7: Dysrhythmias Flashcards
Arrhythmias- SA node
1: sunus bradycardia
2: sinus tachycardia
3: sinus dysrhythmia
4: sinus arrest
Normal Sinus rhythm
- there must always be a P wave
- the P wave should be a rounded shape
- each P wave should be the same shape
- each P wave should be followed by a QRS of normal morphology
- the P-R interval should be 3-5 small squares and constant
- the rhythm should be regular
Arrhythmias- Atria
1: wandering pacemaker
2: premature atrial contractions (PAC)
3: atrial tachycardia (AT)
4: Paroxysmal supraventricular tachycardia (PSVT)
- AVNRT
- AVRT
5: atrial flutter
6: atrial fibrillation
Arrhythmias- AV junction
1: junctional rhythm
2: premature junctional contractions
3: junctional ectopic tachycardia
Arrhythmias- Ventricles
1: ventricular escape complexes and rhythm
2: premature ventricular complexes
3: ventricular tachycardia
4: ventricular fibrillation
Arrhythmias- Conduction
1: AV blocks
- 1-4th degree blocks
2: Bundle branch blocks
- RBBB
- LBBB
- Hemi-blocks
dysrhythmia- dx
Holter monitor
-portable ECG recorder for 24hr recording- for arrhythmia that occur less than daily
Treadmill testing
-dysrhythmias exacerbated by stress
Electrophysiologic studies (EP)
-electrodes are placed inside the right atrium and ventricle using catheter
-dx of abnormal foci or tract, SA, AV node disorder, placement of permanent pacemaker
Sinus arrhythmia
Phasic variation of R-R interval with respiration
Heart rate increases during inspiration and decreases during expiration
Sinus arrest
Failure of sinus node to initiate impulse- normal rhythm followed by an absent P wave and an absent ORS causes -sick sinus syndrome -ischemia -digitalis toxicity -excess vagal tone
Sick sinus syndrome
causes: degenerative process damaging the sinus node
-Sarcoidosis
-Amyloidosis
-Chaga’s disease
-Cardiomyopathies
sx: sinus bradycardia, sinus arrest or SA block, alternating episodes of tachyarrhythmia and bradycardia
Tx: no tx for asymptomatic, permanent pacing for symptomatic pts
Wandering atrial pacemaker (WAP)
Transient shifts in location of dominant pacemaker
EKG
-continual changes in the P-wave morphology. P waves vary in size, shape, and directions
-at least 3 different P waves must be present
-varying P-R intervals
Tx: not needed
Multifocal atrial tachycardia (MAT)
WAP associated with tachycardia (>100bpm)
Narrow QRS complexes
causes
-cor pulmonale, digitalis toxicity, CAD, elderly
Atrial tachycardia (AT)
heart rate: 120-250bpm AV block (by adenosine) does not terminate tachycardia
Premature atrial complexes
Common and benign
Premature P wave (buried in the preceding T wave)
Paroxysmal supraventricular tachycardia (PSVT)
sudden onset, usually initiated by a premature beat and the arrhythmia stops abruptly
Could result in decreased CO, angina, hypotention, CHF
types
1: AV node reentry (AVNRT)- 90%
2: AV reentrant tachycardia (AVRT)
AVNRT- info
Slow AV nodal pathway for anterograde conduction and Fast AV nodal pathway for retrograde conduction
P-wave buried in QRS and not seen
-if P wave is seen: pseudo ‘r’ wave at the end of QRS complex in V1, V2; or pseudo ‘S’ waves maybe seen in LEAD II, III, aVF
-Tachycardia associated with prolongation of PR interval
AVNRT- management
Initial maneuvers -carotid sinus massage -gagging -valsalva maneuver If fails -Adenosine (DOC)** If hemodynamic compromise (hypotension) -DC cardioversion** Chronic -Beta blocker -Ca channel blockers -Class IC antiarrhythmics -Radiofrequency catheter ablation of slow tract
AVRT- info
AV node and 1 or more bypass tracts
Orthodromic tachycardia (narrow qrs complex tachycardia)
-anterograde via AV node and retrograde via accessory pathway
Antidromic tachycardia (wide qrs complex tachycardia)
-anterograde via accessory pathway and retrograde via bundle of His and AV node
Antidromic AVRT
Wolff-Parkinson-White syndrome (WPW) associated with Ebstein's anomaly The bundle of Kent* (accessory pathway) - results in delta waves** EKG -Short P-R interval (0.12sec) -Slurring of upstroke (delta waves) of QRS complex -Secondary ST-T wave change
AVRT- tx
Catheter ablation (choice)
DC cardioversion
Orthodromic: Adenosine or verapamil*
Antidromic: Procainamide or cardioversion
-contraindicated: AV node blockers** (digitalis, adenosine, diltiazem, verapamil, Ca channel blocker, beta-blocker)
Atrial flutter- info
Rhythm disturbance of the atria
Sawtooth flutter waves (P waves) in LEAD II, III, aVF**
-reentrant atrial tachycardia
-rate of ventricular response increases above 140/m-> CO drops and cardiac sx appear*
Complication- CHF, embolization
Atrial flutter- causes
- long standing HTN
- Valvular heart disease (rheumatic)
- Coronary artery disease
- Acute pulmonary embolism*
Atrial flutter- tx
symptomatic Cardiversion -when spontaneous reversion doesnt occur -when there is hemodynamic instability -acute myocardial ischemia Rate control -verapamil, beta-blockers -catheter ablation (if no response to drugs)
Atrial fibrillation
dysrhythmia due to multiple areas of reentry within the atria
complete disorganization of atrial electrical activity
