Bradyarrhythmias: How SSSSSLOW is Too Slow?

Transcription

1 Bradyarrhythmias: How SSSSSLOW is Too Slow? Daniel H. Cooper, MD Assistant Professor, Division of Cardiology, Department of Medicine, Washington University School of Medicine Clinical Cardiac Electrophysiologist and Practicing Physician, Barnes-Jewish Hospital

2 MCE Conferences: Cardiology Review for Primary Care Medicine Bradyarrhythmias: How SSSSSlow is too slow? Daniel H. Cooper, M.D. Washington University School of Medicine July 5 th, 2014

3 Overview Anatomy of the cardiac conduction system Approach to bradycardia History and Physical Exam Diagnostic Evaluation ECG Analysis Management Role of Permanent Pacing Clinical syndromes associated with bradyarrhythmias

4 Bradyarrhythmias Commonly encountered rhythms in both inpatient and outpatient setting, resulting in ventricular rate < 60 bpm Common Questions: Our patient was found to have HR < 50 last night on telemetry What should we do? Does my patient need a pacemaker? Is my patient s pacemaker functioning properly?

5 Cardiac Conduction System Wolf, C. M. and Berul, C. I Molecular Genetics of Cardiac Arrhythmias. els.

6 Approach to Bradycardia Five S s approach to a SSSSSlow heart rate: STABLE: Is the patient hemodynamically unstable? SYMPTOMS: Does the patient have symptoms and do the symptoms correlate with the bradycardia? SHORT-TERM: Are the circumstances surrounding the arrhythmia reversible or transient? SOURCE: Where in the conduction system is the dysfunction? Has it been captured on ECG? SCHEDULE A PACEMAKER: Does the patient need a permanent pacemaker?

7 Causes of Bradycardia Intrinsic Congenital Disease Idiopathic Degeneration Infarction or ischemia Cardiomyopathy Infiltrative disease (sarcoid, amyloid, hemochromatosis) Collagen vascular diseases (SLE, RA, Scleroderma) Surgical Trauma Infectious Disease Extrinsic Autonomically-mediated Neurocardiogenic Syncope Carotid Sinus Hypersensitivity Increased vagal tone Drugs (BB, CCB, digoxin, antiarrhythmics) Hypothyroidism Hypothermia Neurologic Disease Electrolyte Imbalance (hyperkalemia, hypermagnesemia) Hypercarbia/Sleep Apnea Sepsis

8 History and Exam Broad range of symptoms: Asymptomatic Nonspecific (Lightheadeness, Fatigue, Weakness, Exercise intolerance) Overt (Syncope)

9 History and Exam Historical Points of Emphasis Temporal relationship Associated symptoms Precipitating circumstances History of fast rhythms Pertinent comorbidities THOROUGH review of ALL meds

10 History and Exam If bradycardia is ongoing, initial H and P should be truncated, focused on assessing hemodynamic stability Unstable ACLS Hypotension, confusion, decreased consciousness, cyanosis, etc. Stable More thorough examination Focused largely on CV exam and any findings consistent with pertinent comorbidities

11 Diagnostic Evaluation: ECG Cornerstone diagnostic tool in any arrhythmia work-up Rhythm Strips: Leads that provide best view of atrial activity (II, III, AVF, V1) Evidence of sinus node dysfunction (P wave intervals) Evidence of AV conduction abnormalities (PR interval, dropped beats) Evidence of either old or acute manifestations of ischemic heart disease

12 Diagnostic Evaluation Snapshot 12 lead ECG may not be sufficient to reveal arrhythmia Continuous Monitoring Exercise (treadmill) ECG Eval sinus node response to exertion (chronotropic incompetence) and look for exercise induced conduction block hour HOLTER Monitor If symptoms are frequent 30-day Event Recorder If symptoms are less frequent Implantable loop recorder (ILR) Rare, but significant events

13 ECG Analysis: Sinus Node Dysfunction Sinus Bradycardia Regular rhythm < 60 bpm QRS complexes preceded by sinus P waves Upright II, III, AVF; Biphasic V1 Young: common, well-tolerated, normal variant Elderly: higher resting HRs, less tolerant

