Wellens Syndrome

Ok, so not every post on EverydayEmergencyMedicine will focus on the basics, some will focus on the rare/odd/funny cases that we see everyday as well.

Case Presentation:

Sorry, the blog post title gives the case away….

Male in his early 50s presents for a sexual transmitted infection (STI) check, along with his new (and younger) significant other; he is currently asymptomatic.  During the history, patient admits to some shortness of breath and chest discomfort during a recent argument with his significant other, as well as, some shortness of breath with exertion (both walking and intercourse) in the past few days.  Patient, again, has no current complaints.   

The history prompted the patient to have an ECG preformed.  Which showed….

Because of these findings, cardiology was contacted and the patient was admitted.

What does this ECG show?               …         Wellens Syndrome

Wellens Syndrome represents a characteristic T-wave change on electrocardiogram (ECG) that is present during pain-free periods in a patient with intermittent chest pain and symptoms consistent with unstable angina/ischemic chest pain. 

The findings of Wellens Syndrome suggest a high-degree stenosis of the proximal left anterior descending (LAD) coronary artery (i.e., the “Widow Maker”), that if not treated with intervention will lead to a massive anterior myocardial infarction and/or death within two weeks (mean time, 8.5 days) in 75% of patients (i.e., a “Widow Maker”).  Medical Management is ineffective.

Wellens syndrome is characterized by T-wave changes in the precordial leads, mainly V2 & V3 ± V4, during pain free periods, in a patient with a history of chest pain that is consistent with unstable angina/ischemic chest pain.  Type A (or Type I) (75-76% of cases) shows deeply inverted T-waves, while Type B (or Type II) (24-25% of cases) shows biphasic T-wave.  Type A is rarely missed, but Type B is often interpreted as “non-specific T wave changes” by the computer and clinicians. 

Type A (or Type I)

Type B (or Type II)

 

The diagnosis should be made by the history obtained from the patient and ECG only, as cardiac enzymes will be normal or only mildly elevated.  This also helps enforce the importance of serial ECGs and pain-free ECGs in patients with a history of chest pain that is concerning for unstable angina/ischemic chest pain.

These patients do not necessarily need immediate catheterization, but they need urgent catheterization.  These patients should not undergo a stress test, as it places them at risk for an acute anterior wall myocardial infarction.  Cardiac catheterization has demonstrated patients with Wellens syndrome to have a 50% or greater stenosis of the proximal LAD.

Case resolution:

This patient’s ECG showed Wellens Type B (or Type II) … biphasic T waves in leads V2 & V3 (and arguably in leads in V1 & V4 as well), the computer read it as “T wave abnormality, consider anterior ischemia.”  The patient was asymptomatic in the emergency department and had negative cardiac markers and was admitted to cardiology (the patient was reluctant to be admitted).  Cardiology did order a treadmill stress test for the morning, which the patient failed and thus went to cardiac catheritzation and a 95% proximal LAD lesion was found and two stents were placed. 

Had this been missed, the patient likely would have passed in bliss during intercourse with his younger significant other (personal commentary).

References:

Rosen’s 7^th Edition

De Zwaan C, Bar FW, Wellens HJ. Charcteristic electrocardiographic pattern indicating a critical stenosis high in the left anterior descenting artery in patients admitted because of impedning myocardial infarction. Am Heart J. 1982;103:730-6.

J Emerg Trauma Shock. 2009 Sept  Dec; 2(3): 206-208.

Hypothermia

Hypothermia

This will focus on accidental hypothermia; there are numerous secondary causes that will not be the focus of this review. 

Although typically associated with regions of the world with severe winters, hypothermia is also seen in areas with warmer climates, as well as during summer months and in hospitalized patients.  Even with modern supportive care, mortality for patients with moderate to severe accidental hypothermia approaches 40%.

Body Temperature reflects the balance between heat production (cellular metabolism) and heat loss (evaporation, radiation, conduction & convection).  The normal human core temperature is 98.6±0.9^oF (37±0.5^oC).  The human body has limited physiological capacity to respond to cold environmental conditions (basically, peripheral vasoconstriction), thus our behavioral adaptations of clothing and shelter.  In response to a cold stress, the hypothalamus attempts to stimulate heat production through shivering and increased thyroid, catecholamine and adrenal activity.  There is also sympathetic mediated vasoconstriction of peripheral tissues. 

Hypothermia is defined as a core temperature below 95^oF (35^oC).

•          Mild: 93.2 – 95^oF (34-35^oC)
•           Moderate: 86 – 93.2^oF (30-34^oC)
•           Severe:  less than 86^oF (less than 30^oC)

Mild hypothermia is characterized by tachypnea, tachycardia, initial hyperventilation, ataxia, dysarthria, impaired judgment, shivering and “cold diuresis.”  “Cold Diuresis” is renal-fluid wasting due to hypothermia-induced vasoconstriction and diminished release of anti-diuretic hormone.

Moderate hypothermia is characterized by a proportionate reduction in pulse rate and cardiac output, hypoventilation, central nervous system depression, hyporeflexia, decrease renal blood flow, and the loss of shivering.  Patients may begin to display paradoxical undressing.  Atrial fibrillation, junctional bradycardia and other cardiac arrhythmias may also occur.

Patients with severe hypothermia develop pulmonary edema, oliguria, areflexia, hypotension, bradycardia, coma, ventricular arrhythmias and asystole.

Risk Factors for hypothermia include: Age (infants and the elderly), Environmental (exposure, drowning, and an alpine environment), Poverty, Homeless, Drugs / Toxicology and Psychiatric disorders.

