Dysrhythmias. Hyperkalemia & The ECG. Who develops hyperkalemia? 2/13/17. What we will discuss today. Hyperkalemia-related bradycardia

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1 Dysrhythmias What we will discuss today Hyperkalemia-related bradycardia Bradycardia & AV Block William J Brady, MD Professor of Emergency Medicine, University of Virginia wjbrady@virginia.edu Atrial fibrillation complex Wide Complex Tachycardia SVT with aberrant conduction Ventricular tachycardia Undifferentiated wide complex tachycardia Hyperkalemia & The ECG Who develops hyperkalemia? Elevated serum potassium Life- threatening dysrhythmias Mechanisms Slows impulse formation ectopic rhythms & bradycardia Disrupts conduction AV block & bundle branch block Irritates ventricular myocardium Malignant dysrhythmias asystole, VT, & VF Renal dysfunction Acute kidney injury Chronic renal failure End- stage renal disease on hemodialysis Renal tubular acidoses Nephrotic syndrome Heart failure (severe/chronic) Liver failure with cirrhosis (severe/chronic) Severe acidosis Rhabdomyolysis Salt substitutes Medications KCl Spironolactone ACE inhibitors Digoxin etc, etc, etc 1

2 Hyperkalemia & The ECG ECG Abnormalities Prominent T waves QRS complex widening Interval prolongation (PR & QT) Dysrhythmias Bradycardia / AV block Ventricular dysrhythmias Sinoventricular rhythm Hyperkalemia & The ECG In general wide & slow Prominent T Wave Peaking of T wave Tall, narrow, symmetric No J point elevation Best seen in precordial leads Widening of QRS Complex Disruption of conduction Widening - - broad range Minimal Maximal Slow to rapid rhythms Slow, more easily diagnosed Rapid, confused with VT Bundle branch block mimic 2

3 2/13/17 Widening of QRS Complex with bradycardia Sinoventricular Rhythm SA node- mediated Severe manifestation of hyperkalemia Rate: slow to normal & regular QRS complex: maximally widened Sine wave appearance More pronounced widening Sinoventricular Rhythm Comparison with Idioventricular Rhythm Sinoventricular rhythm Malignant Dysrhythmias Slow to normal rate Extremely widened QRS complex Mali gnan t(d Tach ysrhythm ycard ias Vent ricu ias lar+ta chyc ardi a Vent ricu la s thmia ysrhy ck nant(d (&(AV(Blo g li a s M cardia Brady Sinoventricular Rhythm Junc tiona l*bra dyca rdia Junc tiona l*bra dyca r+fibr illatio n rdia thm hy ular*r ntric Idiove thm *Block Heart Idioventricular Rhythm hy ular*r ntric Idiove Bradycardia, block, & ventricular dysrhythmia 3

4 Three Treatment Goals Stabilize cardiac cell membrane Transiently shift potassium into cells Remove potassium from body permanently Hyperkalemia Management Membrane Stabilization Calcium Intracellular Potassium Shift Bicarbonate Adrenergic agonists Glucose / insulin Magnesium Premanent Potassium Removal GI binding resins Loop diuretics Hemodialysis Hyperkalemia: ECG- Guided Management ECG Response to Therapy Suspicion for Hyperkalemia Cardiac Arrest Compromising Dysrhythmia Advanced Life Support & Membrane Stabilization / Cellular Shift Therapies Advanced Life Support & Stabilization / Shift / Removal Therapies 0918 over 15 minutes with appropriate therapy, normalization of ECG QRS Complex Widening Stabilization / Shift / Removal Therapies Sinoventricular Rhythm Prominent T Wave Stabilization / Removal Therapies Widened QRS Complex No ECG Abnormality Consider Stabilization / Removal Therapies Prominent T Wave Normalization 4

