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Benjamin S Abella, MD MPhil

Department of Emergency Medicine


University of Pennsylvania
Benjamin.abella@uphs.upenn.edu
 CC: Chest pain
vs.
1. ABC’s/Stabilization/Resuscitation
 IV, O2, monitor, pulse oximeter
2. ECG
3. +/- 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/G
 Resp: CTAB, easy respirations
 Abd: Soft, NTND
 Ext: 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 demand
 Clot formation
 Accelerated 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 + esmolol
B. 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
abnormalities
 Sinus 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 High Indeterm Low All
Category
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 US
 Pulmonary angiography
 Spiral CT
 MRI

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 uncomfortable
 Vitals: 37ºC, RR 22, HR 120, BP 145/95
 CVS: Tacky, Normal S1, S2, no M/R/G
 Resp: Decreased bs on the right, tachypeic
 Abd: Soft, NTND
 Ext: No calf tenderness or swelling, no
edema, strong distal pulses
 Especially tall, thin male smokers
 Only 10 – 20% occur with exertion
 Most thought to result from rupture of a
subpleural bleb
 Symptoms 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% ptx
o 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, pOx
 The diagnosis of ACS/PE/dissection may
be subtle.