Benjamin S Abella, MD MPhilDepartment of Emergency MedicineUniversity of PennsylvaniaBenjamin.abella@uphs.upenn.edu

CC: Chest pain

vs.

1. ABC’s/Stabilization/Resuscitation IV, O2, monitor, pulse oximeter

2. ECG3. +/- CXR

CC: Chest pain

64 year old man presents with 5 hours of SS chest pressure associated with SOB, nausea and diaphoresis. Gradual onset while shoveling the snow. Improved with rest.

PMH: HTN, DM

Gen: Nontoxic appearing, apprehensive, mildly diaphoretic

Vitals: 37.5ºC, RR16, HR 100, BP 160/95

CVS: RRR, Normal S1, S2, no M/R/GResp: CTAB, easy respirationsAbd: Soft, NTNDExt: No calf tenderness or swelling,

no edema, strong distal pulses

MedPixTM

Epidemiology >6,000,000 Americans have CAD 500,000 deaths/yr. in the U.S. from CAD 250,000 pts. with prehospital cardiac arrest▪ 6% survive to hospital discharge

>4,000,000 E.D. visits per year for acute chest pain

$100 billion per year Etiology

Ischemia: imbalance between oxygen demand and oxygen supply

Fixed atherosclerotic lesion vs. plaque disruption with platelet/thrombi aggregation vs. spasm

Stable angina: transient, episodic chest discomfort that is predictable and reproducible.

Unstable angina: angina that is new in onset, occurs at rest or is similar but somewhat “different” than previous episodes.

Acute myocardial infarction

Substernal chest discomfort > 15 minutes associated with dyspnea, diaphoresis, light-headedness, palpitations, nausea and/or vomiting NSTEMI STEMI

12.5% of acute MI’s are clinically “silent”

Smoking Hypertension Diabetes mellitis Hypercholesterolemia Family history of CAD prior to age 55 in

a first-degree relative Previous history of CAD or peripheral

vascular disease Cardiac risk factors are very poor

predictors of risk for ACS in the E.D

Not helpful in distinguishing patients with ACS from those with noncardiac chest pain unless an alternative diagnosis is clear e.g. pneumothorax

Normal cardiopulmonary exam is most common

S3 in 15-20% with AMI Chest wall tenderness to palpation in

~15% with ACS

The standard ECG is the single best test to identify patients with an AMI upon E.D. presentation

But sensitivity is still far from ideal ST elevation in 50% of AMI’s 1-5% of AMI’s have a normal initial ECG 4 - 23% of pts. with unstable angina

have a normal ECG

CK-MB Sensitivity > 90% for MI 5-6h after symptom onset 50% sensitive shortly after presentation

Troponin Tn-I: similar sensitivity and specificity to CK-MB for

AMI in E.D. patients Tn-T: less sensitive for myocardial injury▪ Independent marker of cardiovascular risk

Marker Elevation Peak Duration

CK-MB 3-12 h 18-24 h 2 days

Troponin-I 3-12 h 18 h 5-10 d

Troponin-T 3-12 h 12 h 5-14 d

Aspirin Inhibits thromboxane A2 … decreases

platelet aggregation Nitrates

Decreases preload and afterload; increases coronary perfusion in obstructed vessels

Beta blockers Decreases infarct size, cardiovascular

complications, and mortality Consider heparin (or enoxaparin),

antiplatelet agents, GIIb/IIIa inhibitors Fibrinolysis or PCI

ST elevation > 0.1 mV in two or more continguous leads or new LBBB

Time to therapy < 12 hours (Class I), 12-24 hours (Class IIb)

Door to balloon time

Epidemiology: 6% of pts. with cocaine-associated

chest pain have an AMI 20-60% have transient myocardial

ischemia Often atypical chest pain Can be delayed for hours to days after

the most recent use

Spasm Increased myocardial oxygen

demandClot formationAccelerated atherosclerosis and

LVH

Diagnosis: ECG less sensitive and specific for MI CK-MB less sensitive Troponin I may be more useful

Prognosis: Favorable short-term prognosis 1 year mortality primarily due to

comorbidities and/or continued cocaine use Treatment:

Benzodiazepines Avoid Beta blockers

>4 million E.D. visits per year for acute chest pain

<15% with ACS 2-6% sent home from ED ultimately with

ACS Chest pain units/Obs

CC: Stroke

51 year old woman brought in by EMS with acute onset of right sided weakness and aphasia.

PMH: HTN

Gen: Somnolent, diaphoretic Vitals: 37.5ºC, RR16, HR 110, BP 180/110 CVS: Tachy, Normal S1, S2, no M/R/G Resp: CTAB, easy respirations Abd: Soft, NTND Ext: No calf tenderness or swelling, no

edema, weak distal pulses Neuro: Right leg/arm 4/5 strength,

+expressive aphasia

Definition: Intimal tear with entry of blood into the media “dissects” between the intima and adventitia

#1 site: ascending aorta at the ligamentum arteriosum

Stanford Classification: A: involves Ascending aorta (w/ or w/o

descending)▪ 80% of dissections

B: descending aorta only DeBakey Classification

Increased risk: Group A: >50 yoa with hypertension Group B: younger pts. with Marfan’s, Ehler-

Danlos, pregnancy Mortality

Type A:▪ Untreated: 75%▪ Surgically treated: 15-20%

Type B:▪ 32-36% with or without surgery

History: >90% with abrupt and severe pain

in the chest or between the scapulae▪ “tearing” or “ripping”▪ Can be dull or pressure-like▪ Anterior chest ~ ascending aorta; Back ~

descending Nausea, vomiting, diaphoresis

common

Associated symptoms based on progression of dissection:▪ Carotid arteries: stroke▪ Spinal arteries: paraplegia▪ Abdominal aorta/renal arteries/iliacs:

