emergency medicine pocketbook

Pocket Emergency Third Edition
MEDICINE

JOHN D. ANDERSON, MD
NIR HARISH, MD, MBA
Denver Health Residency in Emergency Medicine

NICHOLAS G. MALDONADO, MD
ALEXANDER Y. SHENG, MD
The Harvard Affiliated Emergency Medicine Residency Program

Edited by
RICHARD D. ZANE, MD, FAAEM
Professor and Chair
Department of Emergency Medicine
University of Colorado School of Medicine
Aurora, Colorado

JOSHUA M. KOSOWSKY, MD
Assistant Professor, Harvard Medical School
Vice Chair for Clinical Affairs, Department of Emergency Medicine
Brigham and Women’s Hospital
Boston, Massachusetts

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CONTRIBUTORS

John D. Anderson, MD
Denver Health Residency in Emergency Medicine
Denver Health Medical Center
Department of Emergency Medicine
University of Colorado School of Medicine
Denver, Colorado

Nir Harish, MD, MBA
Denver Health Residency in Emergency Medicine
Denver Health Medical Center
Department of Emergency Medicine
University of Colorado School of Medicine
Denver, Colorado

Nicholas G. Maldonado, MD
The Harvard Affiliated Emergency Medicine Residency Program
Department of Emergency Medicine
Brigham and Women’s Hospital
Massachusetts General Hospital
Boston, Massachusetts

Alexander Y. Sheng, MD
The Harvard Affiliated Emergency Medicine Residency
Department of Emergency Medicine
Brigham and Women’s Hospital
Boston, Massachusetts

ACKNOWLEDGMENTS

To our patients who trust that we are always there and know what to do, when to do it,
and allow us the privilege of caring for them during the most vulnerable moments of
their lives. For Siobhan, Jake, Gaby, and Finn whose support made everything possible.

RICHARD D. ZANE, MD

To all those from whom I continue to gain wisdom—my teachers, my colleagues, my
students, and perhaps foremost, my patients. And to Devorah, Harry, Jake, and Judah,
whose support means the world to me.

JOSHUA M. KOSOWSKY, MD

PREFACE

Sir William Olser wrote, “He who studies medicine without books sails an uncharted sea,
but he who studies medicine without patients does not go to sea at all.” Emergency
medicine is a thrilling specialty, demanding exceptional abilities and an increasingly
expansive fund of knowledge—patterns of illness and injury, a whole range of
diagnostics and therapeutics, all at one’s ngertips in real time at the bedside with lives
on the line. In this context, we have designed Pocket Emergency Medicine as a life raft for
the busy physician, resident, physician assistant, nurse practitioner, or student.

Unlike many traditional textbooks, we have chosen to organize chapters around
presenting conditions rather than diagnoses. In this way, the book mirrors the way
patients present to the emergency department and allows the reader to develop the
thought processes that guide appropriate diagnostic and therapeutic interventions. Each
chapter begins with a general approach to a particular condition, followed by a succinct
discussion of important diagnostic categories, highlighting essential elements of the
history, physical examination, testing, and treatment speci c to these diagnoses.
Sprinkled throughout the text are “clinical pearls”—focused bullet points, emphasizing
important clinical findings or warning about common clinical errors.

This book was written by a group of talented emergency medicine residents from the
Denver Health and Harvard A liated Emergency Medicine Residency programs. The
residents undertook studious research on their individual topics, guided by an acute
awareness of the needs of busy emergency department providers. Chapters were edited
by an experienced team of senior emergency medicine faculty from the Departments of
Emergency Medicine at The University of Colorado School of Medicine, Brigham and
Women’s Hospital and Harvard Medical School. The editors bring over 25 years of
experience in clinical and academic emergency medicine, ensuring the accuracy and
integrity of the text. The result, we think you’ll agree, is a supremely useful immediate
reference for the emergency medicine practitioner.

RICHARD D. ZANE, MD
JOSHUA M. KOSOWSKY, MD

CONTENTS

SECTION I: CARDIOVASCULAR

Electrocardiography
Chest Pain
Acute Coronary Syndrome (Overview)
STEMI
UA/NSTEMI
Prinzmetal’s (Variant) Angina
Cocaine-induced Angina
Stress Testing
Cardiac Catheterization
Post-PCI Complications
Post-MI Complications
Pulmonary Embolism and DVT
CHF/Acute Pulmonary Edema
Aortic Dissection
Thoracic Aortic Aneurysm
Pericarditis and Pericardial Effusion
Cardiac Tamponade
Myocarditis
Syncope
Hypertension and Hypertensive Emergencies
Hypotension and Shock
Hypovolemic Shock
Cardiogenic Shock
Septic Shock
Neurogenic Shock
Dysrhythmia
Bradycardia
AV Node Block
Tachycardia/Palpitations
Pacemaker and AICD Malfunction

SECTION II: PULMONARY

Cough
Dyspnea (Shortness of Breath)
Hemoptysis

SECTION III: GASTROINTESTINAL

Abdominal Pain
Nausea and Vomiting
Gastrointestinal Bleed

Difficulty Swallowing
Diarrhea
Constipation
Jaundice
Rectal Pain (PROCTALGIA)

SECTION IV: INFECTIOUS DISEASE

Fever
Abscess
Soft Tissue Infections
Viral Infections
Rabies
Tetanus
Parasitic Infections
Vector-Borne Infections
Bioterrorism

SECTION V: NEUROLOGY

Altered Mental Status
Vertigo
Facial Droop
Headache
Seizure
Stroke
Weakness/Fatigue

SECTION VI: RENAL & GENITOURINARY

Dysuria
Urinary Tract Infections
Flank Pain
Hematuria
Acute Renal Failure
Testicular Torsion/Torsion of Testicular Appendix
Phimosis and Paraphimosis
Priapism
Emergencies in Dialysis Patients

SECTION VII: OBGYN

Vaginal Bleeding
Preeclampsia and Eclampsia
Hyperemesis Gravidarum
Emergency Delivery
Female Pelvic Pain

Vaginal Discharge (Sexually Transmitted Infection)
Pelvic Inflammatory Disease and Tubo-ovarian Abscess

SECTION VIII: DERMATOLOGY

Rash
Viral Exanthems
Bacterial Exanthems
Fungal Exathems
Allergic/Inflammatory Exanthems
Neoplastic/Other Exanthems
Dermatologic Emergencies

SECTION IX: ENDOCRINE & METABOLIC

Acid–Base Disorders
Abnormal Electrolytes
Hyperglycemic Emergencies (DKA/HHS)
Thyroid Emergencies
Adrenal Insufficiency

SECTION X: ENVIRONMENTAL

Dehydration
Bites and Stings
Occupational Exposure
Burns
Carbon Monoxide Poisoning
Dysbarism
Electrical Injury
High-Altitude Illness
Hypothermia
Hyperthermia
Lightning Injury
Drowning
Botulism

SECTION XI: HEMETOLOGY & ONCOLOGY

Allergic Reactions, Anaphylaxis, and Angioedema
Oncologic Emergencies
Sickle Cell Disease
Abnormal Bleeding: Platelet Disorders and Coagulopathy
Transfusions
Approach to the Transplant Patient

