Life Threatening EKG s In the Toxicology Patient

Transcription

1 Life Threatening EKG s In the Toxicology Patient Dean Olsen, DO Faculty, New York City Poison Control Center Director Emergency Medicine Residency Nassau University Medical Center Assistant Professor Pharmacology, Toxicology New York College of Osteopathic Medicine

2 Disclosure I have no financial or academic conflicts of interest.

3 Objectives Review 5 life threating arrythmias seen in poisoning Learn the characteristics that distinguish these from other common arrythmias encountered in the emergency department Learn the pathophysiology behind these arrythmias Develop a treatment plan based on current literature and/or mechanistic principals 3

4 Disclaimer There is very little literature to guide us RCT- none Case series- few Case reports- many- most bad! Animal studies- Few Much of this is based on theory, extrapolation and opinion 4

5 Concept: Resist the urge to shock these Arrythmias

6 Peri-mortem Gestures Lipid emulsion therapy Used for bupivacaine toxicity Lots of case reports and animal studies for other drugs Mechanism Lipid sink Free fatty acid substrate Increase viscosity Dose: 20% Lipid emulsion: 1.5 ml/kg then 0.25 ml/kg/min (may double) Methylene Blue Nitrate scavenger Causes vasoconstriction May increase blood pressure Dose: 1-2 mg/kg IV 6

7 Arrythmia 1 7

8 Case 1 27 Year old female BIBEMS agitated diaphoretic found on the street Witnesses report patient acting bizarre and agitated on street 8

9 Vital Signs Blood pressure 180/110 Heart rate 170 Respirations 36 Temperature Extremely agitated and diaphoretic 9

10 Emergency Department Course Cardiac monitor, oxygen, IV access and blood drawn Lorazepam 2mg IV EKG obtained 10

11 What is the cause? Patient admits to cocaine use prior to being picked up by EMS What is the treatment for this patients Arrhythmia? Sodium bicarbonate 1-2meq/kg bolus 11

12 Sodium Channel Blockade 12

13 Cocaine Cocaine induced wide complex tachycardia From sodium channel blockade (similar to TCA) Sinus tachycardia that s aberrantly conducted Usually associated with acidosis Does not respond to electricity 13

14 Cocaine Sodium Channel Blockade Treatment: 1. Sedation with benzodiazepines 2. Sodium bicarbonate 3. Lidocaine 4. Amiodarone? 5. Intralipid?? Avoid Type 1A antidysrhythmics Beta blockers Epinephrine

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16 Parker RB et al: Comparative effects of sodium bicarbonate and sodium chloride on reversing cocaine-induced changes in the electrocardiogram J Cardiovasc Pharmacol Dec;34(6):864-9 Dog model used Randomized to treatment of NS vs NaHCO3 HaHCO3 superior in reversal of arrhythmia Reversal of arrhythmia associated with reversal of acidosis 16

17 Literature review Highlights the data on using NaHCO3 above Lidocaine in the treatment of cocaine induced wide complex tachycardia 17

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19 Lange et al: Annals Internal Med, 1990 June 15; 112 (12) Randomized double blind placebo controlled study Patients administered cocaine on cath table Randomized to beta blocker vs placebo Statistically significant decrease in coronary artery diameter 19

20 Sodium Channel Blockade 20

21 Case 47 year old female took an overdose in a suicide attempt Patient arrives in the ED obtunded and has a witnessed generalized tonic-clonic seizure Vitals P 140 BP 90/60 R 12 T 99.3 Skin: dry Pupils: 6mm not reactive; absent bowel sounds 21

22 Case What is the most likely cause of this patients clinical condition? A. Cocaine B. TCA C. Digoxin D. Zoloft E. Anxiety The patients parents bring in an empty bottle of amitriptyline 22

23 Case The best initial treatment for this patent is? A. Procainamide B. Lidocaine C. Beta blocker D. Sodium bicarbonate 23

24 Case The patient receives NaHCO3 and the ECG improves ph 7.6 and ECG QRS widens to 155ms; Management? Lidocaine Procainamide Hypertonic saline Amiodarone

25 Case report of alkalemic patient with wide QRS that improved with hypertonic saline 7.7% NaCl IV bolus

26 Sodium Channel Blockers Common TCA Quinidine Propafenone Mexiletine Disopyramide Chloroquine Not So Common Procainamide Flecanide Uncommon Sedating H1 blockers Carbamazepine Cocaine Cyclobenzaprine 26

