Pt Exam 4

Front 1

The beta-blocker esmolol (shown above) was specifically designed to be metabolized very _____________ because of its ____________ group.

Back 1

*D. … quickly…

Front 2

Cardiac glycosides bind and partially inhibit _____________ and result in ___________ contraction of cardiac muscles.

Back 2

Na+K+ATPase …

Front 3

Based on your knowledge of cis and trans ring fusions, which of the cardiac glycosides shown above is the most potent inhibitor?

Back 3

cis-trans-cis

Front 4

Which choice below correctly identifies the structure of the cardiac glycoside with the shorter duration of action?

Back 4

The one with the extra OH is digoxin. A shows digoxin which is more hydrophilic than B.

Front 5

The natriuretic peptides are first produced as a long precursor protein and are then cut by a protease into two pieces (cartoon shown above). Which part binds to its specific receptor and is most responsible for the natriuretic response?

Back 5

the processed peptide that is circularized via a disulfide bond

Front 6

If the antiarrhythmic drug quinidine has two pKa values, 4 and 10, what is the predominating ionization state of this molecule at a pH of 7.0?

Back 6

one ionized, one not. The one in the ring with the double bond is not

Front 7

Paroxysmal nocturnal dyspnea occurs as a result of:

Back 7

Return of extravascular fluid to the vascular circulation

Front 8

Decreased peripheral resistance which lowers the arterial diastolic pressure decreases cardiac oxygen demand?

Back 8

Yes

Front 9

A decrease in the effort spent in isovolemic systole decreases oxygen demand

Back 9

TRUE

Front 10

A reduction in the surface area of the ventricular endocardium at the end of the ventricular filling period increases cardiac oxygen demand

Back 10

TRUE

Front 11

Increasing the capacitance of the venous system would be expected to decrease the cardiac oxygen demand

Back 11

True

Front 12

Dcreasing the arterial runoff would be expected to decrease the cardiac oxygen demand

Back 12

FALSE

Front 13

Increasing the diastolic pressure would be expected to decrease the cardiac oxygen demand

Back 13

FALSE

Front 14

Hypertension of pregnancy would be expected to decrease the cardiac oxygen demand

Back 14

FALSE

Front 15

Giving phenylephrine to a patient in NYHA Class IV CHF would be expected to: Decrease the afterload

Back 15

FALSE

Front 16

Giving phenylephrine to a patient in NYHA Class IV CHF would be expected to: Increase the cardiac oxygen demand

Back 16

True

Front 17

Giving phenylephrine to a patient in NYHA Class IV CHF would be expected to: Decrease the extracellular fluid volume

Back 17

FALSE

Front 18

Giving phenylephrine to a patient in NYHA Class IV CHF would be expected to: Decrease the preload

Back 18

FALSE

Front 19

About the problem of unrecognized digitalization, Actually, it is seldom a problem with digitalis therapy

Back 19

FALSE

Front 20

About the problem of unrecognized digitalization, It can lead to a hypertensive emergency

Back 20

FALSE

Front 21

About the problem of unrecognized digitalization, Most of the digitalizing dose is already within the body

Back 21

TRUE

Front 22

About the problem of unrecognized digitalization, An acute allergic response may result

Back 22

FALSE

Front 23

Why is dobutamine ineffective as a chronic cardiac stimulant?

Back 23

Downregulation of its receptors prevents efficacy

Front 24

Why have the bipyridine cardiac stimulants fallen out of therapeutic favor?

Back 24

They have proarrhythmogenic actions.

Front 25

Is nesiritide a TNF-alpha antagonist.

Back 25

No

Front 26

Does nesiritide increase the levels of circulating renin and, thus, makes CHF worse.

Back 26

no

Front 27

Does nesiritide promotes renal sodium excretion and reduces the extracellular fluid volume.

Back 27

Yes

Front 28

Is nesiritide much more useful for chronic CHF than for acute CHF.

Back 28

no

Front 29

Does Inhibition of the sodium pump lead to decreased activity of the sodium/calcium exchanger.

Back 29

yes

Front 30

Is the Prolonged refractory period of the AV-node leading to fewer action potentials going down the Bundle which results in hemodynamic improvement.