5 ETIOLOGY BRADYARRHYTHMIA Bradyarrhythmia Bradycardia & AV Block Primary Cause 20% Acute Coronary Syndrome 45% 90% STEMI 85% Inferior 15% Anterior Bradyarrhythmia Chronic Heart Disease 5% Secondary Cause 80% Toxicologic 20% Other 20% Shock Respiratory s/p ROSC Vasovagal Misc Bradycardia & AV Block Frequency of Occurrence AV Block Bradycardia Pathophysiology Primary & Secondary Disorders Primary disorders Defect within pacemaking / conduction system More common in elderly Secondary disorders ACS most common Inferior common, usually reversible, variable risk Anterior uncommon, not reversible, high risk Secondary disorders other causes Toxicology and many others 5

6 Bradycardia & AV Block Site of Block Bradycardia & AV Block Site of Block Sinus & Atrial Bradycardias, I AVB & II/Type 1 AVB Junctional Bradycardia Atrial AV Node Ventricular Bundle of His Atrial AV Node Ventricular Bundle of His Bradycardia & AV Block Site of Block Bradycardia & AV Block Response to Therapy Minimal autonomic innervation & reduced response to medical Rx Atrial AV Node Idioventricular Bradycardia, II / Type 2 AVB & III AVB Ventricular Bundle of His Rich autonomic innervation & increased response to medical Rx Atrial AV Node Ventricular Bundle of His 6

7 2/13/17 Bradycardias General Comments Bradycardias Sinus Bradycardia Sinus bradycardia SA node Normal variant in healthy, athletic individuals Most common compromising dysrhythmia Frequent in ACS, particularly inferior STEMI Junctional Rhythm Junctional bradycardia AV node Rarely normal variant Escape rhythm (first default) Idioventricular bradycardia ventricular conduction system or myocardium Escape rhythm (second default / final) AV Block General Comments Idioventricular Rhythm Atrial Fibrillation With Slow Response AV Blocks First Degree AVB First & second degree / type I AV block Rarely compromising Can be considered normal variants If new in compromising situations, can serve as potential warning of higher grade AV block Second Degree / Type I AVB Second degree / type II & third degree AV block Second Degree / Type II AVB Frequently compromising Always abnormal Third Degree AVB 7

8 Atropine AHA Bradycardia Algorithm Guidelines 2015 Parasympatholytic medication Enhances SAN automaticity Promotes AVN conduction Less influence on intraventricular conduction Initial intervention Dosing Adult: Initial mg with max 0.04 mg / kg Pediatric dose: 0.01 mg / kg Glucagon Atropine Use of atropine in unstable bradyarrhythmia More likely to respond to initial dose to higher dose, initial & cumulative to bradycardia than AV block Rare adverse event Stimulates camp synthesis Independent of beta receptor stimulation Positive chronotropic effects Use in atropine- resistant cases Impact may be TRANSIENT Most experience with toxicology Beta- & calcium channel blocker Data is limited, mainly in TOX literature 8

9 and anecdote! Bolus dosing Glucagon Adult: 2-5 mg over 1 minute Pediatric: 50 mcg/kg Peak effect within 5-7 minutes May repeat if no response in 10 minutes Additional doses unlikely to benefit Continuous infusion, if positive response Adult: 2-5 mg/hr Pediatric: 70 mcg/kg/hr Half- life 30 minutes Adverse effects: emesis & hyperglycemia Vasopressors Dopamine 2-10 mcg/kg/min Chronotropic effect via B- 1 stimulation More obvious at lower doses Also B- 2 & A- 1 Epinephrine 2-10 mcg/min Chronotropic effect via B- 1 stimulation More obvious at lower doses Also B- 2 & A- 1 Isoproterenol 1-4 mg/min Potent chronotropic effect via B- 1 stimulation B- 2 stimulation No alpha effect Cardiac Pacing Transcutaneous & Transvenous Temporary in nature Transcutaneous hours Transvenous hours to days Variables to adjust Energy delivery Pacing rate Determinations to make Electrical capture pacing spike with QRS complex Mechanical capture electrical beat with pulse 9