27 TCA 27

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31 Tricyclic Antidepressants Treatment Arrhythmia Does not respond to electricity Sodium bicarbonate 1-2 meq/kg IV bolus Hypertonic saline Lidocaine / amiodarone? Seizures Benzodiazepines Paralyze if needed Intubate / Hyperventilate ph

32 Tricyclic Antidepressants What not to do Procainamide Quinidine Dilantin Beta blockers 32

33 Arrythmia 2 33

34 Case 2 35 year old male s/p overdose HR 35 BP 50s systolic Normal mental status Skin cool, diaphoretic No purposeful movement EKG obtained 34

35 Case 2 Patient found in vicinity of open bottles of atenolol and verapamil 35

36 Beta and Calcium Channel Blockers 2 sets of problems that may or may not be inter-related Bradycardia Improved rate may not translate to improved perfusion Many patients tolerate rates in the 30 s Hypotension Is it rate or contractility? 36

37 Beta and Calcium Channel Blockers Hypotension associated with beta and calcium channel blockers Drug induced cardiogenic shock Ultimate problem is decrease in intracellular calcium Switching of metabolism of myocardium from fatty acids to glucose for fuel 37

38 BETA-BLOCKER β1 Agonist 1 receptor 5 AMP ATP Adenylate cyclase G s protein Ca ++ PDE c-amp protein kinase A L-type voltagesensitive calcium channels Ca ++ Ca ++ Actin-myosin complex Myocardial Cell Sarcoplasmic reticulum Ca ++ CALCIUM CHANNEL BLOCKER 38

39 5 AMP ATP glucagon Adenylate cyclase 1 receptor G s protein catecholamines Calcium channel Ca ++ Ca ++ PDE Ca ++ c-amp protein kinase A Ca ++ Ca ++ Sarcoplasmic reticulum Ca ++ Ca ++ amrinone Actin-myosin complex High dose insulin and glucose Ca ++ 39

40 Beta and Calcium Channel Blockers Treatment 1. Vasopressors 2. Calcium 3. Glucagon 4. High dose insulin therapy 5. Amrinone 6. Intralipid Therapy 7. Bypass, ECHMO or IABP 40

41 Euglycemic Insulin Therapy Rational Myocardial cells normally use primarily fatty acids for metabolism Calcium channel blockers cause myocardial cells to become carbohydrate dependent At the same time CCB s also inhibit the ability of myocardial cells to use these carbohydrates by inhibiting insulin release and increasing myocardial resistance to insulin Decrease substrate delivery to myocardium through decreased blood flow further worsens contractility 41

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43 Euglycemic Insulin Therapy Dose 1u/kg bolus Higher doses may be of benefit 43

44 Euglycemic Insulin Therapy 1u/kg/h infusion Dextrose infusion to keep serum glucose normal Titrate drip as high as possible with keeping serum glucose normal 44

45 Arrythmia 3 45

46 Case 3 16 year old male presents with history of taking grandmothers heart medication in suicide attempt Presents with alteration in color perception confusion and vomiting Intubated for agitation and confusion HR 45 regular BP 120/70 ECG 46

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48 Case 3 Over the next 30 minutes the patient began to have multiform PVCs that degenerate to ventricular fibrillation No response to defib x 3 Diagnosis and treatment? A. Calcium channel blocker OD; give pressors B. ACE inhibitor OD; standard ACLS C. Diuretic OD; give fluids and ACLS D. Digoxin OD; give Digibind 48

49 Cardiac Glycosides Prior to Digibind survival following cardiac arrest was almost 0 (Bismuth) 49

50 In the multi-center study of Digibind survival for cardiac arrest patients was 54% Most other causes result in 10% or less The most treatable cause of arrest?? 50

51 Na-Ca Exchanger Na-K ATPase 3Na + 2K + K + Voltage sensitive potassium channel Ca ++ 3Na + Na + Voltage sensitive sodium channel Ca ++ Ca ++ Sarcoplasmic reticulum Actin-myosin complex Myocardial Repolarization L-type voltagesensitive calcium channel 51

52 Na-Ca Exchanger 3Na + Na-K ATPase 2K + K + Cardiac Glycosides Voltage sensitive potassium channel Ca ++ 3Na + Na + Voltage sensitive sodium channel Ca ++ Ca ++ Sarcoplasmic reticulum Actin-myosin complex Myocardial Repolarization L-type voltagesensitive calcium channel 52

