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Slide 1

Paul A. Berger, III, D.O.FellowDivision of Pulmonary And Critical CareDepartment of Internal MedicineUniversity of Kansas Medical Center

Calcium Channel Blocker and Beta Blocker Overdose

“A Dab Will Do Ya”

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Slide 2

› No disclosures to report

Disclosures

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Slide 3

› Introduction

› Pathophysiology and Pharmacokinetics– Toxic Effects

› Review of Toxin Induced Cardiovascular Failure

› Differential and Work-Up

› Therapy Options– “Newer” and More Controversial Therapies

› Conclusion

› References

Objectives

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Slide 4

Why Is This Important To Us?

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Slide 5

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Slide 6

Introduction

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Slide 7

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Slide 8

› Increasing prevalence of cardiovascular disease

› Increasing use of cardiovascular medications

› Annual Report of the American Association of Poison Control Centers– 102,766 CV Medication Exposures

– CCBs most often implicated

› Identifying and treating patients with toxic effects is complex

› ABC’s and Resuscitative Protocols

› “Interesting” Therapies

Introduction

Clin Tox 2014; 52: 926-944EB Medicine 2014; 16(2)

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Slide 9

Pathophysiology and Pharmacokinetics

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Slide 10

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Slide 11

› Atomic number 20

› Alkaline earth metal

› Most abundant metal by mass in most animals

› Critical role in intracellular messaging and myocytecontraction

Calcium

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Slide 12

› Developed in the 1960’s

› Hypertension, cardiac dysrhythmias, and angina

› #1 cause of fatal CV medication exposures

› Three main classes– Dihydropyridines (Nifedipine)

– Phenylalkylamines (Verapamil)

– Benzothiazapines (Diltiazem)

Calcium Channel Blockers

Clin Tox 2014; 52: 926-944EB Medicine 2014; 16(2)

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Slide 13

› Affinity to L-type Calcium Channels– Dihydropyridines: Vascular smooth muscle

– Phenylalkylamines: Vascular and Cardiac

– In an OD situation receptor selectivity is lost

› Blocking of L-type Calcium Channels– Interferes with release of Ca from sarcoplasmic reticulum

– Interferes with formation of actin-myosin complex

– Decreases inotropy and chronotropy

– Smooth muscle relaxation


Emerg Med Clin N Am 2014; 32: 79-102Clin Tox 2014; 52: 926-944EB Medicine 2014; 16(2)

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Slide 14

› Well absorbed in gastrointestinal tract

› Metabolized via cytochrome system– Risk of drug/drug interactions

› Highly protein bound

› Large volume of distribution

› HD is not useful in OD situation



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Slide 15 Calcium Channel Blockers

Emerg Med Clin N Am 2014; 32: 79-102

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Slide 16

› Developed in the 1960’s

› Hypertension, CHF, thyrotoxicosis, angina, ACS, and essential tremor

› Two Beta Receptors of Importance– Beta-1: Cardiac myocytes

– Beta-2: Lungs and vascular smooth muscle

Beta Blockers


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Slide 17

› Beta-1– G coupled, cyclic-AMP receptors

– Calcium release from sarcoplasmic reticulum

– Increases inotropy and chronotropy

› Beta-2– Less well understood mechanism

– Smooth muscle relaxation

› Selective or Non-selective– Non-selective: Propranolol

– Selective: Metoprolol

Beta Blockers


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Slide 18

› Lipophilicity (Propranolol)– Increased CNS penetrance

– Increased risk of seizures (Therapeutic dosing)

– Decreased level of consciousness (Overdose)

› Membrane stabilizing activity (Propranolol or Acebutolol)– Sodium channel blockade / Cardiac fast channels

– QRS widening

– Increased risk of dysrhythmia

– Seizure activity and diminished consciousness

Beta Blockers


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Slide 19 Beta Blockers


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Slide 20 The Role Of Calcium In Myocardial Contraction

EB Medicine 2014; 16(2)