Abdominal/flank pain▪ Coronary arteries: aortic insufficiency; pericardial

effusion/tamponade▪ Laryngeal nerve compression: hoarseness▪ Tracheal compression: dyspnea/stridor/wheezing ▪ Esophageal compression: dysphagia

Physical Exam: Symptoms/signs as above Most commonly: normal heart and lungs▪ Aortic insufficiency murmur in 16-20%

Unequal, decreased, or absent peripheral pulses only found in 50%

CXR 85% with some abnormality▪ widened mediastinum most common▪ left pleural effusion; indistinct aortic knob;

displaced, calcified intima > 6mm from outer aortic wall

CT vs. TEE vs. aortogram

Considering it? 2 large bore IV’s, monitor, T&C, ECG

Blood pressure: Decrease the shear force on the intima

to minimize progression▪ Lower arterial blood pressure▪ Decrease LV contractility

Goal: SBP 100-110 mm Hg; HR 60-80

Options:A. Nitroprusside + esmololB. Labetalol

Early CT surgery involvement

CC: Chest pain

40 year old woman brought in by EMS with acute onset pleuritic right sided chest sharpness associated with SOB.

PMH: HTN

Gen: Well appearing, mildly uncomfortable

Vitals: 38ºC, RR 22, HR 120, BP 150/85 CVS: RRR, Normal S1, S2, no M/R/G Resp: CTAB, easy respirations Abd: Soft, NTND Ext: No calf tenderness but mild left-

sided swelling, no edema, strong distal pulses

MedPixTM

650,000 cases/year in the U.S. Mortality

2-10% if diagnosed and treated 30% if undiagnosed #3 cause of death overall #1 cause of nonsurgical maternal death in the

peripartum period The source is lower extremity DVT in 80-

90% of cases Upper extremity DVT in 10-15% Others: pelvic vein thrombosis; fat emboli; septic

emboli; right heart thrombosis

Virchow’s triad:1. Venous stasis

▪ Prolonged travel; bed rest; etc.2. Hypercoagulability

▪ Pregnancy; malignancy; estrogen therapy; deficiencies of protein C, protein S, AT III

3. Endothelial damage▪ Recent surgery, trauma

#1 risk factor = prior DVT/PE 10-15% of patients will have no

identifiable risk factor at the time of presentation

“Classic Triad”: Dyspnea, hemoptysis, pleuritic CP in

only 20% of pts.Three notable findings:

Pleuritic chest pain in 74% Dyspnea in 84% Respiratory rate > 16 in 92%

Heart rate > 100 in only 44%

Kline, 2003

Often normal> 40% with nonspecific ST and T

wave abnormalitiesSinus tachycardia is the most

common rhythm disturbance.S1Q3T3 is seen in only 6% of

patients with PE.

Normal in ~30% and a concerning finding in the setting of

dyspnea and hypoxemia w/o RAD Atelectasis in ~50% Elevated hemidiaphragm in 40% Hampton’s Hump: Pleural based wedge

shaped infiltrate Westermark sign: Proximally dilated

pulmonary artery with abrupt cut-off Needed for subsequent interpretation of

the V/Q scan

Clinical Likelihood Probability, %

Scan Category

High Indeterm Low All

High 96 88 56 87

Intermediate 66 28 16 30

Low 40 16 4 14

Normal 0 6 2 4

Total 68 30 9 28

Normal Ventilation

Abnormal Perfusion

LE Doppler USPulmonary angiographySpiral CTMRI

Garg, 1999

Considering it: IV, O2 prn, monitor, pulse ox.

High pretest probability: Anticoagulate 1st, then order your study Heparin 80 U/kg i.v. bolus; 18 U/kg/hr i.v.

drip Low (+/- intermediate) pretest

probability: Study 1st, then anticoagulate if appropriate

Consider thrombolytics if unstable

CC: “can’t catch my breath”

40 year old man presents with acute onset of SOB and pleuritic right sided chest sharpness.

PMH: none

Gen: Mildly uncomfortableVitals: 37ºC, RR 22, HR 120, BP

145/95CVS: Tacky, Normal S1, S2, no M/R/GResp: Decreased bs on the right,

tachypeicAbd: Soft, NTNDExt: No calf tenderness or swelling,

no edema, strong distal pulses

Especially tall, thin male smokersOnly 10 – 20% occur with exertionMost thought to result from

rupture of a subpleural blebSymptoms vary with size and rate

of progression of pneumothorax

Acute pleuritic CP in 95%Dyspnea in 80%Decreased breath sounds over the

affected lung in 85%Tachypnea > 24 in only 5%Hyperresonance in <1/3

Tension pneumothorax: Clinical presentation of pneumothorax

with hemodynamic compromise Treatment is immediate needle

decompression“Non-tension” spontaneous

pneumothorax Upright PA CXR is 83% sensitive

Tube thoracostomy Minicatheter or standard chest tube

Catheter aspiration Single or sequential

Observation x 6 hrs. with repeat CXR:o Stable; minimal/no symptoms; <25% ptxo No significant comorbidities

Remember the “Big Five” life threatening causes of chest pain Acute coronary syndrome Aortic dissection Pulmonary embolism Tension pneumothorax Esophageal rupture

ABCs; IV, O2, monitor, pOxThe diagnosis of ACS/PE/dissection

may be subtle.