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Toxic Bradycardia and Hypotension

Toxic Bradycardia and Hypotension. Alyssa Reed, R1. Thanks to Dr Mark Yarema. CASE. It is 330 am when the paramedics patch to tell you they are on scene with a man who has a pulse of 45 and SBP of 80 What medical conditions could cause this?. Medical Causes of Bradycardia. MI

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Toxic Bradycardia and Hypotension

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  1. Toxic Bradycardia and Hypotension Alyssa Reed, R1 Thanks to Dr Mark Yarema

  2. CASE • It is 330 am when the paramedics patch to tell you they are on scene with a man who has a pulse of 45 and SBP of 80 • What medical conditions could cause this?

  3. Medical Causes of Bradycardia • MI • Sick Sinus Syndrome • Hyperkalemia • Hypothermia • Increased ICP • Vasovagal • Physiologic (athletes)

  4. CASE CONTINUED… • The patient arrives. Vitals are unchanged after 2L N/S and 2 mg of atropine. He is obtunded but breathing spontaneously. His wife says he has a history or atrial fibrillation, angina, hypertension and depression. The paramedics found a lot of pill bottles beside him and suspect an overdose. They left the bottles behind. • What medications cause bradycardia?

  5. TOXIC BRADYCARDIA • Beta Blockers • Calcium Channel Blockers • Cardiac glycosides (digoxin) • Cholinergic agents • Clonidine/Imidazolines (alpha2 agonists) • Opioids/Sedative Hypnotics • Phenylpropanolamine (alpha1 agonists) • Sodium channel blockers Can we eliminate any of these based on clinical presentation?

  6. TOXIC BRADYCARDIA • Beta Blockers • Calcium Channel Blockers • Cardiac glycosides (digoxin) • Cholinergic agents • Clonidine/Imidazolines (alpha2 agonists) • Opioids/Sedative Hypnotics • Phenylpropanolamine (alpha1 agonists) • Sodium channel blockers

  7. THE “BIG FOUR” • Beta Blockers • Calcium Channel Blockers • Cardiac Glycosides • Sodium Channel Blockers

  8. Introduction

  9. Maybe put in some physiology and table 17.11 page 393 of lilly

  10. CASE • 40M brought by EMS after an OD. Drug unknown. Pulse is 50 and SBP is 90. • Which of the four do you think is most likely responsible?

  11. Na Channel Blockers • Class IA Antiarrhythmics • Quinidine • Procainamide • Disopyramide • Class IC Antiarrhythmics • Flecainide • Propafenone • Cocaine • TCAs • Diltiazem/Verapamil • Propranolol • Carbamazepine

  12. Presentation • QRS widening • Hypotension • Seizures • Altered Mental Status • Membrane Stabilizing Activity • Decreased perfusion

  13. Management • Sodium Bicarbonate • 50ml = 50mEq = 1ampule • Indications • QRS > 100ms • Persistent hypotension despite adequate fluid resus • Dysrhythmias • Dosing • Bolus 3 amps • 3 amps in a bag of D5W and infuse and 2-3x maintenance • Hypertonic Saline

  14. CASE • A 55M is brought in by the paramedics with a pulse of 40 and SBP of 78. His BG is 18. He is AOx3. • He has a history of “heart problems” and no other medical history • K 4.0 • Which of the “big four” is likely responsible? (see next ECG to help eliminate)

  15. Put in ECG that is slow and narrow

  16. Calcium Channel Blockers • All block L-type calcium channels • Heart* • Contractile Tissue • Pacemaker cells • Vascular Smooth Muscle* • Endocrine (including beta pancreatic cells) • Retina • Skeletal muscle

  17. 1) Myocyte depolzn triggers opening of LTCC 2) Causes release of stored Ca from SR 3) Contract Put in a pic of the channels and depolarization

