.... Imaging

Routine computed tomography ( CT) imaging of the head

is not warranted unless directed by the history and

physical. Indications include signs and symptoms suggestive of a cerebrovascular etiology such as an antecedent

headache, focal neurologic deficits on physical exam, or a

prolonged recovery phase after the syncopal event. Chest

radiographs may be helpful to evaluate for signs of cardiomegaly, aortic dissection, or congestive heart failure

(CHF). Indications include syncope that occurs without

prodrome or is preceded by chest pain or shortness of

breath.

CHAPTER 19

J

J J ,..,

* 1

- - "" t' �� � ,1 � _,,

II I,\ vi

iI . � r� v

t

,...

I IJ � ... �j� l j;; 1- foo UI � r--.� 3 v

r-

���

r

I

,....�

l

11

I �� r -

�5

Figure 19-1. ECG demonstrating Brugada syndrome. Note the classic rSR appearance in leads v1 and v2 with a

downsloping ST-segment elevation.

MEDICAL DECISION MAKING

Manage all syncopal patients in a standardized stepwise

fashion. Start with a broad differential focusing on lifethreatening causes of syncope. Review the patient's initial vital signs and obtain a bedside capillary glucose.

Obtain a STAT ECG and place the patient on the cardiac

monitor. Take a careful and detailed history including

any bystander accounts. Review the patient's past medical history and note all current medications. Focus the

physical exam on the cardiovascular and neurologic systems. Tailor any ensuing laboratory and imaging studies

to abnormalities discovered during the history and

physical exam. After excluding any acute life threats,

focus on the more benign causes, keeping in mind that

often times the exact etiology is not identified in the ED

( Figure 19-2).

TREATMENT

Rapidly determine hemodynamic stability and initially

focus on supportive care. Obtain IV access, start supple ­

mental oxygen in hypoxic or dyspneic patients, and initiate continuous cardiac monitoring. Check a bedside

glucose and give supplemental dextrose as indicated. The

remainder of treatment should focus on the inciting

event.

Cardiac syncope. Follow standard advanced cardiac life

support guidelines for any cardiac rhythm disturbances.

Avoid agents that primarily reduce the cardiac preload (eg,

nitroglycerin) in patients with hypertrophic cardiomyopathy

or aortic stenosis. With concern for PE or aortic dissection,

obtain appropriate imaging and tailor t reatment to the results.

Cerebrovascular syncope. If SAH is suspected, obtain

an emergent head CT and dictate further management

accordingly.

Orthostatic syncope. Initiate volume resuscitation

with isotonic saline as tolerated. If internal hemorrhage is

suspected (eg, ruptured ectopic, AAA, GI bleed), begin

aggressive fluid resuscitation and proceed with the appropriate confirmatory studies. Identify and avoid any potentially contributing medications that the patient might be

taking (eg, beta-blockers, nitrates).

Reflexive/vasovagal syncope. Often no additional

treatment is necessary. Attempt to identify the precipitat ­

ing event to limit further occurrences.

DISPOSITION

.... Admission

Admit all patients with either clinical findings or risk factors

concerning for cardiac syncope to a monitored setting.

Although there is no consensus regarding which items should

prompt serious concern, patients with any of the following

generally warrant admission: age >45 years, abnormal vital

signs including hypoxia or a systolic BP <90 mmHg, ECG

abnormalities, an underlying history of CHF or coronary

SYNCOPE

Syncopal or near-syncopal episode

IV, cardiac monitor, pulse oximetry,

bedside gl ucose, and full set of vita l signs

History and physical exam (focus on

cardiovascular & neurologic systems)

I mmediate ECG, further

imaging or labs as dictated by H&P

Benign etiology establ ished and

addressed, no risk factors

for cardiac syncope

Discharge with close

outpatient follow-up

Figure 19-2. Syncope diag nostic algorithm. ECG, electroca rd iogram; H&P, history and physica l examination.

artery disease (CAD), a laboratory hematocrit <30%, an

abnormal physical exam, a positive stool guaiac test, syncope

that occurs either with exertion or without prodrome, and

syncopal episodes that were accompanied by shortness of

breath.

� Discharge

Patients with a low risk for a cardiac etiology (normal

physical exam, no history of CAD or CHF, normal ECG,

age <45 years) can be safely discharged home. This

assumes the exclusion of all other noncardiac life threats.

