CLINICAL PRESENTATION

An acute asthma presentation is due to a decrease in expiratory airflow and is characterized by progressive symp ­

toms of shortness of breath, a nonproductive cough, and

89

• Pea k expiratory flow rate and forced expiratory vol ume

in 1 second are objective measures of the severity of a

patient's asthma exacerbation and should be followed

serially to measure improvement.

wheezing in all lung fields. Symptoms may develop over a

period of hours, days, or weeks, but often there is an acute

worsening that prompts the patient to seek medical care.

The most common trigger of acute asthma is an upper

respiratory tract infection, but other factors may lead to

sudden worsening of symptoms (Table 21-1).

..... History

Obtaining a thorough history may not be possible in an

acute asthma exacerbation. A focused history should be

obtained in parallel with initiation of therapy to reverse

Table 21-1. Acute asthma triggers.

Environmental allergens

Exercise-induced

Gastroesophageal reflux disease

Tobacco smoke

Occupational exposures

Inhaled irritants

Stress-induced

Environmental changes (weather)

Air pollutants

CHAPTER 21

Table 21-2. Risk factors for morta l ity in asthma.

Chronic steroid usage

>2 canisters of short acting beta-2 agonists per month

2"2 hospital izations in the past year

2"3 emergency department visits in the past year

History of intensive care unit admissions

Previous intubations for asthma

Cardiopulmonary comorbidities

Illicit drug use

low socioeconomic status or inner-city residence

airflow obstruction, regardless of the trigger. Once the

patient has improved and is able to provide more history,

an attempt should be made to characterize the triggering

event, rapidity of symptom onset, and the severity of the

exacerbation, which will help guide further treatment

and disposition. Characterization of the severity of the

patient's underlying asthma may help predict mortality

(Table 21-2).

Attempting to define the patient's underlying longterm asthma control does not aid in the management of an

acute exacerbation, but will be important to understand

when prescribing outpatient therapeutic regimen and

follow-up. Patients should be asked about the frequency

and duration of their current asthma symptoms and recent

beta-agonist usage.

Numerous medical conditions can present in a similar

fashion to asthma, including pulmonary embolism (PE),

pneumonia, congestive heart failure (CHF), acute myocardial infarction (AMI), or chronic obstructive pulmonary

disease (COPD). The initial history should focus on differentiating asthma from other life-threatening causes of

shortness of breath and wheezing.

...... Physical Examination

Patients may present with a wide spectrum of severity,

from an increase in coughing to obvious respiratory distress with tachypnea and accessory muscle use. Mental

status should be assessed initially because alterations in

consciousness may affect the patient's ability to protect

their airway. A diminished level of consciousness is an

indicator of impending respiratory arrest. The neck

should be palpated for tracheal deviation and crepitus, as

might occur with spontaneous pneumothorax. The lung

exam is variable and demonstrates prolonged expiration

with wheezing. However, the severity of the airflow

obstruction cannot be gauged by the loudness of the

wheezing. The patient who is audibly wheezing may still

have good air movement on auscultation, whereas the

quiet sounding chest with little air movement is a sign of

severe disease because there is not enough airflow to produce a wheeze. Percussion of the thorax reveals hyperresonance due to air trapping. Evaluation of extremity

edema will help differentiate asthma from other causes of

difficulty breathing.

 

may occur. Be especially suspicious if there are signs of

unilateral leg swelling. Entertain the thought of pulmonary embolism in any patient who is short of breath,

especially if the cause of dyspnea is unclear.

DIAGNOSTIC STUDIES

Diagnostic studies will vary based on the clinical presentation and physical exam.

� Laboratory

Pulse oximetry is a rapid, noninvasive test that is useful

to screen for hypoxia. An Sa02 >98% predicts a Pa02 >80

mmHg. An Sa02 >90% predicts a Pa02 >60 mmHg. This is

important because an Sa02 of 90% is at the precipitous edge

of the oxygen dissociation curve; the patient may drop from

90% to 70% far quicker than from 95% to 90%. An arterial

blood gas is the only way to directly measure the Pa02 and

the pCO r The pCO 2 is useful in the management of patients

with chronic obstructive pulmonary disease, asthma, or

sleep apnea. The complete blood count can help in assessing

whether anemia is a cause of dyspnea. A metabolic panel

can elucidate the patient's renal status as well as give further

information about the patient's acid-base status (bicarbonate). Blood cultures are important in cases of pneumonia.

Remember to obtain before starting antibiotics.

� Electrocardiogram

ECG is useful to assess for cardiac ischemia, arrhythmias,

and even pericarditis or pericardial effusion.