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Slide 21

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Slide 22 The Toxic Effects

› Calcium Channel Blockers– Inhibition of Calcium influx through L-type channels

– Inhibition of myocardial fast sodium channels

– Inhibition of insulin release from pancreatic islet cells› Hypoinsulinemia and Hyperglycemia

– Inhibition of glucose uptake in peripheral tissues

› Beta Blockers– Inhibition of beta receptors -> reduction in cAMP

– Inhibition of Calcium influx through L-type channels

– Inhibition of myocardial fast sodium channels

Clinical Tox 2011; 49: 277-283Emerg Med Clin N Am 2014; 32: 79-102Clin Tox 2014; 52: 926-944EB Medicine 2014; 16(2)

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Slide 23

› Calcium channel blockade triggers the heart to change metabolism– Carbohydrate metabolism (Stressed State)

– Free fatty acid oxidation (Non-Stressed State)

The Toxic Effects

Emerg Med Clin N Am 2014; 32: 79-102Clin Tox 2014; 52: 926-944

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Slide 24

› Profound vasodilation!!!

› Decreased systemic vascular resistance!!!

› Bradycardia!!!

› Conduction delays!!!

› Lactate accumulation!!!

› Metabolic acidosis!!!

› Altered mental status!!!

› Seizures!!!

The Toxic Effects

SHOCK!!!

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Slide 25

The FUN Stuff

Review of Toxin Induced Cardiovascular Failure

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Slide 27 Adverse Cardiovascular Events After Overdose


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Slide 28 Toxin Induced Cardiovascular Failure

The Flowchart of Death!!!


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Slide 29 Examples Of Shock And Physiology

Epocrates.com

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Slide 30 EKG Manifestations of CCB and BB Toxicity

› Normal Sinus Rhythm

› Sinus Tachycardia

› Sinus Bradycardia

› PR Prolongation

› Variable Atrioventricular Blocks

› Junctional Rhythms

› Bundle Branch Blocks

› QT ProlongationClinical Tox 2011; 49: 277-283Emerg Med Clin N Am 2014; 32: 79-102Clin Tox 2014; 52: 926-944EB Medicine 2014; 16(2)

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Slide 31 Effects of Toxic Ingestion


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Slide 32

Differential And Work-Up

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Slide 33

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Slide 34

› Short list with Bradycardia and Hypotension

› Acute Coronary Syndrome (Inferior MI with various blocks)

› Hyperkalemia

› Endocrine disorders (Hypothyroid)

› Hypothermia

› Poisoning– Clonidine

– Cholinergic toxicity

Differential Diagnosis


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Slide 35

› ABC’s

› IV Access

› EKG

› Review medications!!! (Regular vs Sustained Release)

› Laboratory studies (Blood / Urine)

› CT Head with altered mental status

› Consider the Blood Sugar Level

› Identify the “type” of shock if unstable

Clinical Work-Up

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Slide 36

› Variability of presentation depending on ingestion

› Verapamil and Diltiazem -> Bradycardia and Heart Blocks

› Nifedipine -> Hypotension +/- Reflex tachycardia

› Beta Blockers -> 1st degree heart block with QRS interval prolongation– High risk for ventricular dysrhythmia

Clinical Work-Up


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Slide 37

Therapeutic Options

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Slide 38

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›ABC’s!!!›TEAMWORK!!!› Consultation with Toxicologist / Poison Control Center

– Improved mortality

Initial Treatment

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Slide 40

› Prevention of absorption (Seems like a good idea)

› Caution

› Do not induce emesis

› Activated charcoal– Non-sustained product

– 1-2 hours post ingestion (no effect ~ 6 hours)

– 50% reduction at 2 hours from ingestion

– 25 – 100 grams + Sorbitol

GI Decontamination


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Slide 41

› Whole bowel irrigation– Sustained release medication

– Hemodynamically stable

– Polyethylene glycol 1500 – 2000 mL/h (until clear)

– Beware:› Prone to rapid decompensation

› Non-intubated aspiration risk

GI Decontamination


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Slide 42

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Slide 43 Insulin and Glucose