Further work-up including Holter monitoring or tilt-table

testing can be arranged in the primary care setting.

SUGGESTED READING

Chen L, Benditt D , e t al. Management of syncope in adults: An

update. Mayo Clin Proc. 2008;83:1280-1293.

Huff J, Decker W, et al. Clinical policy: Critical issues in the

evaluation and management of patients presenting to the ED

with syncope. Ann Emerg Med. 2007;49:43 1-444.

Quinn J. Syncope. ln: Tintinalli JE, Stapczynski JS, Ma OJ, Cline

DM, Cydulka RK, Meckler GD. Tintinalli's Emergency

Medicine: A Comprehensive Study Guide. 7th ed. New York,

NY: McGraw-Hill, 20 1 1, pp. 399-405.

Quinn J, McDermott M, et al: Prospective validation of the San

Francisco rule to predict patients with serious outcomes. Ann

Emerg Med. 2006;47:448-454.

Dyspnea

Shari Scha bowski, MD

Chua ng-yuan Lin, MD

Key Points

• Determine whether an immed iate life threat is present.

• Answer 3 key questions when approaching patients in

moderate to severe respiratory distress.

• Diagnose causes of dyspnea by using a structured stepby-step anatomic approach.

INTRODUCTION

Dyspnea, from the patient's perspective, is known as

"shortness of breath." This is a sensation of breathlessness

or "air hunger" manifested by signs of difficult or labored

breathing, often owing to a physiologic aberration.

Tachypnea is rapid breathing. Dyspnea may or may not

involve tachypnea. Hyperventilation is ventilation that

exceeds metabolic demands, such as can be caused by a

psychological stressor (eg, anxiety attack).

From the physician's perspective, dyspnea is caused by

impaired oxygen delivery to tissues. This can begin at the

mechanical level, with any possible cause of airway

obstruction, and can end at the cellular level, with any

chemical inability to offload oxygen to tissues. If time

permits, a systematic walk-through from airway to tissue

can help elucidate the more difficult diagnoses. However,

treatment for life-threatening severe respiratory distress

must be initiated during, or even before, the diagnostic

work-up.

CLINICAL PRESENTATION

Start your initial assessment of the severity of the presenta ­

tion with these 3 questions:

1. Does the patient need to be intubated immediately?

84

 

� Imaging

Obtain a head computed tomography (CT), searching for

signs of hypertensive encephalopathy or intracranial hem ­

orrhage in patients presenting with altered mental status,

papilledema, focal neurologic deficits, or seizure. Order a

chest x-ray (CXR) to look for signs of flash pulmonary

edema or aortic dissection in patients with chest pain, back

pain, or shortness of breath. Pursue CT angiography of the

chest and abdomen in patients with suspicion of aortic

dissection.

MEDICAL DECISION MAKING

Rapidly evaluate all patients with severe hypertension for

the presence of hypertensive emergency (hypertensive

encephalopathy, intracranial hemorrhage, flash pulmonary

edema, acute coronary syndrome, aortic dissection, and

HYPERTENSIVE EMERGENCIES

Severe hypertension (BP > 1 80/1 1 0)

History and physical exam, re-measure BP

Gradual normal ization of

BP over 24-48 hours with

oral anti-hypertensives

Figure 1 8-1. Hypertensive emergency diagnostic algorithm. BP, blood pressure; ECG, electroca rdiogram.

acute kidney injury). Utilize the history and physical exam

to help narrow the differential diagnosis and obtain the

appropriate laboratory and imaging studies to both confirm

end-organ injury and guide further therapy (Figure 1 8-1

and Table 18-1).

TREATMENT

Hypertensive emergency requires immediate BP reduc ­

tion to limit continuing end-organ damage. The goal is

not to normalize the BP ( < 140/90 mmHg), but rather to

Table 1 8-1. Hypertensive emergency diag noses with findings.

