male patients or postmenopausal females, hypertension,

dyslipidemia, diabetes mellitus, smoking, family history of

CAD, truncal obesity, and a sedentary lifestyle. It is important to remember that these risk factors are based on large

demographic analyses and cannot be used to predict the

presence or absence of CAD in a given patient. Approximately half of all patients presenting with ACS have no

identifiable risk factors outside of age and sex.

CLINICAL PRESENTATION

� History

A thorough history is the most sensitive tool for the detection of ACS, and an experienced clinician will always be

wary of its variable presentation. Chest pain is the most

common presenting complaint. Myocardial ischemia is

classically described as pressure-like or squeezing sensation

located in the retrosternal area or left side of the chest.

Inquire about the quality, duration, frequency, and in ten ­

sity of the pain. Determine whether there is radiation of

pain, associated symptoms, and provoking and palliating

factors. Symptoms commonly associated with myocardial

ischemia include nausea, diaphoresis, shortness of breath,

and palpitations. Anginal pain can radiate in almost any

direction depending on the individual patient and the

affected region of the heart, but radiation to the shoulder,

arm, neck, and jaw is most common. It should be noted

that the intensity of pain is not predictive of the overall

severity of the myocardial insult, and even minimal symptoms can correlate with significant mortality.

Up to a third of patients with ACS will present with

symptoms other than chest pain. Also known as "anginal

equivalents;' these presentations further complicate the

accurate diagnosis of ACS. Possible complaints include

dyspnea, vomiting, altered mental status, abdominal pain,

and syncope. Patients at an increased risk of atypical pre ­

sentations include the elderly, women, diabetics, polysubstance abusers, psychiatric patients, and nonwhite

minorities. These patients have a near 4-fold increase in

mortality owing to inherent delays in their diagnosis, treatment, and disposition. Always obtain a detailed social history and inquire about any recent and chronic substance

abuse. Habitual tobacco use has been proven to be an

independent risk factor for CAD, whereas cocaine use can

not only induce significant coronary spasm in the acute

setting, but also accelerate the atherosclerotic process when

chronically abused.

� Physical Examination

There are no physical findings specific for ACS, and the

exam is frequently normal. Obtain a complete set of vital

signs and closely monitor unstable patients. Bradycardia is

common with inferior wall ischemia owing to an increase

in vagal tone, whereas tachycardia may represent compensation for a reduction in stroke volume. Concurrent hypertension increases the myocardial 02 demand and may

exacerbate the underlying ischemia, whereas acute cardio ­

genic shock has an extremely poor prognosis.

Carefully auscultate the heart for any abnormal sounds.

Acute changes in ventricular compliance may result in an

S3, S4, or paradoxically split S2. The presence of a new

systolic murmur may signify either papillary muscle infarction with secondary mitral valve insufficiency or ventricu ­

lar septal infarction with secondary perforation. Look for

signs of acute congestive heart failure (CHF), including

jugular venous distension, hepatojugular reflux, and inspiratory crackles. Perform a rectal exam to look for evidence

 

ment. Patients with potential cardiac presentations

frequently complain of pain that is worse with exertion

and improved with rest. Pain that is worse with cough or

deep inspiration (pleuritic pain) is typically associated

with either pleurisy, a musculoskeletal etiology, or pulmo ­

nary embolism. Epigastric pain that is worse with meals

usually signifies a gastrointestinal etiology. Pain that is

aggravated by emotional stress may point to an underlying

psychiatric etiology. Finally, inquire about any associated

symptoms. For example, nausea and diaphoresis have been

associated with a higher likelihood for ACS.

Unfortunately, the long-term risk factors for underlying

heart disease (high cholesterol, smoking, hypertension, diabetes, family history) have not been shown to help in the

differentiation of acute chest pain patients in the ED. Nonetheless, this history should be taken. A history of an underlying hypercoagulable state ( eg, pregnancy, malignancy) should

alert you to a possible pulmonary embolism (PE), whereas a

history of an underlying connective tissue disorder ( eg,

Marfan syndrome) should prompt an evaluation for aortic

dissection. Ask about any illicit drug habits, as cocaine use

has been associated with accelerated atherosclerosis, acute

MI, and aortic dissection.

� Physical Examination

Note the general appearance of the patient. Those with

ACS or other serious etiologies may be clutching their

chest and frequently appear anxious, pale, and diaphoretic.