Back 30

no

Front 31

Does Increased secretion of renin which leads to increased sodium retention which allows the heart to beat more strongly.

Back 31

no

Front 32

Consequences of excessively elevated venous pressure can include Jugular venous distension

Back 32

yes

Front 33

Consequences of excessively elevated venous pressure can include Bilateral basilar rales

Back 33

yes

Front 34

Consequences of excessively elevated venous pressure can include Hepatojugular reflux

Back 34

yes

Front 35

The Nernst equation is:

Back 35

Eion=RT/zF ln [ionout]/[ionin]

Front 36

The PR interval of the electrocardiogram is due to

Back 36

AV nodal conduction time.

Front 37

Phase 4 in all regions is primarily dependent on inward-rectifier K channel function.

Back 37

True

Front 38

The conduction velocity in FAST tissue is regulated by sodium channel activity.

Back 38

True

Front 39

Sodium channel inactivation is voltage-dependent.

Back 39

True

Front 40

Automaticity in SLOW tissue is partly dependent upon the funny current.

Back 40

True

Front 41

Sodium channel inactivation increases conduction velocity.

Back 41

FALSE

Front 42

Arrhythmias are due to Abnormalities of impulse conduction.

Back 42

True

Front 43

Arrhythmias are due to Abnormalities of impulse generation.

Back 43

True

Front 44

Arrhythmias are due to Abnormalities of impulse hyperpolarization.

Back 44

FALSE

Front 45

Triggered activity is induced by prior action potentials.

Back 45

True

Front 46

Early afterdepolarizations are due to abnormal repolarization (phase 3).

Back 46

True

Front 47

Late or delayed afterdepolarizations are due to calcium overload in cells.

Back 47

True

Front 48

Catecholamines promote delayed afterdepolarizations.

Back 48

True

Front 49

Reentrant arrhythmias are caused by a two-way conduction block with refractoriness at the site of block.

Back 49

FALSE

Front 50

Reentrant arrhythmias Some may be treated with Na+ channel blockers.

Back 50

True

Front 51

Reentrant arrhythmias Some may be treated with Ca++ channel blockers.

Back 51

True

Front 52

Reentrant arrhythmias Some may be treated with agents which prolong repolarization.

Back 52

True

Front 53

Ca++ channel blockers. antiarrhythmic drugs

Back 53

YES

Front 54

Are K+ channel blockers antiarrhythmic drugs

Back 54

NO

Front 55

ß-adrenergic receptor antagonists. antiarrhythmic drugs

Back 55

YES

Front 56

Na+ channel blockers. antiarrhythmic drugs

Back 56

YES

Front 57

Agents that prolong action potential duration. antiarrhythmic drugs

Back 57

YES

Front 58

Quinidine is used only for supraventricular and ventricular arrhythmias.

Back 58

YES

Front 59

Torsades de pointes occurs only with lidocaine.

Back 59

NO

Front 60

A lupus-like syndrome occurs with

Back 60

procainamide

Front 61

Concealed conduction controls the ventricular rate in atrial fibrillation.

Back 61

Yes

Front 62

Prolongation of action potentials is an important component of class IA agents.

Back 62

Yes

Front 63

Lidocaine is used for supraventricular and ventricular arrhythmias.

Back 63

no

Front 64

Lidocaine is orally effective.

Back 64

no

Front 65

Lidocaine has CNS toxic effects resulting in paresthesis and convulsions.

Back 65

yes

Front 66

Lidocaine is a class III antiarrhythmic agent.

Back 66

no

Front 67

Lidocaine is contraindicated for digitalis-induced triggered activity.

Back 67

no

Front 68

Propranolol non-selectively blocks -adrenergic receptors.

Back 68

yes

Front 69

Propranolol is useful for ventricular arrhythmias due to stress or exercise.

Back 69

yes

Front 70

Propranolol suppresses AV conduction thereby contributing to its efficacy in supraventricular arrhythmias.

Back 70

yes

Front 71

Propranolol prevents sympathetic activation and induction of low-output congestive heart failure.

Back 71

yes

Front 72

Propranolol use can be rapidly terminated with no adverse effects following chronic therapy.

