Senior Report 7.2

Case Presentation by Dr. Andrew Klutman

CC:  73 yo male brought in by EMS for confusion and difficulty in breathing

HPI: According to EMS, up until yesterday the patient was his normal self other than his worsening chronic back pain. He woke up and simply did not feel well. As the day progressed he became more tired and slept most of the day.  In the middle of the night, the patient had trouble sleeping. He started developing a cough and began running a slight fever. His wife woke found him sleeping in the recliner this morning. She attempted to wake him up but had difficulty arousing him which is when she called EMS. Upon arrival the patient’s saturations were in the high 80’s so EMS placed him on a non-rebreather. The patient is unable to provide any history

ROS: Unable to obtain due to clinical condition

PMH: CAD – NSTEMI, HTN, DM, COPD and chronic back pain
Surgical Hx: Hernia repair, right knee replacement 3 years ago
Allergies: None
Medications: Insulin, metformin, carvedilol, aspirin
Social: 20+ pack year history for tobacco, occasional alcohol and no illicit drugs

Physical Exam:
Vitals: T 38.2 HR 125 BP 130/86 RR 20 Sats 96% on a non-rebreather
General: Patient is drowsy but will open his eyes to stimulation
Eyes: Eyes are non-icteric, non-injected, pupils are round, equal and reactive to light
HENT: Head is normal cephalic, atraumatic. Neck is supple without nuchal rigidity. Patient does have a gag reflex. No JVD
CV: Tachycardic but regular rhythm. No murmurs. Palpable pulses in his upper and lower extremities
RESP: Diffuse crackles. Patients respirations are deep and slightly tachypnic.
Abdomen: Soft, non-distended, no obvious tenderness to palpations. Fecal occult negative, good rectal tone.
Extremities: Though he does not follow commands he does move all extremities spontaneously.
Skin: Warm to touch but no obviously rashes or lesions.
Neuro: Patient will not follow commands but does move extremities spontaneously. He does speak some words you can understand but do not make sense. He opens his eyes spontaneously.  His eyes are noted to move past midline.  No clonus.

Labs:

Electrolytes: Na-132 K-3.1 Cl-92 CO2-14 BUN-60 Cr-2.1 Glu-310

CBC: WBC-18 HGB-9.9 PLT-199 HCT-100

INR: 1.73 PT:

Lactate: 4.1

Troponin: .489

VBG: pH-7.29 pCO2-19.7

TSH: 1.734

ECG:
ECG 7.1

Chest XR:
CXR 7.1

Head CT:
CT Head 7.1 Torres

1. What is the correct interpretation of the patient’s acid-base status
a.  Acute respiratory acidosis and chronic metabolic alkalosis
b. Chronic metabolic acidosis and acute respiratory alkalosis
c. Acute metabolic acidosis with incomplete respiratory compensation
d. Acute respiratory acidosis with incomplete metabolic compensation

2. What do you feel is the most likely diagnosis
a. NSTEMI
b. CVA
c. CHF
d. Salicylate toxicity

3. How would you treat this patient’s underlying problem?
a. Initiate heparin for an NSTEMI
b. Stroke consult – consider TPA
c. Early goal directed therapy
d. Serum/urine alkalization with NaCO3

Bonus Question (academic purposes only)

Would you intubate this patient, why, why not and any special concerns?

Answers and Discussion

1) B – its the only one with a mixed metabolic acidosis and respiratory alkalosis
2) D
3) D – Initiate alkalization in order to minimize CNS toxicity

Question 1.  Typically when considering salicylate toxicity most of us know to look for an acute respiratory alkalosis characteristic of salicylate toxicity.  The mechanism of action is stimulation of the CNS respiratory center causing hyperpnea (rapid, deep breaths) ultimately leading to a fall in pCO2 and a respiratory alkalosis.  This respiratory alkalosis predominates in the early stages, usually within 24 hours, of salicylate toxicity.  Later stages of severe salicylate toxicity is characterized by accumulation of organic acids, mainly lactic acid and ketones, causing a metabolic acidosis as well.  Salicylates drive the metabolic acidosis by uncoupling oxidative phosphorylation leading to increased energy production and utilization within the cells causing increased dependence upon an anaerobic metabolism.  In this case, the patient’s lactate was elevated above 4 and if a UA was obtained it would likely show ketones. The interesting aspect of salicylate toxicity is that there are no “givens.” Just because there is not an anion gap does not mean that it is not the underlying cause. Depending upon when the patient presents in their toxicity course will determine what acid/base disorder you may see. Therefore, you can have any combination of acid-base discrepancies. Depending on timing, level of toxicity, co-ingestions and underlying co-morbidities you may not appreciate a respiratory alkalosis which is seen early but not necessarily late in their toxicity. However, looking at this patient we have:

