Cards: Arrhythmias

Question 1

What are the side effects of amiodarone?

Answer 1

Although highly effective, amiodarone has multiple toxicities. Amiodarone therapy is associated with risks for thyroid toxicity, hepatotoxicity, lung toxicity, photosensitivity, corneal and lenticular deposits, optic neuropathy, and other neurologic adverse effects.

Question 2

What do you need to monitor people on amiodarone?

Answer 2

Patients on amiodarone require routine monitoring of thyroid and liver function, pulmonary function testing at baseline and with symptoms, and periodic ophthalmologic evaluation.

Question 3

What does amiodarone interact with?

Answer 3

Amiodarone interacts with several medications. Patients on amiodarone require lower doses of warfarin, statins, and digoxin.

Question 4

What is the mechanism of digoxin?

Answer 4

Digoxin is an oral positive inotropic agent that acts on the sodium-potassium exchanger and has vagal properties that lead to decreased atrioventricular (AV) nodal conduction. As a result of its vagal mechanism, it primarily controls the heart rate at rest and is less effective during activity.

Question 5

What is the mechanism of adenosine?

Answer 5

Adenosine is an A1-receptor blocker that can inhibit AV conduction. Adenosine is frequently used as a therapeutic agent to terminate supraventricular tachycardia.

Question 6

What are some reversible causes of bradycardia?

Answer 6

Physicians should maintain a high suspicion for reversible causes of bradycardia, including elevated intracranial pressure, hypothyroidism, hyperkalemia, Lyme disease, and medication effects (most commonly AV nodal blockers, especially β-blockers and digoxin).

Question 7

What is the diagnostic evaluation for sinus bradycardia?

Answer 7

The diagnostic evaluation of bradycardia includes (1) establishing a correlation between the rhythm (bradycardia) and symptoms and (2) excluding severe conduction abnormalities that require urgent intervention. Evaluation includes a careful history, a focused laboratory evaluation (including an assessment of thyroid function), resting 12-lead electrocardiogram (ECG), exercise treadmill testing to assess the heart rate response to exercise (chronotropic competence), and ambulatory ECG monitoring based on the nature and frequency of the patient’s episodes or symptoms. Rarely, electrophysiologic testing can be used to help ascertain if sinus node dysfunction is present.

Question 8

What are the most common intrinsic and extrinsic causes of sinus bradycardia? What are some of the less common ones?

Answer 8

The most common intrinsic cause of inappropriate or pathologic sinus bradycardia (sinus node dysfunction) is age-related myocardial fibrosis in the vicinity of the sinus node. The most common extrinsic cause of sinus bradycardia is medication effect.

Other, less common, causes of sinus node dysfunction include right coronary ischemia, intracranial hypertension, postsurgical scarring after cardiothoracic surgery, and infiltrative or inflammatory disorders (such as sarcoidosis).

Question 9

What is first degree AV block? How does it look on the EKG? What is it associated with an increased risk for?

Answer 9

AV block is classified as first degree, second degree, or third degree. First-degree AV block is characterized by prolonged AV conduction, which manifests on the ECG as a PR interval greater than 200 msec. First-degree AV block is not a true block because all P waves conduct to the ventricles. It has been associated with an increased risk of atrial fibrillation, pacemaker implantation, and all-cause mortality in long-term follow-up.

Question 10

What happens to p waves with second degree AV block?

Answer 10

In second-degree AV block, some P waves conduct to the ventricle and some do not.

Question 11

Describe a Mobitz Type 1 AV Block. EKG findings, where it is often localized, prognosis, what improves it

Answer 11

When progressive PR prolongation is observed prior to a blocked beat, second-degree Mobitz type 1 (Wenckebach) block is present. Second-degree Mobitz type 1 block is characterized by grouped beating and progressive shortening of the R-R intervals. Mobitz type 1 block is almost always localized to the AV node. It generally carries a benign prognosis and frequently improves with exercise or increased sympathetic tone.

