Management of Peri-arrest Arrhythmias Presented: Dr Hesham Faisal, MD, MRCP, EDICConsultant Intensivist SFH-Dammam
Objectives• ECG and rhythm information interpretation within the context of total patient assessment• The concept of symptomatic &/or unstable• Basic ECG interpretation• Tachy-arrhythmias and Brady-arrhythmias• ECG strips
Symptomatic Bradycardia and Tachycardia• ACLS providers treatment decisions – Should not depend solely on rhythm interpretation and neglect clinical evaluation. – must evaluate the patient’s symptoms and clinical signs (ventilation, oxygenation, HR, BP, level of consciousness, and signs of inadequate organ perfusion) – Must define the cause of the patient’s instability in order to properly direct treatment.• unstable – vital organ function is acutely impaired or cardiac arrest is ongoing or imminent• Symptomatic – arrhythmia is causing symptoms (palpitations, lightheadedness, or dyspnea) – patient is stable and not in imminent danger
The Electrocardiogram• Relationship of the ECG to Electrical Events in the Heart – ECG Components • P Wave • QRS Complex • T Wave • U Wave
The Electrocardiogram– Refractory Periods • Absolute • Relative
Bradycardia• HR <60 beat/minute• Symptomatic bradycardia < 50 beat/minute• hypoxemia is a common cause of bradycardia• Assessment: – signs of increased work of breathing (tachypnea, intercostal retracions, suprasternal retracions, paradoxical abdominal breathing) – Hypoxemia as determined by pulse oximetry• Action: – provide supplementary oxygen. – Attach a monitor to the patient, – evaluate blood pressure – establish IV access. – If possible, obtain a 12-lead ECG to better define the rhythm.
Dysrhythmias Originating in the SA Node Rules of Interpretation Sinus BradycardiaRate Less than 60Rhythm RegularPacemaker Site SA nodeP Waves Upright & normalPRI NormalQRS Normal
Bradycardia• Signs & Symptoms of poor perfusion – Hypotension – acute altered mental status – ischemic chest discomfort, – acute heart failure, hypotension, or other signs of shock,• the patient should receive immediate treatment.
A first-degree AV block (generally benign) Rules of Interpretation First-Degree AV Block Depends on underlyingRate rhythmRhythm Usually regularPacemaker Site SA node or atrialP Waves NormalPRI > 0.20 SecondsQRS Usually < 0.12 seconds
Second Degree, Mobitz type I block, the block is at the AV node; the block is often transient and asymptomatic Rules of InterpretationMobitz Type I Second-Degree AV Block Atrial, normal; ventricular,Rate normal to slow Atrial, regular;Rhythm ventricular, irregularPacemaker Site SA node or arial Normal, some P waves notP Waves followed by QRS Increases until QRS isPRI dropped, then repeatsQRS Usually < 0.12 seconds
Second Degree Mobitz type II block block is usually below the AV node often symptomatic potential to progress to complete AVblock . Rules of InterpretationMobitz Type II Second-Degree AV Block Atrial, normal;Rate ventricular, slow May be regular orRhythm irregularPacemaker Site SA node or atrial Normal, some P waves notP Waves followed by QRS Constant for conductedPRI beats, may be > 0.21 secondsQRS Normal or > 0.12 seconds
Third Degree AV block AV node,bundle of His, or bundle branches Rules of Interpretation Third-Degree AV Block Atrial, normal;Rate ventricular, 40–60 Both atrial and ventricularRhythm are regular SA node and AVPacemaker Site junction or ventricle Normal,with noP Waves correlation to QRSPRI No relationship to QRSQRS 0.12 seconds or greater
Treatment of BradycardiaAtropine:• first-line drug for acute symptomatic bradycardia (Class IIa, LOE B)• Dose: 0.5 mg IV every 3 to 5 minutes to a maximum total dose of 3 mg• Use cautiously in the presence of acute coronary ischemia or MI• ineffective in cardiac transplant patient• Avoid in type II second-degree or third degree AV block with a new wide-QRS complex
Treatment of BradycardiaTranscutaneous pacing (TCP):• unstable patients who do not respond to atropine (Class IIa, LOE B)• patient should be prepared for transvenous pacing and expert consultation should be obtained.
