Sunday, April 25, 2021

Cardiac Arrhythmias Case File

Posted By: Medical Group - 4/25/2021 Post Author : Medical Group Post Date : Sunday, April 25, 2021 Post Time : 4/25/2021
Cardiac Arrhythmias Case File
Eugene C. Toy, MD, Manuel Suarez, MD, FACCP, Terrence H. Liu, MD, MPH

Case 15
A 25-year-old man complains of palpitations and tachycardia with skipped heart beats. He is found to be diaphoretic following a  brief episode of syncope accompanied by urinary incontinence after participating in a pick-up basketball game. He went to the emergency  department (ED)  because the  palpitations  would not  subside. The patient's older male sibling also suffers from the same condition. The patient's  neurological examination is unremarkable. A magnified snapshot  of the ECG tracing is shown  (Figure   15-1). These episodes have occurred twice before, after similar physical stimuli. At the last occasion, the tachycardia terminated  after a bout of hiccups. His  vital  signs are: respiratory  rate (RR)  22 breaths/minute,  blood  pressure  (BP)  100/50 mm Hg,  and heart  rate  (HR)  of 150  beats/minute and regular. His oxygen  saturation (O2sat) is 94% on  ambient air (RA). Other values include temperature of 98°F, weight 70 kg, height  72  in. His  electrolyte  levels were: sodium (Na+) 140  mEq/L,  potassium (K+) 4 mEq/L, chloride (CI-) 105 mEq/L, bicarbonate (HCO3m-) 23 mEq/L.

Magnified ECG tracing

Figure 15-1. Magnified ECG tracing.

 What is the most likely diagnosis? 
 Why is the diagnosis so important for correct treatment? 
 What is the next step in therapy? 


Cardiac Arrhythmias

Summary: A 25-year-old man has palpitations, tachycardia with HR of 150 beats/ minute, and a QRS complex with a slurred upstroke of the R wave representing Wolff-Parkinson-White syndrome (WPW), a life-threatening supraventricular arrhythmia. He has a normal blood pressure.
  • Most likely diagnosis: WPW. The classical findings of short PR interval (rapid AV conduction via accessory pathway) and a "delta wave" (representing pre-excitation of the portion of the ventricle that begins to depolarize by the bypass tract) .
  • Importance of diagnosis: This i s an important diagnosis since the usual treatments for supraventricular tachycardias such as blocking the AV node will make the WPW arrhythmia worse, which can lead to the patient's death.
  • Treatment: The drugs of choice are adenosine, procainamide, or amiodarone, which prolong conduction in the aberrant track and slow repolarization; adenosine may also be used with pure WFW but is contraindicated with concomitant atrial fibrillation.

  1. To develop an approach to diagnosing the different types of cardiac arrhythmias.
  2. To recognize the most common types of supraventricular and ventricular arrhythmias.
  3. To be familiar with a rational workup and treatment of the cardiac arrhythmia.
This 25 -year-old patient has a tachycardia with HR of 150 beats/minute, the classic shortened PR interval, and "delta wave" of WPW. The first priority is to recognize and stabilize the patient with this life-threatening arrhythmia. Synchronized electric cardiac defibrillation (ECD) is indicated in all hemodynamically unstable patients with arrhythmias. Advanced cardiac life support (ACLS) measures, including cardiopulmonary resuscitation (CPR ) , may be needed if the patient fails ECD and the heart rhythm deteriorates into ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT). Continuous monitoring of vital signs and ECG should be employed. Rapid sequence intubation (RSI) and mechanical ventilation (MV) and pacing with an external on IV pacemaker may be required. Replacement of intravascular volume, usually with intravenous (IV) normal saline (NS) , will increase preload and ventricular volume, BP, and CO. The electrolyte levels should be assessed and corrected if abnormal. Continuous infusion of antiarrhythmic drugs may be employed in order to maintain normal sinus rhythm (NSR). The next priority is to determine the etiology of the cardiac arrhythmia. Electrical activity occurs

normal ecg intervals and duration

before mechanical activity in the heart; P waves occur before atrial contraction; QRS complex occurs prior to each ventricular contraction, and T waves occur prior to each ventricular repolarization. The accepted duration or interval time of these waves is seen in Table 15-1.