Question 12

Describe a Mobitz Type 2 AV Block. EKG findings, where it is often localized, prognosis, what improves it

Answer 12

When the PR interval is constant prior to nonconducted P waves, the second-degree block is termed Mobitz type 2 block. When 2:1 block is present, Mobitz type 1 versus type 2 block cannot be differentiated. Mobitz type 2 block usually represents block lower in the conduction system and has a higher risk of progression to complete heart block.

Question 13

What is 3rd degree AV block?

Answer 13

Third-degree AV block, or complete heart block, is defined as the failure of any P waves to conduct to the ventricles, and it is characterized by AV dissociation on the ECG.

Question 14

When is a permanent pacemaker indicated?

Answer 14

Pacemakers are indicated in patients with:

• symptomatic bradycardia in the absence of a reversible cause,
• persistent resting heart rate below 40/min
• evidence of AV conduction disturbances that have a high likelihood of progressing to complete heart block or life-threatening sudden asystole
• cases of syncope where there is also chronic bifascicular block

Question 15

In new onset conduction disease, describe the role of temporary and permanent pacing?

Answer 15

When a patient develops new-onset conduction disease in the setting of an acute coronary syndrome, temporary pacing may be required, but decisions on permanent pacing should be delayed until a patient has been revascularized and stabilized to determine whether the arrhythmia persists.

Question 16

What are SVTs?

Answer 16

Supraventricular tachycardias (SVTs) are a group of arrhythmias that arise in atrial tissue or the AV node.

Question 17

What do SVTs look like on EKG and why?

Answer 17

Because conduction of supraventricular impulses below the AV node is conducted normally, the ECG in SVT usually reveals a narrow-complex tachycardia, although the QRS complexes can be wide (>120 msec) in the presence of bundle branch block, aberrancy, pacing, or anterograde accessory pathway conduction (antidromic tachycardia).

Question 18

What are some SVTs from the atrium?

Answer 18

SVTs include abnormal electrical activity arising in the atrium (premature atrial contractions, tachycardia, atrial fibrillation and flutter, multifocal atrial tachycardia)

Question 19

What are some SVTs from the AV node?

Answer 19

AV node (junctional tachycardia, AVNRT, atrioventricular reciprocating tachycardia [AVRT]).

Question 20

What is an arrhythmia that can be seen with digoxin intoxication?

Answer 20

Junctional tachycardias are less common in adults, but they can occur in patients with digoxin intoxication and other conditions.

Question 21

What are ways to terminate SVT?

Answer 21

A recent randomized trial demonstrated that a modified Valsalva maneuver, with supine repositioning and passive leg raise after the Valsalva strain, is more effective than a standard Valsalva maneuver for restoration of sinus rhythm in patients with SVT.

Question 22

What is the modified valsalva maneuver and why is it important?

Answer 22

A recent randomized trial demonstrated that a modified Valsalva maneuver, with supine repositioning and passive leg raise after the Valsalva strain, is more effective than a standard Valsalva maneuver for restoration of sinus rhythm in patients with SVT.

Question 23

What does termination of an SVT with adenosine suggest? What if there is continued atrial activity?

Answer 23

Termination with adenosine often suggests AV node dependence (AVNRT and AVRT), whereas continued atrial activity (P waves) during AV block can help identify atrial flutter and atrial tachycardia.

Question 24

When symptomatic, what are the first line treatments for atrial tachycardia?

Answer 24

when symptomatic, first-line treatment of an acute episode is an intravenous β-blocker or nondihydropyridine calcium channel blocker (diltiazem or verapamil).

Question 25

What is first and second line for hemodynamically unstable atrial tachycardia?

Answer 25

In patients with hemodynamically unstable focal atrial tachycardia, synchronized cardioversion is recommended as first-line therapy. Second-line treatment includes antiarrhythmic drug therapy.

Question 26

Who gets catheter ablation for atrial tachycardia?

Answer 26

Patients who require ongoing management of symptomatic focal atrial tachycardia should undergo catheter ablation as an alternative to pharmacologic therapy. In general, success rates for ablation of atrial tachycardia are lower than those for other SVTs.