Diagnosis

Hypertensive encephalopathy

Intracranial hemorrhage

Acute pulmonary edema

Acute coronary syndrome

Aortic dissection

Acute renal failure

Findings on H&P, Labs, and Imaging

AMS, headache, vomiting and papilledema; labs and a head frequently normal

Headache, coma and focal neurologic deficits; a head with hemorrhage

SOB, chest pain and inspiratory crackles on lung exam; elevated BNP; CXR with cardiomegaly

and pulmonary edema

Chest pain, SOB; elevated troponin; ECG with ischemic changes

Severe chestjback pain; unequal pulses; CXR with wide mediastinum, a chest with dissection

Decreased urine output, hematuria; peripheral edema; urinalysis positive for protein and RBCs ± casts,

acutely elevated BUN and creatinine

AMS, altered mental status; BNP, B-type natri u retic peptide; BUN, blood u rea nitrogen; CT, computed tomography; CXR, chest x-ray;

ECG, electroca rdiogram; RBCs, red blood cel ls; SOB, shortness of breath.

CHAPTER 18

 

Beta-blockers are generally considered the first-line

therapy for acute dissection given their ability to reduce

both blood pressure and heart rate. Because of its short

duration of action and rapid onset, esmolol is an excellent

first-line agent. Start with a loading dose of 500 meg/kg

given over 1 minute followed by a continuous infusion at

50 meg/kg/min. If the desired ventricular response has not

been achieved within 5 minutes, repeat the loading dose

and increase the infusion to 1 00 meg/kg/min. If the desired

ventricular response has not been achieved within another

CHAPTER 17

5 minute span, give a third and final loading dose of

500 meg/kg and increase the infusion up to a max rate of

200 meg/kg/min.

Patients frequently remain hypertensive despite achieving the ideal heart rate. In such situations, begin a continuous

infusion of an arterial vasodilator such as nitroprusside

(0.3-3.0 mg!kg/min). Alternative vasodilators including nicardipine or clevidipine are acceptable. Regardless of which

medication is used, never initiate vasodilator therapy until the

heart rate is adequately suppressed with beta-blockers to

avoid reflex tachycardia and propagation of the dissection.

As an alternative, labetalol is a reasonable single agent

due to its selective a1 and nonselective beta-blocking properties. Give an initial dose of 1 0-20 mg as a slow N bolus

over 2 minutes. If the desired blood pressure and heart rate

are not achieved within 10 minutes, administer escalating

doses (ie, 20 mg, 40 mg, 80 mg, 1 60 mg) at 1 0-minute

intervals to a cumulative maximum dose of 300 mg.

Labetalol can also be given as a continuous infusion. Start

the infusion at 0.5 mg/min and increase by 0.5 mg/min

every 15 minutes to a max dose of 2.0 mg/min as necessary.

If necessary, additional boluses of N labetalol can be given

while concurrently titrating the infusion to more rapidly

achieve the goal heart rate and blood pressure. Stanford

type A dissections require prompt cardiothoracic consultation for operative repair, whereas type B dissections are

typically managed medically.

DISPOSITION

� Admission

All patients with an acute aortic dissection require hospital

admission to an intensive care unit setting.

� Discharge

A patient in whom aortic dissection has been ruled out

should be discharged only when there was an initial low

clinical suspicion and all other concerning etiologies for

the presenting complaints have been excluded. Patients

with known chronic aortic dissections can be safely discharged provided their blood pressure is adequately con ­

trolled and their presenting complaint is unrelated to the

underlying dissection. At times subspecialty consultation

may be necessary to assist with disposition.

SUGGESTED READING

Klompas M. Does this patient have an acute thoracic aortic

dissection? J Am Med Assoc. 2002;287:2262-2272.

Upadhye S, Schiff K. Acute aortic dissection in the emergency

department: Diagnostic challenges and evidence-based management. Emerg Med Clin N Am. 201 2;30:307-327.

Wittels K. Aortic emergencies. Emerg Med Clin N Am. 20 1 1;

29:789-800.

Hypertensive Emergencies

Erik K. Nordqu ist, MD

Key Points

• Hypertension is a very common fi nding in emergency

department patients. Evidence of acute end-organ

dysfunction in the setting of hypertension is rare but

requires emergent diagnosis and treatment.

• Depend on the history and physical to guide the clinical

eva luation of patients with severe hypertension.

INTRODUCTION

Hypertension affects up to 30% of the total adult population and is one of the most common medical conditions in

the United States. Of these individuals, nearly 75% have

inadequately controlled blood pressure (BP) (beyond normotensive limits of 140/90 mmHg), and only half are taking their medications correctly as prescribed. That said,

fewer than 1% of all patients with hypertension will ever

develop a hypertensive emergency.