To measure the temperature in a hypothermic patient requires a low-reading thermometer.  Most standard thermometers only read down to 93^oF (34^oC).  If the patient is conscious, a rectal probe thermometer is practical (although, to be truly accurate, needs to be inserted 15cm).  If the patient is intubated, an esophageal probe is preferred and is most accurate (inserted into the lower 1/3 of the esophagus). 

What studies to obtain?

•  Finger stick glucose!  Do not miss the patient who is hypothermic secondary to hypoglycemia.  Remember, if the patient does not have glucose, the body cannot generate heat to help rewarm itself.  Also, insulin release is decreased in hypothermia, so hyperglycemia is common.
• ECG
•   Hypothermia causes characteristic ECG changes because of slowed impulse conduction through potassium channels.  This results in prolongation of all the ECG intervals.  There also maybe elevation of the J point, producing the characteristic Osborn J Wave (from the distortion of the earliest phase of membrane repolarization).                            
• BMET
• Resuscitation is futile if K >10
• Check frequently during the resuscitation
• CBC
• There is 2% drop in Hct for each 1^oC drop in temp
• Thrombocytopenia is common
• Lactate – elevated from shivering and poor tissue perfusion
• PT/PTT – often coagulopathy is clinically evident but laboratory studies appear normal as the test is run at 98.6F (37C)
•  Fibrinogen
• Creatine phosphokinase
• Arterial blood gas – acidosis often present due to severe respiratory depression and CO₂ retention as well as lactic acid production
• CXR – pneumonia (aspiration) is a common complication
• Toxicology screen
• ETOH

 

Management

• ABCs
• There is an alteration in ACLS algorithm for patients with severe hypothermia (less than 86^oF (less than 30^oC)).  In patients with severe hypothermia, begin CPR and attempt defibrillation once.  Withhold typical ACLS medications and any further defibrillation attempts until the patient’s core temp is >86^oF (>30^oC).  These patients will require active internal rewarming (information below).
• Peripheral pulses may/will be difficult to assess, check a central pulse for up to a minute and consider using doppler.
• Establish two large bore (14 or 16 gauge) peripheral intravenous lines and start an infusion of warmed (100.4 – 107.6^oF (38 – 42^oC)) isotonic crystalloid.  This will only really prevent further heat loss!  If central venous access is needed, use the femoral approach, if possible (to avoid the guide wire irritating the right atria and causing an arrhythmia, which can occur with the internal jugular or subclavian approach).
• Treatment of cardiac arrhythmia.  Handle these patients with care!  Movement has been reported to trigger arrhythmias, including lethal ventricular fibrillation.  Remember, bradycardia is expected and pacing is not required unless the bradycardia persists despite rewarming to 90-95^oF (32-35^oC).
• Typical progression is sinus bradycardia to atrial fibrillation to ventricular fibrillation to asystole.
• 
  
• Rewarming Therapies

o   Passive External Rewarming (PER).  This is the treatment of choice for patients with mild hypothermia.  Removal all wet and cold clothing and then cover the patient in blankets or other types of insulation (aluminum foil).  Set room temp to 82^oF. PER requires the patient to have a physiologic reserve sufficient to generate heat by shivering and an increased metabolic rate.  If the patient’s temperature does not rise by 0.5-2^oC/hr., reconsider the diagnosis (are they septic, hypoglycemic, hypovolemic, endocrine source, etc.) and consider starting AER.

o   Active External Rewarming (AER).  AER is indicated for moderate to severe hypothermia and for a patient with mild hypothermia who is unstable, lacks physiologic reserve or fails PER.  AER is a combination of warmed blankets, heating pads (watch for body surface burns from decreased sensation and reduced blood flow), radiant heat, warm baths, or forced warm air, which are applied to the patients skin. 

§  Core Temperature After Drop is a risk during AER.  This occurs when the truck and extremities are warmed simultaneously.  Cold, academic blood that has pooled in the extremities returns to the core and can cause a drop in temperature and pH.  This can trigger cardiac dysrhythmias. 

§  Rewarming shock can occur when peripheral vasodilation and venous pooling results in relative hypovolemia and hypotension.

o   Active Internal Rewarming is indicated for severe hypothermia and those who fail to respond to AER. 

§  Airway rewarming is utilized by use humidified air at 40-45^oC. 

§  Pleural irrigation can be accomplished by placing two thoracotomy tubes (36 to 40 French), one placed anterior and one posterior, and instilling warmed IVF into the anterior chest tube and allowed to drain out the posterior chest tube.  If the patient is pulseless, use the left thoracic (bath the heart in the warm fluid), if the patient has a pulse, use the right thoracic to avoid triggering an arrhythmia by irritating the heart with tube insertion.

§  Bladder irrigation is another option

o   Extreme options (not readily available in many EDs): ECMO, hemodialysis, cardiopulmonary bypass

• Medications

o   Glucose, if the patient is hypoglycemic

o   Naloxone

o   Thiamine, as patients are often alcoholics (also, Wernicke’s)

o   Hydrocortisone, if the patient has a history of adrenal insufficiency

o   Antibiotics, for suspected sepsis

Remember, the patient is not dead until they are “warm and dead.”  But, how warm is warm?  Target a temperature of 89.6^oF (32^oC) in adults and a temperature of 95^oF (35^oC) in children. 

If the body is frozen and chest compressions are impossible; or if the nose and mouth are blocked by ice; or if the patient’s potassium is >10, then resuscitation can be withheld. 

References:

Tintinalli Sixth Edition

Accidental hypothermia in Adults. Up-To-Date

Circulation. 2005;112:IV-136-IV-138.

Brown, et al. Accidental Hypothermia. N Engl J Med 2012;367:1930-8.