Episode 48 – Urine Drug Screen, Cocaine, and PCP

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

We review a post by Dr. Seth Trueger (@MDaware) on false positives of common medications in the urine drug screen.  We delve into posts by Dr. Bryan Hayes (@PharmERToxGuy) on false negatives for benzodiazepines and opioids in the urine drug screen.

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Core Content

We delve into core content on cocaine and phencyclidine (PCP) using Rosen’s (8th edition), Chapter 154 and Tintinalli (8th edition)

Cocaine

Cocaine
Cocaine

Note: Beta-blockers are contra-indicated in cocaine induced hypertension and chest pain.  Much of the ischemia induced by cocaine is thought to be due to vasospasm, predominantly from alpha-1 receptor effects.  Beta-blockers block the relaxation provided by beta-2 stimulus on muscles, leaving alpha-1 constricting vessels, “unopposed.”  This is largely theoretical/based on canine literature as there are only two human studies on this, (a) 10 humans given propranolol + cocaine with vasospasm and (b) 9 humans given labetalol + cocaine without vasospasm [4,5]. However, recent papers attempting to dispel this teaching don’t quite prove the point. One retrospective chart review looked at cocaine positive urine screens in patients with chest pain and found no worsened troponins. Cocaine stays positive in the urine for 3 days so it is not clear that these were patients presenting with cocaine associated chest pain [6].

Generously Donated Rosh Review Questions

  1. An 18-year-old man is brought to the ED by the police after being found running around a parking lot, screaming at bystanders. He reportedly smoked phencyclidine (PCP) earlier that day. His vital signs are notable for a heart rate of 130 beats per minute and a blood pressure of 150/86 mm Hg. On physical exam, he is diaphoretic, with vertical nystagmus and equal pupils and appears acutely agitated.

A. Administer haloperidol for acute agitation

B. Administer IV fluids for presumed rhabdomyolysis and benzodiazepines for agitation

C. Apply physical restraints; this is adequate treatment for most cases

D. Monitor for traumatic injuries; they are the most common cause of morbidity and mortality with PCP use

E. Urinary acidification to increase PCP elimination

Answer

The most common cause of morbidity and mortality in patients with phencyclidine (PCP) intoxication is rhabdomyolysis. Fluid hydration with normal saline is the initial therapy for rhabdomyolysis. Creatinine kinase (CK) should be obtained in patients with PCP intoxication. If abnormal, serial levels should be obtained until a downward trend is noted. Serum creatinine should also be monitored for evidence of renal insufficiency. PCP is a dissociative anesthetic drug that works on the NMDA glutamate receptor. People who abuse PCP can have sensations of euphoria initially, but this can be followed by an emergence reaction that is characterized by dysphoria and psychosis. If initial calming measures such as placing the patient in a calm environment fail and chemical restraints are needed, benzodiazepines are the treatment of choice. Benzodiazepines are also the preferred medication for acute agitation. Haloperidol (A) may cause dysrhythmias and hypotension. It also lowers the seizure threshold and may precipitate PCP-induced movement disorders. PCP is a weak base and its excretion is increased in acidic urine. Physical restraints (C) may be required for patients with PCP intoxication, but they should be used in conjunction with chemical restraints (preferably benzodiazepines). An agitated patient fighting against physical restraints is at risk for worsening rhabdomyolysis, which, if unrecognized, can precipitate cardiac arrest. Traumatic injuries (D)frequently occur in PCP-intoxicated patients; however, rhabdomyolysis with subsequent renal insufficiency is the most common cause of associated morbidity and mortality. Patients with PCP intoxication should be evaluated for suspected trauma, and any injuries should be stabilized and treated. Acidification of the urine (E) can cause a metabolic acidosis, which is potentially harmful and has not demonstrated improved outcomes. For these reasons, urinary acidification is not routinely recommended.

2. A 39-year-old woman presents with chest pain and difficulty breathing that began shortly after smoking crack cocaine. Vital signs are BP 190/85 mm Hg, HR 105, RR 18, T 99.1℉. The ECG demonstrates ST segment depression and T wave inversions in the lateral leads.

A. Diazepam

B. Metoprolol

C. Morphine

D. Phenylephrine

Answer

Diazepam, a benzodiazepine, should be administered to this patient who is hyperadrenergic from cocaine intoxication. Signs and symptoms of cocaine intoxication include, dilated pupils, diaphoresis, tachycardia, hypertension and hyperthermia. Many patients experience euphoria, though some will develop acute psychosis. Benzodiazepines decrease the cocaine-induced hyperadrenergic state. Reduction of sympathetic tone induces coronary and peripheral vasodilation. Coronary artery dilation directly improves myocardial blood flow. Peripheral vasodilation reduces preload and afterload. Reductions in preload and afterload decrease blood pressure and improve myocardial oxygen demand. Several factors, including, excess sympathetic stimulation, dehydration, hyperthermia, and cocaine-induced cardiac sodium channel blockade, may cause patients with cocaine intoxication to develop dysrhythmias. These contributing factors should be treated with benzodiazepines, IV fluid resuscitation and temperature management. In some patients, cocaine-induced cardiac sodium channel blockade may cause wide complex tachycardia that should be treated with sodium bicarbonate. Hyperthermia should be managed aggressively with a target temperature of less than or equal to 102.0℉. Severe agitation, aggression or psychosis should be initially managed with benzodiazepines. Most antipsychotic agents have pronounced anticholinergic side effects. This may worsen dysrhythmias.and decrease sweating, further complicating temperature management