Question 27

What patient profile is multifocal atrial tachycardia typically seen in? What is the treatment?

Answer 27

Multifocal atrial tachycardia, characterized by multiple (≥3) P-wave morphologies and a heart rate greater than 100/min, is frequently seen in patients with end-stage COPD. Treatment is usually directed at the underlying etiology and electrolyte disturbances, although β-blockers and calcium nondihydropyridine calcium channel blockers can be used cautiously.

Question 28

What is the most common cause of SVT?

Answer 28

AVNRT is the most common type of SVT, accounting for two thirds of all patients with SVT (excluding atrial fibrillation and atrial flutter). AVNRT is caused by reentrant conduction within the AV node, utilizing both the fast and slow pathways

Question 29

How is acute AVNRT managed?

Answer 29

Beyond acute termination with physical maneuvers, adenosine, or synchronized cardioversion, treatment to prevent recurrent AVNRT includes AV nodal blocking therapy with β-blockers or nondihydropyridine calcium channel blockers.

Question 30

Who with AVNRT gets catheter ablation?

Answer 30

Patients who have recurrent AVNRT or do not tolerate or prefer to avoid long-term medical therapy are usually referred for catheter ablation, which has a high success rate.

Question 31

If a patient has AVNRT and is not a candidate for ablation or betablocker/dilt, what can they be treated with?

Answer 31

Antiarrhythmic drug therapy with flecainide or propafenone may be considered in patients who are not candidates for catheter ablation and in whom β-blockers and nondihydropyridine calcium channel blockers are ineffective; however, flecainide or propafenone are contraindicated in patients with structural or ischemic heart disease.

Question 32

What is first line therapy for WPW?

Answer 32

First-line therapy for Wolff-Parkinson-White syndrome (preexcitation with symptoms) is catheter ablation.

Question 33

For atrial fibrillation, if rate control is ineffective, then what is tried next?

Answer 33

Rhythm control next. Then, In patients who have refractory symptomatic atrial fibrillation despite antiarrhythmic drug therapy, catheter ablation with pulmonary vein isolation is an effective rhythm control therapy.

Question 34

What is considered in CHADSVASC scoring?

Answer 34

The CHA2DS2-VASc score for estimating stroke risk in atrial fibrillation is similar to the CHADS2 score but better differentiates low- and intermediate-risk patients; in addition to heart failure, hypertension, age, diabetes mellitus, and previous stroke, the CHA2DS2-VASc score incorporates lower age (65-74 years), sex, and the presence of atherosclerotic disease.

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Question 35

How is atrial flutter managed?

Answer 35

In many respects, atrial flutter is managed similar to atrial fibrillation, including stroke prevention. However, owing to the atrial rate and the ratio of conduction through the AV node (for example, 2:1 or 4:1), rate control of atrial flutter can be difficult and often requires large doses of AV nodal blockers. Therefore, atrial flutter is usually managed with a rhythm control strategy. Catheter ablation of typical atrial flutter is often preferred owing to a high success rate and lower complication rate relative to other ablation procedures. In asymptomatic patients in whom rate control can be achieved, a medical rate control strategy is acceptable.

Question 36

What is a wide complex tachycardia?

Answer 36

A wide-complex tachycardia is any tachycardia (heart rate ≥100/min) with a QRS complex of 120 msec or greater. The differential diagnosis includes supraventricular rhythms with aberrant conduction (such as underlying bundle branch block), preexcitation, paced rhythms, and ventricular tachycardia.

Question 37

Who are PVCs most common in?

Answer 37

PVCs are more common in patients with hypertension, left ventricular hypertrophy, prior myocardial infarction, and other forms of structural heart disease.

Question 38

If treated, how do you manage PVCs?

Answer 38

Treatment for PVCs usually begins with β-blocker or nondihydropyridine calcium channel blocker therapy.

Question 39

What is sustained and unsustained VT?

Answer 39

VT can present as nonsustained or sustained VT (>30 seconds).