› Historical perspective

› Experimentation on treating verapamil poisoned canines

› Over 20 years ago

› Circulatory shock, acidosis, and mild hyperglycemia responded well with epinephrine and glucagon

› Tachyphylaxis and hemodynamic collapse with increased amounts of CCB

› Insulin infusion with slow and steady hemodynamic improvement– Sustained contractility and organ perfusion– Protection from increased doses of CCB


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Slide 44

› High-dose insulin euglycemic therapy has become the mainstay

› First line intervention

› Insulin supports the heart metabolically during shock states

› Metabolism changes from free fatty acids to glucose in stress states

› Insulin promotes carbohydrate metabolism– Increases glucose uptake by myocytes

– Increases lactate uptake providing secondary energy substrate

› 0.5 – 1U/kg of regular insulin, followed by infusion of 1U/kg/hr

› Consider ideal body weight

Insulin And Glucose


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Slide 45

› Insulin is titrated to achieve MAP goal

› Concurrent glucose administration followed by infusion– 25g Dextrose with initial insulin bolus

– 0.5g/kg/hr infusion

– Consider higher glucose concentration infusion

› Complications: Hypoglycemia and Hypokalemia

› Frequent glucose monitoring

Insulin and Glucose


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Slide 46

› Seems like a natural reversal agent

› Evidence is weak

› Dosage not well defined / no dose-effect relationship

› 10 – 20mL of 10% CaCl2 or 30 – 60mL 10% Calcium gluconate– Which provides more calcium?

› CaCl2 via central access, Calcium gluconate via peripheral

› CaCl2 syringe present in Accudose, Calcium gluconate usually delivered in IVPB

› Single dose?– Efficacy not well defined– Too much Ca2+ can be harmful

Calcium


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Slide 47

› Commonly used, variable success

› Not necessarily failure of treatment, too profound of toxicity

› Standard dosing may not be adequate– Push the limits

› No single agent has been shown to be superior

Vasopressors


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Slide 48 Vasopressors and Inotropes

www.aaemrsa.org

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Slide 49

› Studied since the 1960’s– Increased chronotropic and inotropic effects

› Produced by the pancreas, glucose homeostasis

› Increases cAMP– Decreased in CCB / BB OD

› Negative inotropic and chronotropic effects

› Bypasses normal catecholamine driven production of cAMP

› Early use may provide benefit

› 3 – 5mg over 1-2 min, repeat 4 – 10mg , maint 2 – 5mg/h

› Nausea / Vomiting

Glucagon


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Slide 50

› Used for the bradycardic and hypotensive patient

› Rarely effective in CCB or BB OD

› Studies provide limited evidence

› 0.5 – 1mg every 2 minutes, up to 3mg may be trialed

Atropine


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Slide 51

› Widened QRS– Indicative of sodium channel blockade

› If the QRS shortens, consider infusion

› Not routinely used for treatment of CCB / BB OD

Sodium Bicarbonate


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Slide 52

› Amrinone, Enoximone, Milrinone

› Prevent degradation of cAMP

› Possible efficacy with concomitant use with Glucagon

› Side effect: Hypotension– May not be a valued therapy option in already hypotensive patient

› Long half-life

Phosphodiesterase Inhibitors


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Slide 53

› Transvenous or Transthoracic

› Consideration for patient refractory to other therapies

› Goal HR ~ 50 – 60 bpm

› Efficacy is uncertain– While HR rises, inotropy does not necessarily rise

Pacing


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Slide 54

› Extracorporeal Membrane Oxygenation

› Itra-Aortic Balloon Pump

› No clear guidelines– ARDS Studies

› Few reports of good outcomes

› Refractory to all other therapies

ECMO / IABP


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Slide 55

› Both CCBs and BBs are highly protein bound

› Large volume of distribution

› Hemodialysis is not indicated and is not useful

› Unless…– Atenolol, Acebutolol, Nadolol, or Sotalol

– Unique hydrophilic properties

– Minimal protein binding

Hemodialysis


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Slide 56

The “Newer” and More Controversial Therapies

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Slide 57

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Slide 58

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Slide 59 Lipid Emulsion Therapy