Patients presenting with a systolic BP :?: 180 mmHg or a

diastolic BP :?:l l O mmHg are classified as having severe

hypertension. Evaluating a patient with severe hyperten ­

sion should focus on the rapid distinction between hypertensive emergency or hypertensive urgency, as the

treatment and disposition differ dramatically. Hypertensive

emergency is defined as an acute elevation in BP ( :?: 180/l lO

mmHg) associated with active end-organ damage, specifically ongoing injury to the brain, heart, aorta, kidneys,

and/or eyes. Hypertensive urgency is less clearly defined,

but can be thought of as a severe elevation in blood pressure without evidence of acute end-organ dysfunction.

The suggested mechanism behind hypertensive emer ­

gency requires a sudden increase in systemic vascular

75

• Emergent blood pressure control is contraindicated

in asymptomatically hypertensive patients without

evidence of end-organ dysfunction.

resistance due to an unregulated surge in circulating vasoconstrictors. This spike in BP causes undo stress on the

vascular wall with consequent endothelial injury. The

injured endothelium produces pathologic increases in vascular permeability, activation of the platelets and coagulation cascade, and the localized deposition of intraluminal

fibrin. Secondary fibrinoid necrosis of the arteriolar endorgan circulation results in significant tissue hypoperfusion and consequent organ system dysfunction.

Most individuals presenting with hypertensive emer ­

gency will carry a previous diagnosis of hypertension. When

determining the goals for BP treatment, it is important to

understand the effects of longstanding hypertension on the

cerebral circulation. Chronic hypertension forces a shift in

cerebral autoregulation, allowing patients to tolerate significant elevations in blood pressure without any signs of cerebral end-organ damage. Consequently, the overaggressive

reduction of systemic BP in this setting, even if only

decreased to normotensive limits, may lead to secondary

hypoperfusion and ischemia of the central nervous system

(CNS). Always remember that treating blood pressure based

on numbers alone, without considering the clinical context,

can be altogether quite harmful for the patient.

CLINICAL PRESENTATION

� History

CHAPTER 18

Patients with severe hypertension require a rapid evaluation for evidence of end-organ damage. Start with a

focused history and comprehensive review of systems,

inquiring about the presence of chest pain, back pain,

shortness of breath, hematuria or decreased urine output,

and neurologic complaints including numbness, weakness, headache, confusion, and visual disturbances.

A more detailed history related to specific diagnoses

follows. 

 

dissections are managed medical ly.

• Complications of acute dissection include myocardial

infarction, cardiac tamponade, aortic valve insufficiency,

stroke, renal failure, paralysis, limb ischemia, and death.

extend distally (antegrade), proximally (retrograde), or in

both directions. Rarely, the false lumen will rupture

through the adventitia, resulting in immediate hemodynamic collapse. The majority of aortic dissections originate in the ascending aorta (65%), the aortic arch ( 10%),

or just distal to the ligamentum arteriosum (20%). The

Stanford classification system divides aortic dissections

clinically into types A and B. Type A dissections involve the

ascending aorta, whereas type B dissections involve only

the distal aorta (origin of the intimal tear is distal to the left

subclavian artery) (Figure 17-1).

CLINICAL PRESENTATION

..... History

The classic presentation of an acute thoracic aortic dissection is that of a 55- to 65-year-old male with chronic hypertension who develops a sudden onset of severe sharp or

tearing chest pain radiating to the intrascapular area. Keep

in mind that this is a fairly rare condition that often presents

in an atypical manner. When obtaining the history, identify

relevant risk factors and inquire about the quality, radiation,

and intensity at onset of the pain. Type A dissections present

most commonly with anterior chest pain (71 %) and less

commonly with either back ( 47%) or abdominal pain (21 o/o ).

AORTIC DISSECTION

Figure 1 7-1. Stanford classification of aortic

d issections A. Type A. B. Type B. (Reprod uced with

permission from Brunicardi FC, Andersen D, Billiar T,

et al. Schwartz's Principles of Surgery. 8th ed. New

York: McGraw-Hill Education, 2005.)

Additional presenting complaints include syncope (13%)

and stroke-like symptoms (6%). Type B dissections present

most often with acute back (64%) and chest (63%) pain

with increasing rates of abdominal pain (43%). Atypical

presentations include patients with intermittent symptoms,

pleuritic or positional pain, and isolated syncope. Painless

aortic dissections have also been reported. Corresponding

visceral symptoms including diaphoresis, nausea, vomiting,

and pallor are often present.