This "sick vs not sick" mentality will guide the rapidity of

your examination. As with all emergency patients, assess

the vital signs and ensure adequate airway, breathing, and

circulation (ABCs). Note abnormal vital signs to help

guide your differential diagnosis. A detailed examination

of the heart, lungs, abdomen, extremities, and neurologic

systems will ensure that no emergent causes of chest pain

are overlooked. Listed next are some emergent presenta ­

tions matched with potential physical exam findings.

ACS. Vital signs will vary widely depending on the re ­

gion of ischemia or infarction. For example, an inferior

wall MI may present with bradycardia and hypotension

owing to increased vagal tone. Murmurs and abnormal

heart sounds such as an S3 or S4 may be present. I nspiratory crackles on 1 ung exam are consistent with secondary

pulmonary edema.

Tension pneumothorax. Look for the classic signs of

decreased breath sounds, tracheal deviation, and res piratory distress. Consider spontaneous pneumothorax in

young, thin patients with an acute onset of chest pain

and shortness of breath.

Pericardia! tamponade. Although usually limited to

patients in extremis, patients may exhibit the classic

signs of Beck's triad (hypotension, diminished heart

CHEST PAIN

sounds, and jugular venous distension). Pulsus paradoxus > 10 mmHg has shown a high sensitivity but low

specificity for tamponade, as any condition causing increased intrathoracic pressure may demonstrate this.

Pulmonary embolism. Dyspnea is the most common

complaint of patients with PE. They may also describe a

pleuritic-type chest pain, especially those with segmental

PEs that cause secondary infarction of the parietal pleura.

Patients with significantly large (massive or submassive)

PE are generally ill-appearing and hemodynamically unstable owing to the sudden severe increase in pulmonary

vascular resistance. A detailed examination of the heart

and lungs may reveal rales, gallops, or a prominent P2.

Lower extremity exam may reveal unilateral swelling consistent with a deep venous thrombosis.

Aortic dissection. The pain is often most severe at onset

and typically extends above and below the diaphragm.

These patients are often hypertensive and may have a

pulse deficit in either the radial and/or femoral arteries.

A marked discrepancy in blood pressure compared between each arm (>20 mmHg) is highly suggestive.

DIAGNOSTIC STUDIES

Perform an electrocardiogram (ECG) within 10 minutes of

presentation for all patients who complain of chest pain or

have signs and symptoms concerning for ACS. Obtain cardiac

markers including a troponin assay ± CK-MB analysis in all

patients with suspected ACS. D-dimer can aid the evaluation

of low-risk patients in whom PE is a diagnostic possibility.

CXR should be ordered on most patients in the ED with

chest pain. Posteroanterior and lateral views are ideal, but a

portable anteroposterior view is sufficient for patients who

require continuous cardiac monitoring. Acute aortic dissection may present with a widened mediastinum or abnormal

aortic contour. Pneumothoraces and subcutaneous air are

readily identified. Pneumomediastinum ± a left-sided pleural

effusion (owing to the relative thinness of the left esophageal

wall) is seen with esophageal rupture (Boerhaave syndrome).

 

Newer generation CT angiography is the modality of

choice to diagnose pulmonary embolism and aortic dissection and may have an evolving role in the evaluation of

patients with potential coronary artery disease.

Transthoracic echo is often readily available and clinically useful to evaluate for possible pericardia! effusions

and tamponade physiology, ventricular hypokinesis in

patients with ACS, and right ventricular strain in patients

with massive PE. A bedside transesophageal echo is very

sensitive for diagnosing acute aortic dissection in patients

who are not candidates for CT angiography.

MEDICAL DECISION MAKING

A detailed history and physical exam in combination with

an ECG and/or chest radiograph may provide sufficient

evidence to exclude a myriad of emergent conditions.

CHAPTER 13

Patient presenting with

chest pain

Rapidly address ABC's, IV access,

supplemental 02 and cardiac mon itor

Immediate ECG and CXR

Absent breath

sounds with

shock

Pain radiates to

the back with wide

mediastinum on CXR

ECG with ischemia

or positive troponin

Pleuritic CP,

hypoxia, + CT

angiogram

History of vomiti ng,

mediastinal air on

CXR

Hypotension,

JVD, muffled

heart tones

.&. Figure 13-1. Chest pain diagnostic algorithm. BMP, basic metabolic panel; BP, blood pressure; CBC, complete blood

count; CP, chest pain; CT, computed tomography; CXR, chest x-ray; ECG, electrocardiogram; JVD, jugular venous distention.