› Use has increased dramatically in the management of CV instability in overdose of cardiotoxic medications

› Initially described for treatment of cardiovascular collapse related to local anesthetic toxicity

› Exact mechanism of action is not completely known– Enhances fatty acid transport across the mitochondrial membrane

improving cellular energy

– Increasing cardiac myocyte calcium levels -> increased inotropy

– New medium allowing for lipid soluble drug equilibration (pulling toxin from the tissue)

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Slide 60

› 20% Lipid Emulsion

› 1.5mL/kg bolus over 2 – 3min, followed by a 0.25mL/kg/min infusion

› A repeat bolus may be given for asystole or PEA

› Will interfere with certain laboratory testing

› Consider following Triglycerides

Lipid Emulsion Therapy

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Slide 61

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Slide 62 L-Carnitine

› Refractory shock despite maximal therapy

› 6g L-Carnitine IV, followed by 1g every 4 hours

› Theory– Reversal of free fatty acid metabolism from glucose in the myocytes

– Decreasing insulin resistance

– Increasing uptake and oxidation of free fatty acids

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Slide 63

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Slide 64 Methylene Blue

› Accumulation of cGMP in vascular smooth muscle results in vasodilation and decreased response to vasopressors

› Production of cGMP decreased through inhibition of nitric oxide synthase and guanylate cyclase

› 2mg/kg over 20min, followed by 1mg/kg/hr infusion

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Slide 65

All good things must come to an end!

Conclusion

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Slide 66

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Slide 67

› Do not allow yourself to be lulled into complacency

› Do the puzzle pieces fit together?

› Critical thinking is REQUIRED

› Not a time to be cavalier, to colleagues and families

› Not everyone will have a good outcome

› TEAMWORK!!! COMMUNICATION!!! DEDICATION TO THE DETAILS!!!

Conclusion

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Slide 68

› Abeysinghe N, Aston J, and Polouse S. Diltiazem overdose: a role for high dose insulin. 2010. Emerg Med J; 27(10).

› Aggarwal N, Kupfer Y, Seneviratne C, and Tessler S. Methylene blue reverses recalcitrant shock in B blocker and calcium channel blocker overdose. 2013. BMJ Case Reports.

› Bechtel LK, et al. 2008. Verapamil toxicity dysregulates the phosphatidylinositol 3-kinase pathway. Acad Emerg Med; 15: 368-374.

› Doepker B, Healy W, Cortez E, and Adkins EJ. 2013. High-dose insulin and intravenous lipid emulsion therapy for cardiogenic shock induced by intentional calcium-channel blocker and beta-blocker overdose: a case series. JournEmerg Med; 46(4): 486-490.

› Engebretsen KM, Kaczmarek KM, Morgan J, and Holger JS. 2011. High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning. Clinical Tox; 49: 277-283.

› Greene SL, Gawarammana I, Wood DM, Jones AL, and Dargan PI. 2007. Int Care Med; 33: 2019-2024.

› Jang DH, Nelson LS, and Hoffman RS. Methylene blue in the treatment of refractory shock from an amlodipine overdose. 2011. Ann Emer Med; 58(6).

› Jang DH, Nelson LS, and Hoffman RS. Methylene Blue for Distributive Shock: A potential new use of an old antidote. 2013. J Med Toxicol; 9: 242-249.

› Jang DH, Spyres MB, Fox L, and Manini AF. Toxin-Induced Cardiovascular Failure. 2014. Emerg Med Clin N Am; 32: 79-102.

References

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Slide 69

› Kline JA. Insulin for Calcium Channel Toxicity. 2014. Ann Emer Med; 63(1): 92-93.

› Louters LL, et al. 2010. Verapamil inhibits the Glucose Transport Activity of GLUT1. J Med Toxicol; 6: 100-105.