Back 72

no

Front 73

Side effect? procainamide -- cinchonism

Back 73

no

Front 74

Side effect? quinidine --- polymorphic ventricular tachycardia

Back 74

yes

Front 75

Side effect? bretylium --- NE release

Back 75

yes

Front 76

Side effect? amiodarone --- pulmonary toxicity

Back 76

yes

Front 77

Side effect? verapamil --- constipation

Back 77

yes

Front 78

Ventricular arrhythmias can be treated with one or more agent from the following classes? class I

Back 78

yes

Front 79

Ventricular arrhythmias can be treated with one or more agent from the following classes? class II

Back 79

yes

Front 80

Ventricular arrhythmias can be treated with one or more agent from the following classes? class III

Back 80

yes

Front 81

Ventricular arrhythmias can be treated with one or more agent from the following classes? class IV

Back 81

no

Front 82

An antiarrhythmic agent which may induce severe pulmonary toxicity, has a 1-2 month half-life and is used primarily for life-threatening ventricular arrhythmias is

Back 82

amiodarone

Front 83

Which of the following antiarrhythmic agents prolongs action potentials and inhibits b-receptors but does not block sodium channels, has optimal pharmacokinetics, is orally effective and has low toxicity?

Back 83

sotalol

Front 84

can potentially cause torsades de pointes diltiazem

Back 84

no

Front 85

can potentially cause torsades de pointes ciprofloxacin

Back 85

no

Front 86

can potentially cause torsades de pointes terfenadine

Back 86

yes

Front 87

can potentially cause torsades de pointes sotalol

Back 87

yes

Front 88

Associated with atrial fibrillation? Hypertension

Back 88

yes

Front 89

Associated with atrial fibrillation? Myocardial ischemia

Back 89

yes

Front 90

Associated with atrial fibrillation? Hypokalemia

Back 90

yes

Front 91

Associated with atrial fibrillation? Hypothyroidism

Back 91

no

Front 92

Associated with atrial fibrillation? Hyperthyroidism

Back 92

yes

Front 93

Hemodynamic consequences of atrial fibrillation can include decreased sympathetic tone

Back 93

no

Front 94

Hemodynamic consequences of atrial fibrillation can include decreased cardiac output

Back 94

Yes

Front 95

Hemodynamic consequences of atrial fibrillation can include arterial embolization

Back 95

Yes

Front 96

Hemodynamic consequences of atrial fibrillation can include decreased atrial kick

Back 96

Yes

Front 97

In a patient who presents with atrial fibrillation and is hemodynamically unstable, the first therapeutic step is

Back 97

direct current cardioversion

Front 98

Candidate for anticoagulation therapy? A 56 y/o man with embolic stroke secondary to atrial fibrillation and with no documented cerebral bleeding

Back 98

yes

Front 99

Candidate for anticoagulation therapy? A 56 y/o man with PVCs and ventricular dysfunction

Back 99

no

Front 100

Candidate for anticoagulation therapy? A 56 y/o man with hypertension and myocardial ischemia

Back 100

no

Front 101

What factors that need to be considered for initiation of chronic antiarrhythmic therapy

Back 101

risk of antiarrhythmic treatment, type and complexity of arrhythmias, and patients' hemodynamic response

Front 102

Flecainide and encainide have been shown to be safe in all patients

Back 102

no

Front 103

Flecainide and encainide have been shown to increase mortality in patients who survive a MI

Back 103

yes

Front 104

Flecainide and encainide have been shown to possess proarrhythmic effect

Back 104

yes

Front 105

Due to the increased risk of hypotension, ACEI should be avoided in patients with severe heart failure

Back 105

FALSE

Front 106

Treatment with ACEI should be started only after digoxin and diuretics are shown to be ineffective

Back 106

FALSE

Front 107

ACEI should be used with caution in patients with elevated serum potassium concentrations

Back 107

True

Front 108

Patients with New York Heart Association class IV heart failure are at significantly increased risk for the development of ACEI-induced renal failure?

Back 108

True

Front 109

Patients taking NSAIDS are at significantly increased risk for the development of ACEI-induced renal failure?

Back 109

True

Front 110

Patients with concurrent hypokalemia are at significantly increased risk for the development of ACEI-induced renal failure?

