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of the heart rhythm Can cause syncope, sudden death, palpitations or no symptoms May be classified according to origin or speed
Slow
heart rate
Types
Respiratory sinus arrhythmia Sinus bradycardia Sick sinus syndrome (SSS) Types I, II, III
In
Changes in vagal tone during respiration Inhalation increase HR Exhalation decrease HR If HR < 60 bpm during exhalation sign of good autonomic tone benign
Presentation
Workup
Found
Physiologic - Increased vagal tone Pathologic inferior wall MI, electrolyte disorders, infection, sleep apnea, drugs (beta blockers, digitalis), hypothermia, increased ICP, hypothyroidism, cholestatic jaundice Mostly asymptomatic but may include syncope, dizziness, SOB, chest pain, exercise intolerance Slow regular HR on auscultation and palpation
Presentation
Workup
and Management
Treat underlying cause if due to drugs, endocrine disorder etc IV atropine increase rate by blocking vagal stimulation to SA node Persistent bradycardia - pacemaker
Umbrella
term for abnormalities of SN impulse formation/propagation e.g. sinus bradycardia, sinus arrest Causes
Intrinsic age related changes (fibrosis), CAD Extrinsic medications, autonomic hyperactivity
Presentation
Cerebral irritability, labile mood swings, forgetfulness, dizziness, falls, syncope Cardiac palpitations, angina, CHF, SCD (rare) GI symptoms, oliguria Exercise intolerance, fatigue, SOB
Workup
and Management
Thyroid function, electrolyte testing ECG, Holter monitoring Asymptomatic no treatment reqd Chronic, symptomatic SND pacemaker therapy
Decreased intensity of S1; short blowing diastolic murmur at apex No treatment if asymptomatic Treat associated/underlying condition if appropriate
2nd
degree AV block
Progressive prolongation of PR interval until atrial impulse fails to conduct no QRS complex Block originates from AV node
Mobitz I (Wenckebach)
Mobitz II
Unexpected dropped impulse without progressive lengthening of PR interval Block originates in bundle of His
Causes
Cardioactive drugs exert negative effects on AVN e.g. digoxin, beta blockers, CCBs Inflammatory dx endocarditis, myocarditis, Lyme disease Infiltrative amyloidosis, hemochromatosis, sarcoidosis Metabolic hyperkalemia, hypermagnesemia, Addisons, hyperthyroidism Tumors, trauma, following surgical procedures, EtOH poisoning, acute MI Mobitz I generally asymptomatic syncope, bradycardia Mobitz II lightheaded, dizzy, syncope, chest pain, regularly irregular heartbeat, hypoperfusion
Presentation
Workup
and Management
If asymptomatic no specific therapy reqd Symptomatic atropine and transcutaneous pacing Suspect MI anti-ischemic regimen Drugs decrease dose/discontinue medication
Mobitz II
3rd
Ventricular pacemaker takes over escape rhythm = 20-40 bpm Can progress to sudden death Causes
Acute MI Cardiac meds beta blockers, CCBs, digitalis Endocarditis, Lyme disease, rheumatic fever
Presentation
Neck veins cannon a waves, Variable intensity S1, slow pulse If have heart failure rales, S3 gallop, peripheral edema, hepatomegaly CHF
Decreased CO Tachypnea, rales, JVD Hypoperfusion altered mental state, hypotension, lethary
Workup
and Management
CBC, electrolytes, ECG, CXR If transient IV atropine Chronic block dual chamber pacing
ECG widened QRS (>0.12 s); deep S waves in lead I and V6, tall late R waves in V1/V2 (like bunny ears/M pattern) Causes isolated congenital anomaly, or assoc with cardiac/pulmonary conditions Presentation wide physiological splitting of S2
Left
Premature
ECG early P waves (differ in morphology from normal P waves from sinus node), normal QRS Presentation
Normal heart found in 50% of pts on Holter monitoring Diseased heart ischemic precusor may have palpitations Asymptomatic no treatment, monitor Symptomatic beta blockers
Management
Premature
ECG slower conduction since from ventricles wider QRS; P wave buried in QRS Presentation
Can be asymptomatic Hypotension, diminished pulse, hypoxia, cannon a waves in JVP, sympathetic activation (if catecholamines are cause)
Asymptomatic no treatment Symptomatic beta blockers Risk sudden death if recurrent PVCs + heart disease implantable cardiac defibrillator (ICD)
Management
Fast
heart rate
Types
ECG rate >100 bpm, regular rhythm, normal P waves, shorter PRI and QRS
Mainly in young women Persistent increase in resting HR unrelated to or out of proportion with level of physical/emotional stress Cause generally secondary phenomenon exercise, emotion, PE, infection Management
Beta blockers slow sinus rate Ivabradine (If channel blocker) if BB not tolerated
Multiple foci in atria fire continuously atrial rate ~400 bpm but impulses not all conducted to ventricles ventricular rate 75-175 bpm irregularly irregular pulse Causes - raised atrial P, increased atrial muscle mass, atrial fibrosis, inflammation and infiltration of atrium
Classic rheumatic heart disease, thyrotoxicosis, EtOH Most common HTN, heart failure
Symptoms