› Montiel V, Gougnard T, and Hantson P. 2011. Diltiazem poisoning treated with hyperinsulinemic euglycemia therapy and intravenous lipid emulsion. Euro J of Emerg Med; 18: 121-123.

› Nirav P, Pugh ME, Goldberg S, and Eiger G. Hyperinsulinemic Euglycemia Therapy for Verapamil Poisoning: A Review. 2007. Am J Crit Care; 16: 498-503.

› Palatnick W and Jelic T. 2014. Emergency Department Management of Calcium Channel Blocker, Beta Blocker, and Digoxin Toxicity. EB Medicine; 16(2).

› Rosser G, and Dubrey SW. Massive Calcium Channel Blocker Overdose: Intravenous Insulin and Glucose as Therapy. 2012. BMJ Case Reports.

› St Onge M, Ajmo I, Poirier D, and Laliberte M. L-Carnitine for the treatment of a calcium channel blocker and metformin poisoning. 2013. J Med Toxicol; 9: 266-269.

› St. Onge M, et al. Treatment for calcium channel blocker poisoning: A systematic review. Clin Tox 2014; 52: 926-944.

› Woodward C, Pourmand A, and Mazer-Amirshahi M. 2014. High dose insulin therapy, an evidence based approach to beta blocker/calcium channel blocker toxicity. DARU Jour Pharm Sciences; 22.

References

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Slide 70

Calcium Channel Blocker Overdose - AmlodipineCase Study #1

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Slide 71 Background

› 45 year old male - unemployed, divorced, 1 estranged son

› Medical/Surgical History: HTN, Pancreatitis, Testicular Cancer s/p Orchiectomy 1996 , Kidney Stones s/p stent placement, Depression, Drug/Alcohol Abuse

› Psych/Social History: 5 previous suicide attempts

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Slide 72 More background

› 8 previous ED visits over past 3 years

› 3 days prior to admission: First inpatient admission to hospital – Librium overdose

› Left AMA

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Slide 73 ARRIVAL

› Found down by mother, brought to ED via EMS

› Initial GCS: 5

› Initial VS: 35.0° C axillary, HR 114, RR 5-6, 99% on NRB, 115/70

› Required immediate intubation in ED

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Slide 74 Initial ED assessment

› GEN: GCS 5, responsive to noxious stimuli only

› HEENT: Pupils constricted but equal

› HEART: Tachy regular, no S3, S4, or murmurs

› LUNGS: Distant, otherwise CTA B/L,

› ABD: S/ND,

› EXT: Upper extremity tattoos present, warm, acyanotic, cap refill < 3

› NEURO: Unable to fully assess

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Slide 75 Labs on arrival

› Na: 143

› K: 3.4

› Ca: 3.6

› BUN: 8

› Creatinine: 1.00

› Mg: 1.3

› Phos: 3.5

› Lactate: 3.5

› Positive for alcohol/benzodiazepines

› ABG (post intubation):

› pH: 7.42/pCO2 42/pO2 189/Bicarb 27/Base Excess 2.0

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Slide 76 ED Course (~3 hours)

› Intubated upon arrival

› HR 110s/Normotensive

› Within 1 hour of arrival, profoundly hypotensive (60s-70s/40s) with HR 80s

› Sedation switched from Propofol/Fentanyl to Versed/Fentanyl and eventually stopped

› Overdose medications determined by pharmacy: Seroquel, Hydroxyzine and Amlodipine

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Slide 77 ED course continued

› EKG: No evidence of dysrhythmias or QT prolongation

› Given 3L NS bolus

› Norepinephrine initiated

› Calcium Gluconate

› Magnesium Sulfate

› Immediate transfer to MICU

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Slide 78 MICU Arrival @ ~2230

› Central Access obtained – R TL IJ

› Right radial arterial line placed

› Norepinephrine drip increased to maximum dose

› Vasopressin, Epinephrine, Phenylephrine and Dopamine drips initiated to maintain MAP>60mmHg

› Initial Insulin bolus of 83 units given (1unit/kg)