  18. Calcium Channel Blockers 2 Major Clasess • Dihydropyridines • Preferentially block L-type calcium channels in the vasculature • Potent vasodilators with little negative effect upon cardiac contractillity or conduction • Non-dihydropyridines • Preferentially block L-type calcium channels in the myocardium • Negative inotropic effects and decrease AV node conduction

  19. Q: Why is brady not listed as complication of the dihydropyridines?

  20. CCB OD Presentation • Hypotension • Bradydysrhythmias (or reflex tachycardia) • Normal mental status • Hyperglycemia • disruption of fatty acid metabolism creating relative insulin resistance and decreased release of insulin from β panc cells • Pulmonary Edema • Heart failure + vasodilation and extravasation • Ileus • Decreased smooth muscle function in bowel

  21. CCB OD Dx • No urine or serum test readily available • ECG • CXR • Lytes (including Ca, Mg) • Blood Glucose • ABG What are some of the ECG findings/rhythms in CCB OD?

  22. CCB OD and the ECG • Bradysrhythmias • AV block of all degrees • Sinus arrest • AV dissociation • Junctional rhythm • Asystole • Reflex Sinus Tach • Nifedipine OD

  23. OD General Approach • ABCs • GI Decontamination • Activated charcoal (50G in adult, 1g/kg in peds) • Gastric Lavage • Whole Bowel Irrigation (polyethylene glycol 2L/hr adults, 500cc/hr peds) • Enhanced Elimination • Hemodialysis • Antidotes • Supportive care

  24. CCB OD Mx • HYPOTENSION • Fluids • Calcium • Glucagon • Pressors • BRADYCARDIA • Atropine • Calcium • Glucagon • Pacer

  25. Atropine • Given routinely to symptomatic bradycardic patients • Often ineffective • Adults: 0.5-1 mg IV Q3min to a max of 3mg • Peds: 0.02mg/kg IV with a min dose of 0.1mg and a max of 1mg

  26. Calcium • CALCIUM CHLORIDE • 10% solution • 1g/10ml • 1g = 13.6 mEq • Central line • Dose: 1g over 10 min (10cc) Q15 to a max of 6 g and can infuse 1-2g/hr if responsive • CALCIUM GLUCONATE • 10% solution • 1g/10ml • 1g = 4.5 mEq • Peripheral line • Dose: 3g (30cc) over 10 min

  27. Glucagon • Increases intracellular levels of cAMP • Opens Ca channels • Animal models • increase in heart rate • Little effect on MAP • Bolus: 5mg over 1-2 min, to max of 15mg (this is diluted in 10cc N/S) • Maintenance: infusion of response dose mg/hr • Vomiting and aspiration risk • Phenol toxicity

  28. Glucagon Catecholamine pressors Glucagon Gs Amrinone ATP cAMP Phosphodiesterase AMP

  29. Pressors Q: What would be the ideal properties of a pressor in CCB tox? A: Direct-acting agent with +chronotropy, inotropy, and vasoconstrictive effects Q: What would you use? A: Norepinenphrine is initial choice Dopamine not because indirect effects and little alpha Can increase pulmonary edema and ischemic vascular dz and renal failure

  30. Insulin and Glucose • CJEM 2006 Prediger and Yarema • Systematic review of 13 papers • 20 cases of CCB OD (17 adult, 3 pediatric) • Most effective at treating hypotension (n=15) • 3 patients converted to sinus from AV block • Dosing and length of treatment varied widely • AE: asymptomatic hypoglycemia (n=8),hypokalemia (n=4) • Conclusion: HDIG is safe and effective treatment of CCB overdose

  31. Insulin and Glucose • The heart usually metabolizes free fatty acids but in shock state it needs glucose • In CCB OD cardiac glucose uptake is impaired b/c • Decreased insulin release (calcium mediated) • CCB toxicity induces a state of insulin resistance (myocardium and rest of body) • Acidosis and low perfusion limits glycolysis and carbohydrte delivery to the heart • Insulin acts as a pressor • Improved glucose delivery and uptake to the heart and improving cardiac performance