When this is not adequate, a thoughtful use of laboratory

studies combined with the pretest probability of disease

will guide decision making (Figure 13-1).

TREATMENT

� Acute Coronary Syndrome

Provide supplemental 0 2, administer a loading dose aspirin

(162-365 mg), and begin sublingual nitroglycerin (0.4 mg

every 5 minutes) on all ACS patients without known contraindications (eg, allergy, hypotension). Further antithrombotic

(eg, clopidogrel) and anticoagulation (eg, low-molecularweight heparin) therapy will differ by institution and cardiologist. Of note, the preceding interventions are often only

temporizing measures, as early revascularization is definitive,

especially in those patients presenting with an ST -elevation MI.

� Aortic Dissection

Patients with an aortic dissection require an immediate

and aggressive reduction in both heart rate and blood pressure. The goal of treatment is to maintain a heart rate

<60 bpm and systolic blood pressure < 100 mmHg. There

are multiple medication options for this purpose, and

often concurrent infusions are required to meet the pre ­

ceding targets. When utilizing dual therapy, it is of utmost

importance to control the heart rate before dropping the

blood pressure to avoid a "reflex tachycardia" and conse ­

quent expansion of the underlying dissection.

� Pulmonary Embolism

Treatment will vary based on the hemodynamic impact of

the embolism. Anticoagulate stable patients with either

low-molecular-weight or unfractionated heparin. Hemo ­

dynamic instability may necessitate the use of thrombolytic

therapy.

..... Boerhaave Syndrome

Esophageal rupture is uncommon and classically presents

with the sudden onset of chest pain after vomiting. Initiate

broad-spectrum antibiotic coverage while arranging for

definitive surgical repair.

..... Pneumothorax

Place all patients with a pneumothorax on s upplemental 02

via a nonrebreather mask. Those with a tension pneumothorax require immediate needle decompression followed

by chest tube thoracostomy. Simple pneumothoraces can be

treated with tube thoracostomy or simple observation.

..... Pericardia! Tamponade

The recognition of tamponade is much easier in the age of

bedside ultrasonography. Perform immediate pericardio ­

centesis in unstable patients while arranging for an operative pericardia! window via cardiothoracic surgery.

DISPOSITION

...,_ Admission

Admit all patients with concerning presentations to a

monitored bed. The following chapters discuss the

CHEST PAIN

disposition of patients with specific conditions m

greater detail.

..... Discharge

Many patients with chest pain can be discharged with close

primary care follow-up and a list of strict indications for

reevaluation. Take care to exclude emergent causes and

discharge only those cases with a clear nonemergent etiology (eg, chest wall pain, zoster, dyspepsia). If clinical doubt

exists, it is certainly prudent to err on the side of caution

 

Anaphylaxis

Anaphylactic shock can be rapidly fatal and requires

immediate treatment. Administer normal saline boluses,

N antihistamines, and N corticosteroids to all patients.

Give intramuscular epinephrine (1:1,000 solution) in 0.3-

to 0.5-mg doses as needed to maintain systemic perfusion.

In patients refractive to the preceding, administer 0.3- to

0.5-mg doses of N epinephrine (1:10,000 solution) over a

2- to 3-minute duration. Actively search for and remove

any ongoing allergen exposure ( eg, retained soft tissue bee

stinger).

SHOCK

� Obstructive Shock

Cardiac Tamponade

Administer 1-2 L of normal saline followed by emergent

bedside pericardiocentesis. Perform an emergency department

thoracotomy in patients with penetrating thoracic trauma

who fail to respond.

Pulmonary Embolism

Administer small boluses of normal saline (250-500 mL)

followed by vasopressor support in unstable patients.

Fibrinolysis is the treatment of choice for massive PE presenting with profound hypotension (MAP <60), severe

refractive hypoxemia (Sp02 <90 despite supplemental 02),

or cardiac arrest.

Tension Pneumothorax

Administer 1-2 L of normal saline while performing

emergent needle thoracostomy followed by chest tube

placement.

� Cardiogenic Shock

The goal of treatment is to improve cardiac output while

at the same time reducing myocardial workload.