Electrolytes: Na-132 K-3.1 Cl-92 CO2-14 BUN-60 Cr-2.1 Glu-310

VBG: pH-7.29 pCO2-19.7

The first step is to decide if this is acidosis or alkalosis. So obviously this is an acidosis as the pH is less than 7.38. Step 2 is deciding the primary process. Here we have a low HCO3 and CO2 so this a metabolic acidosis. Next is to access compensation. As we decided that this is a primary metabolic acidosis we can use Winter’s formula; PCO2=1.5(HCO3) + 8 (+/- 2). Applying the formula we expect a PCO2 of 27-31. As his pCO2 is below that value, the patient has a metabolic acidosis along with a primary respiratory alkalosis.

Question 2.  The reason I chose this case is because in my 2 years and 7 months of residency I have developed new appreciation for the power of the endocrine system, influenza and now aspirin. Bottom-line, aspirin may improve mortality in an MI but it can cause some serious problems. Looking at this patient his aspirin toxicity could easily have been mistaken for heart failure, dementia, sepsis, MI and DKA. Unfortunately chronic aspirin toxicity frequently has a delayed diagnosis due to it’s similarities to the diagnosis listed above. Instead, it is often diagnosed days after admission when the ICU consults Dr. Hedge or Dr. King. Think about it, how many times have you honestly considered aspirin toxicity in an elderly patient, on aspirin, with mental status changes. Unless you are Craig Sharkey, I would be willing to bet rarely.

So how can you make the diagnosis? Early symptoms include tinnitus, vertigo, nausea, vomiting and diarrhea. But how often are ED Doc’s privileged to early symptoms? As discussed above, most clinicians “hang their hats” on a respiratory alkalosis.  But what about a patient with COPD or other chronic CO2 trappers? Could this patient have a normal pCO2 and HCO3 and still be in physiological respiratory alkalosis? I feel that he most definitely could have but as most of us realize, there definitely would be some ethical problems conducting toxic substance ingestion randomized controlled trials in humans to prove this. So, what else can we look for?

The SDS provides great incite. Generally salicylate levels above 40mg/dL are considered toxic. Salicylate levels should be obtained every 2 hours in patients until 2 consecutive levels show a downward trend below 40 and the patient is asymptomatic with a normal respiratory rate. Levels may not begin to rise until 5-6 hours after ingestion due to pylorospasm, bezoar formation or enteric coated pills. Also of note, 10-30 g of acute aspirin ingestion for adults and 3g for children is usually considered fatal. Chronic ingestion and toxicity is harder to quantify.  My point was to illustrate that in this patient a therapeutic aspirin level should at least perk your interest for possible chronic toxicity.

Vital signs are frequently not useful in suspecting ASA toxicity either. Do not let vital signs talk you out of aspirin toxicity. Low grade fevers are common.  This may occur due to ASA uncoupling oxidative phosphorylation in mitochondria. The uncoupling causes generation of heat ultimately leading to fever. Toxic aspirin patients typically present with hyperpnea as well. These patients take deep, rapid breaths so paying attention to their breathing can be pivotal. Along the same lines, tachycardia is frequently present. These patients can be agitated, dehydrated due to vomiting/diarrhea and increased osmotic diuresis, and in general distress.

Though not always necessary, imaging can help in completing the diagnosis. This patient has an chest x-ray showing non-cardiogenic pulmonary edema.  This can be very subtle on x-ray or very prominent as in this case. The edema is most likely related to increased membrane permeability and acidosis. The patient also had a head CT that showed cerebral edema. The progressive acidemia facilitates the ability of salicylic acid to cross the blood brain barrier leading to cerebral edema again likely through increased membrane permeability.

Finally, salicylate toxicity can also cause thrombocytopenia.

Question 3.   As with all resuscitations of critically ill patients, we follow the ABC’s upon presentation. The exception is intubation as it should only be reserved for patients with obvious respiratory failure or impending collapse. Even the brief apnea during RSI is enough to worsen the patients acidosis causing the protonation of anions to salicylic acid allowing them to cross the BBB and worsening the patients CNS toxicity. Once intubated, the acidosis is exacerbated with ventilator asynchrony and relative ventilator related hypoventilation. If you must intubate these patients, shoot for tidal values in the 6-8 mL/kg and high ventilation rates. Also avoid deep sedation or long acting paralytics which blunt the patients ability to breath over the vent.  You need to match the patient’s own minute ventilation if you intubate them.  If you do not, their Co2 will rise and worsen their acidosis which can be fatal.