10 2/13/17 Electrical Capture Capture Pseudo- capture Mechanical Capture Pacer Spike ECG Artifact Paced QRS Complex Marker Palpable pulse corresponding to paced electrical beat No electrical capture Small complexes after spike are artifact pseudo- capture Partial electrical capture Ultimately, sustained perfusion corresponding to paced rhythm Complete (100%) electrical capture Vince DiGiulio Atrial Fibrillation #2 NCT seen in ED Variable heart history usually elderly Atrial Fibrillation with bundle branch block No P waves Varying R- R intervals Rapid rate with extremely rapid rates, irregularity is not apparent Pathophysiologic issues Rapid ventricular response No atrial contraction - - loss of atrial kick Thromboembolism 10

11 Atrial Fibrillation Diagnosis is usually straightforward But treatment plan is less easily determined Traditionally, treatment has focused on rate & rhythm control strategies Ignores the COMPLEX presentation in patient with critical illness which is quite common in the ED Complex Atrial Fibrillation Atrial fibrillation with rapid ventricular response Significant additional physiologic stressor simultaneously occurring Atrial fibrillation with RVR & critical illness Complex AF = AF with RVR + Significant Clinical Event Atrial Fibrillation Traditional Treatment Goals Goal #1 - determination of stability If unstable...electrical cardioversion If stable, consider goal #2 Goal #2 - rate control Gain control of the AV node Calcium channel / beta blocker / digoxin Goal #3 - rhythm conversion Medication Electrical Anticoagulation Atrial Fibrillation Contemporary Treatment Goals Goal #1 - determination of stability If unstable...determine cause of instability and treat accordingly Goal #2 - rate control Not always rate control agent Treat underlying event IVF, antibiotics, etc Goal #3 - rhythm conversion Not always needed Not always possible Not always correct 11

12 Complex Atrial Fibrillation Complex Atrial Fibrillation 416 patients with AF - - rate vs rhythm control & adverse event Adverse effect: 55/135 (41%) in rate/rhythm Rx vs 20/281 (7%) in non- rate/non- rhythm Rx Conclusions: In ED patients with complex atrial fibrillation, attempts at rate & rhythm control are associated with a nearly 6- fold higher adverse event rate than that for patients who are not managed with rate or rhythm control success rates of rate or rhythm control attempts appear low. Scheuermeyer FX et al, Ann EM 2015;;65:511 Strategy Adverse Event Rate Success Rate / Rhythm Control 41% 18% (#135) 19% rate 416 patients with AF - - rate vs rhythm control & 13% adverse rhythmevent Adverse Supportive effect: Therapy 55/135 (41%) in 7% rate/rhythm Rx vs NA 20/281 (7%) in (#281) non- rate/non- rhythm Rx Conclusions: In ED patients with complex atrial fibrillation, attempts at rate & rhythm control are associated with a nearly 6- fold higher adverse event rate than that for patients who are not managed with rate or rhythm control success rates of rate or rhythm control attempts appear low. Scheuermeyer FX et al, Ann EM 2015;;65:511 Complex Atrial Fibrillation In ED patients with complex atrial fibrillation attempts at rate & rhythm control are associated with a nearly 6- fold higher adverse event rate than that for patients 416 who patients are not with managed AF - - rate with vs rate rhythm or rhythm control control and & adverse event Adverse effect: 55/135 (41%) in rate/rhythm Rx vs 20/281 (7%) success in non- rate/non- rhythm rates of rate or rhythm Rx control attempts appear Conclusions: low. In ED patients with complex atrial fibrillation, attempts at rate & rhythm control are associated with a nearly 6- fold higher adverse event rate than that for patients who are not managed with rate or rhythm control success rates of rate or rhythm control attempts appear low. Scheuermeyer FX et al, Ann EM 2015;;65:511 Complex Atrial Fibrillation In this setting, consider AF with RVR as sinus tachycardia 416 patients with AF - - rate vs rhythm control & adverse event Adverse effect: 55/135 (41%) in rate/rhythm Rx vs 20/281 (7%) in non- rate/non- rhythm Rx & treat accordingly Conclusions: In ED patients with complex atrial fibrillation, attempts at rate & rhythm control are associated with a nearly 6- fold higher adverse event rate than that for patients who are not managed with rate or rhythm control success rates of rate or rhythm control attempts appear low. Scheuermeyer FX et al, Ann EM 2015;;65:511 12

