CO Poisoning

HPI:      57 yo M w/ PMHx of HTN, HLD presents with concern for carbon monoxide poisoning. Pt reports he was using a gas-powered saw in an enclosed bathroom to cut concrete. After some time, he began to feel hot and dizzy. When he stood up to walk out of the bathroom, he reported being unable to walk straight. He then began to feel lightheaded and developed a headache. He has also developed photophobia since. He reports no other problems. Smokes approximately 1ppd.

 

Exam: Vital Signs WNL

GEN: Alert, with no distress

CV: RRR, S1S2 present, No M/R/G

Pulm: CTAB, Non-labored

Neuro: CN II-XII intact, Strength 5/5 in all extremities, Normal Sensation/Coordination

 

Labs:    CarboxyHb lvl 19.3%

ABG showed normal pH, pCO2, pO2, Bicarb

CBC, CMP, Troponin, EKG, and CXR negative for acute process

 

Dispo:  He was placed on a NRB and symptoms began improving. After discussion with Poison Control and Jewish, pt was transferred to Jewish to receive a hyperbaric O2 treatment. He felt much improved after the treatment and was discharged in good condition.

 

The suspicion for carbon monoxide poisoning is based primarily on history. Most symptoms are non-specific. Mild to moderate CO poisoning presents with headache (most common), nausea, dizziness. Don’t forget to ask about LOC. Severe CO toxicity can produce neurologic symptoms (seizures, syncope, or coma) and/or end organ damage. If CO toxicity is suspected based on history, a careful and detailed neurologic exam should be performed.

 

If sufficient concern after history and physical, the diagnosis is made by an elevated carboxyhemoglobin level measured off an arterial blood gas sample. Nonsmokers should have baseline level of less than 3% carboxyhemoglobin. Smokers may have baseline levels of 10-15%. Once the diagnosis of CO poisoning is confirmed, an EKG should also be performed. CMP should also be considered to evaluate for electrolyte abnormalities and to assess renal function. Troponin should be obtained in patients with EKG abnormalities, cardiac comorbidities, and older patients.

 

CO binds hemoglobin with greater affinity than oxygen. This results in impaired oxygen transport. CO can also precipitate an inflammatory cascade that results in CNS lipid peroxidation and delayed neurologic sequelae. The half-life of CO can be changed by manipulating O2 delivery to the patient. CO half-life is approximately:

·      250 to 320 minutes on room air

·      90 minutes on high-flow oxygen via a NRB face mask

·      30 minutes with 100 percent hyperbaric oxygen

 

Some evidence suggest that HBO treatment can decrease the chance of delayed neurologic sequelae. Patients can often be discharged soon after HBO treatment is completed.

 

Recommendations for Hyperbaric Oxygen from Rosen’s 9E:

·      Carboxyhemoglobin (COHb) independent of clinical findings

o   >25% with no clinical findings

o   >15% in pregnancy or fetal distress

 

·      Or an elevated COHb with one or more of the following findings:

o   Syncope

o   Coma

o   Seizure

o   Altered mental status (GCS <15) or confusion

o   Abnormal cerebellar function

o   Prolonged CO exposure with minor clinical findings

 

Suggested treatment algorithm from UpToDate:

 

 

 

 

References:

 

Walls, Ron M., et al. “Inhaled Toxins.” Rosen’s Emergency Medicine: Concepts and Clinical Practice, Elsevier, 2018.

 

Clardy, Peter F, et al. “Carbon Monoxide Poisoning.” UpToDate, 28 Feb. 2017, www.uptodate.com/.

Prolonged QT

58 yo F presents to the ED for cough, chest pain, and fatigue for 1wk. She has sharp, atypical sounding chest pain. But she is 58 and has risk factors: HTN, HLD, 0.5ppd smoker x48yrs. Better get an EKG.

Prolonged QT EKG

Initial EKG

Awesome, no STEMI. Done with EKG right? Hope you didn’t miss that really long QT interval.

First, how do we measure the QT?

QTc imageWe usually talk about QTc rather than just the QT. This is because the QT interval varies depending on the HR. Using a correction equation standardizes the interval so it can be interpreted regardless of the HR. The EKG computer does give a calculation of the QTc, because we are obviously not hand calculating this on every patient. You should compare what the computer calculates to your gestalt when you review the EKG. If there are any concerns or discrepancies, you should hand calculate the QTc. MDCalc has an easy to use calculator. Above is the Bazett’s formula, which seems to be the most commonly used. Other formulas do exist. QTc is considered prolonged if > 440ms in men or > 460ms in women.

Next, why do we care?

ecg_hypokalaemia_torsades

This is the start of Polymorphic VT. There are several things that can cause this rhythm. Long QT is one possible cause. When Polymorphic VT is caused by a prolonged QT we give it a special name, torsades de pointes. The mechanism behind this is demonstrated on the above EKG. As the QT interval becomes more prolonged, there is a higher chance for an R-wave to hit on just the right part of the T-wave and cause this rhythm. QTc > 500ms seems be associated with higher risk.

So what causes prolonged QT?

Many things can cause prolonged QT. The most common etiologies are electrolyte abnormalities and drugs. Hypokalemia, hypomagnesemia, and hypocalcemia are well known to cause prolonged QT. Potassium and calcium are included on the CMP but don’t forget about magnesium. Drugs are also a big cause of prolonged QT. The list of drugs is long. Probably too long to memorize. However, there are some common medications and medication classes that you should know. The big classes are, Antiarrhythmics (like Amiodarone), Antihistimines (like Diphenhydramine), Macrolides (like Erythromycin), Antipsychotics (like Haloperidol), and TCAs (like Amitriptyline). This is not a complete list, just some highlights. If you really want to know if a specific medication is associated with prolonged QT, www.crediblemeds.org is a good source.

Other causes worth mentioning are structural heart disease, cardiac ischemia, and stroke. Some people do have Congenital Long QT Syndrome, but this should not be the leading diagnosis in the ED. Also those people are still at high risk for developing Polymorphic VT.

How did our patient do?

Her medications were reviewed and she was not on any of the most common offenders. Then routine labs came back. Unremarkable, except for K of 2.9! Repeat EKG after potassium repletion.

Normal EKG

EKG after K repletion

 

References:

  • www.uptodate.com
  • http://lifeinthefastlane.com/ecg-library/basics/qt_interval/
  • http://hqmeded-ecg.blogspot.com/2013/10/polymorphic-ventricular-tachycardia.html
  • bjsm.bmj.com/content/43/9/657/F3.large.jpgamp