› ~0000: Insulin drip initiated at 35 units/hr, subsequent increases to 45units/hr, 68units/hr, 88units/hr, 110units/hr, 130units/hr to eventual rate of 166units/hr Q15 minute FSBS

› Several amps D50 administered

› Continuous D10 infusion

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Slide 79 MICU Arrival continued…

› 5mg Glucagon given IVP, followed by infusion at 5mg/hr

› Methylene Blue: 2mg/kg for 20 min, followed by 1mg/kg continuous infusion

› 1L NS Bolus x8.5 with NS infusion at 200mL/hr

› Banana Bag at 150mL/hr

› 1L LR Bolus followed by LR at 150mL/hr

› 0.45% Sodium Chloride + 100mEq Sodium Bicarbonate at 125mL/hr

› Hydrocortisone

› Cefipime, Vancomycin, Levaquin

› Q1 hour labs

› Q10-15 minutes FSBS

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Slide 80 Why did we administer these medications?

› High dose insulin: positive inotropic effects; increased intracellular glucose transport;

› Glucagon: increases heart rate and myocardial contractility, and improves atrioventricular conduction

› Methylene Blue: has several actions that may counteract the effect of increased nitric oxide synthase stimulation

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Slide 81 Electrolyte replacement

› 140 mEq KCl IV given over 7 hours; 80 mEq KCL given via OGT

› 1g Calcium Gluconate

› 1g Calcium Chloride

› 3g Magnesium Sulfate

› 16mmol Potassium Phosphate

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Slide 82 What exactly is going on?

› Severe metabolic acidosis

› Distributive shock

› Anuric Renal Failure

› Pulmonary edema secondary to shock resuscitation

› Development of severe ARDS

› Thrombocytopenia

› Multiple electrolyte abnormalities

› Possible septic shock with developing leukocytosis

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Slide 83 The next 12 hours…

› 1 unit PRBCs

› 4g magnesium sulfate, 70 mEq IV KCL, 30mmol Potassium Phosphate

› 2L LR Bolus

› 16 hours following admission: CRRT initiated – pt with PROFOUND hypotension (50s/20s)

› Insulin drip decreased to 41.5 units/hr

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Slide 84 Per MICU attending physician…

“The patient is profoundly ill. His physiology is secondary to a combination of issues including multiple mechanisms from his poly-ingestion and SIRS response with distributive shock. We

will continue aggressive supportive care, but he has shown very little progress throughout the day despite great efforts. Contwith multiple vasopressors, aggressive ventilator measures,

CRRT, electrolyte repletion, empiric antibiotics, blood product repletion and monitoring. Updated mother and other family

multiple times throughout the day. Very poor prognosis. ”

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Slide 85 24 hours later…

› Opened eyes to voice, began following simple commands

› Net + 28L fluid!!!

› Severe ARDS, paralyzed with Cisatracurium due to dyssynchrony with vent

› Only 2 pressors (Norepinephrine and Vasopressin)

› Elevated bladder pressures (highest 25)

› Shock Liver

› Insulin drip off, D50 q4hrs for hypoglycemia

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Slide 86 Nursing care the first 24 hours…

› 4-5 RNs first several hours

› 12-16 IV pumps running with continuous medications

› MULTIPLE titrations/rate changes/IV bag changes

› Q1 hr labs

› Q15 minute – q1hr FSBS

› Ventilator management

› Paralytic administered/titrated with train of four assessment

› CRRT initiation/management

› General nursing care/assessment

› Other medications

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Slide 87 Overall course

› 4 days later: Off all vasopressors

› 5th day: STAT urology consult due to significant penile/scrotal edema

› 8 days later: CRRT stopped

› 9th day: Extubated to nasal cannula (significant delirium/encephalopathy)

› AWAS monitoring

› 12 days later: transferred to floor

› 16th day: transferred to inpatient psychiatry

› 22 days later: Discharged home.