...,.. Physical Examination

The physical examination should initially focus on the

general appearance of the patient and an assessment of his

or her vital signs. Patients with acute dissections are t ypically very uncomfortable and ill-appearing. Palpate peri ph ­

eral pulses in all 4 extremities and measure the blood

pressure in both arms, taking note of any discrepancies.

The presenting blood pressure cannot be used to either

diagnose or exclude this condition, as roughly half of

patients will have an elevated blood pressure, whereas an

equal proportion will be either normotensive or hypoten ­

 

Tiffany BR, eds. Cardiac Emergencies. New York, NY: McGraw

flill, 2006, pp. 219-236.

Moffa DA. Cardiac conduction blocks. In: Peacock WF, Tiffany

BR, eds. Cardiac Emergencies. New York, NY: McGraw-Hill,

2006, pp. 250-268.

Piktel JS. Cardiac rhythm disturbances. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Clince DM, Cydulka RK, Meckler GD,

eds. Tintinalli's Emergency Medicine: A Comprehensive Study

Guide. 7th ed. New York, NY: McGraw-fUll, 20 11, pp. 129-1 54.

Walters DJ, Dunbar LM. Atrial arrhytlunias. In: Peacock WF,

Tiffany BR, eds. Cardiac Emergencies. New York, NY: McGrawflill, 2006, pp. 237-249.

Aortic Dissection

David A. Wa ld, DO

Key Points

• Always consider aortic dissection in patients presenting

with the acute onset of chest or thoracic back pain.

• Initiate a rapid reduction in heart rate and blood pressure in all patients with a high clinical suspicion for aortic dissection before obtaining confirmatory diagnostic

imaging.

INTRODUCTION

Acute aortic dissection is a rare but potentially life-threatening

condition. Although the true incidence is unknown, it is

estimated that there are between 6,000 and 10,000 new

cases annually in the United States. Aortic dissection is

more prevalent in men and in patients with advanced age,

with approximately 75% occurring in patients between

40 and 70 years of age. Younger patients with aortic dissection usually have a history of an underlying connective

tissue disease. Of note, about half of all aortic dissections

in women under the age of 40 years occur in the third trimester or early postpartum period.

Risk factors for acute aortic dissection include chronic

hypertension, a bicuspid aortic value, coarctation of the

aorta, or inherited connective tissue disorders such as

Ehlers-Danlos and Marfan syndromes. Vascular inflammatory disorders such as giant cell arteritis or Takayasu arte ­

ritis are additional risk factors for dissection.

Aortic dissection results from a tear in the intimal layer

of the vessel wall. Common inciting factors include the

chronic conditions listed previously, as well as illicit drug

use or blunt thoracic trauma. High-pressure pulsatile

blood will travel through this tear into the media layer of

the aorta, thereby separating the intima from the adventitia. This creates a false lumen for aortic blood flow that can

70

• Stanford type A (proximal) dissections typically require

surgical intervention, whereas Stanford type B (dista l)

 

>200 msec) and requires no urgent intervention. Search

for and address any predisposing conditions. Bradycardic

rhythms that feature more P waves than QRS complexes

typically represent second- or third-degree AV blocks.

Second-degree AV block is divided in Mobitz types I

(Wenckebach) and II. Type I presents with a PR interval

that progressively elongates until an impulse is not conducted to the ventricles, resulting in a dropped QRS on the

ECG. A progressively decreasing interval between c onsecutive R waves is classic for this dysrhythmia. In seconddegree AV block type II, although the PR interval remains

constant, occasional P waves will not be conducted to the

ventricles, resulting in a dropped QRS. Type II is more

CHAPTER 16

Figure 1 6-2. Dysrhythmia diag nostic algorithm.

serious than type I and typically represents a conduction

blockade distal to the AV node. Complete disruption of

signal conduction between the atria (P waves) and ventri ­

cles (QRS complexes) represents third-degree or complete

heart block. The P waves and QRS complexes march inde ­

pendently of one another with no consistency between the

two. The QRS complexes are referred to as escape beats and

can be either narrow (junctional) or wide (ventricular)

depending on their site of origin (Figure 16-3).