14 ECG Analysis: Sinus Node Dysfunction Sinus Arrest or Sinus Pause Failure of sinus node to depolarize Period of atrial asystole (no P waves) Accompanied by either ventricular asystole or escape beats from junction or ventricle 2-3 Second Pauses Not uncommon in healthy, asymptomatic, sleeping adults > 3 Second Pauses If during daytime, awake hours raises concern for sinus node dysfunction

15 ECG Analysis: Sinus Node Dysfunction Sinus Exit Block Appropriate firing of SA node, with failure of impulse to exit the perinodal tissue Indistinguishable from sinus pause/arrest on ECG, except that the R-R interval will be a multiple of the preceding R-R

16 ECG Analysis: Sinus Node Dysfunction Tachy-Brady Syndrome Alternating tachy and brady arrhythmias, usually in setting of atrial fibrillation Rapid atrial rate during tachycardia suppresses sinus node output and results in sinus node dysfunction when tachyarrhythmia treminates

17 ECG Analysis: AV Conduction Disturbances Atrioventricular conduction can be Diverted (fascicular or bundle branch block) Delayed (first-degree AV block) Occasionally interrupted (second-degree AV block) Frequently, but not always, interrupted (advanced or high-degree AV block) Completely absent (Complete or third-degree AV block)

18 ECG Analysis: AV Conduction Disturbances 1 st Degree AV block AV conduction delay, PR >200ms Block is a misnomer

19 ECG Analysis: AV Conduction Disturbances Mobitz type I 2 nd degree AV block (Wenckebach) Progressive delay in AV conduction with successive atrial impulses until an impulse fails to conduct PR lengthens, RR shortens, Group beating Block is usually within the AV node and portends a more benign natural history

20 ECG Analysis: AV Conduction Disturbances Mobitz type II 2 nd degree AV block Abrupt AV conduction block without evidence of progressive conduction delay PR remains unchanged before and after dropped beat Natural history is more malignant, indicating more significant distal conduction disease and risk for progression to complete heart block

21 ECG Analysis: AV Conduction Disturbances 2 nd degree 2:1 AV block Difficult to classify given no consecutive PR intervals to measure Clues to a more benign (Mobitz 1), proximal process Concomitant 1 st degree AV block, narrow complex QRS Periodic Wenckebach Improved (1:1) conduction with higher sinus rates or exercise Clues to more distal block (Mobitz 2) Concomitant bundle branch block or fascicular block Conduction worsens at higher rates or with exertion

22 ECG Analysis: AV Conduction Disturbances 3rd Degree (Complete) AV block All atrial impulses fail to conduct to the ventricles AV dissociation

23 ECG Analysis: AV Conduction Disturbances Advanced or high-degree AV block More than 1 consecutive P wave fails to conduct to the ventricles However, there is evidence of AV conduction somewhere on the tracing to avoid the complete designation Mangram et al. NEJM 2000; 342: 703

24 Management Bradyarrhythmias that lead to significant symptoms or hemodynamic compromise are cardiovascular emergencies. Atropine 0.5 to 2.0 mg IV Proximal Disease Atropine responsive Symptomatic sinus bradycardia, 1 st degree AV block, Mob I 2 nd degree block Distal Disease NOT responsive and could be worsened by atropine

25 Management Identify reversible causes and withhold potential offending or exacerbating agents. Consider temporary pacing if unresponsive to pharmacologic interventions. Indications: Transient, symptomatic 2 nd or 3 rd degree AV block (electrolyte imbalance, drug overdose) CHB or 2 nd Degree Mob II AV Block in setting of acute MI Temporary transvenous pacing preferred Transcutaneous Pacing: less reliable, more discomfort

26 Management: Who gets a PPM? Once HD stability confirmed or established attention focuses on need for permanent pacing. If symptomatic 1) Consider reversibility of causative factors 2) Temporal relationship of symptoms and arrhythmia If asymptomatic 1) Is it reversible? 2) Does the conduction abnormality have a natural history that portends progression to higher degrees of heart block?