SECTION XII: MUSCULOSKELETAL & RHEUMOTELOGICAL

Leg Pain and Swelling
Lower Back Pain
Joint Pain

SECTION XIII: OTOLARYNGOLOGY/DENTAL/OPHTHALMOLOGY

Ear Pain
Hearing Loss
Sore Throat
Sinusitis
Epistaxis
Eye Pain/Redness
Vision Change and Vision Loss
Toothache

SECTION XIV: PEDIATRICS

Resuscitation
Abdominal Pain
Cyanosis
Pediatric Fever
Jaundice
Limp
Pediatric Seizure
Nausea and Vomiting
Pediatric Meningitis (See 5d)
Neonatal Complaints
Congenital Heart Disease
Respiratory Complaints
Diabetic Ketoacidosis
Hypoglycemia
Fluid and Electrolyte Abnormalities
Pediatric Exanthems
Urinary Tract Infection

SECTION XV: PSYCHIATRIC PATIENT

Psychiatric Patient

SECTION XVI: TOXICOLOGY

General Approach to The Intoxicated Patient
Anticholinergic Ingestion
Psychopharmacologic Ingestion
Alcohols
Drugs of Abuse
Analgesic Overdose

Cardiac Medication Overdose
Caustic Ingestions
Cellular Asphyxiates

SECTION XVII: AIRWAY MANAGEMENT

Airway Management
RSI
Cricothyrotomy

SECTION XVIII: TRAUMA

Primary Survey
Head Trauma
Maxillofacial Injury
Eye Injury
Neck Trauma
Cervical Spine Trauma
Thoracic/Lumbar/Sacral Spine Trauma
Thoracic Trauma
Abdominal Trauma
Genitourinary Trauma
Hip/Pelvic Trauma
Extremity Injury
Wound Management
Abuse

SECTION XIX: APPENDIX

Abbreviations
Pediatric Advanced Life Support (PALS)
Mechanical Ventilation
Analgesia & Conscious Sedation
ICU Medications
Equations
Procedures

INDEX

ELECTROCARDIOGRAPHY

Approach

• Correct pt, correct date, correct lead placement, comparable calibration (mV, paper
speed)

• Rate, rhythm, axis
• Waves (P, Q, R, T, U waves) & segments (PR, QRS, QT intervals, & ST segment)
• Conduction & bundle blocks
• Atrial enlargement, ventricular hypertrophy
• Ischemia/infarction
• Miscellaneous (stigmata of electrolyte abx, syncope, tox, PMs, PE, etc.)







Adapted from: Wang K, Asinger RW, Marriott H. ST-segment elevation in conditions
other than acute myocardial infarction. N Eng J Med. 2003;349:2128–2135.

CHEST PAIN

Approach

Obtain & review an ECG w/i 10 min of pt arrival & compare w/ prior if available. If
pain persists, repeat q15–20min; consider R-sided & posterior leads if high probability
w/ initially nl appearing ECG.
• Intervene early w/ IV, O2, & cardiac monitoring

• CXR for all nontrivial CP
• Give ASA 325 mg if considering a cardiac etiology & you do not suspect aortic

dissection
• Give NTG for pain
• Obtain PQRST of pain & recheck after pain medication is given
• Obtain CAD hx: Prior MI, CABG, catheterization, stress test, angina
Risk stratify: Age >50, HTN, DM, HL, +FH, smoking, cocaine; use of risk stratification

models such as TIMI, GRACE, or PURSUIT can be useful to assist in decision making
w/ regard to tx options in pts w/ suspected ACS.
• Always consider immediately life-threatening causes of CP

ACUTE CORONARY SYNDROME (OVERVIEW)

Approach

• See Approach above

Definitions

• ACS: Represents a clinical spectrum ranging from UA through NSTEMI & STEMI
ACS develops when a vulnerable or high-risk plaque undergoes disruption of the
fibrous cap which is a stimulus for thrombogenesis w/ ultimate imbalance b/w
myocardial O2 supply & demand

• UA (subtotal coronary thrombosis, angina that is new onset, crescendo, OR at rest,
usually <30 min, ±ST depression &/or TWI)

• Rest angina: Angina occurring at rest & prolonged, usually >20 min
• New-onset angina: New-onset angina of at least CCS class III severity
• Increasing angina: Previously diagnosed angina that has become distinctly more

frequent longer in duration, or lower in threshold (ie, increase by 1 or more CCS
class)

• NSTEMI (same as UA but w/ +troponin)
• STEMI (total coronary thrombosis, angina usually at rest >30 min, ST elevations,

+troponin)
• Note: Most troponin elevations in ED are not due to primary ACS, but demand

ischemia

History (NEJM 2005;294:2623)

• Typical sxs
• Angina (substernal pressure/pain/tightness, radiation to neck/jaw/arms,
precipitated by exertion/relieved w/ rest or NTG); w/ ACS, new onset, crescendo, or
at rest
• Associated sxs: Dyspnea diaphoresis, N/V, palpitations, LH; ∼23% MIs lack typical
sxs (AJC 1973;32:1)

Physical Exam

• Usually unremarkable exam

Evaluation

• ECG: ST change (up or down), TWI, LBBB that is new. Q wave or PRWP suggests prior
MI → CAD. Always check ECG w/i 10 min, w/ changes in sxs, at 6–12 h & c/w
baseline. If pain persists, repeat q15–30min.

• It is reasonable to obtain supplemental ECG leads V7–V9 in pts whose initial
ECG is nondiagnostic to r/o MI due to L circumflex occlusion

• Sgarbossa’s criteria: In setting of old LBBB, STEMI Dx requires ≥1 mm STE concordant
w/ QRS (sens 73%, spec 92%) or ≥5 mm discordant (sens 31%, spec 92%) any lead
(NEJM 1996;334:481).

Cardiac Biomarkers

• Requires serial testing at 6 & 12 h after sx onset. It is reasonable to remeasure positive
biomarkers at 6- to 8-h intervals 2–3 times or until levels have peaked, as an index of
infarct size & dynamics of necrosis.

• Troponin (I or T) is most sens & spec. Also seen in myocarditis, CMP, severe CHF,
cardiac trauma, cardioversion, sepsis, ICH, renal failure.

• Cardiac index, CI = (CK – MB/CK) × 100. CI <3 suggests skeletal source, CI 3–5 →
indeterminate, CI >5 suggests cardiac source

Figure 1.1

• Other labs: Chem 7, CBC, coags, T/S (if intervention planned), tox (if cocaine

suspected)
• CXR: Check for cardiomegaly, pulmonary edema
• Echo: If ECG is not interpretable (prior LBBB, paced) & suspicion for ACS is high, can

obtain echo to evaluate for regional wall abnlty.
• CTCA: May be useful for evaluating pts w/ intermed & low PreTP for CAD w/ nl serial

ECGs/biomarkers (Circulation 2006;114:1761; JACC 2006;48:1475; NEJM
2012;366(15):393; NEJM 2012;367(4):299)

Treatment

• See STEMI & UA/STEMI for details

Disposition

• If hx & initial ECG/biomarkers are non-Dx: Repeat ECG/biomarkers at 3 & 6 h from
1st set & if suspicion for ACS is low, may monitor for recurrent sx. If no ACS, can
evaluate for inducible ischemia via stress test.

• Stress testing may be done as an outpt if low risk (age <70, no prior CAD, CVD, PAD;
no rest angina) at 72 h (0% mortality, <0.5% MI, [Ann Emerg Med 2006;47:427])

• If STEMI or UA/NSTEMI: Admit (see below)

Pearls

• Give ASA if you suspect ACS & there are no CIs. It provides the greatest
morbidity/mortality benefit of any tx in the ED for ACS (50–70% drop D/MI for
UA/NSTEMI, NEJM 1988;319:1105; 23% drop death in STEMI, ISIS-2, Lancet
1988;ii:349).