� Imaging

CXR can help to assess the bronchial tree, alveoli, and

interstitium. It is also useful for evaluating bony structures,

the mediastinum, heart silhouette, and even aberrations of

the pleural space. Chest CT can be useful to assess mass

lesions, consolidations, effusions/exudates or pulmonary

emboli. Soft tissue plain radiograph or CT of the neck can

be used in stable patients to determine the presence of

epiglottitis, foreign body, or neck abscesses.

MEDICAL DECISION MAKING

As stated previously, the first goal of a dyspnea work-up

is to determine whether the patient is in extreme respiratory distress. If the patient is unable to oxygenate, ventilate, or preserve the airway, the patient must be intubated

immediately ( question 1). Next, if the patient has signs

of a reversible cause of dyspnea, such as asthma, CHF,

anaphylaxis, or tension pneumothorax, initiate treatment as soon as possible (question 2). Finally, once the

patient is stable, begin the diagnostic work-up (question

3, begin walking down respiratory system anatomically)

(Figure 20- 1).

ABCs

IV, 02, mon itor, pulse

oximetry, lung exam

Answer 1:

Can patient

No oxyg enate, ventilate,

maintain airway?

Yes

DYSPNEA

Hypoxic? � g ive oxygen Answer question 2:

Is the cause of

severe respiratory

d istress rapidly

reversible?

Yes Bronchospasm? � beta-agonists vs. steroids vs. epinephrine

-----� Hypertensive pulmonary edema?� nitroglycerin, lasix

Pneumothorax?� needle decompression, chest tube, etc .

Allergic reaction? � steroids vs. epinephrine

No, and

unstable

No immediate

i nterventions

available/necessary

Answer question 3:

Can the patient run?

Yes

Obtain history from

patient, family,

careg ivers

Walk anatomically down

respiratory system

-ECG

-Radiographs/CT

-ABG, labs

 

blood gas is the only way to directly measure the Pa02 and

the pCO r The pCO 2 is useful in the management of patients

with chronic obstructive pulmonary disease, asthma, or

sleep apnea. The complete blood count can help in assessing

whether anemia is a cause of dyspnea. A metabolic panel

can elucidate the patient's renal status as well as give further

information about the patient's acid-base status (bicarbonate). Blood cultures are important in cases of pneumonia.

Remember to obtain before starting antibiotics.

� Electrocardiogram

ECG is useful to assess for cardiac ischemia, arrhythmias,

and even pericarditis or pericardial effusion.

� Imaging

CXR can help to assess the bronchial tree, alveoli, and

interstitium. It is also useful for evaluating bony structures,

the mediastinum, heart silhouette, and even aberrations of

the pleural space. Chest CT can be useful to assess mass

lesions, consolidations, effusions/exudates or pulmonary

emboli. Soft tissue plain radiograph or CT of the neck can

be used in stable patients to determine the presence of

epiglottitis, foreign body, or neck abscesses.

MEDICAL DECISION MAKING

As stated previously, the first goal of a dyspnea work-up

is to determine whether the patient is in extreme respiratory distress. If the patient is unable to oxygenate, ventilate, or preserve the airway, the patient must be intubated

immediately ( question 1). Next, if the patient has signs

of a reversible cause of dyspnea, such as asthma, CHF,

anaphylaxis, or tension pneumothorax, initiate treatment as soon as possible (question 2). Finally, once the

patient is stable, begin the diagnostic work-up (question

3, begin walking down respiratory system anatomically)

(Figure 20- 1).

ABCs

IV, 02, mon itor, pulse

oximetry, lung exam

Answer 1:

Can patient

No oxyg enate, ventilate,

maintain airway?

Yes

DYSPNEA

Hypoxic? � g ive oxygen Answer question 2:

Is the cause of

severe respiratory

d istress rapidly

reversible?

Yes Bronchospasm? � beta-agonists v

volume may not be achieved. On the physical exam, gross

asymmetric chest wall expansion or abdominal distention/ascites can be clues of diaphragmatic dysfunction or

impairment. Look for asymmetric diaphragmatic excursion on a good inspiratory CXR.

Chest wall. Chest wall expansion is important for

unimpeded respiration. Any disorder that restricts wall

motion may cause dyspnea (ie, paresis/paralysis, neuro ­

muscular junction or muscular dysfunction, pain from

contusion or rib fractures). Do not underestimate splinting from chest wall pain-even from apparently minor

injuries. Inspection of the chest wall during respiration will

help you to assess this aspect of breathing. Use CXR to look

for rib fractures and/or pulmonary contusion (haziness at

site of trauma).