The morphology of P waves can also suggest certain atrial diseases such as the P mitrale. Abnormal P-wave morphology may be seen in mitral valve regurgitation, or the peak in the second half of the P wave seen in left atrial enlargement. The early, tall notch in first half of P wave is seen in right atrial enlargement or P pulmonale. The morphology of the P wave can be upright, biphasic, or inverted in the inferior leads (II, III, a VF) and is best seen in those leads. The inferior leads are looking directly at the atria. A large negative P wave seen in lead V1 is also indicative of left atrial enlargement.

Drugs such as digoxin, β-blockers (BBs) , and calcium channel blockers (CCBs) are used to treat the more common supraventricular arrhythmias (SVTs) . These agents block the AV node and are contraindicated in WPW. The drugs of choice for treating WPW are adenosine, procainamide, or amiodarone which prolong conduction in the aberrant track and slow repolarization; adenosine is contraindicated with atrial fibrillation. In unstable patients, immediate ECD should be used. Hypoxemia and any electrolyte imbalances, especially of K+ and Mg+ should be corrected. Atrial tachycardia may arise from any area of the right or left atrium and the most common arrhythmic pathway is reentry. Reentrant tachycardia is associated with structural heart disease such as Ebstein anomaly but also seen with digitalis toxicity. Atrial fibrillation (AF) in WPW can lead to a rapid rhythm, which may degenerate into ventricular fibrillation (V). Sudden death may occur in 0.2% of affected individuals over 3 to 10 years.

Approach To:
Cardiac Arrhythmias

Arrhythmias can be classified according to their origin. Supraventricular arrhythmias (SVTs) usually have a narrow QRS with visible retrograde P waves (P waves seen after the QRS complex ) and originate above the AV node. P waves may also appear to be absent because they become buried in the QRS complex. Ventricular arrhythmias generally have a wide QRS complex ( >0.12 ms) similar to a bundle branch block pattern with AV disassociation and can be monomorphic or polymorphic. Arrhythmias are also classified according to rate. Tachycardia is defined as a rate > 100 beats/minute. Bradycardia is classified as a rate <60 beats/minute. Common signs and symptoms o f these arrhythmias are palpitations, lightheadedness, dyspnea, chest pain, syncope or presyncope, and fatigue. Syncope requires a loss of blood flow to both cerebral hemispheres at the same time. Evaluation of an arrhythmia is based on a recent ECG, an old ECG if available for comparison, a CBC, electrolyte determinations, TSH, ABG or O2sat, glucose, BUN , and creatinine levels. ECD is indicated for hemodynamically unstable patients regardless of the rhythm.

Tachyarrhythmias (>100 beats/minute) 
  • Sinus tachycardia: Normal sinus rhythm (NSR) is defined as an SA nodal rhythm with a frequency of 60 to 100 beats/minute. Heart rates >100 beats/minute originating in the SA node are defined as a sinus tachycardia (ST). ST is associated with anxiety, pain, fever, dehydration, stress, and drugs both therapeutic and recreational. Atrial tachycardias arise from ectopic atrial foci and/or the pulmonary veins. Valsalva maneuvers and/or carotid massage can terminate the SVTs. ST, as in multifocal atrial tachycardia (MAT), is defined as an ectopic atrial rhythm with >2 different P-wave morphologies at a rate >100 beats/minute. MAT is typically seen in patients with COPD or other pulmonary disease processes. MAT responds to treatment of the underlying COPD, especially hypoxia with hypercapnia. Antiarrhythmic therapy area is usually unnecessary since MAT is self-limiting and responds to treatment of the underlying cause. 
Supraventricular tachycardia (SVT): SVT is a regular and rapid rhythm with a narrow QRS, with rates between 160 and 180 beats/minute. The most common type, atrioventricular nodal reentry tachycardia (AVNRT), involves reentry electrical activity within the atrioventricular node (AVN). A late P wave can be seen in the final portion of the QRS complex, which is consistent with retrograde P-wave conduction via the AVN. SVT is a benign rhythm in the absence of structural disease. A true SVT should respond to treatment with IV adenosine if it is unresponsive to vagal maneuvers. Adenosine breaks the arrhythmia and causes a long pause in the electrical activity, which resets the AV node for normal AVN conduction (see Figure 15-2 ) .
  • Atrial flutter: Atrial flutter is recognized b y sawtooth P waves with a regular pattern. All P waves have the same morphology and are conducted at regular rates. The P-wave rate and pulse rate varies from 240 to 350 beats/minute. Conduction of P waves to QRS varies from 2 to 1 or 3 to 1 P waves for every QRS complex conduction leading to a heart rate of 100 to 150 beats/minute. Flutter may turn into AF over time. One must rule out secondary noncardiac causes of atrial flutter such as hyperthyroidism, high caffeine intake, overuse of vasoconstricting nasal sprays, β2 agonists, theophylline, and substance abuse with alcohol, cocaine, or amphetamines.
  • Atrial fibrillation: AF is the most common sustained ectopic atrial tachyarrhythmia. AF is an irregularly irregular rhythm on ECG without any discernible P waves being recognized (chaotic pattern as atria fibrillate).