27 Permanent Pacing Points of Emphasis - Placement of anchored, intracardiac leads for purpose of maintaining adequate HR - Alleviate symptoms - Prevent collapse/syncope/death - Complications ~ 1-2% - Modern day PPMs try to more closely mimic normal physiologic pacing - Lower rate limit (LRL) determines lowest HR that will be allowed before pacing begins - Pacing Spikes: - Low amplitude - Sharp - LBBB QRS

28 Pacemaker Malfunction Categories of Pacemaker Malfunction: Failure to Pace Failure to Capture Undersensing Pacemaker-Mediated Tachycardia ***Disclaimer: PPM malfunction is rare if the device has been implanted for any amount of time.***

29 Pacemaker Malfunction If pacemaker malfunction is suspected 1) Start with 12 lead ECG telemetry is not good enough. 2) Try to talk yourself out of PPM malfunction odds are against you. 3) If no pacing output consistently seen when expected or if PMT suspected, consider placing a magnet over device. Magnet behavior for PPM = Switches to asynchronous pacing mode VVI VOO DDD DOO Magnet behavior for ICD = Turns off tachy therapies (Shocks, ATP) only 4) Formal Interrogation (Ask for card in wallet) 5) PA and Lateral CXR

30 Indications for PPM: SND Real-World Translation Patients with symptomatic sinus bradycardia in the absence of reversible causes are great candidates for pacemakers. If necessary medical therapy (i.e. BB in CAD) is causing symptomatic bradycardia, then a PPM should be offered to allow continuation of therapy. If during a syncope of unknown etiology workup, an EP study reveals evidence of significant SND, a PPM is reasonable. If symptoms are less clearly related to bradycardia, but the patient has rates <40 bpm while awake, a PPM is reasonable. If asymptomatic or if symptoms are demonstrated to occur clearly when patient is not bradycardic, then PPM is not indicated.

31 Indications for PPM: AV Block(I) Real-World Translation Patients with symptomatic advanced heart block (CHB or advanced 2 nd degree) are great candidates for pacemakers. Patients with advanced heart block (CHB or advanced 2 nd degree) who require medically necessary therapy that cause bradycardia are great candidates for pacemakers. If asymptomatic, but high risk features are present, then a PPM should be offered. SR + asystole > 3 s Escape rhythm < 40 bpm sub AV node escape AF + pause > 5s Escape >40 bpm but CHB and cardiomyopathy Don t forget the special cases. Neuromuscular disease + advanced heart block Post-op CHB not expected to recover Exercise-induced advanced heart block

32 Indications for PPM: AV Block(II) Real-World Translation It is reasonable to put a PPM in anyone with CHB, even if they don t have high risk features. Some patients with markedly prolonged PR intervals or second degree AV block develop symptoms similar to pacemaker syndrome PPM is reasonable for them. If asymptomatic, Mobitz II 2 nd degree block is present, then look at the QRS. Narrow = PPM is reasonable Wide = PPM should be performed (Class I) Due to unpredictable progression of AV block in patients with neuromuscular disease, one could consider PPM even with 1 st degree AVB. Do NOT put PPMs in patients with asymptomatic 1 st degree block, asymptomatic Mobitz I 2 nd degree AV block, or in patients with more advanced block that is expected to resolve.

33 Clinical Scenarios Which patient(s) should get a PPM with this presenting ECG? a. 18 y/o man while resting after school b. 45 y/o woman hospitalized night before gastric bypass surgery at 3 A.M. c. 45 y/o asymptomatic man with CAD while talking to family member d. 25 y/o woman with myotonic dystrophy and syncopal spells Mangram et al. NEJM 2000; 342: 703

34 Indications for PPM: Chronic Bifascicular Block Real-World Translation What is bifascicular block? ECG evidence of impaired conduction below the AV node in the right and some portion of the left bundle So, does LBBB (LAFB+LPFB) count without RBBB? Not really Bifascicular Block + Mobitz II or worse = PPM Alternating Bundle Branch Block = PPM Syncope + Bifascicular Block + Other causes excluded = Reasonable to offer PPM Any fascicular block + neuromuscular disease = could consider PPM