Treatment of BradycardiaAlternative Drugs:• unresponsive for atropine• Temporizing measure awaiting TCP• overdose of a β blocker or Ca channel blocker.Dopamine• 2-10 mcg/kg/minute and titrate to patient responseEpinephrine• 2 -10 mcg/min and titrate to patient responseIsoproterenol• 2 to 10 mcg/min by IV infusion, titrated according to heart rate and
Tachycardia• Heart rate > 100 beats/minute• clinical significance ≥ 150 beats/minute• hypoxemia is a common cause of tachycardia,Assessment: – signs of increased work of breathing (tachypnea, intercostal retracions, suprasternal retracions, paradoxical abdominal breathing) – Hypoxemia as determined by pulse oximetryAction: – provide supplementary oxygen. – Attach a monitor to the patient, – evaluate blood pressure – establish IV access. – If possible, obtain a 12-lead ECG to better define the rhythm immediate cardioversion should not be delayed if the patient is unstable
Unstable tachycardiaEvaluate• unstable tachycardia• with severe signs and symptoms related to a suspected arrhythmia – acute altered mental status, – ischemic chest discomfort, – acute heart failure, – hypotension, or other signs of shockTreat:• Immediate Cardioversion• Selected cases of regular narrow complex tachycardia: Adenosine
Synchronized Cardioversion• establish IV access before cardioversion• sedation if the patient is conscious• shock delivery that is timed (synchronized) with the QRS complex• avoids shock delivery during the relative refractory period of the cardiac cycle when a shock could produce VF• recommended to treat 1. unstable atrial fibrillation →120 - 200 J 2. unstable SVT → 50 - 100 J 3. Unstable atrial flutter → 50 - 100 J 4. unstable monomorphic (regular) VT → 100 J.
The Electrocardiogram– Refractory Periods • Absolute • Relative
Stable tachycardiaEvaluate:• narrow-complex or wide-complex tachycardia• rhythm is regular or irregular• Wide complexes QRS morphology is – monomorphic – PolymorphicTreat:• Tailored accordingly
Narrow–QRS-complex (SVT) tachycardiasQRS< 0.12 second in order of frequency• Sinus tachycardia• Atrial fibrillation• Atrial flutter• AV nodal reentry• Accessory pathway–mediated tachycardia• Atrial tachycardia (including automatic and reentry• forms)• Multifocal atrial tachycardia (MAT)• Junctional tachycardia (rare in adults)
Sinus Tachycardia physiologic compensation rather than the cause of instability Rules of Interpretation Sinus TachycardiaRate >100 (220-age )Rhythm RegularPacemaker Site SA nodeP Waves Upright & normalPRI NormalQRS Normal
Supraventricular Tachycardia (Re-entry SVT) Rules of Interpretation Paroxysmal Supraventricular TachycardiaRate 150–250Rhythm RegularPacemaker Atrial (outside SA Node)Site Often buried inP Waves preceding T wavePRI Usually normalQRS Usually normal
Treatment of stable PSVTVagal Maneuvers• Valsalva maneuver or carotid sinus massage• preferred initial therapeutic choices for the termination of stable PSVT• may transiently slow the ventricular rate & assist rhythm diagnosisAdenosine (Class I, LOE B)• 6 mg rapid IV push followed by a 20 mL saline flush• 12 mg rapid IV push• Defibrillator should be available• Side effects: flushing, dyspnea & chest discomfort
Treatment of stable PSVTcalcium channel blockers (Class IIa, LOE B)• verapamil – 2.5 mg to 5 mg IV bolus over 2 minutes – repeated doses of 5 -10 mg q 15-30 minutes to a total dose of 20 mg – Contraindicated in impaired LV function or heart failure• Diltiazem – 15 -20 mg IV over 2 minutes – maintenance infusion dose is 5-15 mg/hourIV β-blockers (Class IIa, LOE C)• metoprolol,atenolol, propranolol, esmolol• used with caution in patients with COPD or CCF
Wide-Complex TachycardiaEvaluation1. Stable or unstable patient – Unstable → immediate cardioversion2. 12 lead ECG3. Regular or irregular a. Regular VT or SVT with aberrancy b. Irregular atrial fibrillation with aberrancy or polymorphic VT/torsades de pointes
Therapy for Regular stable Wide- Complex TachycardiasIV adenosine• safe for both treatment and diagnosis (Class IIb, LOE B).• should not be given for unstable or irregular or polymorphic widecomplex tachycardias• 6 mg rapid IV push → 12 mg → 12 mg• defibrillator should be availableStable likely VT• IV antiarrhythmic (procainamide, amiodarone or sotalol)• Or elective cardioversion