AV nodal reentrant tachycardia

Figure 15-2. AV nodal reentrant tachycardia. H R of 150 beats/minute with narrow complex tachycardia. (Reproduced, with permission, from  Longo DL, Fauci AS, Kasper DL, et al. Harrison's Principles of internal Medicine. 18th ed. New York, NY: McGraw-Hill Education; 201 2. Figure e30-l3.)

Regularization of the R-R interval (becomes less irregular) in AF at heart rates of <60 can be a sign of digoxin toxicity. AF can be classified as:
  1. Acute <48 hours
  2. Chronic AF persisting for >48 hours
  3. Paroxysmal AF
  4. Indeterminate AF
This classification helps choose treatment options. Treatment of AF requires anticoagulation with warfarin (Coumadin) to reduce stroke rates in patients who have a CHADS2 score >2. In patients whose CHADS2 score is < 2 , treatment with ASA is recommended. Stools should be checked for occult blood or any signs of active bleeding before starting heparin or warfarin (Coumadin). Dabigatran, a new oral direct thrombin inhibitor, can be used as an alternative to warfarin in nonvalvular AF. Dabigatran does not require frequent blood tests for international normalized ratio (INR) or prothrombin time (PT) monitoring.

An echocardiogram or a transesophageal echo study is excellent for the evaluation of valvular disease causing AF. The identification of intracardiac thrombi must be excluded prior to cardioversion. Clots in the left atrial appendage are commonly found. When clots are present, anticoagulation is needed for a period of 4 weeks prior to performing elective ECD. Over 80% of patients with AF have some form of underlying heart disease, frequently atrial septal defects are found. In the elderly the primary underlying cause is hypertension. To treat AF or any SVT, Valsalva maneuvers or carotid massage should be attempted to increase vagal tone, to slow A VN conduction, and to cause increased refractoriness. ECD is used in all unstable patients regardless of tachyarrhythmia. IV heparin should be given for any AF of unknown duration, and an evaluation for intracardiac thrombi should be done before attempting ECD to NSR. Anticoagulation should continue for 1 month post ECD in A F patients. ECD is an alternative to pharmacological cardioversion of AF of any duration. AF treatment requires anticoagulation, no matter whether treated with rhythm control or conversion to NSR. If the heart rate exceeds 110 beats/minute the patient may need additional AVN blockade. A recommended INR range of 2.0 to 3.0 is optimal for patients with a CHADS2 score >2. To determine whether the risk of stroke is high enough to warrant chronic anticoagulation in AF, risk stratification scores have been developed. One such stratification scheme is known as CHADS2 score (with 1 point each for the presence of the following, with a maximum score of 6):
  • Congestive heart failure (CHF)-1 point
  • Hypertension- 1 point
  • Age >75 years- 1 point
  • Diabetes-1 point
  • Stroke or transient ischemic attack (TIA)-2 point
Patients are given 2 points for a history of stroke or TIA (the strongest risk factors) and 1 point for all other risk factors. The risk of stroke is the lowest in patients with a CHADS2 score of 0 (1.2 %). The risk is 18% per year for a CHADS2 score of 6 (maximum score). Patients with a CHADS2 score of 23 and patients with a history of stroke are at high risk and should be considered for chronic anticoagulation dosing with warfarin. Patients with a CHADS2 score of 1 or 2 should be assessed on an individual basis for ASA versus warfarin therapy. Cerebrovascular accident (CVA) rate in nonrheumatic AF is 5% . Risk factors for stroke are a history of previous TIA or CVA, an MI, hypertension, age >65 years, diabetes, left atrial enlargement, and left ventricular dysfunction.