• Women, diabetics, & elderly pts often present w/o CP; anginal equivalents: SOB,
fatigue, weakness

STEMI

Definition

• Total coronary thrombosis, angina usually at rest >30 min, ST elevations, +troponin

Evaluation

• ≥0.2 mV precordial leads, ≥0.1 mV limb leads, & ≥0.5 mV in R-sided & posterior
leads in at least 2 contiguous leads

Treatment

• Decide whether the pt will receive lysis or PCI as soon as possible

• If PCI is to be performed, call cardiology/PCI lab (if one is available) as early as
possible (potentially even before the pt arrives in the ED – if reliable prenotification of
STEMI via EMS)

• If pt will be transferred for PCI, call for transfer early, & ensure their door-to-balloon
time is <90 min

• Antithrombotic/adjunctive therapy, should not delay transfer for PCI

Routine Medical Therapies “MONAB”

• Morphine: Drug of choice for pain relief in pts w/ STEMI; typical dose 0.05–0.1 mg/kg
IV

• O2: Appropriate only in hypoxic pts w/ O2 saturation <90%, as routine O2 use may

cause higher risk of death for pts w/ confirmed AMI
• Nitrates: No mortality benefit, but may ameliorate sxs; typical dose 0.4 mg SL q5min

× 3 doses; CI w/ hypotension, RV infarct, concomitant PD inhibitor use w/i 24–48 h.
• Aspirin: 23% ↓ in death (ISIS-2, Lancet 1988;2:349); typical dose 162–325 mg PO
• Beta-blockers: Oral BB should be administered w/i 24 h of STEMI w/o CIs. Routine IV

should not be used & recommended in those w/o CIs or w/ ongoing ischemia.
Increased risk of cardiogenic shock in those >70 y/o, SBP <120 mmHg, HR >110
bpm (COMMIT/CCS-2, Lancet 2005;366:1622); when used, typical dose Metoprolol
tartate 5 mg IV
• Other: Often started as inpts include oral BBs, statins, ACE inhibitors/ARBs

Fibrinolysis

• Fibrinolytic therapy should be given to pts w/ STEMI & onset of sxs w/i previous 12 h
when it is anticipated that primary PCI cannot be performed w/i 120 min of 1st
medical contact

• Indications: Sx <12 h & either STE ≥1 mm in ≥2 contig. Leads or LBBB not known to
be old; benefit if sx >12 h less clear; reasonable if persistent up to 24 h sx & STE.

• Door-to-needle time should be ≤30 min
• ∼20% ↓ mortality in anterior MI or new LBBB; 10% ↓ mortality in IMI
• ∼1% risk of ICH; high-risk groups include elderly (∼2% if >75 yr), women, low

weight
• Fibrin-specific lytic (front-loaded tPA) 14% ↓ mortality c/w SK (1% abs Δ; GUSTO,

NEJM 1993;329:673) although ↑ ICH (0.7% vs. 0.5%); 3rd-generation bolus lytics
easier to administer, but no more safe or efficacious

• Fibrinolytic agents:
Tenecteplase (TNK-tPA): Single IV weight-based bolus
30 mg for weight <60 kg
35 mg for 60–69 kg
40 mg for 70–79 kg
45 mg for 80–89 kg
50 mg for ≥90 kg
Reteplase (rPA): 10 U + 10 U IV bolus given 30 min apart
Alteplase (tPA): Bolus 15 mg, infusion 0.75 mg/kg for 30 min (max 50 mg), then 0.5
mg/kg (max 35 mg) over 60 min; total dose not to exceed 100 mg

Adjunctive Antithrombotic Therapy for Fibrinolytic Therapy

• ASA (162–325 mg PO) & Clopidogrel (300 mg LD for pts ≤75 y/o, 75 mg for pts >75
y/o) should be administered to pts w/ STEMI who receive fibrinolytic therapy (ISIS-2,
Lancet 1988;2:349; CLARITY-TIMI 28, NEJM 2005;352:1179; COMMIT, Lancet
2005;366:1607)

• Pts w/ STEMI undergoing reperfusion w/ fibrinolytic therapy should receive
anticoagulation therapy for minimum of 48 h, w/ recommended regimens:
UFH weight-based infusion w/ IV bolus 60 U/kg (max 4000 U) followed by infusion
of 12 U/kg/h (max 1000 U) to maintain aPTT ∼50–75 s for 48 h or until
revascularization
Enoxaparin: If <75 y/o, 30 mg IV bolus, then 15 min later, 1 mg/kg SC q12h; if >75
y/o; no bolus, 0.75 mg/kg SC q12h; if CrCl <30 mL/min, 1 mg/kg q24h
Fondaparinux: Initial 2.5 mg IV, then 2.5 mg SC the following day, CI in CrCl <30

Indications for Transfer for Angiography After Fibrinolysis

• Immediate transfer for cardiogenic shock or severe acute HF irrespective of time delay
from MI onset

• Urgent transfer for failed reperfusion or reocclusion
• As part of an invasive strategy in stable pts w/ PCI b/w 3 & 24 h after successful

fibrinolysis

Primary PCI (NEJM 2007;356:47)

• Should be performed w/i 90 min of arrival by skilled operator at high-volume center
• Superior to lysis: 27% ↓ death, 65% ↓ re-MI, 54% ↓ stroke, 95% ↓ ICH (Lancet

2003;361:13)
• Transfer to center for 1° PCI may also be superior to lysis (DANAMI-2, NEJM

2003;349:733) if can achieve acceptable door-to-balloon times (as above)

Adjunctive Antithrombotic Therapy for Primary PCI

• ASA 162–325 mg PO (crushed/chewed) should be given before primary PCI (Circulation
1987;76:125; Eur Heart J. 2009;30:900; NEJM 2010;363:930)

• A loading dose of a P2Y12 receptor inhibitor should be given as early as possible or

at the time of primary PCI in pts w/ STEMI:
• Clopidogrel 600 mg PO (NEJM 2010;363:930; ARMYDA-6 MI, J Am Coll Cardiol

2011;58:1592; CURRENT-OASIS 7, Lancet 2010;376:1233)
• Prasugrel 60 mg PO (NEJM 2007;357:2001; TRITON-TIMI, Lancet 2009;373:732);

should not be used in pts w/ a prior h/o stroke or TIA
• Ticagrelor 180 mg PO (PLATO, Circulation 2010;122:2131)
*(Consider deferring decision regarding timing of P2Y12 receptor inhibitor use to

cardiology, given potential need for CABG)
• It is reasonable to begin tx w/ an IV GPIIb/IIIa receptor antagonist in the precatheter

setting to pts w/ STEMI for whom primary PCI is intended (JAMA 2004;292:362;
RELAx-AMI, J Am Coll Cardiol 2007;49:1517)
• Abciximab: 0.25 mg/kg bolus, then 0.125 mcg/kg/min (max 10 mcg/min)
• Tirofiban (high-bolus dose): 25 mcg/kg IV bolus, then 0.15 mcg/kg/min; ↓ by 50%

in CKD
• Eptifibatide: (double bolus): 180 mcg/kg IV bolus, then 2 mcg/kg/min; a 2nd 180

mcg/kg bolus given 10 min after 1st bolus; ↓ by 50% in CKD, avoid in dialysis pts
• For pts undergoing primary PCI, the following anticoagulant regimens are

recommended:
• UFH w/ GP IIb/IIIa inhibitor: 50–70 U/kg bolus to achieve therapeutic ACT
• UFH w/o GP IIb/IIIa inhibitor: 70–100 U/kg bolus to achieve therapeutic ACT
• Bivalirudin: 0.75 mg/kg IV bolus, then 1.75 mg/kg/h infusion w/ or w/o UFH;

preferred over UFH w/ GP IIb/IIIa inhibitor in pts at high risk of bleeding

Nonprimary PCI

• Facilitated PCI: Lytic before PCI harmful (Lancet 2006;367:569; Lancet 2006;367:579), &
partial dose lytic no better than no lytic (FINESSE, NEJM 2008;358:2205); upstream
GPI also shows increased mortality