  32. Insulin and Glucose • Disrupt state of carbohydrate dependence and insulin resistance • Animal models • Improved survival with hyperinsulinemia/euglycemia compared to calcium, pressors and glucagon • Positive inotropic effects • Bolus: 0.1U/kg IV of regular insulin • Infusion: 0.2-0.5 U/kg/hr • Glucose: 25-50 g of dextrose at beginning or can infuse at 0.5 g/kg/hr

  33. Other Therapies • Phosphodiesterase Inhibitors • Amrinone , milrinone • Increase cAMP by preventing degradation of it by phosphodiesterase enzyme • May exacerbate hypotension • ICU setting with pulmonary artery catheter • Sodium Bicarbonate • Prolonged QRS or lactic acidosis • 1amp= 50mEq • Put 3 amps in 1L D5W and infuse and two times maintenance

  34. Invasive Mx • Transvenous pacing • Does not counteract negative inotropic effects • Successful capture may not correct hypotension • Intraaortic balloon pump • Cardiopulmonary bypass

  35. Summary • Block L-type channels • Vascular smooth muscle • Cardiac muscle cells and pacemaker cells • Hypotension, brady or tachy, preserved mental status, hyperglycemic • Mx • Early WBI • Fluids/atropine • Calcium • Glucagon • Pressors • Insulin and glucose

  36. CASE • 50F brought in by EMS. Patient is altered. T= 37, P= 50, RR= 12, SBP= 74, O2=90%RA, BG 3.5 • Hx of “heart problems” and hypertension • Which of the big four do you suspect?

  37. Beta Receptors Beta 1 • Primarily in the heart • Increase 1) heart rate, 2) contractility, and 3) AV conduction • Decrease AV node refractoriness Beta 2 • Primarily in bronchial and peripheral smooth muscle • Also in liver, uterus, heart • Vasodilation, bronchodilation, gluconeogenesis, glycogenolysis Beta 3 • Adipose tissue and heart • Thermogenesis

  38. Beta Blockers • Structurally resemble isoproterenol (pure β agonist) • Competitively inhibit endogenous catecholamines (ex. Epinephrine) at the B-receptor • These catecholamines normally bind to the receptor and result in activation of adenyl cyclase, resulting in cAMP • cAMP augments: • Inotropy (myocardial contraction) • Dromotropy (cardiac conduction) • Chronotropy (heart rate)

  39. How would you expect the patient to present?

  40. Clinical Presentation • Bradycardia • Hypotension • Unconsciousness • Respiratory arrest or insufficiency • Hypoglycemia (uncommon in adults) • Seizures (esp. propranolol) • Symptomatic Bronchospasm • VT or VF • Mild hyperK Rosen’s Table 150-8

  41. βB Properties • Membrane-Stabilizing Activity (MSA) • Inhibition of myocardial fast sodium channels • Can result in wide QRS and other dysrhythmias • Lipophilicity • High lipid solubility= rapidly cross BBB • Cause altered LOC (independent of hypoperfusion) • Intrinsic Sympathomimetic Activity (ISA) • Partial agonist effect at beta receptor site • Cause less bradycardia and hypotension • DO NOT completely protect

  42. Noncardioselective βB Rosen’s Table 150-3

  43. Cardioselective βB Rosen’s Table 150-3

  44. βB OD and the ECG • Increased PR from decreased conduction velocity down AV node • Bradycardia from decreased automaticity within SA node • Ventricular tachydysrhythmias with MSA βB • Wide QRS with MSA βB • QT prolongation with sotalol OD

  45. Which beta blocker might cause this dysrhythmia?

  46. βB OD Mx • HYPOTENSION • Fluids • Glucagon • Epinephrine • Isoproterenol • BRADYCARDIA* • Atropine • Glucagon • Pacemaker • Epinephrine • Isoproterenol * Only tx if third degree block or symptomatic

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