Atrial rate: 350-600/m-> P waves are replaced by fine, undulating fibrillatory waves (“F” waves)**
R-R interval is irregular
Peripheral emboli**- 15% risk of stroke
Atrial fibrillation- physical exam
Variation in intensity of first heart sound (S1)**
Heart rate is irregular
Absence of ‘a’ wave in Jugular venous pulsation** (no atrial contraction)
Atrial fibrillation- tx
Rate control- beta blocker, Ca channel blocker, digoxin
Anticoagulant therapy
-Heparin and Warfarin if A-fib > 2days old**
Restoration of rhythm- cardioversion
-hemodynamically instable: IV heparin-> immediate cardioversion**
-hemodynamically stable:
–48hrs of A-fib: continue cate control and anticoagulation for 3 weeks before attempting cardioversion**
Rhythm control
-Type IA, IC, III
-Amiodarone (Class III): DOC following cardioversion**
Junctional escape rhythm
SA node fails to discharge-> AV node becomes the dominant pacemaker
causes
-Inferior MI, cardiac surgery, digoxin toxicity
EKG
-inverted or absent P-wave before QRS complex or P after QRS
-narrow QRS
Premature ventricular complexes (PVC)
MC ventricular rhythm disturbance
Two successive PVCs are called “couplet”
-Monomorphic VT: 3 or more PVC >100bp with similar morphology
-Multifocal or polymorphic VT: morphology varies*
-Bigeminy VT: PVCs successively alternate with a sinus beat
Discordant ST segment and T wave changes (T wave is opposite the major deflection of the QRS)
Full compensatory pause- double the preceding R-R interval following PVC
PVC- causes, tx
- excess caffeine, alcohol, tobacco
- emotional stress
- sympathomimetics
- hypoxia, hyperkalemia, hypokalemia
no tx w/o significant sx
Beta blocker can be used in MI
Ventral tachycardia- sx
Sustained VT: -lasts >30 sec -associated with hemodynamic instability -syncope, dizziness, palpitations Nonsustained VT: -lasts <30 sec -not associated with hymodynamic compromise -Asx or transient palpitations
VT- dx
Intermittent canon ‘a’ waves in Jugular veins and Variable first heart sound (S1)**
VT- tx
Hemodynamic instability: DC cardioversion**
Stable pts
-Lidocaine (DOC)**
-Procainamide
Recurrent sustained or sx non-sustained VT:
-Implanted cardioverter/defibrillator (ICD)
Torsades de Pointes- info
VT characterized by polymorphic QRS* associated with prolonged QT* (often >0.6sec)
Risk of sudden death**
Torsades de Pointes- causes
Congenital anomaly: familial long QT syndrome
Drugs: Quinidine, Disopyramide, Phenothiazine, Tricyclic antidepressants**
Electrolyte imbalance: hypokalemia, hypomagnesemia**
Torsades de Pointes- tx
Acute
-IV magnesium** (slows down the heart-> watch out for cardiac arrest)
-Beta blocker, Mexiltine, Phenytoin
Chronic
-Beta blocker
-if recurs
–Left-sided cervicothoracic sympathetic ganglionectomy
–Dual chamber permanent pacing
–Cardioverter/Defibrillator (ICD) for congenital forms
Ventricular escape beats- Idioventricular rhythm
there is a lack of impulses from SA or AV nodes
Ventricular fibrillation- info
chaotic ventricular rhythm-> no ventricular contraction
no P wave no QRS complex
LETHAL!! in 3-5 mins
V fib- tx
Immediate cardioversion and CPR
First degree AV block
delay in conduction from sinus node to the ventricle
all impulses are conducted
P-R interval >0.2sec
Second degree AV block
intermittent failure of AV conduction Type I (Mobitz type I or Wenkebach): MC: AV node (qrs narrow) -Progressive lengthening of the P-R interval-> failure of a P wave to conduct and an absent QRS Type II (Mobitz type II) -Abrupt failure of AV conduction -no preceding gradual P-R prolongation
Second degree AV block type I- tx
Most case dont require tx Electrophysiologic mapping if -no identifiable acute cause -elderly pt -Severe coronary artery disease -calcified aortic disease Permanent pacing if -Block within the bundle of His (qrs wide)* -History of dizziness or syncope
Third degree heart block-info
Complete heart block
- total dissociation btw P wave and QRS complex
- Giant cannon wave in jugular vein may be seen when atria contracts against closed AV valve**
Third degree heart block- AV node
Narrow QRS complex
Asx
Heart rate >50bmp
Tx: pacemaker, Atropine
Third degree heart block- Bundle of His
Wide QRS complex
Ventricular rate 30-40bpm
Unresponsive to ANS influence*
Tx: permanent pacing**
Right bundle branch block
S2 is widely split due to delayed closure of pulmonic valve
Secondary R wave (R’) in right precordial LEADs: V1, V2
Wide S wave: V5, V6
Left bundle branch block
Paradoxical splitting of S2 due to delayed closure of aortic valve** (during inspiration, splitting gets smaller)
Broad R wave: V5, V6
Deep S wave: V1, V2
What to focus on..
Ddx- sinus tachycardia (p-qrst), paroxysmal supraventral tachycardia (pseudo R wave, sudden onset)
Sinus arrest (no p and qrs)
WAP (at least 3 p wave morphology, with tachycardia-> MAT)
PAC (narrow qrs) PVC (wide qrs)- both with premature p wave
PSVT- know tx: AVNRT (adenosine)
Antidromic AVRT: delta waves. contraindication
Atrial flutter/ fibrillation- dx, complication, PE, tx schedule.
premature ventricular complexes- dx
V-tach: management, sx
Torsades de pointes: ekg
V-fib: ekg, tx
AV block: just know all blocks
RBBB, LBBB
