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V1 monophasic R wave / biphasic (qR or RS) / triphasic with R > R
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- Premature atrial beat (PAB)
V1 monophasic R wave / biphasic (qR or RS) / triphasic with R > RV6 R/S ratio < 1 Common causes of BBBClinically normal individual Lenegre’s disease (idiopathic fibrosis of the conduction tissue) Lev’s disease (calcification of the cardiac skeleton) Cardiomyopathy Dilated, Hypertrophic (concentric or asymmetric) Infiltrative Tumor, Chagas’ disease, Myxedema, Amyloidosis Ischemic heart disease MI (acute/old), CAD Aortic Stenosis (AS) Infective endocarditis Cardiac trauma Hyperkalemia Ventricular hypertrophy Rapid heart rates Massive PE Hemiblocks Watch for intermittent change in QRS axis and/or pattern ½ of LAD infarctions cause ant. hemiblock (also can get RBBB)
QRS usu. 0.1 to 0.12 Q1S3 LAD from late depolarization (r/o inferior MI, LVH, horizontal heart) Posterior hemiblock RAD (r/o lateral MI, RVH, lung disease) Normal or wide QRS S1Q3 Other slow (or no) rhythms Asystole PEA (pulseless electrical activity – many causes) SSS (sick sinus syndrome) BTS (SSS with intermittent tachycardia) Normal Atrial foci 60-80 Junctional foci 40-60 Ventricular foci 20-40
Atrial flutter 250-350 Atrial fibrillation 350-450
Ventricular flutter – rapidly becomes V fib Ventricular parasystole – simultaneous pacing of A and V Types of Tachycardias Regular narrow complex Sinus, atrial, AV-reentrant, WPW, atrial flutter, junctional tachycardia Irregular narrow complex Atrial fibrillation, multifocal atrial tachycardia, atrial flutter with variable block Wide complex QRS > 0.12 with normal conduction or > 0.14 with RBB or > 0.16 with LBB Ventricular tachycardia (VT), Torsades de Pointes (drugs that cause), supraventricular (SVT) with aberrant conduction, hyperkalemia, TCA toxicity Note: hyperkalemia can cause complete AV block even without widened QRS Diagnosis and Treatment Synchronized countershock Vagal maneuvers Adenosine P1 receptors in AV node / given as 6 then 12 mg IV / chest discomfort, transient hypotension / may terminate reentrant tachycardia / SVT may stop then recur / preexcitation tachycardia should not be affected AV nodal agents
1 mg/kg bolus, 1-4 mg/min / SE: confusion, seizures Magnesium torsades (especially drug-induced) / 1 g MgSO4 given IV Calcium membrane stabilization Atrial Arrhythmias Atrial Tachycardias (follow links for specifics) Sinus tachycardia Sinus node re-entry Atrial tachycardia Unifocal / Multifocal Atrial flutter Atrial fibrillation AV Junctional Tachycardia AV re-entry (WPW) orthodromic / antidromic
epinephrine caffeine, amphetamines, cocaine, other B1 agonists
low O2 (to some extent) Atrioventricular Relationship atrioventricular dissociation sinus capture beats fusion beats Regular atrial arrhythmias sinus tachyarrhythmia paroxysmal atrial tachycardia (PAT) (see other) atrial flutter with constant conduction (see other) Supraventricular Tachycardia (SVT) Tachyarrhythmia originating above ventricle (includes PAT, AT, JT, etc.) may have widened QRS (resembling PVT) – BBB or aberrancy can try vagal maneuvers 1st, then meds // Note: do not attempt carotid massage if there is a bruit!!! Brugada’s Criteria (VT versus SVT with aberrancy) absence of RS complex in all precordial leads? interval from R to nadir of S > 100 msec in any precordial lead? AV dissociation? Are there morphology criteria for VT in both V1 & V6? (suggesting BBB) If yes to any → VT If no to all → SVT w/ aberrancy Premature atrial beat (PAB)P1 looks different / can merge with T-wave SA pacing will be reset to P1 Non-conducted PAB may resemble 3rd degree heart block
PAT with block is typical for digitalis toxicity Note: Must have AV blocking when controlling SVT’s / do not use only a single class IC agent (e.g. flecainide) to control an atrial tachycardia because you might convert a 240 (A) 120 (V) to a 200/200
5% over 60 yrs / 10-15% over 80 yrs Causes: mitral valve disease, thyrotoxicosis, HTN, CAD, MI, pulmonary embolism, pericarditis / stress, fever, excessive alcohol intake, volume depletion, idiopathic Prognosis: 60% of new onset AF convert spontaneously within 24 hrs / atrium greater than 4.5 cm and long duration of Afib are more likely to have chronic/relapsing AF Work-up: TSH, consider PE w/u, more… Treatment: Control ventricular response Rate control: Digoxin, B-blockers, Amiodarone vs. His ablation and pacemaker B-blockers reduce relapse (60% 40%) and when they do relapse, the HR will be lower (may also increase chance of conversion) Digoxin – good for rate control (not conversion) / peak action at 90 mins Ca channel blockers (verapamil, diltiazem) – for rate control (not conversion) Cardioversion - immediate DC conversion if hemodynamically unstable AFFIRM trial suggest no need to cardiovert most patients with chronic Afib; benefit may be seen more with younger, healthier women as well as patients whose heart failure is so severe that NSR would be of major benefit; some studies (PIAF/STAF/RACE) show that rhythm control may actually have worse outcome for elderly, CAD or non-CHF patients / for CHF patients, sometimes amiodarone is the best option (in spite of many side effects) [NEJM] AF present > 48 hrs or unknown duration Plan 1: 10 days (some say 21) anticoagulation therapy cardioversion 4 weeks post-anticoagulation Plan 2: if no thrombus seen on TEE (85% of cases) cardioversion 24-48 hrs later 4 weeks post-anticoagulation [plan 2 has higher initial success rate and lower bleeding events due to shorter duration of anticoagulation, but chance of long-term NSR is same] Spontaneous cardioversion (50% within 24 hrs) Direct current (DC) conversion – success rate 90%, low rate of ventricular arrhythmia, premedication before DV conversion has no effect on short term maintenance of NSR Chemical Cardioversion – variable success (ventricular arrhythmia rate 0-10%) Class III/Ia are more dangerous for hypertrophied hearts (prolonged QT and torsades) Class I are more dangerous for functionally (ischemic) and anatomically (fibrosis, infiltration) challenged hearts (ventricular tachyarrhythmias) Examples of efficacy: amiodarone (30%/1 hr, 80%/24 hrs), procainamide (65%/1 hr), quinidine (?), propafenone (90%/1hr), digoxin (50%/1 hr) If thrombus present (15% of cases): LA appendage > LA cavity (6:1) / 80% will resolve on repeat TEE within 2 months of anticoagulation Anticoagulation: heparin in short term then coumadin long-term; by 2003, Lovenox still not officially recommended; older patients with chronic or paroxysmal AF without contraindications should receive long-term warfarin (INR 2 to 3). ASA 325 mg/day (20% risk reduction) Risk of stroke: increased with diabetes, > 65 yrs, HTN, CHF, rheumatic heart disease, prior CVA or TIA, TEE showing spontaneous echo contrast in LA, left atrial atheroma, left atrial appendage velocity < 20 cm/s Investigational: focal atrial ablation, atrial pacing/defibrillators Download 3.95 Mb. Share with your friends:
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