Benjamin S Abella, MD MPhil Department of Emergency Medicine University of Pennsylvania [email protected]

 CC: Chest pain

vs.

1. ABC’s/Stabilization/Resuscitation  2. ECG IV, O2, monitor, pulse oximeter 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

MedPix TM

 

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 S 3 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

CK-MB Troponin-I Troponin-T

Elevation

3-12 h 3-12 h 3-12 h

Peak

18-24 h 18 h 12 h

Duration

2 days 5-10 d 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 B: younger pts. with Marfan’s, Ehler-Danlos, pregnancy Mortality  Group A: >50 yoa with hypertension 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

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   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

Scan Category High Intermediate Clinical Likelihood Probability, % High Indeterm

96 66 88 28

Low

56 16

All

87 30

Low Normal Total

40 0 68 16 6 30 4 2 9 14 4 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 1 st , then order your study  Heparin 80 U/kg i.v. bolus; 18 U/kg/hr i.v. drip Low (+/- intermediate) pretest probability:  Study 1 st , 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, O 2 , monitor, pOx The diagnosis of ACS/PE/dissection may be subtle.