Administer IV fluids judiciously to avoid undesired elevations in the left ventricular preload and secondary pulmonary edema. Begin inotropic and vasopressor support in

patients who remain hypotensive despite IV fluids. Firstline therapy is often a combination of dopamine and

dobutamine (as dobutamine monotherapy will exacerbate

hypotension), with norepinephrine reserved for patients

who fail to respond. Of note, all of the aforementioned

modalities are temporizing measures pending definitive

revascularization (ie, percutaneous coronary intervention

or fibrinolysis).

DISPOSITION

Admit all patients in shock to a critical care bed.

SUGGESTED READING

Cherkas D. Traumatic hemorrhagic shock: Advances in fluid

management. Emerg Med Pract. 20 1 1;13:1-20.

Dellinger, RP, Levy, MM, et al. Surviving Sepsis Campaign:

International guidelines for management of severe sepsis and

septic shock: 2008. Grit Care Med. 2008;36:296-327.

Otero RM, Nguyen HB, Rivers EP. Approach to the patient in

shock. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ,

 

and admit for inpatient observation.

SUGGESTED READING

Anderson JL, Adams CD, Antman EM, et al. ACC/ AHA 2007

Guidelines for the management of patients with unstable

angina/non ST-elevation MI: A report of the ACC/AHA

task force of practice guidelines. Circulation. 2007;116:

el48.

Fesmire FM, Brown MD, Espinosa JA, et a!. Critical issues in the

evaluation and management of adult patients presenting to

the emergency department with suspected pulmonary embolism. Ann Emerg Med. 20 1 1;57:628-652.

Green GB, Hill PM. Chest pain: Cardiac or not. I n: 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. 36 1-367 .

Swap CJ, Nagumey JT. Value and limitations of chest pain his ­

tory in the evaluation of patients with acute coronary syn ­

dromes. JAMA. 2005;294:2623-2639.

Acute Coronary Syndromes

Ch ristopher Ross, MD

Key Points

• Consider acute coronary syndrome (ACS) in the initial

assessment of all patients presenting with chest pa in

and/or d ifficu lty breathing.

• Atypical presentations are common, especially in

women, the elderly, and diabetics.

• Obta in an emergent el ectroca rdiogram in all

patients with concern for ACS to ra pidly identify

INTRODUCTION

Acute coronary syndrome (ACS) encompasses a spectrum

of disease that includes unstable angina (UA), nonST-segment elevation myocardial infarctions (NSTEMI),

and ST-segment elevation myocardial infarctions (STEM!).

The distinction between the 3 is based on historical factors,

electrocardiogram (ECG) analysis, and cardiac biomarker

measurements. ACS is the leading cause of mortality in the

industrialized world and accounts for more than 25o/o of all

deaths in the United States. More than 5 million patients

per year present to U.S. emergency departments with

symptoms concerning for ACS, although fewer than lOo/o

will be diagnosed with acute myocardial infarctions (AMI).

That said, between 2o/o and 4o/o of all patients with ACS are

initially misdiagnosed and improperly discharged from the

ED, resulting in significant morbidity and mortality and

accounting for the leading source of malpractice payouts

in the United States.

The pathophysiology of myocardial ischemia can be

broken down into a simple imbalance in the supply and

demand of coronary perfusion. Atherosclerosis is responsible for almost all cases of ACS. This insidious process

begins with the deposition of fatty streaks in the coronary

50

 

Gentle downward pressure applied to the cricoid cartilage (Sellick's maneuver) at the onset of induction and

paralysis has been historically advocated to limit the potential for aspiration. A growing body of literature has begun to

question the utility of this maneuver as it not only fails to

prevent aspiration but can limit adequate visualization of

the vocal cords and impair successful insertion of the ETT. If

cricoid pressure is applied, release inlmediately if the patient

begins to vomit to prevent secondary esophageal rupture.

� Difficult Airway Adjuncts

Multiple devices have been designed to assist with the

management of difficult airways. Laryngeal mask airways

AIRWAY MANAGEMENT

Figure 1 1-5. Schematic demonstrati ng use

of bougie.

(LMA) conform to the natural curvature of the oropharynx and are designed for blind insertion into the supraglottic region. Proper insertion creates an airtight seal over

the larynx, allowing for mechanical ventilation. LMA

insertion does not prevent aspiration, though, and is not

considered a definitive airway.

Introducer bougies are very useful in patients whose

vocal cords cannot be adequately visualized. They are

essentially long flexible rubber sty lets with a distal curve at

their tip, which, when blindly inserted along the inferior

margin of the epiglottis, will naturally angle upward into

the larynx and through the vocal cords. Successful endotracheal placement can be detected as the tip of the bougie

skips along the tracheal rings. The ETT is then inserted

blindly over the bougie and into the airway (Figure 1 1-5).