Pleural space. The pleural space is a potential space

present to facilitate movement of the lungs within the

chest wall. If the space is filled with fluid (ie, effusion, pus,

blood) or air, dyspnea can occur. If the pleural space is

occupied, it will typically cause decreased breath sounds

on the effected side. Fluid causes decreased resonance,

whereas air causes increased resonance. Abnormalities

will typically be seen on CXR; the addition of a lateral

decubitus radiograph of the chest may be helpful. Look

for extra-lucent edges that indicate a pneumothorax and

lenticular, dependent, or meniscal opacifications

consistent with an effusion.

Cardiac. The heart pumps deoxygenated blood to the

lungs and oxygenated blood to the tissues. Any impairment

of pump function (ie, ischemia, dysrhythmia, valvular

dysfunction, septal defects, pericardial fluid) can cause

dyspnea. Do not hesitate to initiate relevant cardiac workups when a patient presents with dyspnea. On the physical

exam, assess for cardiac murmurs, gallops, and rhythm

aberrations. These are important clues to expand the differential to cardiac problems.

Hemoglobin. There must be enough healthy red blood

cells to carry the oxygen to the tissues (ie, no significant

anemia), and the hemoglobin must be unadulterated so

that oxygen can bind in the lungs and release at the tissues

(ie, no CO or CN poisoning). A lack or impairment of

hemoglobin can also manifest as dyspnea. Consider a stool

guaiac exam if there is any clinical or historical signs of

anemia (eg, pallor, cachexia). Replete with a blood transfusion as necessary.

Blood volume. Adequate circulating volume is necessary to deliver red blood cells to the lungs and then distribute them throughout the body. Determine the volume

status by assessing vital signs, pulses, mucus membranes,

skin turgor, amount of secretions, etc.

Blood vessels. Blood must be able to flow freely to all

parts of the lungs to pick up oxygen. A PE may obstruct

blood flow to lung tissue and effect gas exchange, resulting in dyspnea. Unfortunately, the physical exam may

not reliably assist with this diagnosis, although wheezing

 

..... History

Relevant questions to answer during history taking include

the following: What makes the dyspnea worse? Is it exertional? Is it positional? When does the dyspnea occur? Has

the patient felt this dyspnea, or similar dyspnea, before?

What are the circumstances surrounding the dyspnea?

What is the patient's medical condition; any predisposi ­

tions toward dyspnea? While asking those questions, consider the following factors.

Positional dyspnea. In an upright position, fluid is

dependent and aeration is maximized at the apices. The

upright tripod position is the optimal position for effective

respirations: The diaphragm is able to reach full excursion;

there is no restriction of chest wall movement; the airway

is maximally patent. A history of dyspnea when lying down

suggests congestive heart failure ( CHF) or pericardia!

effusions.

Exertional dyspnea. If oxygen delivery is compromised, any increase in cardiac work and oxygen demand

will exacerbate the problem. This applies to every cause of

dyspnea, from primary pulmonary disease to cardiac disease to anemia. Determine whether there are recent

changes to how easily a patient starts feeling dyspneic. Be

especially concerned if there is new dyspnea at rest.

Transient dyspnea. If defined events of dyspnea are

described that resolve without intervention, this suggests a reversible or transient cause (ie, dysrhythmia,

pulmonary embolism [ PE ] , perceived dyspnea with

panic attacks ).

Recurrent dyspnea. The past predicts the future. "The

last time I had these symptoms it was my ". Fill in

the blank: asthma, PE, CHF, dysrhythmia.

Past medical history. A baseline pulmonary disease, cardiac disease, history of bleeding, or bleeding disorder may

manifest unexpectedly as a patient complaint of dyspnea.

Exposures. Several exposures can provoke dyspnea,

including cleaning products, angiotensin-converting

enzyme inhibitors, allergens, irritants, carbon monoxide.

DYSPNEA

In these cases, there is a temporal relationship between

exposure and onset of dyspnea.

Activities of daily living. Baseline exercise tolerance is

important historic information that helps you to judge the

severity of the acute process in addition to providing information regarding cardiac status. Ask about whether the

patient can do day-to-day chores. A patient who reports

trouble changing clothes or doing dishes tells much about

their baseline-and how quickly they may decompensate

in the emergency department.

 

• Do not hesitate. Initiate treatment in cases of respiratory

distress immediately, even if the diagnostic work-up is

incomplete.

This may be demonstrated by the patient's:

a. Failure to oxygenate

b. Failure to ventilate

c. Failure to protect the airway

If "yes" to any of the above, intubate immediately. If the

patient cannot oxygenate, there will be anoxic injury, espe ­

cially brain injury, within seconds to minutes. The inability

to perform the act of breathing (failure to ventilate) leads

to carbon dioxide buildup, and the ensuing acidosis can

lead to cardiac dysfunction. Finally, if the patient cannot

maintain an open airway (due to brain injury, mechanical

occlusion, etc.), there will be threat to both oxygenation

and ventilation, warranting immediate intubation.