In nonvalvular AF, the use of warfarin with a target INR of 2 to 3 reduces the stroke risk by 68%, which usually outweighs the bleeding risk. In patients without risk factors, ASA may be sufficient and will decrease the stroke rate by 42%. In patients older than 65 , heart rate control may be the best, especially when compared to the expected side effects of antiarrhythmic drugs used to maintain rhythm control. The goal is to maintain a heart rate < 100 beats/minute. BBs and CCBs are the drugs of choice for this purpose. Digoxin is not recommended as a single agent especially when the heart rate activity becomes uncontrolled during exercise. Oral or IV agents can lead to cardioversion in 70% to 90% of those cases with the onset of AF within the past 48 hours, but are less effective in treating chronic AF cases appearing after 48 hours. Amiodarone and dronedarone are useful medications when any structural heart disease is present, otherwise propafenone or flecainide is used. Most antiarrhythmic drugs are also proarrhythmic on their own. IV heparin should be started immediately in patients with newly diagnosed AF. Risks of ECD in AF include thromboembolism, tachyarrhythmias, and bradyarrhythmias.

Surgical procedures. Catheter ablation is now frequently done to eliminate the aberrant conducting pathway. This is 99% effective with a mortality of only 1% to 3%. The Maze surgical procedure, in which a series of incisions are made in a maze-like pattern to reduce effective atrial size and prevent reformation of AF waves.

Atrioventricular Nodal Block (AVNB)
  • First-degree heart block: The PR interval is >0.20 seconds on the ECG. All P waves are conducted and this condition requires no specific treatment. It is benign in most patients.
  • Second-degree heart block: This heart block is characterized by intermittent nonconduction of P waves and "dropped" ventricular beats. Second-degree heart block is of 2 types, Mobitz I and Mobitz II.
  • Mobitz type I second-degree heart block: Mobitz type I second-degree heart block is characterized by a progressive prolongation of the PR interval until a dropped beat occurs (also called Wenckebach block) and does not progress to complete heart block. It is transient and usually requires no treatment. Type I may be associated with a bradycardia.
  • Mobitz type II: Mobitz II second-degree heart block is characterized by nonconduction of P waves and subsequent "dropped" ventricular beats without the progressive prolongation of the PR interval (see Figure 15-3). This is considered malignant since it tends to proceed to complete heart block or third-degree heart block. Mobitz II heart block is associated with evidence of additional disease in the conduction system, such as bundle branch block (BBB) or bifascicular or trifascicular block. Mobitz type II heart block suddenly and unpredictably progresses to complete heart block and is usually treated with a pacemaker.
  • Third-degree heart block: Third-degree heart block is also referred to as complete heart block or atrioventricular disassociation (AVD). In third-degree
Second-degree heart block

Figure 15-3. Second-degree heart block with bradycardia with ventricular HR of 30 beats/minute. This is Mobitz  II heart block with P waves of 60 beats/minute. (Reproduced, with permission, from Longo  DL,  Fauci AS, Kasper DL, et al. Harrison's Principles of Internal Medicine. 18th ed.  New York, NY: McGraw-Hill Education; 201 2. Figure  e30--3.) 

heart block, the P rate i s higher than the QRS rate and marches a t the same interval through the rhythm. Insertion of a pacemaker is usually required for relief of third-degree heart block.

