action potentialDuration of the diastolic interval

193
Q

What type of afterpolarizations interrupt phase 3 of the nodal action potential?

A

Early afterpolarizations (EADs)

194
Q

What type of afterpolarizations interrupt phase 4 of the nodal action potential?

A

Delayed Afterpolarizations (DADs)

195
Q

When are EADs usually exacerbated?

A

At slow heart rates and thought to contribute to the development of long QT arrhythmias

196
Q

When are DADs usually exacerbated?

A

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
Q

Wolff-Parkinson-White is an example of what type of conduction abnormality?

A

Reentry

198
Q

What three things must be present for reentry to occur?

A

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
Q

What are the oldest group of anti arrhythmic drugs?

A

Sodium channel blockers, Class I

200
Q

Thiocyanate toxicity affects which organ system the most and what type of symptoms are seen?

A

Neurotoxicityhyperreflexia, confusion, psychosis and miosis, may progress to seizures and coma

201
Q

How does thiocyanate toxicity affect the endocrine system?

A

Can cause hypothyroidism, inhibits the uptake and binding of iodine

Pharm II Final (12 decks)

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