13 Complex Atrial Fibrillation Common Scenarios Septic shock Hemorrhage with shock Alcohol withdrawal Sympathomimetic ingestion Acute respiratory failure Acute, chronic, or acute / chronic AF with compromising event & tachycardia Wide Complex Tachycardia VENTRICULAR TACHYCARDIA. ABERRANT SVT AVNRT ST w/ BBB WPW AFIB METABOLIC TOXIC. etc, etc, etc Afib with RVR & critical illness AFIB w/ BBB WPW AVRT Wide QRS Tachycardia in the ED Classically Reported Wide QRS Tachycardia in the ED In Reality VT 13

14 Wide QRS Tachycardia in the ED University of Virginia ED Experience SVT with Aberrancy Clinical Presentation Age Increasing age - - increasing incidence of VT Age > 50 favors VT Age < 50 favors SVT PMH Congenital Heart Disease with surgery favors SVT CAD / MI / CHF favors VT Symptoms largely not helpful Physical Examination Establishing rhythm diagnosis Not helpful Determining appropriate therapy Helpful Hemodynamic stability Not predictive of rhythm diagnosis Common incorrect belief Ventricular Rate Rate: SVT > VT VT: bpm - - ~170 bpm SVT: bpm - - ~180 bpm Overlap No value 14

15 2/13/17 Regularity VT - - usually very REGULAR AV Dissociation Ventricular focus produces WCT Continued SAN activity produces P waves VT Focus SVT - - regular & irregular PSVT & atrial flutter - - regular Atrial fibrillation & MAT irregular Limited value, when irregular Fusion & Capture Beats Less common Strongly favors VT P Waves Concordance - Positive & Negative Strongly Favors VT SAN- initiated impulse causes depolarization of ventricle Positive Concordance Partial fusion beat Complete capture beat Fusion beat Fusion of SV & V impulses Intermediate width QRS Capture beat Supraventricular impulse activates ventricles Results in narrow QRS Strongly favors VT Negative Concordance 15

16 Management 1. Known SVT with aberrant conduction 2. Known VT 3. Unknown WCT Management 1. Known SVT with aberrant conduction If unstable, consider electrical cardioversion AVNRT (PSVT) Vagal maneuver, adenosine, calcium / beta- blocker, electrical cardioversion with sedation Atrial fibrillation / atrial flutter Complex (treat cause) vs not (rate control) WPW Avoid AVN blockers (calcium / beta- blockers, amiodarone, adenosine) Procainamide electrical Management 2. Known VT If unstable, consider electrical cardioversion Amiodarone 150 mg IV / 5-10 minutes Procainamide 17 mg/kg over 45 minutes Magnesium 2 gm IV over 5-10 minutes Electrical cardioversion with sedation Management 3. Unknown WCT Exclude ST with BBB, metabolic, & toxic issues Treat underlying cause(s) If Afib, is it complex? Treat underlying cause(s) Remainder If unstable, consider electrical cardioversion Procainamide 17 mg/kg over 45 minutes Electrical cardioversion with sedation 16

17 So, the bottom line.. 1. Treat the patient & ECG, not just the ECG 2. Exclude sinus tachycardia with BBB, toxic, & metabolic issues 3. Remember that VT occurs in older patients with compromised left ventricles 4. If in doubt, assume VT & treat accordingly 17