Dysrhythmias Originating in the Ventricles Rules of Interpretation Ventricular TachycardiaRate 100–250Rhythm Usually regularPacemaker Site Ventricle If present, notP Waves associated with QRSPRI NoneQRS >0.12 seconds, bizarre
Irregular TachycardiasIrregular narrow-complex or wide-complex tachycardia:1. atrial fibrillation (with or without aberrant conduction)2. MAT3. sinus rhythm/tachycardia with frequent atrial premature beats
AF Rules of Interpretation Atrial Fibrillation Atrial rate 350–50Rate Ventricular rate variesRhythm Irregularly irregularPacemaker Site Atrial (outside SA Node)P Waves None discerniblePRI NoneQRS Normal
Treatment of AFRate control• >48 hours are at increased risk for cardioembolic events• Avoid Electric or pharmacologic cardioversion unless the patient is unstable• IV β –blockers or calcium channel blockers such as diltiazem• Digoxin and amiodarone – Congestive heart failure• wide-complex irregular rhythm (AF with pre-excitation) – Avoid AV nodal blocking agents such as adenosine, calcium channel, β blockers, digoxin
MAT Rules of Interpretation Multifocal Atrial TachycardiaRate More than 100Rhythm IrregularPacemaker Site Ectopic sites in atria Organized, nonsinus PP Waves waves; at least 3 forms Varies depending onPRI source of impulseQRS Variable
PACs Rules of Interpretation Premature Atrial Contractions Depends on underlyingRate rhythm Usually regular exceptRhythm for the PACPacemaker Site Ectopic sites in atria Occurs earlier thanP Waves expected Varies dependent onPRI foci of impulseQRS Usually normal
Dysrhythmias Originating in the Atria Rules of Interpretation Atrial Flutter Atrial rate 250–350Rate Ventricular rate variesRhythm Usually regularPacemaker Site Atrial (outside SA node)P Waves F waves are presentPRI Usually normalQRS Usually normal
Dysrhythmias Originating in the Ventricles• Torsade de Pointes – Polymorphic VT. – Caused by the use of certain antidysrhythmic drugs. – Exacerbated by coadministration of antihistamines, azole antifungal agents and macrolide antibiotics, erythromycin, azithromycin, and clarithramycin.
Polymorphic (Irregular) VT torsades de pointes• requires immediate defibrillation with the same strategy used for VF – stop medications known to prolong the QT interval – Correct electrolyte imbalance• magnesium is commonly used – Polymorphic VT associated with familial long QT syndrome• isoproterenol or ventricular pacing – Polymorphic VT with bradycardia and drug-induced QT prolongation• IV amiodarone and β–blockers – myocardial ischemia induced Polymorphic VT
Dysrhythmias Originating in the Ventricles Rules of Interpretation Artificial Pacemaker Rhythm Varies withRate pacemaker May be regular orRhythm irregular Depends uponPacemaker Site electrode placement None produced byP Waves ventricular pacemakers; pacemaker spikePRI If present, variesQRS >0.12 seconds, bizarre
Dysrhythmias Resulting from Disorders of Conduction• Pre-excitation Syndromes – Excitation by an impulse that bypasses the AV node • Wolff-Parkinson- White Syndrome (WPW) – Short PRI and long QRS duration – Delta waves – Treat underlying rhythm.
ECG Changes Due to Electrolyte Abnormalities and Hypothermia• Hyperkalemia – Tall Ts • Suspect in patients with a history of renal failure.• Hypokalemia – Prominent U waves• Hypothermia – Osborn wave (“J” wave) – T wave inversion, sinus bradycardia, atrial fibrillation or flutter, AV blocks, PVCs, VF, asystole
Summary• The goal of therapy for bradycardia or tachycardia is to – rapidly identify and treat patients who are hemodynamically unstable or symptomatic due to the arrhythmia• Drugs or when appropriate, pacing may be used to control unstable or symptomatic bradycardia• Cardioversion or drugs or both may be used to control unstable or symptomatic tachycardia• ACLS providers – should closely monitor stable patients pending expert consultation and – should be prepared to aggressively treat those with evidence of decompensation