• Rescue PCI (after full dose lytics & persistent STEMI or cx): Beneficial if <50% ST
segment resolution by 90 min (NEJM 2005;353:2758)

• Routine angio ± PCI w/i 24 h of successful lysis: ↓ D/MI/Revasc (Lancet
2004;364:1045)

• Late PCI (median day 8) of occluded infarct-related artery: No benefit (NEJM
2006;355:2395)

Disposition

• Admit to cardiology → cath lab → CCU

Pearls

• Mortality 6% w/ reperfusion tx (PCI or lytic), ∼20% w/o
• Predictors of mortality: Age, time to therapy, anterior MI, LBBB, heart failure

(Circulation 2000;102:2031)
Guideline: O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the

management of STEMI: A report of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll
Cardiol. 2013;61(4):e78–e140.

UA/NSTEMI

Definition

• UA (subtotal coronary thrombosis, angina that is new onset, crescendo, OR at rest,
usually <30 min, ±ST depression &/or TWI); see above for CCS classification
• Rest angina: Angina occurring at rest & prolonged, usually >20 min
• New-onset angina: New-onset angina of at least CCS class III severity
• Increasing angina: Previously diagnosed angina that has become distinctly more
frequent longer in duration, or lower in threshold (ie, increase by 1 or more CCS
class)

• NSTEMI (same as UA but w/ +troponin)
• Consider calling cardiology for +Tn, ongoing CP

Routine Medical Therapies “MONAB”

• Morphine: Reasonable to use if there is uncontrolled ischemic CP despite NTG; typical
dose 0.05–0.1 mg/kg IV

• O2: Supplemental O2 should be administered to pts w/ UA/NSTEMI w/ an arterial

saturation less that 90%, respiratory distress, or other high risk features for hypoxia

• Nitrates: Pts w/ ongoing ischemia should receive NTG SL (0.4 mg) q5min for a total of
3 doses, after which assessment should be made about need for IV NTG if no CIs (CI w/
hypotension, RV infarct, concomitant PD inhibitor use w/i 24–48 h)

• Aspirin: 23% ↓ in death (ISIS-2, Lancet 1988;2:349); typical dose 162–325 mg PO
• Beta-blockers: Oral BB should be administered w/i 24 h of NSTEMI w/o CIs. Routine

IV should not be used. It is reasonable to administer IV BBs to UA/NSTEMI pts who do
not have 1 or more of the following: (1) signs of HF, (2) e/o low-output state, (3)
increased risk of cardiogenic shock, (4) other CIs to BB therapy (RAD, heart block,
etc.).
• Other: Often started as inpts include oral BBs, statins, ACE inhibitors/ARBs

Conservative vs. Early Invasive Strategy (JACC 2002;40:166)

• Conservative approach = selective angiography
• Medical tx w/ pre-d/c stress test
• Angio only if recurrent ischemia or strongly +ETT

• Early invasive approach = routine angiography w/i 24–48 h
• 25% ↓ MI, 34% ↓ rehospitalization for ACS & nonsignificant 8% ↓ death c/w cons
(JAMA 2005;353:1095), but results dominated by peri-PCI MI; post-d/c benefits of
INV c/w prior data
• No benefit to PCI w/i 24 h compared to PCI w/i 72 h (N Engl J Med 2009;360:2165)

• General tx approach
• If low-risk pt (–Tn, no ST ↓, & TRS 0–2)
• If ↓ EF, recent PCI, prior CABG then → INV strategy
• If not, then → CONS strategy (stress test once stabilized, before d/c)

• If high-risk pt (+Tn, ST ↓ >0.5 mm, or TRS ≥3) → INV strategy
• In those where an initial conservative strategy is selected, if recurrent sxs/ischemia,

HF, or serious arrhythmias appear, then diagnostic angiography should be performed

Antiplatelet Therapy

• ASA 162–325 mg PO (crushed/chewed) should be given as early as possible in pts w/
UA/NSTEMI (VA Cooperative Study, NEJM 1983;309:396; NEJM 1988;319(17):1105)

If ASA allergy: Clopidogrel (300–600 mg LD followed by daily maintenance dose) should
be administered

• Early invasive strategy
• Before PCI:
• Clopidogrel (NEJM 2001;345:494; PCI-CURE, Lancet 2001;358:527); or
• Ticagrelor (PLATO, NEJM 2009;391:1045); or
• An IV GP IIb/IIIa inhibitor, where eptifibatide & tirofiban are preferred
• At the time of PCI:
• Clopidogrel if not started before PCI; or
• Prasugrel (TRITON-TIMI, NEJM 2007;357:2001); or
• Ticagrelor (PLATO, NEJM 2009;391:1045); or
• An IV GP IIb/IIIa inhibitor, where eptifibatide & tirofiban are preferred

• Initial conservative strategy is selected, clopidogrel (300–600 mg LD) or ticagrelor
(180 mg LD) should be added to ASA & anticoagulation therapy as soon as possible
after admission

A loading dose of a P2Y12 receptor inhibitor is recommended for UA/NSTEMI pts for

whom PCI is planned. One of the following regimens is used:
a. Clopidogrel 600 mg PO (J Am Coll Cardiol 2006;48:1339; CURRENT-OASIS 7, Lancet

2010;376:1233)
b. Prasugrel 60 mg PO (TIMI, Lancet 2009;373:732); should not be used in pts w/ a

prior h/o stroke or TIA
c. Ticagrelor 180 mg PO (PLATO, Circulation 2010;122:2131)
• In those where an initial conservative strategy is selected, it may be reasonable to add
eptifibatide or tirofiban to anticoagulant & oral antiplatelet therapy
• Tirofiban: 0.4 mcg/kg IV bolus over 30 min, then 0.15 mcg/kg/min; ↓ by 50% in

CKD (PRISM-PLUS; NEJM 1998;338:1488)
• Eptifibatide: 180 mcg/kg IV bolus, then 2 mcg/kg/min; ↓ by 50% in CKD, avoid in

dialysis pts (PURSUIT, NEJM 1998;339(7):436)

Anticoagulant Therapy

• Anticoagulant therapy should be added to antiplatelet therapy in UA/NSTEMI pts as
soon as possible after presentation

• For pts undergoing invasive strategy, the following anticoagulant regimens are
recommended:

