.... 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

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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?

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