2. Is the respiratory distress rapidly reversible?

Recognizing and promptly intervening on the rapidly

reversible causes of severe respiratory distress can prevent

the need for intubation. Delays in therapy may cause the

patient to quickly decompensate. Some of these reversible

causes (and their solutions) are as follows:

Hypoxia (administer oxygen)

Bronchospasm (beta -agonists/ steroids/ epinephrine)

Hypertensive pulmonary edema (nitrates/diuresis)

Pneumothorax (needle decompression/chest tube)

Allergic reaction (steroids/ epinephrine/ antihistamine)

3. Can he run?

Imagine the patient had to run for his or her life (in

many ways, this is what the patient is doing). How

long could the patient go before he or she collapsed?

What is the patient's physiologic reserve? For example,

is the patient young and healthy or elderly with

comorbidities? Consider all of the following in this

assessment: airway, chest walUmusculature, diaphragmatic excursion, posture, age, body mass index, cardiopulmonary status, and baseline exercise tolerance.

The decision to intubate or to wait is based on the

patient's ability to maintain the work of breathing. If

the patient is stable, set time limits and reassess

response to therapy frequently. If the patient has poor

reserve or already has respiratory fatigue, it may be

wiser to intubate electively rather than during a crashing situation.

 

CLINICAL PRESENTATION

...... History

A comprehensive history is critical and may identify the

etiology in up to 40% of cases. It is very important to

clarify all of the events immediately preceding, during, and

after the episode. Interview all family members and emer ­

gency medical service personnel present during the event.

Inquire about any concerning prodromal symptoms

including headache (ie, subarachnoid hemorrhage [SAH] ),

chest pain (ie, myocardial infarction [MI] , aortic dissec ­

tion, PE), and abdominal or back pain (ie, ruptured

abdominal aortic aneurysm [AAA] or ectopic pregnancy).

Obtain a detailed past medical history and review all current medications. Patients with significant cardiac histories

are at higher risk of arrhythmia, whereas elderly patients

on multiple medications are predisposed to orthostatic

syncope.

Antecedent dizziness, nausea, and diaphoresis or

symptoms occurring after moving from a recumbent or

sitting to upright position suggest a benign vasovagal

or orthostatic episode respectively. Syncope that occurs

either suddenly without prodrome or with physical exertion suggests arrhythmia or structural heart disease (aortic stenosis, hypertrophic cardiomyopathy). A prolonged

recovery period after syncope indicates a cerebrovascular

etiology (stroke, seizure, SAH), as classically all patients

should regain consciousness within several seconds of the

event.

...... Physical Examination

Always obtain triage vital signs and repeat when abnormal.

Obtain blood pressure (BP) measurements in both arms,

looking for unequal pressures suggestive of aortic dissec ­

tion. Consider orthostatic vitals, comparing recumbent

SYNCOPE

and standing vital signs. Significant BP findings include a

drop in systolic BP by :2:20 mmHg or an absolute value ::;90

mmHg when standing. Orthostasis suggests volume depletion or medication side effects. The cardiovascular exam

should include a detailed auscultation of the heart, listening for arrhythmias or any murmurs suggestive of underlying structural heart disease. A detailed neurologic exam

should identify any focal neurologic deficits. Perform a

rectal exam with stool guaiac analysis to assess for gastrointestinal ( GI) blood loss.

DIAGNOSTIC STUDIES

...... Laboratory

Routine laboratory evaluation is useful only when indicated by the history and physical exam. Obtain a rapid

bedside glucose in all patients with an altered sensorium.

Beside urine pregnancy testing is important for all females

of reproductive age. Check a complete blood count in all

patients with a history of bleeding or a positive stool

guaiac. Order a basic metabolic panel with any concern for

cardiac dysrhythmia secondary to significant electrolyte

abnormalities. Finally, check cardiac markers in patients

with antecedent chest pain or shortness of breath.

...... Electrocardiogram

Although the yield is relatively low ( <5%) for discerning

the source of a syncopal event, obtain an electrocardiogram (ECG) in all patients to rapidly identify any emergent

life threats. Concerning abnormalities on ECG include the

following:

1. Signs of ischemia or strain (Q waves, T wave, and

ST-segment changes, right bundle branch block)

2. Signs of conduction anomalies (prolonged QRS or QT

intervals, atrioventricular blocks, sinus pauses/arrest)

3. Signs of ectopy or arrhythmia (frequent premature

ventricular contractions, pre-excitation, Brugada crite ­

ria, significant bradycardia <50 bpm) (Figure 19-1)

4. Signs of cardiomyopathy (left ventricular hypertrophy

with or without strain pattern)

 

.... 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