Sinus node dysfunction
Sinus node dysfunction (SND) has also been called sick sinus syndrome (SSS), and refers t o abnormalities i n the formation of sinus node impulses. These conditions include sinus bradycardia, sinus pause/arrest, chronotropic incompetence, and sinoatrial exit block. SND is frequently associated with various SVTs, such as AF and atrial flutter. When associated with SVTs, SND is often termed tachy-brady syndrome or SSS, is seen frequently in the elderly, and is a common cause for the insertion of a pacemaker.

Treatment: The treatment of bradycardia begins with removing all drugs that are capable of causing a bradycardia. Atropine is used in an emergency or cases of symptomatic bradycardia. Atropine IV therapy and external or internal pacing are the main treatment options. Vagal maneuvers and constipation (straining) should be avoided since they can worsen bradycardia. Pacing is indicated for the treatment of symptomatic bradycardia, tachy-brady syndrome, complete heart block, and asymptomatic patients with asystolic pauses > 3 seconds or ventricular escape rhythms of <40 beats/minute. Permanent pacing improves survival in complete heart block especially if syncope has occurred previously.
Drug therapy: One should consider a BB or CCB such as verapamil to treat AVN reentrant tachycardia. CCBs slow calcium channel influx and decrease AVN conduction and increase AVN refractoriness. Amiodarone has the least proarrhythmic effect and is the drug of choice for any patient with LV dysfunction or structural heart disease. Dronedarone has a similar therapeutic effect as amiodarone without the iodine load of amiodarone. One should monitor the QT interval on patients on antiarrhythmic drugs and compare it to baseline ECGs. Watch patients closely for potential side effects of antiarrhythmic drugs. All patients on amiodarone need to be evaluated every 6 to 1 2 months with pulmonary function tests, diffusing capacity for carbon monoxide (DLCO), chest x-ray, thyroid- stimulating hormone level, and liver function tests. This testing evaluates the most common side effects seen with the use of amiodarone. The iodine content of amiodarone is so high that CT scans may appear to have contrast even when done without contrast. When using procainamide, one should follow CBC and WBC values since it has been associated with agranulocytosis. Procainamide can also cause a drug-induced lupus with positive ANA (RNA not DNA) values.

To evaluate and diagnose an arrhythmia, one needs to obtain a 12-lead ECG as well as continuous ECG monitoring. Vital signs including O2 saturation should be monitored. Ischemic heart disease (IHD) should be suspected, and old ECGs should be compared with the current ones. Reversible causes of ventricular arrhythmias such as drugs, electrolyte abnormalities, CAD, ischemia, IHD, hypoxia, or drug toxicity should be sought.

Ventricular Tachycardia
Ventricular tachycardia (VT) is defined both as a wide- or narrow-complex tachycardia with continuous rapid depolarizing bursts in the ventricular His-Purkinje system. VT needs rapid attention and reversal with ECD as it is the main cause of sudden death. VT is a reentrant pathway arrhythmia with abnormal impulse conduction. It is often comorbid with underlying structural heart disease, most commonly ischemic heart disease (IHD) , electrolyte imbalances such as ↓K+ and ↓Mg+, drug toxicity with QT-prolonging drugs (psychiatric medications) , prolonged QT syndrome, valvular heart disease, nonischemic cardiomyopathy (viral, alcohol, etc). VT is subdivided into sustained VT lasting > 30 seconds or requiring termination with ECD and nonsustained VT consisting of 3 straight PVCs with PVCs being <30 seconds. The morphology of the QRS can also be used to evaluate the origin and cause of VT. Concurrent treatment for IHD and CAD is begun because of their high correlation as underlying disorders in VT.

In families with a history of VT and death, one must consider a history of long QT syndrome. VT is also seen in arrhythmogenic right ventricular dysplasia and Brugada syndrome with RBBB. The symptoms and presentation that patients display depend upon the ventricular rate, duration of the arrhythmia, and presence of underlying heart disease.