The base-line treatment of salicylate toxicity is sodium bicarb. The goal is to first correct the CNS acidosis and decreased the BBB permeability to salicylic acid. It is theorized that it’s the CNS toxicity that kills these patients. The secondary affects of bicarb is alkalization of the urine facilitating aspirin excretion. The initial dose of bicarb is 1-2 mEq/kg IV bolus. Then you should start the patient on a bicarb infusion of 100-150 mEq in D5.  This is made by placing 3 amps of NaHCO3 in a liter of D5water. The rate is titrated to a urine pH of 7.5-8 which commonly comes out to 1.5-2 times maintenance. Hypokalemia also needs to be corrected to facilitate urine alkalinization.  You also need to check serum pH frequently to be sure you are not over alkalinizing them.  Your target serum pH is 7.45-7.5.  These patients will need a foley to monitor urine output, check Q1H urine pHs until your target is reached.  It is also imperative that you know they are making urine.  Place a arterial line for frequent blood draws and blood pressure monitoring.

In our patient, he has altered mental status which is likely due to the CNS toxicity and edema, but also neurohypoglycopenia (decreased cerebral glucose). In animal models, it has been demonstrated that even if the patient is normoglycemic or even hyperglycemic, they have low CNS glucose. As expected, no studies have been conducted on humans but the recommendation is to maintain a normal glucose level of 80-120 or even slightly higher.

The big question here is when do we perform hemodialysis. The serum salicylate hard number is > 100 mg/dL. Talking with the Toxicologist, much of it depends on the clinical picture. For instance, our patient has a rather poor clinical picture. He has renal failure, altered mental status, pulmonary and cerebral edema which each alone is an indication for dialysis. Pulmonary edema greatly complicates fluid resusitation and bicarb therapy. Renal failure hinders bicarb therapy and aspirin secretion. And as discussed above, altered mental status and cerebral edema carries an extremely high mortality. So be rather aggressive in patients with the above findings or those who mental status are not improving with conventional treatment.  Lastly, contact your toxicologist regarding activated charcoal.

Key Points:

  1. In altered mental status, especially in the elderly, really look at the SDS.
  2. If any salicylate level is detectable, consider chronic salicylate poisoning.
  3. Toxicity can look like just about anything, do not write it off too soon.
  4. Clinical picture really drives the necessity for dialysis.
  5. Intubate with extreme caution.

 

Additional information and resources:

American college of Medical Toxicology page for salicylism for more information.

http://www.acmt.net/cgi/page.cgi/zine_service.html?aid=4210&zine=show

UpToDate: Salicylate (aspirin) poisoning in adults.

http://www.uptodate.com/contents/salicylate-aspirin-poisoning-in-adults?source=search_result&search=salicylate+toxicity&selectedTitle=1%7E61

Rosen’s

Your local friendly Toxicologist

Intern Report 7.4

Case Presentation by Dr. Nile Chang, MD

A 29 year old African-American pregnant female, G3P2, 38 weeks pregnant per LMP, presents with 2 weeks of progressively worsening shortness of breath and dyspnea with exertion, orthopnea, and ankle edema. She also reports occasional cough worse when she lies down. She reports having gained 15 pounds over the last month. She saw her OBGYN about a month ago and “everything has been fine”.  Her previous pregnancies were notable for full-term vaginal births without complications. She denies fevers, chills, vomiting, headache, or rash.

PMH:
No significant medical history
No significant surgical history
Allergies: no known drug allergies

Physical exam:

General: In mild distress, tachypneic
Vitals: T – 97.6 Pulse- 80 RR- 28 BP- 170/85 O2Sat-88% on RA
HEENT: Normocephalic, Atraumatic, PERRLA, no JVD or distended neck veins
Respiratory: Breath sounds clear and equal bilaterally, no wheezes, rhonchi, or rales, no accessory muscle use
Cardiac: Regular rhythm and rate, no murmurs, rubs or gallops
Abdomen: Gravid, non-tender, soft, no rigidity, rebound, or guarding
Skin: Warm and dry without diaphoresis
Extremities: Palpable pulses in equal bilaterally in all extremities. 2+ pitting edema in both lower extremities
Neurologically: A&Ox3, normal speech, symmetrical strength, DTRs 2+ at the patella and symmetrical, no clonus