Question 40

How should VT be managed, with:

• All patients with VT
• ischemic CM who present with VT
• CM and heart failure
• structural heart disease or CM and sustained VT/VF
• pts with an ICD

Answer 40

All patients with VT should undergo resting ECG, exercise treadmill testing to provoke the arrhythmia, and cardiac imaging to evaluate for structural heart disease.

• ischemic cardiomyopathy who present with VT should undergo an ischemia evaluation and revascularization if indicated
• cardiomyopathy and heart failure should receive optimal medical therapy in order to reduce their risk of ventricular arrhythmia.
• structural heart disease or cardiomyopathy and sustained VT/VF should undergo ICD implantation for secondary prevention. amiodarone is first-line antiarrhythmic drug therapy.
• In patients with an ICD, if VT recurs despite β-blocker therapy, antiarrhythmic drug therapy should be considered. Patients with recurrent VT despite medical therapy should be considered for EP study and catheter ablation, which has been shown to reduce ICD shocks and thus improve quality of life.

Question 41

What is long QT syndrome?

Answer 41

Long QT syndrome is one of the most common inherited arrhythmias and is defined by the presence of a prolonged QTc interval (>440 msec in men and >460 msec in women) accompanied by unexplained syncope or ventricular arrhythmia.

Question 42

What is Brugada disease?

Answer 42

Brugada syndrome, an autosomal dominant disorder associated with mutations in the sodium channel gene, is characterized by right precordial ECG abnormalities, including ST-segment coving (ST-segment elevation that descends into an inverted T wave) in leads V1 through V3 with or without right bundle branch block ( Figure 20 ), VF, and cardiac arrest. Brugada syndrome is more common in men and in persons of Asian descent. Arrhythmic events often occur at night during sleep. T

Question 43

What is sudden cardiac death?

Answer 43

SCD is defined as instantaneous death or sudden collapse within 1 hour of symptoms. Unwitnessed death is considered SCD if the patient was known to be well within 24 hours of the event.

Question 44

How are patients in cardiac arrest managed?

Answer 44

Patients with cardiac arrest require immediate cardiopulmonary resuscitation (CPR) and advanced cardiac life support. The two most important interventions for patients in cardiac arrest are high-quality CPR chest compressions and rapid defibrillation in patients with VT/VF arrest.

Question 45

Describe what meds are given and when during a cardiac arrest

Answer 45

Once CPR has been started, the 2010 AHA guidelines on CPR and emergency cardiovascular care dictate management based upon the presence or absence of a shockable rhythm. In patients with asystole or pulseless electrical activity (PEA), CPR is continued with reassessment of rhythm status for a shockable rhythm every 2 minutes. Epinephrine (1 mg intravenously) should be given every 3 to 5 minutes, although vasopressin (40 units intravenously) can replace the first or second dose of epinephrine. Atropine is not recommended for the treatment of asystole or PEA arrest. Further management of PEA arrest should include ascertainment and treatment of any correctable etiology (for example, tamponade). In patients with VT/VF, a shock is advised with immediate resumption of CPR and reassessment of the rhythm in 2 minutes. Epinephrine should be given after the second shock and every 3 to 5 minutes thereafter. If VT/VF continues despite three shocks and epinephrine, amiodarone should be given as a bolus.

Question 46

How is symptomatic bradycardia treated during a cardiac arrest?

Answer 46

atropine

Question 47

Describe post-resuscitation care for cardiac arrest

Answer 47

Post-resuscitation care includes therapeutic hypothermia in patients who remain comatose. Complications of therapeutic hypothermia include ventricular arrhythmias during rewarming and infectious complications, including sepsis. Hemodynamics and oxygenation should be optimized in the post-arrest setting. Moderate glycemic control is also recommended. Patients with evidence of acute coronary syndrome should undergo immediate catheterization and revascularization provided there are no contraindications.

Question 48

Who gets an ICD for secondary prevention after a cardiac arrest?

Answer 48

Patients with sustained ventricular arrhythmias or cardiac arrest without a reversible etiology have a class I recommendation for secondary prevention ICD placement.