• UFH w/ GP IIb/IIIa inhibitor: 50–70 U/kg bolus to achieve therapeutic ACT
• UFH w/o GP IIb/IIIa inhibitor: 70–100 U/kg bolus to achieve therapeutic ACT
• Bivalrudin: 0.75 mg/kg IV bolus, then 1.75 mg/kg/h infusion w/ or w/o UFH;

preferred over UFH w/ GP IIb/IIIa inhibitor in pts at high risk of bleeding
• For pts in whom a conservative strategy is selected, regimens using either enoxaparin,

UFH, or fondaparinux are recommended:
• UFH weight-based infusion w/ IV bolus 60 U/kg (max 4000 U) followed by infusion

of 12 U/kg/h (max 1000 U) to maintain aPTT ∼50–75 s for 48 h or until
revascularization
• Enoxaparin: If <75 y/o, 30 mg IV bolus, then 15 min later, 1 mg/kg SC q12h; If
>75 y/o; no bolus, 0.75 mg/kg SC q12h; If CrCl <30 mL/min, 1 mg/kg q24h
• Fondaparinux: Initial 2.5 mg IV, then 2.5 mg SC the following day, CI in CrCl <30

Disposition

• Admission to CCU, step-down unit, or ward bed, depending on risk & whether
conservative or early invasive approach is chosen

• Consider admitting to a CP/observation unit if pt deemed low risk, –Tn, &
nondiagnostic ECG. Reconsider/admit pts w/ recurrent sxs, ECG changes, +Tn.

Guideline: Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the
management of patients with UA/NSTEMI: A report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll
Cardiol. 2007;50(7):e1–e157.

Guideline: Anderson JL, Adams CD, Antman EM, et al. 2012 ACCF/AHA focused update
incorporated into the ACCF/AHA 2007 guidelines for the management of patients with
UA/NSTEMI: A report of the American College of Cardiology Foundation/American
Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol.
2013;61(23):e179–e347.

PRINZMETAL’S (VARIANT) ANGINA

Definition

• Distinct syndrome of ischemic CP classically occurring at rest & associated transient
STE as a result of coronary artery spasm

• Although VA results from focal coronary spasm, the exact etiology is unknown

History

• Usually younger pts (35–50 y/o), smokers, F>M; often occurs in the AM, precipitated
by hyperventilation or cold, but not exertion

• No known cardiac hx & may have had a negative coronary angiogram
• Associations: EtOH use, family h/o migraine, Raynaud’s syndrome, pericarditis, &

primary MV prolapse

• Sxs include substernal pressure that radiates to jaw & arm, usually in morning hours
awakening from sleep; pain is typically responsive to NTG

Evaluation

• EKG reveals transient STE in a distribution of a sp coronary artery & reciprocal STΔs;
these episodes may induce a variety of conduction disturbances or arrhythmias

• Stress testing may induce no STΔs, STDs, or STEs; STEs may be seen during recovery
phase of stress testing

• Angiography → nonobstructive CAD; intracoronary acetylcholine injection (90% sens)
• Provocative testing w/ ergonovine or hyperventilation (not performed in ED)

Treatment

• High-dose CCB (nifedipine, verapamil, diltiazem), nitrates (SL prn); d/c smoking

Disposition

• Admit, given risk of MI & arrhythmia during acute episodes

COCAINE-INDUCED ANGINA

Definition

• Cocaine-induced angina is caused by multiple cardiovascular effects of cocaine,
including increased HR, BP, contractility, & end-systolic wall stress (from
sympathomimetic effects) which all lead to increased myocardial demands as well as
cocaine-induced coronary arterial vasoconstriction resulting in decreased O2 supply

• Acute thrombosis of coronary arteries after cocaine use can also occur & use has been
a/w premature coronary atherosclerosis

• Overall incidence of cocaine-associated MI is 0.7–6% of those presenting w/ CP after
ingestion (Acad Emerg Med 2000;36:469; COCHPA, Acad Emerg Med 1994;1:330)

History

• CP (pressure-like) that may be a/w dyspnea, anxiety, palpitations, diaphoresis,
dizziness, or nausea

• Sxs typically occur w/i 3 h of ingestion, but cocaine metabolites may persist up to 24
h to cause delayed or recurrent vasoconstriction

• RF for cocaine-induced MI: Male gender, current smoker, nonwhite

Evaluation

• Similar to ACS (see above)
• Urine toxicology: Usually detects the cocaine metabolite benzoylecgonine which has a

urine t1/2 of 6–8 h, & can be detected for up to 24–48 h after use (range 16–66 h)
• Chronic cocaine users may have cocaine detectable in urine for weeks after last

ingestion

Treatment

• Pts should be treated similarly to possible ACS (see “routine medical therapies” above)
• IV BZD
• Antihypertensives: IV NGT, sodium nitroprusside, or phentolamine; avoid BBs as an

unopposed α-adrenergic effect can lead to worsening coronary vasoconstriction & BP
• STEMI: Early PCI
• Drug-abuse counseling

Disposition

• EDOU if sxs controlled & cardiac markers negative
• Admit to cardiac unit if +cardiac markers or ongoing CP

Pearls

• Cx: Arrhythmia & heart failure (∼90% occur w/i 12 h of presentation)
• Ventricular tachyarrhythmias immediately after cocaine use result from the local

anesthetic (sodium channel) effect on the myocardium & may respond to sodium
bicarbonate therapy in addition to standard therapies (ie, lidocaine)
• Cocaine-associated CP may be caused not only by myocardial ischemia but also by
aortic dissection, thus maintain high index of suspicion
Guideline: McCord J, Jneid H, Hollander JE. Management of cocaine-associated chest
pain and myocardial infarction: A scientific statement from the American Heart
Association Acute Cardiac Care Committee of the Council on Cardiology. Circulation.
2008;117:1897–1907.

STRESS TESTING

Approach

• Noninvasive eval for CAD is done in the ED for pts after “r/o MI”
• It should not be done on pts w/ high-risk ACS, ongoing CP

Indications

• Dx CAD, assess Δ clinical status in pt w/ known CAD, localize ischemia

Contraindications

• Absolute: Severe acute illness – AMI w/i 48 h, high-risk UA, PE/aortic
dissection/pericarditis, CHF, arrhythmias – or underlying, severe AS

• Relative: Inability to exercise, high-degree AVB, severe HTN, LM CAD, mod valvular
stenosis, HCMP, severe electrolyte abnl

Findings

• HR: A “diagnostic” exercise test requires minimum 85% of max predicted HR (220 –
age)

• METS (max exercise capacity), also displayed in minutes
• ECG changes: Downsloping or flat ST ↓ predicts CAD, but does not localize dz; ST ↑ an

even better predictor
• Duke Treadmill Score (NEJM 1991;325:848) = Duration of exercise in minutes – (5

× max ST dev, in mm) – (4 × angina index*)
*Angina index: 0 none, 1 nonlimiting, 2 limiting:

Score >+5 → predicted 4-yr survival 98%; average annual mortality 0.25%
Score –10 to 4 → predicted 4-yr survival 94%; average annual mortality 2–3%
Score <–10 → predicted 4-yr survival 81%; average annual mortality 5%
• Imaging: Either radionucleotide defect or echo wall motion abnlty; reversible defect →
ischemia; fixed defect → infarct
• Myocardial viability: To find cardiac muscle that can be “saved” by intervention. Can
be done w/ multiple modalities: MRI (sens >95%, spec ∼70%), PET (sens ∼90%,
spec ∼75%), dobutamine stress echo (sens ∼70%, spec ∼85%), rest redistribution
thallium (sens ∼90%, spec ∼55%).