Labs:

WBC: 10.2
HGB: 11.3
Plt: 335

Na: 133
K: 4.0
Cl: 100
HCO3: 22
BUN: 13
Cr: 1.2

Alb: 3.2
TP: 8
T.Bili: 0.3
D Bili: 0.1
ALT: 35
AST: 50
Alk Phos: 165

pH: 7.43
pCO2: 27
PO2: 56
FiO2:21

Urinalysis: normal

Fetal Doppler: 132 bpm

7.4 1

7.4 2

7.4 3
Questions:

Q1. Which of the following findings is least likely to be found on echocardiogram for this patient?
a) Dilated Left Ventricle
b) Reduced diastolic filling
c) Reduced LV ejection fraction
d) Small pericardial effusion

Q2. Which of the following imaging study exposes the fetus to the most amount of ionizing radiation?
a) Chest X-ray
b) Pelvis X-ray
c) CT Pulmonary Angiogram with abdominal shielding
d) V/Q Scan

Q3. Which one of the following pharmacotherapy should not be used to manage this patient?
a) Beta-blocker
b) ACE inhibitor
c) Hydralazine
d) Furosemide

Answers & Discussion:

1) B
2) B
3) B

Dyspnea in pregnancy is a common complaint seen in the ED. Normal physiological changes includes a normal increase in minute ventilation, which often presents as a complaint. However, dyspnea can be a harbinger for several life-threatening emergencies that require prompt evaluation. These emergencies include asthma, pneumonia, pulmonary embolism, and pulmonary edema secondary to preeclampsia or dilated cardiomyopathy.

The patient in this case has a clear clinical picture of pulmonary edema secondary to peripartum dilated cardiomyopathy (PPCM). Her history and physical is notable for worsening shortness of breath, ankle edema, orthopnea, and paroxysmal nocturnal dyspnea, all signs of heart failure. PPCM generally occur in the last month of pregnancy or within the first five months of delivery.

Q1.  Answer: B

PPCM is a dilated, high output form of cardiac failure. Of the answer choices, findings of a dilated left ventricle (a) and reduced LV ejection fraction (c) on echocardiogram is a definitive diagnosis. A small pericardial effusion can also be seen (d). Reduced diastolic filling (b) is more associated with a restrictive cardiomyopathy, not generally seen in PPCM.

In this patient, additional evaluation such as a BNP may also help confirm the diagnosis.

Q2.  Answer: B

When considering radiological imaging in the pregnant patient, one must be cognizant of the potential exposure of ionizing radiation to the developing fetus, and weigh the risk of the exposure against the risk of misdiagnosis.

The ACOG technical bulletin suggest that significant risk is unlikely when the fetus is exposed to less than 100 rads of cumulative radiation during pregnancy. With exposure to 15 rads or greater, there is a 6% chance of severe mental retardation and 15% chance of microsomia. The following table lists the estimated radiation dose to the fetus by imaging modality.

C-spine (<1mrad)
Chest X-ray (1-3 mrad)
KUB (200-500 mrad)
Pelvis X-ray (200-500 mrad)
L-spine (600-1000mrad)
CT Head/Chest (with shielding) (<1000 mrad)
CT Abdomen (3000 mrad)
CT Pelvis (3000-9000 mrad)
V/Q scan (<55 mrad)
CT PE (with shielding) (<50 mrad)

Conventional wisdoms suggest that a V/Q scan was the test of choice to rule out PE, however, more recent studies have shown that CT with PE protocol may provide a similar level of exposure while providing a higher level of sensitivity and specificity. Therefore, pregnancy should not preclude the use of helical CT for the diagnosis or rule-out of PE.

Of the answer choices, a pelvis X-ray (b) have a highest level of exposure (200-500mrad).

Q3.  Answer: B

For the most part, the goals of medical therapy are similar to those in patients with heart failure due to other causes. However, ACE inhibitors (b) and ARBs are contraindicated at any time in pregnancy. However, they are safe to use in women who are breastfeeding.

Because ACE Inhibitors and ARBS are contraindicated in pregnancy, hydralazine (c) is a safe option for antepartum vasodilation and blood pressure reduction.

Beta-blockers (a) are generally safe during pregnancy, with agents that are beta-1 selective (metoprolol) are preferable, as ones that are not (atenolol) may interfere with beta-2 mediated uterine relaxation and peripheral vasodilation.