35 Indications for PPM: Syncope Real-World Translation Response to carotid sinus stimulation: Cardioinhibitory: Increased parasympathetic tone, resulting in slowing of sinus rate or development of prolonged PR or AV Block. Vasodepressor: Reduction in sympathetic tone, resulting in vasodilation and hypotension. PPM reasonable if exaggerated HR response > 3 s asystole If neurocardiogenic (reflex) syncope is associated with significant bradycardia, then PPM could be considered. No guarantee syncope will cease given vasodepressor component.

36 Acute MI Clinical Syndromes Infection and Bradycardia Increased Intracranial Pressure Drug Toxicity/Overdose

37 Acute Myocardial Infarction Bradyarrhythmias are common. Considerations to decide if bradyarrhythmia is self-limiting or irreversible: Which artery is involved? Extent of infarct Prior conduction disease Success of reperfusion

38 Acute Myocardial Infarction Inferior MI: Block typically at level of AV node Bezold-Jarisch Reflex: Heightened vagal tone during 1 st 24 hrs. Typically, responsive to atropine. Beyond 24 hrs, persistent or worsening block may occur. Less responsive to atropine. Methylxanthine may help. Typically, resolves within 1-2 weeks without PPM. Anterior MI: Site of block is typically infranodal. Due to ischemia and tissue necrosis. Typically, does NOT respond to atropine. More likely to persist and require PPM.

39 Infection and Bradycardia Endocarditis Careful monitoring for prolonged PR or heart block Suggests underlying or developing aortic root abscess Lyme Disease Tick-borne illness endemic to the Northeastern US Myocarditis, Conduction Block, LV failure AV block most common With treatment, typically resolves without need for PPM Chagas Disease Protozoan illness endemic to South America Cardiac involvement in 90% of cases Heart failure, ventricular arrhythmias, all degrees of AV block

40 Increased Intracranial Pressure Cushing s Triad/Reflex Bradycardia Hypertension Respiratory Depression Clinical Scenarios that could lead to intracranial hypertension Hepatic failure, CNS tumors, hydrocephalus, trauma Medical Emergency! Immediate treatment required to avoid catastrophic neurologic compromise

41 Drug Toxicity In all patients who present with significant, symptomatic bradyarrhythmias, drug toxicity should be considered.

42 Drug Toxicity: Digoxin Beware digoxin given narrow therapeutic window Elderly Renal Impairment New medications (i.e. amiodarone) Classic Bradyarrhythmia: Enhanced automaticity plus AV block Role of Digibind Can precipitate heart failure, severe hypokalemia. $$$$ Reserved for extreme situations >10 mg ingested Serum digoxin level > 10 ng/ml Life-threatening bradyarrhythmias

43 Drug Toxicity: Beta Blockers If suspected Atropine Glucagon IV Fluids If bradycardia and hypotension persist IV insulin/glucose Calcium Isoproterenol Vasopressors (norepinephrine or milrinone) Temporary transvenous pacing if necessary Role of hemodialysis Atenolol, acebutolol, nadolol, sotalol: May be useful Metoprolol, propranolol, timolol: not useful

44 Drug Toxicity: Calcium Channel Blockers If suspected Glucagon Calcium Temporary transvenous pacing if necessary Which CCB? Nondihydropyridines (verapamil and diltiazem) Severe bradycardia, pauses, high-grade AV block Beware long-acting formulations longer observation Dihydropyridines (amlodipine, nicardipine, nifedipine) Hypotension, reflex tachycardia

45 Summary SSSSSlow HD tolerance of bradycardia is 1st consideration and is variable. Multiple etiologies exist: Different likelihoods of reversibility, recurrence, and progression. Correlate symptoms to rhythm. Determine level of conduction disease. Be aware of syndromes that include bradyarrhythmias as a presenting sign/symptom. Indications are tedious but if you consider referring all patients with complete heart block and any symptomatic bradyarrhythmia you can t go wrong.

46 Comments/Questions