Two additional bradycardias warrant mention. Junctional

bradycardia is a slow regular rhythm with a narrow QRS

complex and absent or abnormal P waves owing to its origin

within the AV node. As this condition typically occurs because

of medication side effects (eg, beta-blockers), carefully elicit a

medical history to help identify the etiology. I dioventricular

rhythms (ventricular escape rhythms) originate in the ven ­

tricles and appear as regular wide QRS complex rhythms at a

rate of 20-40 bpm with no discernible P waves.

..... Tachydysrhythmias

In stable patients, assess for the regularity of the rhythm

and distinguish between a supraventricular (narrow QRS)

versus ventricular etiology (QRS > 100 msec) (Figure 16-4).

A rhythm that is fast, narrow, and regular is typically either

sinus tachycardia, atrial flutter, or SVT. Slowing the heart

DYSRHYTHMIAS

A

8

(

Figure 1 6-3. A. Second-degree AV block (Mobitz type I; Wenckebach). B. Second-degree AV block (Mobitz

type I I). C. Third-degree AV block. (Reproduced with permission from Tintina lli JE, Kelen GO, Sta pczynski JS.

Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York: McGraw-Hill, 2004.)

rate with vagal maneuvers or adenosine aids in identifying

the underlying rhythm and may treat SVT. Although

appropriate concern should arise when using adenosine in

patients with either known or ECG findings concerning for

pre-excitation ( eg, WPW), it is generally safe provided that

the QRS complexes are narrow. Of note, SVT with aberrancy (conduction through an accessory pathway or bun ­

dle branch block) is typically difficult to distinguish from

VT. Always assume VT until proven otherwise, especially in

elderly patients with underlying cardiac disease.

Sinus tachycardia will appear with a P wave preceding each

QRS and regular R-R intervals. Sinus tachycardia is often

secondary to noncardiac issues, including pain, fever, anxiety,

PE, illicit drug use (cocaine), alcohol withdrawal, thyrotoxico ­

sis, volume depletion, and anemia. Focus on identifying and

treating the underlying cause of the tachycardia.

SVT can be subdivided into AV nodal re-entry tachycardias (AVNRT) and atrioventricular re-entry tachycar ­

dias (AVRT) depending on the anatomy of the re-entry

circuit. AVNRT has a re-entry loop contained within the

AV node itself, whereas AVRT requires the presence of an

accessory pathway ( eg, WPW) to complete the re-entry

loop. With AVRT, signals that travel downward through the

AV node and re-enter the atria through the accessory pathway (orthodromic) will exhibit narrow QRS complexes.

The reverse situation is known as antidromic conduction

and will exhibit wide QRS complexes. Wide QRS complexes are also present in patients with underlying bundle

branch blocks (SVT with aberrancy). Regardless of SVT

subtype, discernible P waves preceding the QRS complexes

will be absent and the R-R intervals will be r egular.

Atrial flutter has a classic "saw tooth" appearance from

 

the multiple flutter waves that precede the QRS complexes.

The R-R intervals are usually regular unless there is variable conduction through the AV node. The most common

presenting rate is - 1 50 bpm and occurs when the flutter

waves are conducted through the AV node in a 2:1 ratio.

In addition to atrial flutter with a variable block, atrial

fibrillation (AF) and multifocal atrial tachycardia (MAT)

represent the irregular narrow QRS complex tachycardias.

AF can be identified by irregular R-R intervals without

discernible P waves. Although MAT is often confused with

AF, the distinction is critical, as the treatment varies markedly. MAT will have varying P wave morphologies and

irregular P-R and R-R intervals, but unlike AF, P waves will

precede each QRS. MAT is most common in patients with

underlying pulmonary disease, and as there is no specific

cardiac treatment. Focus on addressing the underlying

lung pathology.

Wide complex tachycardias typically require more

emergent intervention than their narrow complex coun ­

terparts and are often encountered in the unstable or "coding" patient. Besides the aforementioned SVT with

aberrancy, VT and ventricular fibrillation (VF) are the

remaining possibilities. VT presents with a rate > 1 20 bpm,

QRS intervals > 1 20 msec, and no discernible P waves.

Torsade de pointes is a unique subset of polymorphic

VT that features a beat to beat variation in QRS morphology with a progressive twist in QRS axis. This condition

usually arises from abnormal ventricular repolarization.