Diuretics such as furosemide (d) and hydrochlorothiazide should only be used if there are signs of pulmonary congestion, as it may decrease blood flow over the placenta.

References:
1. Rosen’s Emergency Medicine, Concepts and Practices, 7th edition

2. Trauma during pregnancy: ACOG technical bulletin. American College of Obstetricians and Gynecologists. November 1991.

3. ESC Guidelines on the management of cardiovascular diseases during pregnancy. European Heart Journal (2001) 32, 3147-3197

4. Peripartum Cardiomyopathy. UpToDate. Wolters Kluwer Health. 2013.

Intern Report 5.11

Case Presentation by Dr. Adnan Sabic

CC:  Shortness of breath

HPI:  52 year old male presents to the ED with four weeks of SOB and right sided chest pain. His symptoms have gradually progressed in severity and were worse with exertion.  These symptoms started several days after he fell against a counter and struck his right chest wall. He initially had a “small gash and black and blue mark” on his right lateral chest wall but these resolved over the course of the month. He denied similar symptoms in the past. He denied any nausea or vomiting.  He denied any orthopnea or PND symptoms. He did not take any medication for this. He complained of low grade fever. Review of systems is otherwise negative.

PMH: HTN, uncontrolled.

Medication: none

PSH: none

Allergies: NKDA

PFH: Negative for DM, HTN, Ca.

PSH: positive for tobacco use, negative for EtOH or illicit drugs.

Physical exam:

Vital signs: 37.9 C, 111, 26, 160/95 and  98 % RA,

General: WNWD 52 year old male who appears to be tachypneic.

Head: NCAT

Eyes: PERRLA, EOMI

Neck: trachea is midline, no c-spine tenderness, no crepitus

Cardiovascular: S1 &S2, tachycardic, no murmors, no JVD

Respiratory: Tachypnic, clear breath sounds on the left, but absent breath sounds on the right chest in all lung segments.

GI: soft, NT/ND, +BS

MSK: chest wall was non-tender throughout palpation without any crepitance. Rest of the exam is unremarkable.

Neurological: A&O X3, no obvious neurological deficits.

CXR was obtained:

 

 

  Questions

A)  What is your suspected diagnosis?

  1. Hemothorax
  2. Empyema/Intraparenchymal lung abscess
  3. Pneumonia
  4. Unilateral diaphragm perforation

B)  A chest tube was placed and 1500 cc of yellow, exudative fluid was removed from the right chest cavity.  Which of the following are consistent with exudative fluid?

  1. The ratio of pleural fluid protein to serum protein is greater than 0.5
  2. The ratio of pleural fluid LDH and serum LDH is greater than 0.6
  3. The difference between the albumin level in the blood and the pleural fluid is greater than 1.2 g/dL
  4. A&B
  5. All of the above

C)  What is the most common cause of this condition?

  1. Penetrating trauma
  2. Esophageal rupture
  3. Pleural extension of pneumonia
  4. Previous  thoracic surgery
  5. Previous chest tube placement

Discussion:

Answers:

A)     2

B)     4

C)     3

An empyema is a collection of exudate in the pleural cavity. It is most often caused by pleural extension of pneumonia, but it may be also caused by any seeding of the pleural cavity from penetrating trauma, esophageal rupture, previous thoracic surgery or previous chest tube placement. Empyema is also an under recognized complication of blunt thoracic trauma and may be an occult perpetrator in subsequent respiratory failure and need for mechanical ventilation.

In the emergency setting, chest radiography is indicated to differentiate other chest pathology that can present similarly. A CT of the chest may be necessary to assess for underlying pneumonia, lung abscess, tumor, septations or other pleural disease. When 2-view chest radiographs are used to detect pleural fluid, the sensitivity is 67% and the specificity is 70%. Decubitus views increase the degree of confidence. However, decubitus views are often skipped, and the patient instead undergoes a CT examination.

In the absence of trauma or surgery, the diagnosis of empyema would be very unlikely. Clinically, one might suspect empyema if the patient has fever, productive cough, or clinical symptoms consistent with pneumonia. Radiographically and without a known history, it would be difficult to differentiate the two entities. The gold standard for differentiating them is tube thoracostomy and evaluation of the fluid.