Cricothyrotomy is performed by making a percutane ­

ous incision in the cricothyroid membrane through which

a tracheostomy or small ETT can be placed (Figure 1 1-6).

This can be a life-saving intervention in the crashing

patient when less invasive techniques to secure the airway

have failed. Common indications include massive facial

trauma and angioedema. Cricothyrotomy is contraindi ­

cated in children <8 years of age and should be replaced

with needle cricothyrotomy.

Additional difficult airway adjuncts include blind nasatracheal intubation, lighted stylets, Combitubes, fiberoptic

intubation, retrograde wire-guided tracheal intubation,

and percutaneous translaryngeal ventilation.

DISPOSITION

Admit all patients who require airway management to an

intensive care unit setting.

Figure 1 1-6. Cricothyrotomy. A. An 11 blade

scalpel is used to cut the cricothyroid membrane. B. A

skin hook opens the incision and lifts the thyroid

carti lage su periorly so that the tracheostomy tube or

ETT can be inserted into the ai rway. (Reprinted with

permission from Bai l itz J, Bokhari F, Scaletta TA, et al.

Emergent Management of Trauma. 3rd ed. New York:

McGraw-Hill Education, 201 1 .)

SUGGESTED READINGS

Hedayati T, Ross C, Nasr N. Airway procedures. Rapid sequence

intubation. In: Simon RR, Ross CR, Bowman SH, Wakim PE.

Cook County Manual of Emergency Procedures. 1 st ed.

Philadelphia, PA: Lippincott Williams & Wilkins, 201 2, pp.

14-2 1.

 

Roman AM. Noninvasive airway management. In: Tintinalli JE,

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

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 20 11, pp. 183-190.

Vissers RJ, Danzl DF. Tracheal intubation and mechanical venti ­

lation. In: Tintinalli JE, Stapczynski JS, Ma OJ, Clince DM,

Cydulka, RK, Meckler GD. Tintinalli's Emergency Medicine: A

Comprehensive Study Guide. 7th ed. New York, NY: McGrawHill, 20 l l, pp. l 98-2 15.

S hock

La u ren M. Smith, MD

Nihja 0. Gordon, MD

Key Points

• Do not wait for hypotension to diagnose shock.

• Early ide ntification and i n itiation of aggressive

therapy can significantly improve patient

survival.

INTRODUCTION

More than 1 million patients present to U.S. emergency

departments annually with shock, and despite continued

advances in critical care, mortality rates remain very high.

Shock occurs when the circulatory system is no longer able

to deliver enough 02 and vital nutrients to adequately meet

the metabolic demands of the patient. Although initially

reversible, prolonged hypoperfusion will eventually result

in cellular hypoxia and the derangement of critical bio ­

chemical processes. From a clinical standpoint, shock can

be divided into the following subtypes: hypovolemic, cardiogenic, obstructive, and distributive. Hypovolemic

shock results from an inadequate circulating blood volume

owing to either profound dehydration or significant hemorrhage. Traumatic hypovolemia is the most common type

of shock encountered in patients <40 years of age.

Cardiogenic shock occurs when the heart is unable to provide adequate forward blood flow secondary to impaired

pump function or significant dysrhythmia. Myocardial

infarction is the leading cause of cardiogenic shock and

typically occurs once -40% of the myocardium is dysfunctional. Obstructive shock results from an extracardiac

blockage of adequate venous return of blood to the heart

( eg, pericardia! tamponade, tension pneumothorax, and

massive pulmonary embolism [PE) ). Finally, distributive

shock occurs secondary to an uncontrolled loss of vascular

tone (eg, sepsis, anaphylaxis, neurogenic shock, and adrenal

42

• I n itiate early goa l-directed therapy in patients with

septic shock.

• Early revascu larization is key to improving outcome in

patients with cardiogenic shock.

crisis). Neurogenic shock most commonly occurs in

trauma patients with high cervical cord injuries and a

secondary loss of sympathetic tone and should always be

considered a diagnosis of exclusion. Classically these

patients will present with hypotension and a paradoxical

bradycardia. Suspect septic shock in elderly, irnmunocompromised, and debilitated patients who are toxic appearing

despite only vague symptoms. The prognosis for patients

with cardiogenic and septic shock remains grave, with

mortality rates between 30% and 90%.