Back 110

FALSE

Front 111

use of beta-blockers in patients with heart failure Can be added to pre-existing diuretic and ACEI therapy

Back 111

True

Front 112

use of beta-blockers in patients with heart failure The dose should be decreased in patients with a heart rate < 60 beats/min

Back 112

FALSE

Front 113

use of beta-blockers in patients with heart failure Should not be used in a diabetic patient due to the risk of masking hypoglycemia

Back 113

FALSE

Front 114

A patient with congestive heart failure is started on an ACE inhibitor. He returns to clinic in one week for follow-up. Would this necessitate a reduction of ACE inhibitor dose at this time? The serum creatinine has increased from 1.0 to 1.4 mg/dl

Back 114

no

Front 115

A patient with congestive heart failure is started on an ACE inhibitor. He returns to clinic in one week for follow-up. Would this necessitate a reduction of ACE inhibitor dose at this time? The serum potassium has increased from 5.0 to 5.8 mg/dl

Back 115

yes

Front 116

A patient with congestive heart failure is started on an ACE inhibitor. He returns to clinic in one week for follow-up. Would this necessitate a reduction of ACE inhibitor dose at this time? The patient has symptomatic hypotension

Back 116

yes

Front 117

Am I at increased risk of diuretic-induced hypokalemia? Hyperaldosteronism

Back 117

yes

Front 118

Am I at increased risk of diuretic-induced hypokalemia? Hyperactive renin-angiotensin-aldosterone system

Back 118

yes

Front 119

Am I at increased risk of diuretic-induced hypokalemia? Concurrent digoxin administration

Back 119

no

Front 120

Is this a treatments of diuretic resistance? Give larger oral doses

Back 120

yes

Front 121

Is this a treatments of diuretic resistance? Switch to intravenous diuretics

Back 121

yes

Front 122

Is this a treatments of diuretic resistance? Use combination diuretic therapy

Back 122

Yes

Front 123

Contraindications to ACE inhibitor use in patients with congestive heart failure? Systolic blood pressure < 80 mg/dl

Back 123

no

Front 124

Contraindications to ACE inhibitor use in patients with congestive heart failure? Angioedema with previous administration

Back 124

yes

Front 125

Contraindications to ACE inhibitor use in patients with congestive heart failure? Pregnancy

Back 125

yes

Front 126

Diuretics can activate the renin-angiotensin-aldosterone system, thereby worsening heart failure when used alone

Back 126

True

Front 127

The correct step to take in a heart failure patient with azotemia and volume depletion is to decrease the dose of furosemide

Back 127

True

Front 128

Use of an ACEI with a diuretic is more likely to cause potassium depletion than diuretics alone

Back 128

FALSE

Front 129

Triggered activity is dependent on prior action potentials.

Back 129

True

Front 130

Early afterdepolarizations are due to abnormal repolarization (phase 3). (about triggered activity)

Back 130

True

Front 131

Late or delayed afterdepolarizations are related to calcium overload in cells. (about triggered activity)

Back 131

True

Front 132

Hyperkalemia will promote triggered activity.

Back 132

True

Front 133

All new drugs are screened for their block of ________ for risk of inducing _________.

Back 133

delayed-rectifier K+ channels, polymorphic ventricular tachycardia

Front 134

? Regarding reentrant arrhythmias, They occur when impulses propagate between two regions that possess different electrophysiological properties.

Back 134

True

Front 135

? Regarding reentrant arrhythmias, WPW is a form of re-entry which induces atrioventricular tachycardia.

Back 135

True

Front 136

? Regarding reentrant arrhythmias, In functional re-entry, the rotor can randomly propagate around ventricular muscle to induce life-threatening ventricular fibrillation.

Back 136

True

Front 137

? Regarding reentrant arrhythmias, Both anatomic and functional re-entry may be treated by prolonging the action potential duration.

Back 137

True

Front 138

will prolong the QRS complex? lidocaine

Back 138

no

Front 139

will prolong the QRS complex? flecainide

Back 139

YES

Front 140

will prolong the QRS complex? verapamil

Back 140

NO

Front 141

will prolong the QRS complex? sotalol

Back 141

NO

Front 142

will prolong the QRS complex? adenosine

Back 142

NO

Front 143

Which class of antiarrhythmics agent is inherently favorable since they generally do not tend to increase the current intensity for defibrillation, they tend to increase myocardial function and they inhibit MI–associated ventricular fibrillation?