Fatigue, exertional dyspnea, palpitations, dizziness, angina, syncope, blood stasis (2to ineffective contraction) thrombi emboli
Management
Minimize risk of thromboembolism by fully anticoagulating Warfarin (INR of 2-3) or dabigatran (150 mg 2x daily for 3 weeks before)
Indicated for: Have permanent form improve with decreased HR or are >65 years with recurrent atrial tachyarrhythmias Failed cardioversion Combo of digoxin, beta blockers or nondihydropyridine calcium channel blockers (verapamil or diltiazem) Only digoxin if elderly non-ambulant Considered controlled if resting HR <110 bpm If symptoms persist resting HR of 60-80 and exercise of <110 bpm For younger, symptomatic and active patients If no significant heart disease any class 1a, 1c or III drug Reserve amiodarone until others have failed Heart failure or LVH amiodarone only CAD sotalol or amiodarone PAF (paroxysmal atrial fib) left atrial ablation
Indications
a fib related to rheumatic mitral stenosis or with mechanical heart valve Score with CHADS2 CHF, HTN, Age >75, Diabetes, Previous stroke/TIA
If score >2 then need oral anticoag If score <2 then use CHADS2VASc Vascular dx, Age 65-74 and female
Score >2 need anticoag; 1=aspirin or consideration for anticoag; 0=no need
Warfarin
dose to maintain INR of 2-3 Dabigatran 150 mg 2x daily or 110 mg 2x daily for >75 yrs
Organized atrial rhythm with atrial rate of 250-350 bpm ventricular rate one half/one third atrial rate usually travels down the lateral wall of the RA, through the eustachian ridge between the tricuspid annulus and IVC then up the interatrial septum CCW flutter
Causes
Most common COPD Heart disease RHD, CAD, CHF ASD
ECG
Carotid massage increase block saw-tooth baseline - QRS complex appearing after every second or third "tooth" (P wave). Saw-tooth flutter waves are best seen in the inferior leads (II, III, aVF) .
In
pts with severe pulmonary disease (COPD) ECG variable P wave morphology; variable PR/RR intervals
Workup
Treatment
ECG
narrow QRS complexes with no P waves (P waves are buried within the QRS complex). circuit is short/conduction rapid, so impulses exit to activate atria and ventricles simultaneously
Causes
IHD; digoxin toxicity, AV node reentry, atrial flutter with rapid ventricular response, AV reciprocating tachycardia (accessory pathway), Excessive caffeine/EtOH
Treatment
Valsalva maneuver, carotid massage, immerse head in cold water Pharm IV adenosine DOC short acting, decrease SA/AV nodal activity
Acute treatment
CI - asthma
Prevention
accessory
conduction pathway premature ventricular excitation - lacks the delay seen in the AV node ECG delta wave deflection before QRS, short PRI, narrow complex Treatment
Radiofrequency catheter ablation of one arm of the reentrant loop (i.e. , of the accessory pathway) is an effective treatment. Avoid drugs active on the AV node (e.g. , digoxin) because they may accelerate conduction through the accessory pathway. Type lA or IC antiarrhythmics are better choices.
rapid
and repetitive firing of three or more PVCs in a row, at a rate ~100-250 bpm AV dissociation (P waves indep. of QRS) Originate below bundle of His Causes
CAD with prior MI - most common cause Active ischemia, hypotension Cardiomyopathies Congenital defects Prolonged QT syndrome Drug toxicity
ECG
wide/bizarre QRS
Presentation
Palpitations, dyspnea, lightheadedness, angina, impaired consciousness (e.g. syncope) May present with sudden cardiac death Signs of cardiogenic shock may be present. Asymptomatic if rate is slow Physical findings - cannon a waves in the neck (2 to AV dissociation atrial contraction during ventricular contraction); varying intensity S1
Treatment
ID and treat underlying causes If hemodynamically stable/systolic BP>90 IV amiodarone, procainamide, sotalol If unstable cardioversion + amiodarone for sinus rhythm If asymptomatic/non-sustained dont need to treat If underlying heart disease ICD placement Pharm 2nd line treatment amiodarone (DOC)
Multiple
foci in the ventricles fire rapidly chaotic quivering of the ventricles no CO Oft begins with VT Causes
IHD most common Antiarrhythmic drugs (esp. if cause torsades de pointes) A. fib with rapid vent. rate in pts with WPW Cant measure BP, no pulse/heart sounds, unconscious, can lead to SCD
Presentation
ECG
No identifiable P waves/QRS complexes very irregular Medical Emergency! Immediate defibrillation and CPR
Treatment
Give 3 sequential shocks to establish new rhythm. Assess rhythm between each shock Give Epinephrine (1 mg IV) decreases defib threshold, increase BF Defib again after 30-60 s Try amiodarone then shocking 2nd line lidocaine, bretylium, procainamide
If above fails
Agabegi,
Elizabeth and Agabegi, Steven. Step Up to Medicine. 2nd Ed. Philadelphia: Lippincott Williams & Wilkins. 2008. Pg. 1830. Kumar and Clarks Clinical Medicine. Ed. By Clark, Michael and Kumar, Parveen. 8th Ed. Edinburgh: Elsevier. 2012. Pg. 697-714. Thaler, Malcom. The Only EKG Book Youll Ever Need. 6th Ed. Philadelphia: Lippincott Williams & Wilkins. 2010. Print.