Patients with nonsustained VT are usually asymptomatic but may complain of palpitations. Patients with sustained VT may present with syncope or nearsyncope or sudden death. VT includes as a group VT, VF, and T dP or long QT syndrome arrhythmias. It is characterized by wide-complex QRS >0.12 seconds and ventricular rate > 100 beats/minute (see Figure 15-4). In VT, these rates are typically from 140 to 250 beats/minute, in VF rates are > 300 beats/minute, and in TdP rates are 200 to 300 beats/minute. When comparing SVT with aberrancy versus VT, a history of structural or ischemic heart disease suggests that

Ventricular tachycardia ECG

Figure 15-4. Ventricular tachycardia. ECG showing AV dissociation (arrows mark P waves), wide­complex QRS. (Reproduced, with permission, from Longo DL, Fauci AS, Kasper DL, et al. Harrison's Principles of Internal Medicine. 18th ed. New York, NY: McG raw-Hill Education; 2012. Figure 233-1 0.) 

the arrhythmia is most likely VT. The presence o f AV disassociation or third degree block also suggests VT. An RBBB morphology QRS >0.14 seconds or an LBBB morphology QRS >0.16 seconds are also more likely to be VT than SVT with aberrancy. A regular R-R interval in VT is more common than SVT with aberrancy. The presence of MI or CAD is almost diagnostic of VT. Profound depression in hemodynamics also point to a VT, but a BP near 100 mm Hg does not exclude it. Large "cannon" a waves of atrial contraction against a closed tricuspid valve caused by the disassociation effect of the third-degree heart block are seen on physical examination.

In unstable patients, VT should be assumed and treated with ECD, delivered in synchronized mode if a pulse is present and in a nonsynchronized mode if a pulse is not present. Definitive treatment of arrhythmias due to reentrant pathways is ablation of those pathways. In the absence of structural heart disease, ablation is the treatment of choice. If structural heart disease is present with an EF <35%, an implanted cardiac defibrillator (ICD) is recommended. ICD use decreased mortality regardless of the etiology in all VT patients with EF <35%.

Drug Therapy
Antiarrhythmic IV drug therapy for VT/VF serves to terminate arrhythmias, to prevent recurrence of arrhythmia, and to prevent life-threatening arrhythmia such as VF (with insertion of an ICD). For acute treatment of sustained monomorphic VT, IV lidocaine, procainamide, or amiodarone may be used. Patients with recurrent VT need chronic therapy. Drug treatment of patients with VT and structural heart disease is inferior to implantation of an ICD. Drugs are used as adjuncts when ICD implantation is contraindicated. Pharmacological treatment for nonsustained VT can be avoided unless there is a history of structural heart disease or long QT syndrome. Here procainamide is the drug of choice. IV magnesium sulfate can be used to suppress polymorphic VT in patients with prolonged QT intervals. Treatment for CHF with BBs, ACEI, and spironolactone will reduce the incidence of sudden death in patients with systolic dysfunction.

Ventricular Fibrillation
Ventricular fibrillation (VF) is an arrhythmia in which there is an uncoordinated and ineffective contraction of the ventricles in the heart, which stops pumping of blood. Although there is electrical activity in the heart, the mechanical activity is missing in this condition. VF is a medical emergency that requires prompt ECD and ACLS. It will likely degenerate into asystole ("flatline") . The condition results in cardiogenic shock (CS) , cessation of effective blood circulation, and sudden cardiac death (SCD) in minutes. If the patient is revived after a sufficient period (roughly 5 minutes) of cerebral hypoxia, the patient sustains irreversible brain damage. Brain death often occurs if NSR or blood flow to the brain is not restored within 90 seconds of the onset of VF. Especially the case if the VF has degenerated further into asystole with complete lack of cerebral and systemic blood flow.

Premature Pre-ventricular Contractions
Premature pre-ventricular contractions (PVCs) originate from the ventricle (wide QRS) and are always followed by a compensatory pause as the electrical system resets. A premature atrial contraction (PAC) with aberrancy can mimic a PVC but there is no compensatory pause. PVCs and arrhythmia rates increase as we age. PVCs appear to be benign unless an underlying left ventricular dysfunction is present. In patients with increased left ventricular dysfunction, PVCs are associated with an increased mortality, while reducing PVC frequency does not reduce mortality. SVT with wide QRS due to a BBB or preexcitation syndrome such as WPW can mimic VT.

Arrhythmias Associated with Long QT
Many common drugs cause TdP. The QT period is rate-dependent. Risk factors for TdP are female sex, hypokalemia, hypomagnesemia, structural heart disease, and a history of long QT or drug-induced arrhythmias.