Back 143

K+ channel blockers

Front 144

Real AE for the drug? procainamide ---lupus-like syndrome

Back 144

YES

Front 145

Real AE for the drug? quinidine --- cinchonism

Back 145

YES

Front 146

Real AE for the drug? lidocaine --- torsades de pointes

Back 146

NO

Front 147

Real AE for the drug? amiodarone --- pulmonary toxicity

Back 147

YES

Front 148

Real AE for the drug? verapamil --- constipation

Back 148

YES

Front 149

widely used for atrial fibrillation, has a very long half-life and interacts with most channels

Back 149

propranolol

Front 150

For the treatment of atrial fibrillation, one may try to control the ventricular rate with ______ or try to re-initiate a normal sinoatrial rhythm with ______.

Back 150

digoxin, quinidine OR propranolol, flecainide OR verapamil, amiodarone

Front 151

_______ has been demonstrated to increase mortality in the CAST trial and ________ has been demonstrated to decrease mortality following infarct.

Back 151

flecainide, amiodarone

Front 152

The following is a natural alkaloid that induces a CNS syndrome of tinnitus and headache, is vagolytic and hypotensive and may induce torsades de pointes?

Back 152

quinidine

Front 153

Place in the correct order of agents allowing recovery from inactivation from fastest to slowest (t increasing from 1 to 10 sec): lidocaine; flecainide; amiodarone

Back 153

lidocaine > quinidine > flecainide

Front 154

pathologic risk factors for stroke? Old age > 85 years old

Back 154

no

Front 155

pathologic risk factors for stroke? Diabetes

Back 155

no

Front 156

pathologic risk factors for stroke? Hypertension

Back 156

YES

Front 157

pathologic risk factors for stroke? Prior embolic event

Back 157

YES

Front 158

risk factors for developing or precipitating atrial fibrillation? Cardiomyopathy

Back 158

YES

Front 159

risk factors for developing or precipitating atrial fibrillation? Thyrotoxicosis

Back 159

YES

Front 160

risk factors for developing or precipitating atrial fibrillation? Hypertension

Back 160

YES

Front 161

risk factors for developing or precipitating atrial fibrillation? Ischemia

Back 161

YES

Front 162

Based on the result of the CAST trial, which antiarrhythmic drugs are proarrhythmic?

Back 162

Encainide, Flecainine, Moricizine

Front 163

not currently available on the market as antithrombotic therapy

Back 163

Ximalagatran

Front 164

Radio frequency catheter ablation is highly successful in long-term management of AV nodal reentry tachyarrhythmias

Back 164

True

Front 165

Radio frequency catheter ablation can result in thermal cell damage

Back 165

True

Front 166

Radio frequency catheter ablation has potential, but major complication is total disruption of AV node

Back 166

True

Front 167

Which of the patient populations is at the highest risk for sudden death from ventricular arrhythmias?

Back 167

Patients with CAD and symptomatic, recurrent sustained ventricular tachycardia

Front 168

In a patient who presents with symptomatic arrhythmias (e.g. atrial fibrillation, ventricular tachycardia (and is hemodynamically unstable, the most appropriate therapeutic action to take immediately is

Back 168

Direct current cardioversion

Front 169

If a patient is hemodynamically stable, the appropriate therapeutic step in the initial management of atrial fibrillation and atrial flutter is

Back 169

control ventricular rate

Front 170

A calcium channel blocker is effective in treatment of ventricular arrhythmias

Back 170

FALSE

Front 171

Ibutilide is approved for converting ventricular arrrhythmias into normal sinus rhythm

Back 171

FALSE

Front 172

Polymorphic and monomorphic ventricular arrhythmias are adverse effects of ibutilide

Back 172

True

Front 173

The best choice for reverting a patient’s atrial fibrillation to sinus rhythm is quinidine

Back 173

FALSE

Front 174

The best choice for maintaining a patient’s atrial fibrillation to sinus rhythm is digoxin

Back 174

FALSE

Front 175

Which of the following patient population would not be a good candidate for dronedarone?