The pathophysiology of shock can be divided into

3 basic categories: a systemic autonomic response, endorgan cellular hypoxia, and the secretion of proinflammatory mediators. The autonomic system initially responds

to widespread tissue hypoperfusion by globally increasing

the overall cardiac output. As tissue perfusion continues

to decline, the body shunts circulating blood away from

less vital structures including the skin, muscles, kidneys,

and splanchnic beds. Reflexively, the kidneys activate the

renin-angiotensin axis, prompting the release of various

vasoactive substances, with the net effect to preserve perfusion to the most critical organs, namely the brain and

the heart.

When the preceding response is inadequate despite

maximal tissue 02 extraction, cellular hypoxia forces a conversion from aerobic to anaerobic metabolism. By nature,

anaerobic metabolism cannot produce enough adenosine

triphosphate to maintain regular cellular function. Tissue

lactate accumulates, resulting in systemic acidosis, and

eventually this breakdown in cellular metabolism leads to

widespread tissue death. Injured and dying cells prompt

the production and secretion of harmful inflammatory

mediators, resulting in the development of the systemic

inflammatory response syndrome, defined by the presence

of fever, tachycardia, tachypnea, and leukocytosis.

CLINICAL PRESENTATION

� History

Vague complaints such as fatigue and malaise may be the

only presenting symptoms, especially in elderly patients.

Friends, family, and emergency medical service personnel

will be vital in obtaining a history in patients with altered

mental status. The past medical history including a list of

active medications might reveal risk factors such as immunosuppression, underlying cardiac disease, and potential

allergic reactions.

� Physical Examination

Although hypotension and tachycardia are the cardinal

features of shock, many patients will presents with normal

vital signs owing to physiologic compensation. Because of

the unmet metabolic demands of the central nervous sys ­

 

Rapid airway eva luation to identify

findings indicative of a difficult airway

Difficult airway

predicted

No difficult airway

predicted

Modified approach including:

• "Awake look" intubation

• Difficult airway adjuncts

(LMA, bougie, fiberoptics, etc.)

Figure 1 1-1. Airway diag nostic algorithm. LMA, laryngeal mask airways; RSI, rapid-sequence intubation.

ridge meant to sweep the tongue to the side during insertion

to improve visualization of the vocal cords. The Miller blade

is straight in appearance and meant to directly lift the

Figure 1 1-2. Proper method of BVM ventilation.

epiglottis away from the vocal cords. It is of particular benefit in patients with very anterior airways and those with a

large "floppy" epiglottis. A size 3 or 4 Macintosh blade is

appropriate for most adult ED patients (Figure 1 1-3).

Certain clinical scenarios warrant unique modifications to standard RSI to attenuate the adverse physiologic

responses to endotracheal intubation. Pretreat head injury

patients with lidocaine (1.5 mg/kg) and a "defasciculating"

dose of a nondepolarizing neuromuscular blocker ( eg,

pancuronium 0.01 mg/kg) to limit the potential spike in

ICP that may accompany ETT placement. Pretreat most

pediatric patients with an anticholinergic agent ( eg, atro ­

pine 0.02 mg/kg) to prevent reflex bradycardia. Pretreat

patients in whom rapid elevations in either blood pressure

or heart rate would be catastrophic (eg, aortic dissection)

with an opioid analgesic ( eg, fentanyl 3 meg/kg) to limit

excessive catecholamine surges. Of note, the clinical utility

of many of these pretreatment regimens has recently come

under considerable debate.

Outside of the pretreatment agents listed previously,

the remaining RSI medications can be divided into either

CHAPTER 11

Figure 1 1-3. Equi pment needed for orotracheal

intubation in an adu lt. From left to right, laryngoscope

handle attached to Macintosh 3 blade, Maci ntosh

4 blade, Miller 4 blade, end-tidal C02 detector,

1 0-ml syringe, and endotracheal tube with stylet.

induction agents or paralyzing agents. Induction agents are

designed to elicit extremely rapid sedation to facilitate ETT

placement. A variety of medications are available, including etomidate (0.3 mg/kg), propofol (1 mg/kg), ketamine

(2-3 mg/kg), and midazolam (0.05-0. 1 mg/kg). Of these,

etomidate is used most frequently in the ED because of its

rapid onset and offset and relative hemodynamic neutrality. Avoid the use of benzodiazepines and propofol in

hypotensive patients and ketamine in patients with paten ­