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Slide 88

Case StudyCCB Overdose- Verapimil

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Slide 89 Background

› 23 yo female presenting with CCB overdose

› AX: Nitro, Doxycycline, Tylenol, Biaxin, Citalopram, Etomidate, Geodon, Lamictal, Peanut.

› HX: depression, previous suicide attempts x4, anorexia nervosa, arthritis, multiple knee and shoulder surgeries, anemia, and sinus tachycardia.

› Prior to arrival pt hanging out with friend described by family as a bad influence.

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Slide 90 Arrival

› Discovered that pt had convinced a physician to prescribe her Verapamil, which she filled earlier that day and proceeded to ingest entire bottle.

› Taken to ED by friend when she began loosing consciousness.

› Pt started seizing in route and was actively seizing upon arrival to ED….The friend left the seen promptly.

› Pt intubated and given Ativan.

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Slide 91 Labs on Arrival

› Lactate 14.4

› ABG- pH 6.74, CO2 48, PaO2 94, HCO3- 6.5

› Glucose 483

› Cr 1.92

› K 4.7

› Anion gap 29

› Ca initially high and quickly dropped

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Slide 92 ED Adventure› Pt in 3rd degree block with HR ~20 and SBP ~60.

› Given calcium, activated charcoal, Epi, bolus of LR, Atropine, 20% lipid emulsion therapy, and high dose insulin therapy.

› Pt bolused with 70 units of insulin and started on gtt at 70u/hr.

› Intravenous pacemaker placed after external pacing failed.

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Slide 93 Some Rationale

Effects of CCB overdose:

› Hypotension from negative effects on inotropy, chronotropy, and peripheral vascular tone.

› Hyperglycemia from blocked release of insulin.

Effects of treatment:

› High dose insulin has inotropic effect.

› Fat emulsion creates lipid ‘sink.’

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Slide 94 Holy moly, now you’re my patient!

› Sooo…does anyone know how to treat CCB overdose?....

......anyone,…anyone…

…..Bueller?

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Slide 95 Arrival to Unit 65

› Pt arrived to the MICU from cath lab around 1430.

› Pt connected to intravenous pacer, although now tachycardiac.

› Insulin running at 280u/hr!

› Lipids infusing.

› Pt on Epi gtt. Tried to titrate off in cath lab, but were unsuccessful.

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Slide 96 Life in room 6502

› Pt’s BP becoming more unstable.

› In light of further BP instability pt was bolused 1L NS, given another small dose of lipids, methylene blue 1% (1mg/kg), 5mg glucagon, ….and started on 3 more pressors.

› NURSING NOTE: Learned that we needed to tell lab to spin off lipids before running results.

› Another 50ml of bicarb given for acidosis.

› Pt started on a D10 gtt once lipids infused.

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Slide 97 Overnight….

› Pt also now requiring large amounts of KCL replacement due to intracellular shifts….200mEq over the next 24hrs

› Overnight pt was weaned off one pressor, but then had to be restarted once she began waking up and needed sedation.

› Pt went through 47 bags of insulin in 24hrs and another 24 250ml bags over the next 24hrs.

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Slide 98 The next day…› Pt off all vasopressors.

› MANY electrolyte replacements

› D20 gtt started to maintain blood glucose > 100 with insulin therapy.

› Blood sugar checks q30mins.

› Insulin therapy titrated down by 10% q30mins as pt’s BP tolerated.

› Pt still had a severe metabolic acidosis.

› Pt had a lactate >2 for 4 days.

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Slide 99 Her Admission

› Insulin gtt titrated off after 72hrs.

› Pt’s K initially high after insulin stopped, but resolved on its own as AKI resolved.

› Pt extubated after 48hrs, floor status in 96hrs, and d/c’d after a 6 day admission.

› Pt developed a clot in R arm where cordis and pacer were. Pt dc’d on warfarin.

› Pt thought by psych to have a conversion disorder.

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and Beta Blocker Overdose N Calcium Channel Blockeraacngkcc.weebly.com/uploads/9/0/8/7/9087132/... · 3/5/2015 · WWhile HR rises, inotropy does not necessarily rise Pacing Clinical