  1. Rao R, Hoffman RS.  Cocaine and other Sympathomimetics. Rosen’s Emergency Medicine (8e). Chapter 154, 1999-2006.e2
  2. “Cocaine and Amphetamines.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (8e). Chapter 187
  3. “Prison Medicine.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (8e). Chapter 301
  4. Lange RA, Cigarroa RG, Flores ED, et al. Potentiation of cocaine, induced coronary vasoconstriction by beta adrenergic blockade. Ann Intern Med. 1990;112:897–90
  5. Boehrer JD, Moliterno DJ, Willard JE, Hillis LD, Lange RA. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med. 1993;94(6):608–610
  6. Ibrahim M, Maselli DJ, Hasan R, Hamilton A. Safety of β-blockers in the acute management of cocaine-associated chest pain. The American Journal of Emergency Medicine. 31(3):613-616.

 

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Episode 47 – Left Bundles and Implantable Cardiac Devices

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

We cover a post from Dr. Smith’s ECG blog investigating ways to read ischemia on a ventricular paced ECG.  In A Patient with Ischemic symptoms and a Biventricular Pacemaker, Dr. Smith asserts that the modified Sgarbossa criteria may work in ventricular paced rhythms as well as Left Bundle Branch Blocks (LBBB).

@FOAMpodcast
@FOAMpodcast

Core Content

We delve into core content on implantable cardiac devices using Rosen’s (8th edition), Chapter 80 and Tintinalli (8th edition)

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Generously Donated Rosh Review Questions

Question 1.  A 44-year-old man with an automatic implantable cardioverter-defibrillator (AICD) in place presents with weakness and palpitations. Vitals are HR 180, BP 83/53, RR 28. His ECG is shown below.  [polldaddy poll=9378494]

rosh reviewAnswer

Electrical cardioversion.  This patient presents with unstable ventricular tachycardia and should immediately be electrically cardioverted. AICDs are placed for a number of indications but the goal is the treatment of ventricular dysrhythmias, particularly ventricular tachycardia (VT) and ventricular fibrillation (VFib). All AICDs have a right ventricular lead that is used for sensing. During insertion, the cardiologist determines the parameters for the device to deliver a shock. Despite the presence of these devices, patients may still present in ventricular dysrhythmias that have not been shocked if the device is malfunctioning. Patients may also experience inappropriate shocks. Regardless of the presence of the device, if a patient presents in an unstable dysrhythmia,electrical cardioversion or defibrillation (depending on the circumstance) should still be performed. This patient presents with ventricular tachycardia and hypotension and device failure. It is recommended that if a shock is to be delivered in a patient with an AICD that the pads not be placed over the device site. Otherwise, the presence of a device is not a contraindication to external electrical cardioversion/defibrillation.
Amiodarone (A) and procainamide (D) are antidysrhythmic agents that can be used in the treatment of stable ventricular tachycardia. Placing a magnet over the AICD site (C) may be beneficial in treating patients who are receiving inappropriate shocks”

Question 2.  A 76-year-old woman presents to the Emergency Department with generalized weakness and fatigue. She had a pacemaker placed one month ago. [polldaddy poll=9378495]

rosh review

Answer

A. Failure to capture can range from complete absence of pacemaker activity to pacemaker spikes being seen but not resulting in depolarization of the myocardium. Complete absence of activity can be due to battery depletion, fracture of the pacemaker lead (which is uncommon with today’s technology) or disconnection of the lead from the generator. Intermittent failure to capture is commonly due to lead displacement and is most likely to happen within the first month of placement. Failure to pace can also be due to impaired endocardium, which despite an intact and normally functioning pacemaker, will not depolarize properly. Causes include ischemia or infarction, hyperkalemia or use of class III antiarrhythmic drugs. Overpacing (B) can occur when atrial flutter develops during dual chamber pacing. The pacemaker may sense the atrial flutter waves resulting in a rapidly paced ventricular rate. A “runaway pacemaker”, a pacemaker that causes extreme increases in pacing rates due to malfunction, is very unlikely with current pacemaker technology. In both of these cases, placing a magnet over the pacemaker will switch it from demand to fixed mode and may terminate the tachycardia. Oversensing (C) occurs when the pacemaker senses electrical activity that is not of cardiac origin and erroneously inhibits the generator. This may result in bradycardia. Undersensing (D) occurs when the pacemaker can not adequately sense the intrinsic electrical activity of the heart. If the pacemaker is in an inhibit mode, this can result in the pacemaker firing inappropriately.

