A 55 year old man is brought in by EMS for altered mental status.

It is the middle of February and he was found sleeping outside. He smells of alcohol, is moaning on the gurney, and responds to painful stimuli.

Vital signs are assessed.

• RR: 13
• HR: 38
• BP: 110/90
• Temp: Cold to touch
• SpO2: Unable to obtain reading

A 12-lead ECG is obtained due to bradycardia and altered mental status.

Sinus bradycardia with a rate of 38. The QRS appears to be wide and there is a large notch or J-wave at the end of the QRS complex. These are classic “Osborn waves” of hypothermia. There is motion artifact due to slight shivering.

At this point the patient’s temperature was found to be 24°C / 75°F by bladder temperature monitoring.

Osborn waves typically have a positive deflection in all leads except aVR and V1. They are known by a number of other names such as the camel-hump sign, late delta waves, hypothermic waves, or prominent J-waves.

In a patient who was found outside in February, they can safely be presumed to represent hypothermia.

The physiologic cause of Osborn waves is not well understood. Since the 1920s many hypothesis have been proposed including anoxia, injury current, acidosis, delayed ventricular depolarization and early ventricular repolarization.

While the treatment of the patient with prominent Osborn waves is based on the precipitating cause, the presence of Osborn waves is related to an increased incidence of ventricular fibrillation.

The patient was aggressively resuscitated with both internal and external warming with warm intravenous fluids and forced heated air blankets.

A repeat 12-lead ECG was performed 2 hours later.

Sinus rhythm with a rate of 60. Osborn waves are still present but they are much smaller.

The patient’s temperature is now 32°C / 89°F.

As the internal temperature improved the patient’s heart rate began to rise and the Osborn waves became less prominent. However, the artifact is worse due to increased shivering.

Rewarming was continued and a third ECG was performed, 3 hours after initial presentation.

Sinus rhythm with a rate of 60. The Osborn waves have resolved. The patient is no longer shivering.

Core temperature at this point was 33°C / 91°F.

Discussion

Osborn waves consist of a positive deflection at the J-point in all leads except for aVR and V1 where the deflection is negative.

Prominent J-waves can be seen in hypothermia, hypercalcemia, neurovascular accident, vasospastic angina, and Le syndrome d’Haïssaguerre (idiopathic ventricular fibrillation or as a normal variant).

While the true physiologic cause of Osborn waves is not known their presence can indicate a progression to ventricular fibrillation.

Osborn waves that are secondary to hypothermia should improve with patient warming.

Hypothermia also causes bradycardia, prolonged PR, QRS and QTc intervals, ventricular ectopy and atrial fibrillation.

Shivering may contribute to poor 12-lead ECG data quality but usually disappears below a threshold temperature.

Resources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1501063
http://lifeinthefastlane.com/ecg-library/basics/hypothermia
http://hqmeded-ecg.blogspot.com/2011/11/osborn-waves-and-hypothermia.html

A 45 year old male with unknown medical history was taken into police custody under concern for trafficking illegal drugs.

While he was in the back of the squad car he told the police he had swallowed a large amount of cocaine and may need to go to the hospital.  Not long afterwards he became unresponsive and paramedics were called to the scene.

Paramedics found the patient minimally arousable.

Vital signs were assessed.

• RR: 12
• HR: 130
• NIBP: 140/69
• SpO2: 95% on room air
• Temp: 36.8 C / 98.2 F
• BGL: 137

The cardiac monitor shows “sinus tachycardia” (the prehospital ECG is unavailable).

During transport paramedics witness tonic-clonic seizure activity and 2 mg of IV lorazepam is given.

On arrival in the Emergency Department the airway is intact, respirations are shallow, and there is no response to painful stimuli.  A nasopharyngeal airway is placed, the patient is ventilated with a bag valve mask, and then intubated via rapid sequence induction.

A 12-lead ECG is acquired.

The QRS is wide at 138 ms. The QTc is prolonged at 596 ms. P waves can be seen in leads aVL and V3. This is most likely sinus tachycardia with toxicologic widening of the QRS.

200 mEq sodium bicarb is given and another 12-lead ECG is obtained.

The QRS is now 130 ms and the QTc is 587ms.

An additional 200 mEq of sodium bicarb is given and the patient is started on a sodium bicarb drip, 150 mEq in 1,000 mL at 150 mL/hr.

30 minutes later the 12-lead ECG is repeated.

The QRS is now 90 msec with QTc 464 msec.

Now the QRS shows a normal duration but there are some troubling ECG findings.

ST-segment elevation is noted in the right precordial leads (V1-V3) and the high lateral leads (I and aVL), with ST-segment depression in the inferior leads (II, III, and aVF). There are Q-waves in leads V1 and V2 with a QR pattern.

This was thought to be secondary to patient’s cocaine use and not from thrombotic disease so the cardiac cath lab was not immediately activated. Cardiac biomarkers remained negative, and the ST-segments normalized during hospitalization.

Discussion

• Cocaine acts like a Class I antiarrhythmic which causes sodium channel blockade and widening of the QRS complex.
• Treatment of toxicologic widening of the QRS consists of sodium bicarbonate (the sodium helps to overcome the blockade caused by the cocaine).
• If QRS does not improve with sodium bicarbonate an alternative diagnosis other than toxicologic widening of the QRS should be considered.
• Cocaine can also cause QT prolongation via blockade of the K+ rectifier channels.
• Other cardiovascular events such as coronary artery spasm, myocardial infarction, hemorrhagic stroke, and aortic dissection related to sympathomimetic properties of cocaine should be considered in the differential diagnosis.