• CT/MR coronary angiography
• Coronary calcium score: Evaluate for CAD & estimate plaque burden based on
quantifying coronary artery calcification
• Can assess significant stenosis w/ sens/spec >85% w/ 64-slice CT, but limited by a
large portion of nonevaluable artery segments (as much as 30%); requires relative
bradycardia (often βB); b/c high NPV → useful for r/o (1) obstructive CAD in pts w/
anginal sxs, (2) CAD in pts w/ intermed & low pretest probability w/ nl serial
ECGs/biomarkers (NEJM 2001;345:1863; JAMA 2006;296:403; JACC 2006;48:1475;
Circulation 2006;114:1761).

Disposition

• For adequate study (HR, METS achieved) & no e/o ECG changes, sxs, or imaging
abnormalities, pt may be discharged home w/ PCP/cards f/u. If low pretest
probability, & nondiagnostic test, pt may be discharged home w/ close f/u & 2nd
testing modality done as outpt.

• For adequate study w/ high-risk test results, consider coronary angiography, ±
admission depending on clinical presentation

Pearl

• Remember that +stress test indicating CAD in a pt who presented to ED w/ CP does
not necessarily mean that CP was caused by CAD. Conversely, most of these tests are
poorly sens/spec, so a negative result should not be particularly reassuring, esp in
high-risk &/or high-PreTP pts.

CARDIAC CATHETERIZATION

Indications

• ACS, high-risk stress test result or indeterminate result & high-risk or high PreTP for
CAD, s/p cardiac arrest (SCD, VT), suspected nonatherosclerotic cause of ischemia (ie,
spasm), systolic dysfxn of unclear etiology, or persistent angina despite tx or w/
systolic dysfxn

Types

• Balloon angioplasty: Effective but has unique cx: Coronary artery dissection &
restenosis from vessel remodeling

• BMS: ↓ restenosis & repeat revasc (to ∼10% @ 12 mo) c/w balloon angioplasty but

requires lifelong ASA & clopidogrel for at least 4 wk
• DES (NEJM 2006;354:483): ↓ restenosis (by ∼75%) & repeat revasc (by ∼50%); to

<5% (by 12 mo); no Δ D/MI over 1 yr c/w BMS; requires lifelong ASA & clopidogrel
for at least 1 yr (Circulation 2007;115:813)

POST-PCI COMPLICATIONS

Approach

• Ask about h/o back pain, noncompliance/recent d/c of antiplt Rx, √ access site
(groin), distal pulses, ECG, CBC, Cr, CK-MB

Treatment

• Bleeding (femoral access site, retroperitoneal)
If hematoma/active bleeding @ groin, apply pressure, reverse/stop anticoag
If retroperitoneal bleed, may c/o back pain, ± Hct drop, ↓ BP, ↑ HR; obtain
abd/pelvic CT (I–), reverse/stop anticoag, consult IR/surgery

• Vascular damage
Pseudoaneurysm: Pain, expanding mass, systolic bruit; obtain US; tx w/ manual
compression, ± thrombin injection/surgery

• AV fistula
Continuous bruit; obtain US; tx w/ surgery ↓ perfusion to LE (from embolization,
dissection, thrombus): ↓ distal pulses; obtain angiogram; consult card &/or surgery
for repair (either percutaneous or operative)

• Renal failure
2° contrast, usually w/i 24 h, peaks 3–5 d

• Stent thrombosis
P/w acute CP & STE. Consult cards/cath lab, for urgent catheterization. Common
causes include underexpanded stent, dissection, or d/c antiplt Rx (JAMA
2005;293:2126).
Late stent stenosis DES > BMS (JACC 2006;48:2584)

• Stent stenosis
P/w more chronic return of prior anginal sx, months after PCI (10% p/w ACS). Occurs
2° postprocedure remodeling, not atherosclerosis. Frequency: Balloon angioplasty
>BMS > DES.

POST-MI COMPLICATIONS

LV Failure

• Presentation ranges from pulmonary edema to frank cardiogenic shock
• Tx

Diuresis for pulmonary edema w/o e/o shock

↓ afterload: IV NTG or nitroprusside
Inotrope: If the above Rx’s fail, give dopamine or dobutamine
Other: For cardiogenic shock, consult cardiology. Avoid diuretics, start w/ inotropes, ↓

afterload. May need IABP. Will need revascularization ASAP (NEJM 1999;341:625).

IMI Complications (Circulation 1990;81:401; Annals 1995;123:509)

• Heart block
2° RCA involvement (supplies AV node), can develop high-degree AV
Block abruptly. Rx: Atropine/place TC pacer pads on pt & prepare for TV pacing, if
necessary.

• Precordial ST ↓
DDx includes (1) anterior ischemia, (2) posterior STEMI, (3) reciprocal Δs. Obtain
posterior leads to r/o posterior STEMI.

• RV infarct
P/w signs of right-sided failure: Hypotension, JVD 2° prox RCA occlusion
Obtain right-sided leads → 1 mm STE in V4R. Avoid nitrates, as these pts are preload
dependent. Give dobutamine for persistently low BP (↑ contractility), consult
cardiology, urgent reperfusion (NEJM 1998;338:933).

Mechanical Complications

• Typically several days post-MI
• Free wall rupture

Tear occurs in the myocardial wall @ junction b/w nl/infarcted muscle, most
commonly in elderly person w/ large MI. P/w PEA, ↓ BP, cardiac tamponade. Tx w/
IV fluids (preload dep.), bedside echo (? peric effusion). Consult surgery/cardiology.
If +effusion & unstable → bedside pericardiocentesis. If stable → operative repair.

• Papillary muscle rupture
Occurs in small MI, IMI > AMI, p/w new murmur. Rx:
Diuretics, vasodilators, IABP, surgery consult for operative repair

• Arrhythmias
AF most common. VT/VF → r/o MI, √ lytes. Monomorphic VT w/i 48 h MI → benign.
AIVR: Slow VT (HR <100), often s/p reperfusion, self-limited/benign. New 2°/3°
AVB → TC pacing ± TV pacing, esp if a/w BBB. TV for new 3° AVB, new BBB + 2°
AVB type II, alternating LBBB/RBBB. Consult cardiology.

• Other
LV thrombus: Anticoagulate
Ventricular aneurysm: Suspect if persistent STE post-MI. Obtain echo for Dx. Consult
surgery, admit.
Pericarditis: Pericardial rub 1–4 d post-MI. ASA, NSAIDs, minimize anticoagulation.
Dressler syndrome: Inflammatory syndrome 2–10 wk post-MI. Fever, pericarditis,
pleuritis. ASA, NSAIDs.