References:

1. Sgarbossa EB, Pinski SL, Barbagelata et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. N Engl J Med. 1996 Feb 22;334(8):481

2.  Smith SW, Dodd KW, Henry TD et al. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med. 2012 Dec;60(6):766-76.

3.Cai Q, Mehta N, Sgarbossa EB, Pinski SL, Wagner GS, Califf RM, Barbagelata A. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: from falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? Am Heart J. 2013 Sep;166(3):409-13. doi: 10.1016/j.ahj.2013.03.032.

PlayPlay

Episode 47 – Left Bundles and Implantable Cardiac Devices

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

We cover a post from Dr. Smith’s ECG blog investigating ways to read ischemia on a ventricular paced ECG.  In A Patient with Ischemic symptoms and a Biventricular Pacemaker, Dr. Smith asserts that the modified Sgarbossa criteria may work in ventricular paced rhythms as well as Left Bundle Branch Blocks (LBBB).

@FOAMpodcast
@FOAMpodcast

Core Content

We delve into core content on implantable cardiac devices using Rosen’s (8th edition), Chapter 80 and Tintinalli (8th edition)

Screen Shot 2016-04-09 at 10.06.12 AM

Generously Donated Rosh Review Questions

Question 1.  A 44-year-old man with an automatic implantable cardioverter-defibrillator (AICD) in place presents with weakness and palpitations. Vitals are HR 180, BP 83/53, RR 28. His ECG is shown below.  [polldaddy poll=9378494]

rosh review

Question 2.  A 76-year-old woman presents to the Emergency Department with generalized weakness and fatigue. She had a pacemaker placed one month ago. [polldaddy poll=9378495]

rosh review

Answers

  1. Electrical cardioversion.  This patient presents with unstable ventricular tachycardia and should immediately be electrically cardioverted. AICDs are placed for a number of indications but the goal is the treatment of ventricular dysrhythmias, particularly ventricular tachycardia (VT) and ventricular fibrillation (VFib). All AICDs have a right ventricular lead that is used for sensing. During insertion, the cardiologist determines the parameters for the device to deliver a shock. Despite the presence of these devices, patients may still present in ventricular dysrhythmias that have not been shocked if the device is malfunctioning. Patients may also experience inappropriate shocks. Regardless of the presence of the device, if a patient presents in an unstable dysrhythmia,electrical cardioversion or defibrillation (depending on the circumstance) should still be performed. This patient presents with ventricular tachycardia and hypotension and device failure. It is recommended that if a shock is to be delivered in a patient with an AICD that the pads not be placed over the device site. Otherwise, the presence of a device is not a contraindication to external electrical cardioversion/defibrillation.
    Amiodarone (A) and procainamide (D) are antidysrhythmic agents that can be used in the treatment of stable ventricular tachycardia. Placing a magnet over the AICD site (C) may be beneficial in treating patients who are receiving inappropriate shocks.
  2. A. Failure to capture can range from complete absence of pacemaker activity to pacemaker spikes being seen but not resulting in depolarization of the myocardium. Complete absence of activity can be due to battery depletion, fracture of the pacemaker lead (which is uncommon with today’s technology) or disconnection of the lead from the generator. Intermittent failure to capture is commonly due to lead displacement and is most likely to happen within the first month of placement. Failure to pace can also be due to impaired endocardium, which despite an intact and normally functioning pacemaker, will not depolarize properly. Causes include ischemia or infarction, hyperkalemia or use of class III antiarrhythmic drugs. Overpacing (B) can occur when atrial flutter develops during dual chamber pacing. The pacemaker may sense the atrial flutter waves resulting in a rapidly paced ventricular rate. A “runaway pacemaker”, a pacemaker that causes extreme increases in pacing rates due to malfunction, is very unlikely with current pacemaker technology. In both of these cases, placing a magnet over the pacemaker will switch it from demand to fixed mode and may terminate the tachycardia. Oversensing (C) occurs when the pacemaker senses electrical activity that is not of cardiac origin and erroneously inhibits the generator. This may result in bradycardia. Undersensing (D) occurs when the pacemaker can not adequately sense the intrinsic electrical activity of the heart. If the pacemaker is in an inhibit mode, this can result in the pacemaker firing inappropriately.

References:

1. Sgarbossa EB, Pinski SL, Barbagelata et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. N Engl J Med. 1996 Feb 22;334(8):481

2.  Smith SW, Dodd KW, Henry TD et al. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med. 2012 Dec;60(6):766-76.

3.Cai Q, Mehta N, Sgarbossa EB, Pinski SL, Wagner GS, Califf RM, Barbagelata A. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: from falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? Am Heart J. 2013 Sep;166(3):409-13. doi: 10.1016/j.ahj.2013.03.032.

PlayPlay