53 Na-Ca Exchanger 3Na + Na-K ATPase 2K + K + Cardiac Glycosides Voltage sensitive potassium channel Ca ++ 3Na + Na + Ca ++ Voltage sensitive sodium channel Ca ++ Sarcoplasmic reticulum Actin-myosin complex Myocardial Repolarization L-type voltagesensitive calcium channel 53

54 Na-Ca Exchanger K+ K+ K+ Na-K ATPase K+ K+ Increased extracellular K+ K+ K+ Ca ++ Actin-myosin complex Ca++ Ca++ Sarcoplasmic Reticulum Ca++ Ca++ Ca++ Ca++ Ca++ K+ More Ca++ Available for contraction 54

55 Cardiac Glycosides Additional Therapeutic Effects Increased vagal tone Decreased SA node firing Decreased AV node conduction 55

56 Toxic Effects Vagal stimulation sinus bradycardia/arrest, PR prolongation, nodal blocks Increased intracellular Ca++ automaticity Increased resting membrane potential Increased delayed after-depolarization's Overall Slowing of normal conduction Increased atrial, AV node, and ventricular ectopy 56

57 Effect Of Digitalis OD On Resting Membrane Potential Phase 1 0mv Phase 2 Depolarization Threshold -65mv Phase 0 Phase 3-90mv Resting Membrane Potential Digitalis OD Myocardial Cell Action Potential Phase 4 57

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59 Digoxin immune Fab Treatment Digibind Antibody to digitalis DO NOT PACE THESE PATIENTS!!! Recommended dose : 20 vials in cardiac arrest Equimolar neutralization is goal (not based on weight) More may not be better Not enough is bad Case reports of patients responding to Digibind post cardiac arrest 59

60 Electricity Digoxin toxicity decreases fibrillation threshold Normal digoxin levels do not appear to do this Consider Digibind or antidysrhythmic before cardioversion 60

61 Arrythmia 4 ame ent rate e 00 PC 5 urations Acct P OB 3 y ear s Mal e S Othe r ech 5 5 m 00 nterv als Sub ectiv e Sy mptom Other specif ied sy mptoms and P si ns inv olv in the O circulatory P O S AC a Contact Pa er 00 5 Conf irmin M c 0 Order M Med Med d A es P ept C nst u ealt h S 3 ate 0 0 ime Speed 5 mm s imb ead ain 0 0 mm m Chest ead ain 0 0 mm m ilters s otch 0 Artif act 00 Stable Of f a a 5 a 3 CO M 5 3 c od es Pa e of

62 Case A 31-year-old male with a history of opioid abuse was brought to the ED after being unresponsive at home Naloxone was given in route HR 103, R 24, BP 140/101, T 37.1 Pt is diaphoretic in the ED

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64 Loperamide (Imodium) Devoid of opioid effects at therapeutic doses (<16mg/day) When taken in large does can cause opioid effects Used to treat withdrawal Used as an agent of abuse in absence of opioids Sodium channel blockade Potassium channel blockade

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67 After some a CO3 and M

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69 Loperamide Treatment Probably will not respond to electricity Naloxone for respiratory depression Sodium bicarbonate Magnesium for qt prolongation

70 Arrythmia 5

71 Case A 55 year old male presents with oral numbness and chest pain after ingesting a plant he thought was ground elder from a private garden about 45 minutes prior The patient goes in to cardiac arrest shortly after arrival and is defibrated

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73 Case His wife arrives with the plant Aconitum napellus Monkshood Aconite Wolf's bane Devils helmet

74 Aconite Sodium Channel activation Myocardium Nerve Delayed after-depolarization Early after-depolarization Prolonged sodium influx Wide complex dysrhythmias with ectopy

75 Aconite Treatment Does not respond to electricity Amiodarone Flecainide Lidocane Procainamide

76 Summary Wide complex tachycardia without ectopy in poisoned patient Think sodium channel blockade Cocaine TCA Sedating H1 blockers Loperamide (Imodium) Treatment NaHCO3 Hypertonic saline Amiodarone? Wide complex tachycardia with ectopy Sodium channel opener Aconite Treatment Class 1 antidysrhythmics

77 Summary Bradycardia with blocks and hypotension Calcium channel blocker or beta blocker Treatment Insulin Ca+ Glucagon Inotropic agents Bradycardia with or without ectopy with normal or high BP Digoxin Plant cardioactive steroid Treatment Digabind on t pace

78 Questions? 78