PULMONARY EMBOLISM AND DVT

Definition

• PE: Thrombosis from a vein that embolizes to the pulmonary arterial system
• DVT: Thrombosis of lower extremity (popliteal, femoral [incl SFV], iliac) or upper

extremity (basilic, cephalic) veins

Approach

• (1) Assess PreTP, (2) perform basic test (labs, CXR, ECG), (3) D-dimer, (4) imaging
studies, to obtain (5) post-TP

• If HD stable perform Dx tests; if unstable, consider empiric tx ± thrombolytics if
potential benefit outweighs risk of bleeding (Chest 2004;126(suppl):401S)

History (Chest 1991;100:598; Am J Card 1991;68:1723)

• RFs: Prior DVT/PE, hypercoagulable state, pregnancy/OCPs, malignancy, prolonged
immobilization, recent surgery, FHx DVT/PE

• PE: Dyspnea (73%), pleuritic CP (66%), cough (37%), syncope, ↓ BP, PEA
• Assess PreTP: May use PERC (to decide whether any testing is necessary) or Wells

criteria (to decide whether D-dimer is sufficient w/u)
• PERC: If (1) low likely by gestalt + (2) “Yes” to all PERC criteria → 1.8% PE miss

rate

Findings

• PE: Unexplained ↑ HR, ↑ RR, ↓ SpO2, fever, JVD

• DVT: Leg edema/pain. Clinical signs DVT ∼50% pts.

Evaluation (PE)

• Obtain ECG (sinus tachycardia, S1Q3T3 not sens/spec, simultaneous TWI in inferior &
anterolateral leads), Hct, PT/PTT, Cr

• CXR: R/o other causes; “classic” PE CXR findings (Hampton’s hump & Westermark’s
sign) not sens/spec

• D-dimer (sens 95–98%, spec 40–55%, ELISA or Rapid Quant. ELISA; Ann Intern Med
2004;140:589, NPV >99% for low pre-TP; JAMA 2006;295:172). Sens/spec vary by
assay/cutoff.
• False+: Pregnancy, trauma, infection, malignancy, inflammatory conditions,
surgery, ↑ age, SCD, AF, ACS, CVA, acute UGIB, DIC

• In pts w/ a low PreTP for PE, a negative quantitative D-dimer assay result can be
used to exclude PE

• In pts w/ an intermediate PreTP for PE, a negative quantitative D-dimer assay result
may be used to exclude PE

• If D-dimer + → more testing (see below)

• For pts w/ low or PE unlikely PreTP of PE who require additional diagnostic testing
(ie, +D-dimer or D-dimer not available), a negative, multidetector CT pulmonary
angiogram alone can be used to excluse PE

• For pts w/ an intermediate or high probability for PE & a negative CTPA result in
whom clinical concern for PE still exists & CT venogram has not already been
performed, consider additional testing (ie, D-dimer, lower extremity imaging, VQ
scanning, traditional pulmonary arteriography) to exclude VTE dz

• Risk stratify: ↑ HR, ↓ BP, ↓ SpO2, CTA RV/LV dimension >0.9, ↑ Tn or BNP, echo e/o
RV dysfxn, D-dimer >4000 all predict bad outcomes

Evaluation (DVT)

• Assign clinical probability using Wells score

• D-dimer: Assays include ELISA & immunoturbidimetric methods (high sens) as well as
whole-blood & quantitative latex agglutination assays (mod sens). There is a wide
variation in the sens, nl reference ranges, & cut-off points among different assays.

• Compression US of proximal veins
• Whole-leg duplex ultrasound (“LENI”)
• CT venography
• See below for diagnostic algorithms in eval of DVT (Chest 2012;141(2)(suppl):e351S)

Figure 1.2 Low pretest probability of DVT.

Figure 1.3 Moderate pretest probability of DVT. A: Starting with D-dimer assessment. B:
Starting with ultrasonography.

Figure 1.4 High pretest probability of DVT.

Treatment

• O2, monitor BP/rhythm, IV fluids for ↓ BP (preload dep)
• Anticoagulation (PE or DVT): Heparin (80 U/kg, 18 U/kg/h IV), enoxaparin (1 mg/kg

SC). ?LMWH superior to heparin for DVT; LMWH may be superior to heparin for ↓
D/major bleeding in PE (Chest 2004;126(suppl):401S; Ann Intern Med 2007;146:369),
relative CI LMWH → renal insufficient, obesity (? unpredictable absorption)
• Thrombolytic: tPA (100 mg over 2 h), for extensive DVT/PE or high clinical suspicion
& HD instability. No mortality benefit w/ RV dysfxn (on echo) alone (NEJM
2002;347:1143), so use is controversial.
• Administer thrombolytic therapy in HD unstable pts w/ confirmed PE for whom the

benefits of tx outweigh the risks of life-threatening bleeding cx
• In centers w/ capability of surgical or mechanical thrombectomy, procedural

intervention may be used as an alternative therapy
• Catheter or surgical thrombectomy (PE): For pts w/ HD instability & massive PE if (1)

CI to lysis, (2) failed lysis w/ tPA, or (3) experienced center & +RV dysfxn. Consult
cardiac surgery.
• IVC filter: When medical tx fails or is contraindicated. No long-term mortality benefit
(NEJM 1998;338:409).

Disposition

• If PE negative → look for other causes

• If +DVT & no suspicion for PE → d/c home after period of observation w/ Lovenox &
Lovenox teaching vs. admission

• Most pts w/ PE can be admitted to tele bed. If e/o HD instability or if thrombolytics
given, then admit to ICU.

Pearls

• Atypical presentation is very common
• Consider massive PE (& potentially thrombolytics) in unexplained PEA arrest
• If you suspect ↓ CrCl in pt who may get CTA, begin renal pretreatment
• Check your hospital’s D-dimer assay → there are many & each has different sens/spec
Guideline: Fesmire FM, Brown MD, Espinosa JA. Critical issues in the evaluation and

management of adult patients presenting to the emergency department with suspected
pulmonary embolism. Ann Emerg Med. 2011;57(6):628–652.

CHF/ACUTE PULMONARY EDEMA

Definition

• CHF: State where heart’s ability to pump is insufficient to meet metabolic needs; can
be L-sided or R-sided & systolic or diastolic (ie, failure w/ nl EF)

• Acute pulmonary edema: Fluid in pulmonary interstitium & alveoli 2° L-sided failure/↑
pressure

Approach

• Determine & tx underlying cause
• Intubate immediately for respiratory failure, but consider CPAP/BiPAP if possible

History

• SOB, DOE, CP, cough, orthopnea, PND; if severe, may have severe respiratory distress
w/ pink/white sputum, altered mental status (AMS)

Findings

• ↑ BP, ↑ HR, ↑ RR, cardiac dysrhythmia
• +S3 (systolic failure) +S4 (diastolic failure)
• L-sided: +rales; R-sided: Leg edema, JVD, ↑ liver size, +hepatojugular reflex

Evaluation

• Primary Dx is clinical
• POC thoracic/cardiac ultrasound: B-lines (“lung rockets”), decreased EF
• ECG: LVH, tachyarrhythmia, L-heart strain, ischemia, e/o old infarction(s)
• CXR (perform @ bedside if unstable): Pulmonary edema, pl effusion, ↑ heart size
• Labs: CBC, lytes, Cr, cardiac markers, BNP or NT-proBNP
• BNP: If dyspnea & BNP >100 → CHF (sens 90%, spec 76%, NEJM 2002;347:161)

• False +: Large PE, cor pulmonale, ESRD; in chronic CHF must compare to “dry
weight BNP”

• NT-proBNP: If dyspnea & NT-proBNP >300 → CHF (sens 99%, spec 60%); ↑ cutoff w/
↑ age; same false+ as BNP

Treatment “LMNOP”

• L: Lasix (2× pts home oral dose given IV, or 80 IV)
• Furosemide PO to IV conversion 2:1 (ie, 40 mg PO equiv to 20 mg IV)
• Furosemide 40 mg = torsemide 10 mg = bumetanide 1 mg
• No difference in IV to PO conversions for torsemide or bumetanide
• If allergy to furosemide/torsemide/bumetanide, can use ethacrynic acid