The fluid obtained by tube thoracostomy is either exudate or transudate. Transudate is produced through pressure filtration without capillary injury while exudate is due to leakage from inflammatory cells. It is critical to identify the fluid as either exudate or transudate in order to make an accurate diagnosis. Light’s criteria, which compares chemistries of the fluid to blood is used to classify the fluid. Fluid is likely exudative if one of the following is true: the ratio of pleural fluid protein to serum protein is greater than 0.5, the ratio of pleural fluid LDH to serum LDH is greater than 0.6, the difference between albumin the fluid and albumin in the blood is less than 1.2 g/dL. Usually protein content of exudate is greater than 35 g/L and cholesterol content is greater than 45 mg/dL.

The definitive management of empyema should be made in consultation with thoracic surgery and infectious disease. The gold standard of treatment has been prompt tube thoracostomy and intravenous antibiotics, but recent literature has suggested a benefit in both intrapleural fibrinolytics and early VATS. Pleural fluid should be sent for analysis and they should be admitted to the hospital for continued therapy.


TWITER 1.1

twiter1A 35-year-old woman presents to the resuscitation room with shortness of breath that began earlier in the afternoon.  The patient has a history of asthma.  On exam, she is in obvious respiratory distress with retractions, accessory muscle use, and faint wheezing on auscultation of her thorax.  She rapidly decompensates and has to be endotrachealy intubated.

Acute asthma exacerbation with respiratory faiulure

  • The most common predictors of fatal asthma seem to be a past medical history of intubation/mechanical ventilation and underuse of steroid therapy
  • Findings suggestive of severe asthma
    • dyspnea so severe the patient is only able to speak a few words at a time
    • poor air movement on auscultation of the lungs
    • use of accessory muscles – reflects diaphragmatic fatigue
    • silent chest – indicates that airflow is dramatically reduced and is no longer adequate to cause wheezing
    • diaphoresis
    • cyanosis – late finding, appearing just prior to respiratory arrest
    • altered mental status – may indicate hypercapnia and often reflects impending respiratory failure
  • Treatment of severe asthma
    • beta2-agonists (onset of action < 5 minutes)
    • anticholinergic agents (onset of action up to 30 minutes)
    • corticosteroids (onset is gradual with initial improvement at 3 hours)
    • heliox
    • magnesium sulfate
    • terbutaline/epinephrine – reserved for patients who are too sick to provide an effective respiratory effort
    • mechanical ventilation – high rate of iatrogenic complications (barotrauma)
      • hypoventilate (8-10 breaths per minute – permissive hypercapnia)
      • I to E ratio increased to at least 1:4

TWITTER notes (This Week In The ER) is an educational resource that presents high-yield, case-based information from actual patient presentations in the Detroit Receving ED.

Answer Tracings Vol 1.1

Case

ECG Interpretation

  • The ECG shows tachycardia (rate just >100 bpm) with a wide QRS complex. A right bundle branch block pattern is present.
  • There is a large upright QRS in AVR suggesting right axis deviation but examination of the other limb leads suggests axis is deviated to the left at near -90 degrees.
  • There are no definite P waves, making the rhythm indeterminate.
  • Is there ST segment elevation somewhere in V1-V4? Hard to say definitely yes or no, but there is no suggestion of reciprocal changes in the inferior leads.

Discussion
Taken together, the patient’s clinical presentation and an ECG suggestive of acute right heart strain (RBBB, axis shift) indicates the possibility of pulmonary embolus. The presentation is also consistent with large vessel acute coronary occlusion (STEMI). In a hemodynamically viable patient, emergency transfer to the cath lab would be a reasonable course. However, with a patient who is intermittently in cardiac arrest, one could consider treatment with thrombolytics, which would address both acute coronary occlusion and PE.

Oh, yes, the patient could also have a dissection, but with this presentation, mortality would be virtually 100%.

Post-mortem examination by the Wayne County Medical Examiner confirmed that the patient expired from massive bilateral pulmonary embolism.

As far as the ECG is concerned, it is trivial, but nevertheless correct, that sinus tachycardia is the most common ECG abnormality associated with pulmonary embolism. More significant and clinically helpful is that right bundle branch block (62%) and axis shifts are commonly present in patients with massive pulmonary embolism. In patients with these findings and a suggestive clinical presentation, pulmonary embolism is a likely diagnosis. In critical situations, treatment with thrombolytics should be considered before a diagnosis can be confirmed by testing.

Reference
Surawicz B, Knilans TK: Chou’s Electrocardiography in Clinical Practice, 5th ed., 2001.

Tracings is a learning module involving actual cases of patients and their ECGs that present to the Emergency Department.  Topics chosesn are dervied from the EM Model for Resident Education.