Cardiac Arrhythmias Case File

https://medical-phd.blogspot.com/2021/04/cardiac-arrhythmias-case-file.html

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.

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? 

ANSWER TO CASE 15:

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.

ANALYSIS

Objectives

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.

Considerations
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

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 V 1 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 O 2sat, glucose, BUN , and creatinine
levels. ECD is indicated for hemodynamically unstable patients regardless of the rhythm.

SUPRAVENTRICULAR ARRHYTHMIAS
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).

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 CHADS 2 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.