• M: Morphine: Venodilator, ↓ dyspnea, ↓ afterload – caution w/ dosing in elderly
*Caution: May be a/w greater frequency of mechanical ventilation, prolonged
hospitalization, ICU admission & mortality (Emerg Med J 2008;25(4)205)

• N: Nitrates (0.4 mg SL or 10–100 mcg/min IV): Caution in pts w/ AS → ↓ BP 2°
preload dep; Nitroprusside if NTG ineffective; nesiritide may ↑ Cr/mortality compared
to noninotropic tx (JAMA 2005;293:1900)

• O: O2: 100% NRB

• P: PPV: CPAP or BiPAP for ↓ SaO2 or NRB; ↓ mort/need for intubation (JAMA

2005;294:3124; Lancet 2006;367:1155), ? ↑ effect CPAP c/w BiPAP. Intubate for
unconsciousness, severe respiratory distress or visibly tiring after LMNOP tx.
• Inotropes: Only for cardiogenic shock. Routine use is a/w increased mortality.
Dopamine, dobutamine, milrinone.
• Other: Sit pt up, Foley (assess ins/outs), IABP/LVAD (for severe cardiogenic shock)

Disposition

• D/C: If mild exacerbation of chronic CHF, benign etiology (ie, dietary indiscretion), &
pt has close f/u

• EDOU: Selected HF pts can be managed by a rapid tx protocol in the OU w/ fewer bed
days & similar readmission rates to admitted pts (Acad Emerg Med 2013;20(6)554)

• Tele: Most pts require admission/Δs to tx regimen before d/c home
• ICU: All intubated pts & those who w/ significant respiratory distress

Pearls

• Ask about or measure increase above dry body weight as in indication of volume
overload

• Look for underlying cause; ask about dietary indiscretion, change in meds

AORTIC DISSECTION

Definition

• Intimal tear → blood enters & traverses the aortic media
• Classification important b/c this impacts management & prognosis

• Can also have intramural hematoma, penetrating ulcer, pseudoaneurysms of thoracic
aorta, & traumatic rupture of thoracic aorta

Approach

• Obtain imaging & consult cardiothoracic surgery early, esp for type A dissection if
clinically suspected

History

• Abrupt onset CP (ascending), interscapular back pain (descending), neck pain;
maximal @ onset, severe, ripping/tearing (∼1/2 pts); syncope, neurologic deficits

Findings

• ↑ BP, though ↓ BP/↑ HR are ominous. Pt is very uncomfortable, other findings depend
on location.

Evaluation (Circulation 2005;112:3802)

• Labs: Type/crossmatch, Hct, Cr (↑ suggests renal artery involvement), PT/PTT;
consider cardiac markers & D-dimer to r/o other life-threatening causes of CP

• ECG: LVH, MI (RCA → IMI); ∼4–8% of thoracic dissections will present w/ signs of
STEMI

• POC cardiac US: Parasternal long-axis & suprasternal notch views may reveal
dissection flap or pericardial effusion

• CXR: nl (20%), wide mediastinum, abnl aortic knob, L apical cap, trachea shift → R,
depressed L bronchus, L pl effusion

• Advanced imaging modalities include TEE, CTA, MRI, angiography

• Angiography: “Gold standard” though rarely used

Treatment (Circulation 2010;121:e266)

• Surgical tx for Stanford A & medical tx for Stanford B
• At least 2 large-bore IVs
• Close BP monitoring/A line
• Initial management of TAD should be directed at decreasing aortic wall stress by

controlling HR & BP:
• In the absence of CIs, IV βB should be initiated to target HR<60
• If IV βB CI, nondihydropyridine CCB (diltiazem, verapamil) should be used
• If SBP >120 mmHg after HR goal achieved, then ACE &/or other vasodilator should

be used to target SBP <120 mmHg
• Standard agents:

βB
• Labetolol: 20 mg q5–10min to max 300 mg, or 1–2 mg/min gtt

• Esmolol: Bolus 0.25–0.5 mg/kg over 1–2 min, then 10–200 mcg/kg/min gtt
Vasodilators

• Nitroprusside: 0.5–3 mcg/kg/min
• Morphine or fentanyl gtt: For pain
• Urgent surgical consultation should be obtained (cardiac surgery for Type A, vascular

surgery for Type B) for all pts diagnosed w/ thoracic aortic dissection regardless of the
location as soon as the Dx is made or suspected
• Acute TADs of ascending aorta should be urgently evaluated for emergent surgical
repair
• Acute TADs of descending aorta should be managed medically unless life-threatening
comp develop (ie, malperfusion, enlarging aneurysm, inability to control BP or sx)
• Consult vascular or thoracic surgery for open repair vs. stent

Disposition

• ICU

Pearls

• Pts may present atypically, sometimes w/ minimal pain, or only neurodeficit or MI
• Pts may appear very well, then suddenly decompensate
• Neurodeficit = presenting complaint in 20% cases & is present in 40%
• Pain patterns frequently change as the dissection migrates
Guideline: Hiratzka LF, Bakris GL, Beckan JA, et al. 2010

ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the diagnosis and
management of patients with thoracic aortic disease. Circulation. 2010;121:e266–e369.

THORACIC AORTIC ANEURYSM

Definition

• Arterial outpouching involving all 3 layers; an aneurysm denotes dilation of a vessel
to 1.5 times its nl diameter. For the thoracic aorta, this value is ∼4.5 cm. Those b/w
1.1 & 1.5 times its nl diameter are considered dilated or ectatic.

• Pseudoaneurysm: Same but <3 layers
• Can occur at the root (annular aortic ectasia) &/or ascending aorta (50%), descending

aorta (40%), aortic arch (10%), or thoracoabdominal aorta (10%). ∼25% of pt may
also have an AAA.
• Most TAAs are caused by degenerative dz resulting in dilation of the aorta
• RFs: Similar to aortic dissection (see above)

• Average rate of expansion 0.10–0.42 cm/yr; TAA >6 cm has high rate of cx

Approach

• Often found incidentally on CT scan or echo; typically asymptomatic though they may
have chest/back pain

• If HD unstable, assume rupture, call surgery

History

• For hx & RFs, see aortic dissection above
• May cause compressive sxs: Hoarseness (compression of recurrent laryngeal nerve),

stridor (compression of trachea/bronchi), dyspnea (lung compression), dysphagia
(esophageal compression), plethora/edema (SVC compression)
• Heart failure sxs may occur 2/2 aortic regurgitation from aortic root dilation
• Embolization of atherosclerotic debris w/ end-organ sxs may occur
• May lead to dissection (see sxs above) or rupture

Evaluation

• CTA: Good sens, quick, noninvasive
• MRI: Best for imaging aortic root
• TTE: Limited eval of root
• TEE: Better than TTE for evaluating the root

Treatment

• BP control: BB, ACEI, avoid intense exercise or Valsalva (ie, weight lifting)
• Lipid profile optimization
• Smoking cessation
• Open vs. endovascular repair (see indications for urgent cardiac surgery consultation

below)

Disposition

• All pts w/ incidental Dx of TAA could be discharged, but should have prompt f/u w/
PCP or cardiologist for BP & lipid optimization as well as serial monitoring