Back 175

severe heart failure

Front 176

What is the advantage of dronedarone over amiodarone

Back 176

d.            *lower risk of thyroid dysfunction due to the absence of iodine

Front 177

The advantage of vernakalant in patients with atrial fibrillation is

Back 177

it has minimal effect on ventricular tissue and therefore less risk for torsades

Front 178

Which of the following agents is the least effective in controlling the ventricular rate in patients with atrial fibrillation:

Back 178

digoxin

Front 179

Which of the following patient-specific conditions is not associated with the potential of precipitating atrial fibrillation?

Back 179

hypothyroidism

Front 180

The following are potential precipitating factors that if present, need to be corrected in the management of arrhythmias:

Back 180

electrolyte abnormalities; acid-base imbalance; Hypoxia

Front 181

Which of the following patient populations is at the highest risk for sudden death from ventricular arrhythmias?

Back 181

patients with CAD and symptomatic, recurrent sustained ventricular tachycardia

Front 182

Which of the following medications has been shown to have a positive effect on mortality in patients who suffered an acute myocardial infarction and who also has a history of congestive heart failure??

Back 182

carvediol

Front 183

Which of the following medications is very effective in converting paroxysmal supraventricular tachycardia?

Back 183

adenosine

Front 184

The following are general goals of therapeutic intervention in patients with atrial fibrillation except? controlling the ventricular rate; maintaining renal function; maintaining sinus rhythm; preventing stroke; reversing unstable vital signs and symptoms

Back 184

maintaining renal function

Front 185

Which of the following mechanisms is the most efficient in increasing the cardiac output?

Back 185

Increasing the venous return

Front 186

In single-cell electrophysiology, Phase 0 corresponds to

Back 186

Sodium influx

Front 187

Which is more efficient as a cardiac reserve mechanism?

Back 187

Changing the preload

Front 188

What effect would acute, large doses of propranolol be expected to have in a decompensated patient with CHF caused by a failure of contraction?

Back 188

Increased symptoms of CHF.

Front 189

What effect would small initial doses of carvedilol be expected to have in a decompensated patient?

Back 189

Decreased preload

Front 190

In a ventricular cell, decreasing the RMP would be expected to increase the conduction velocity

Back 190

FALSE

Front 191

Which of the following is true about the effect of an increased venous return on the afterload? A. It increases the oxygen demand which increases the afterload. B. It increases the preload which increases the afterload. C. The resulting effect is described by Starling’s Law of the heart. D. It increases the preload which decreases the afterload. E. It decreases the preload which increases the afterload.

Back 191

It increases the preload which increases the afterload.

Front 192

Consequenses of chronic renin activation include:

Back 192

Hypertrophy

Front 193

Enalapril is an angiotensin converting enzyme inhibitor. What will enalapril do to the MVO2 in a patient?

Back 193

decrease it

Front 194

Parasympathetic (muscarinic) regulation of heart rate is

Back 194

due primarily to stimulation of a potassium channel that is active during diastole.

Front 195

Reentrant arrhythmias may be effectively treated by

Back 195

prolonging the refractory period

Front 196

An antiarrhythmic agent which will prolong normal action potentials in Purkinjie fibers would most likely stabilize Na+ channels in an inactivated state for

Back 196

for more than 10 seconds

Front 197

An agent which inhibits phase 0 upstroke of action potentials in FAST tissue and prolongs phase 3 repolarization also, is effective for atrial and ventricular arrhythmias, and may induce a lupus-like reaction is

Back 197

procainamide.

Front 198

Lidocaine inhibits

Back 198

open and inactivated Na+ channels

Front 199

An agent that is useful for supraventricular arrhythmias as well as stress-induced ventricular arrhythmias, that indirectly inhibits calcium channels and may promote angina upon rapid withdrawal is

Back 199

propranolol.

Front 200

An agent which has blocks virtually all active channels in the heart, is useful for broad spectrum of ventricular arrhythmias and yet has a very long half-life and strong tissue binding characteristics is

Back 200

amiodarone.

Front 201

. Which of the following agents is used only for supraventricular arrhythmias, is a first-line drug for rate control in atrial fibrillation and also causes hypotension is

Back 201

verapamil

Front 202

Which of the following produces a pharmacological syncope?

Back 202

adenosine

Front 203

Voltage-gated calcium channel(s) mediate

Back 203

phase 0 upstroke of action potentials in SA and AV nodal tissue.