Torsade de pointes (TdP)
Torsade de pointes (TdP) is a form of polymorphic VT associated with a prolonged QT syndrome. For those patients who receive QT-prolonging drugs in the hospital, ECG monitoring of prolonged QT intervals is indicated. TdP should be avoidable if there is an awareness of individual risk factors and ECG signs of drug-induced long QT syndrome (LQTS) are seen. ECG risk factors for TdP include marked QT prolongation to >500 ms (with the exception of amiodarone- or verapamil- induced QT prolongation) . Recognition of these ECG harbingers of TdP allows for treatment with IV magnesium, removal of the offending agent, and correction of electrolyte abnormalities. Other exacerbating factors include the prevention of bradycardia and long pauses where temporary pacing will be necessary.

  • See also Case 4 (Hemodynamic Monitoring), Case 5 (Vasoactive Drugs and Pharmacology) , and Case 16 (Acute Cardiac Failure).


Figure 15-5. EKG.


15.1  A 73-year-old woman is evaluated in the ICU. She has a history of CAD, and has a near-syncopal episode. Her medications include levothyroxine and hydrochlorothiazide. An ECG 2 years ago was normal. On physical examination, her heart rate is 42 beats/minute and regular. The remainder of the examination is normal. Her TSH level is normal. An ECG obtained as part of the current evaluation is shown (Figure 15-5). Of the following diagnoses, which does the ECG in this case confirm?
A. First-degree atrioventricular heart block
B. Mobitz type I second-degree atrioventricular block
C. Mobitz type II second-degree atrioventricular block
D. Third-degree atrioventricular block (complete heart block)
E. AV nodal atrioventricular heart block

15.2  Which of the following is the best treatment for the patient in Question 15.1?
A. Amiodarone
B. β-Blocker therapy
C. Implantable pacemaker
D. Procainamide
E. Lidocaine


15.1  D. The third-degree AV block, or complete heart block, refers to a lack of AV conduction, and lack of conduction of all atrial impulses (P waves) to the ventricles, as seen in this patient's ECG. Mobitz type II second-degree heart block is characterized by a regularly dropped beat without progressive prolongation of the PR interval and is associated with evidence of additional disease in the conduction system, such as BBB or bifascicular or trifascicular block. Mobitz type II heart block suddenly progresses to complete heart block and is usually treated with a pacemaker.

15.2  C. A pacemaker is indicated in patients who have acquired third-degree AV block. Many patients with complete heart block are symptomatic and are treated with a pacemaker. Pacemaker implantation may improve survival for patients with asymptomatic complete heart block; therefore, all patients with complete heart block should be treated with pacemaker implantation.


 The younger the patient with an arrhythmia, the more likely a congenital accessory pathway is present. 
 In WPW,  the treatment of choice is ablation of the accessory pathway. 
 Regularization of AF (at heart rates of 60 beats/minute) can be a sign of digoxin toxicity. 
 In nonvalvular AF, warfarin with a  target  INR of 2.0 to 3.0 decreases stroke risk by 62%. 
 Pacemaker insertion improves survival for  patients with asymptomatic complete heart block. 
 Patients with VT and structural heart  disease is ideally treated with an ICD. 
 Mobitz type II heart  block progresses to complete  heart block and is treated by a   pacemaker. 
 The longer the QT interval, the more the likelihood of an arrhythmia. 
 Antiarrhythmic medications are proarrhythmic themselves. 
 Where the pulmonary veins enter the left atrium, it appears to be a major site for origin of AF. 
 Procainamide is a classic medication causing drug-induced lupus and a positive ANA. 


Dubin D. Rapid Interpretation of EKGs. 6th ed. Tampa, FL: Cover Publication Company; October 1 5 , 2000. 

Loscalzo J. Harrison's Pulmonary and Critical Care Medicine. McGraw-Hill; 2010 . 

Toy E, Simon B, Takenaka K, Liu T, Rosh A. Case Files Emergency Medicine . 2nd e d . New York, NY: McGraw-Hill, Lange.


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