TREATMENT

Address patient airway, breathing, and circulation (ABCs),

provide supplemental 02, ensure adequate peripheral N

access, and initiate continuous cardiac monitoring. Tailor

A

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CHAPTER 16

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Figure 1 6-4. A. Sinus tachycardia. B. Supraventricu lar tachycardia. C. Atrial flutter. D. Atrial fibril lation.

E. Mu ltifoca l atrial tachycardia. F. Ventricular tachycardia. G. Ventricular fibril lation. (B., F. Reproduced with permission

from Ferry DR. Basic Electrocardiography in Ten Days. New York: McGraw-Hill, 2001 . E., G. Reproduced with

permission from Tintinalli JE, Kelen GO, Stapczynski JS. Emergency Medicine: A comprehensive study guide. 6th ed.

New York: McGraw-Hill, 2004.)

the remammg treatment to the patient's underlying

rhythm.

� Bradydysrhythmias

Unstable patients require immediate intervention. Treat those

who are unstable with IV doses of atropine (0.5-1.0 mg) and

epinephrine (0.3-0.5 mg over 2-3 minutes) if refractive.

Initiate transcutaneous pacing and consider placement

of an introducer catheter into the internal jugular or

subclavian vein for transvenous pacing in all patients

who fail to respond. Catecholamine infusions (eg, dopamine)

may be necessary to maintain an adequate HR and blood

pressure.

Whereas second-degree AV block Mobitz type I

typically requires no specific treatment, Mobitz type II and

third-degree heart block require emergent intervention.

Place transcutaneous pacer pads on the chest and initiate

pacing in those that become unstable. To do so, set your

 

• Order a 1 2-lead electrocardiogram on stable patients

and address potentia l etiologies, including acute

coronary syndrome, electrolyte abnormal ities, toxic

ingestions, and medication side effects.

The normal electrocardiogram (ECG) waveform contains a P wave, QRS complex, and T wave. The P wave represents atrial depolarization. It is immediately followed by

the PR interval, which normally lasts between 1 20 and 200

msec in duration. The QRS complex represents ventricular

depolarization and is normally <100 msec in duration.

Delays in intraventricular conduction result in a widened

(> 100 msec) QRS complex. The ST segment represents the

plateau of ventricular depolarization and is normally iso ­

electric in appearance. Finally, the T wave represents ven ­

tricular repolarization. Of note, the segment extending from

the end of a T wave to the beginning of the next P wave,

known as the TP segment, should be used as the isoelectric

baseline when performing any type of ECG analysis.

Bradydysrhythrnias occur either because of depressed

sinus node activity or inhibited electrical signal conduction.

These are common in patients with structural heart damage,

excessive vagal tone, taking certain cardioactive medications,

or with specific electrolyte abnormalities (eg, hyperkalemia).

Tachydysrhythmias occur because of enhanced automaticity

from either the SA node or an ectopic focus and can originate

from both atrial and ventricular sources. Supraventricular

tachycardia (SVT) occurs when re-entry loops are present in

the AV node or accessory conduction pathways.

Rhythms with a wide QRS complex represent ventric ­

ular depolarization that occurs outside of the normal

CHAPTER 16

Table 1 6-1. PIRATES: Causes of atrial fibri l lation.

P PE, pneumonia, pericarditis

Ischemia (coronary artery disease and myocardial infarction)

R Rheumatic heart disease, respiratory failure

A Alcohol ("hol iday heart")

T Thyrotoxicosis

Endocrine (Ca), enlarged atria (mitral valve disease,

cardiomyopathy)

s Sepsis, stress (fever)

conduction system, whereas those with normal QRS durations originate from a focus either superior to or within

the AV node that then travel through standard conduction

pathways.

Cardiac dysrhythmias vary by etiology, severity, and

treatment. Atrial fibrillation (AF), for example, is common and has multiple causes (Table 1 6-1). Although

occasionally symptomatic and/or requiring emergent

intervention, many patients are typically unaware when

they are in AF. Asymptomatic bradycardia is also a very

common rhythm, especially in young, athletic patients. It

can be a normal fmding in some people or result from

medication use at therapeutic levels. Other bradydysrhythmias, such as third-degree heart block, always elicit

emergent concern. Tachydysrhythmias vary in a similar

manner, from an isolated asymptomatic atrial tachycardia

to an emergently life-threatening ventricular fibrillation,

the initial dysrhythmia for the majority of patients in

cardiac arrest.