Front 204

Triggered activity is self-initiating.

Back 204

True

Front 205

WPW re-entrant arrhythmias are self-initiating.

Back 205

True

Front 206

All reentrant arrhythmias may be safely treated with Na+ channel blockers.

Back 206

True

Front 207

The main type of arrhythmia associated with agents such as dobutilide is delayed-afterdepolarizations.

Back 207

True

Front 208

a form of polymorphic ventricular tachycardia due to an early-afterdepolarization.

Back 208

Torsades

Front 209

effectively treated with a Na+ channel blocker/ similar to long QT syndrome

Back 209

Torsades

Front 210

a beta-agonist may be a potentially effective treatment for a prolonged PR

Back 210

True

Front 211

a delayed-rectifier K+ channel blocker may be a potentially effective treatment for prolonged PR

Back 211

FALSE

Front 212

a Ca++ channel blocker may be a potentially effective treatment for a prolonged PR

Back 212

FALSE

Front 213

Digoxin arrhythmias are frequent because digoxin is associated with

Back 213

increased intracellular Ca++.

Front 214

The CAST trials demonstrated that

Back 214

Na+ channel blockers can precipitate deadly recurrent ventricular tachycardias

Front 215

Anatomic re-entry is associated with _______ while functional re-entry is associated with _______.

Back 215

WPW, Circutis, rotors

Front 216

Atrial durg to pretreat before cardioversion

Back 216

ibutilide

Front 217

For AV blockade, use

Back 217

CCB

Front 218

When to use Dig

Back 218

Left ventricular dysfunction is when we DO use it still

Front 219

Dronedarone

Back 219

Less effective for AF than amiodarone, Black Box, no sig incr in thyroid/pulm disorders, not for perm a-fib

Front 220

Antithromb when

Back 220

3-6 weeks b4 cardioversion, warfarin, INR 2-3

Front 221

Ibutilide for

Back 221

Conversion of stable recent onset AF to skinus; Class III activate Na current, prolong repol, IV only, "chemical cardioversion"

Front 222

Dofetilide for

Back 222

Oral "chemical cardioversion, <30% response

Front 223

Other drugs for "chemical cardioversion

Back 223

Propafenone, flecanide, amiodarone

Front 224

IA

Back 224

Mod blockade of Na channel, K channel, decr conduction velocity, prolong repolarization

Front 225

IB

Back 225

Mild blockade of Nat channel, decr conduction velocity, shorten repolarization

Front 226

IC

Back 226

Marke blocakde of na channel, sig decr in conduction velocity, no change in repolarization

Front 227

II

Back 227

Beta blockade

Front 228

III

Back 228

Marked prolongation of repolarization

Front 229

IV

Back 229

Calcium channel blockade

Front 230

Drugs with class I to class IV effections

Back 230

Amiodarone and dronedarone

Front 231

Sotalol classes

Back 231

III, beta blockade

Front 232

No drugs for which AR

Back 232

Atrial tach, sinus tach, premature atrial complexes

Front 233

Supra v tachs

Back 233

Atrial Ars, AV junctional Ars

Front 234

AV junctional ARs

Back 234

AV nodal reentry tach, accessory AV path tach

Front 235

Advantage of vernac….. I

Back 235

Specific to atrial tissue

Front 236

Rate effect of dig

Back 236

Small direct AV node, primary effect is via vagus (incr tone)

Front 237

Antithromb risk factors and therapy

Back 237

Weak/mod/high; aspirin to warfarin

Front 238

PIAF rate control for a-fib

Back 238

Diltiazem

Front 239

PIAF ryhtm control in afib

Back 239

Amiodarone

Front 240

STAF rate control for afib

Back 240

Dig, betab blockers, AV nodal ablation

Front 241

STAF rhythm control for afib

Back 241

Cardioversion + class I or amiodarone as prophylactic)

Front 242

Vernakalant

Back 242

Blocker of cardiac K+ and Na+ channels, atria selective, less risk for torsades, not yet available in US, effective conversion to NSR for recent onset AF

Front 243

Maintenance of NSR (from AF?) with chronic therapy

Back 243

Dofetilide, amiodarone, betapace(sotalol)