cardiac conduction disorders Flashcards
- SINUS ARRHYTHMIA
- SINUS TACHYCARDIA
- SINUS BRADYCARDIA
- SINUS PAUSE/ARREST
- SICK SINUS SYNDROME
- NARROW QRS COMPLEX
- SINUS NODE ARRHYTHMIAS
- PREMATURE ATRIAL CONTRACTIONS
- ATRIAL FIBRILLATION
- ATRIAL FLUTTER
- SVT
- JUNCTIONAL ESCAPE RHYTHM
- AV BLOCKS
ATRIAL/AV NODAL ARRYTHMIAS
- PREMATURE VENTRICULAR
COMPLEXES - VENTRICULAR TACHYCARDIA
- VENTRICULAR FIBRILLATION
VENTRICULAR ARRYTHMIAS
* WIDE QRS COMPLEX
- RIGHT BUNDLE BRANCH BLOCK
- LEFT BUNDLE BRANCH BLOCK
bundle branch block
ECG MORPHOLOGY: IRREGULAR RHYTHM;
IDENTICAL P WAVES, CONSISTENT PR INTERVAL
* PATHOPHYSIOLOGY
* DUE TO RESPIRATORY-RELATED CHANGES THAT
INFLUENCE THE HEART RATE
* HR INCREASES DURING INSPIRATION AND
DECREASES DURING EXPIRATION
* ETIOLOGIES
* NORMAL FINDING
sinus arrhythmia
treatment for sinus arrhythmia
no treatment
- ECG MORPHOLOGY: REGULAR RHYTHM; FAST RATE > 100 BPM;
NORMAL P WAVE - PATHOPHYSIOLOGY
- NORMAL PHYSIOLOGIC RESPONSE TO CATECHOLAMINE
RELEASE OR DUE TO PARASYMPATHETIC WITHDRAWAL - ETIOLOGIES
- FEVER, DEHYDRATION, SHOCK, SEPSIS, ANEMIA, HYPOXIA,
PE, ACS, PAIN, ANXIETY, PHEOCHROMOCYTOMA,
HYPERTHYROIDISM, CHF, EXPOSURE TO STIMULANTS, ETOH
WITHDRAWAL, INAPPROPRIATE SINUS TACHYCARDIA, POTS
DISEASE
sinus tachycardia
treatment for sinus tachycardia
- TREAT UNDERLYING CAUSE
- BETA-BLOCKER FOR INAPPROPRIATE SINUS TACHYCARDIA
- ECG MORPHOLOGY
- SAME AS NORMAL SINUS RHYTHM EXCEPT HR < 60 BPM
- PATHOPHYSIOLOGY
- PHYSIOLOGIC FROM INCREASED VAGAL TONE OR PATHOLOGIC
- ETIOLOGIES
- EXERCISE CONDITIONING, MEDICATIONS, SSS, ACUTE MI, SLEEP
APNEA, HYPOTHYROIDISM, HYPOTHERMIA, INFECTIONS (LYME
DISEASE), INCREASED ICP, VASOVAGAL RESPONSE - SYMPTOMS
- ASYMPTOMATIC; MAY ALSO HAVE LIGHTHEADEDNESS, PRESYNCOPE
OR SYNCOPE, WORSENING ANGINA, COGNITIVE SLOWING, EXERCISE
INTOLERANCE, FATIGUE
sinus bradycardias
sinus bradycardia treatment
- NO TX IF HEMODYNAMICALLY STABLE AND NO SYMPTOMS
- ATROPINE 0.5 MG IV IF SYMPTOMATIC/HEMODYNAMICALLY UNSTABLE
- CAN BE REPEATED EVERY THREE TO FIVE MINUTES, IF NEEDED, TO A TOTAL DOSE OF 3 MG
- TEMPORARY PACEMAKER
- ECG MORPHOLOGY: IRREGULAR; P-P INTERVAL
DISTURBED. - PATHOPHYSIOLOGY
- TRANSIENT LOSS OF SINUS P WAVE LASTING
FROM 2 SECONDS TO SEVERAL MINUTES - < 2 SECONDS: SINUS PAUSE
- > 2 SECONDS: SINUS ARREST
- ESCAPE BEATS/RHYTHM: FROM ECTOPIC
PACEMAKER, NOT SA NODE - ATRIAL PACEMAKER
- JUNCTIONAL PACEMAKER
- VENTRICULAR PACEMAKER
sinus arrest/PA use
P WAVE
PRESENT BUT DIFFERENT
MORPHOLOGY AS THE SINUS
RHYTHM; NARROW QRS; PR
INTERVAL DIFFERENT; RATE 60
AND ABOVE
atrial pacemaker
NO P WAVES OR INVERTED,
NARROW QRS; SLOW RATE UP
TO 40 BPM
junctional pacemaker
NO P WAVES; WIDE QRS,
SLOWER RATE (20 – 40 BPM)
ventricular pacemaker
- ETIOLOGIES
- MEDICATIONS
- DIGOXIN, BETA BLOCKERS, VERAPAMIL, DILTIAZEM
- SINUS NODE DISEASE
- ISCHEMIA, INFLAMMATORY DISEASE,
INFILTRATIVE/FIBROTIC DISEASE, SLEEP APNEA - SYMPTOMS
- PALPITATIONS, CHEST PAIN,
FATIGUE/LIGHTHEADEDNESS
sinus arrest/PA use
sinus arrest/PA treatment
- NO TREATMENT IF ASYMPTOMATIC
- DISCONTINUE OFFENDING DRUG
- PACEMAKER IF NECESSARY
- ECG MORPHOLOGY: SINUS BRADYCARDIA, SINUS
PAUSES/ARREST, ATRIAL TACHYCARDIA, A FIB, A FLUTTER - PATHOPHYSIOLOGY
- INABILITY OF THE SA NODE TO GENERATE A HEART RATE
- RISK FACTORS
- ELDERLY
- INTRINSIC CAUSES
- FAMILIAL SA NODE DISORDERS, IDIOPATHIC
DEGENERATIVE FIBROTIC INFILTRATION,
ISCHEMIA/INFARCTION, INFILTRATIVE DISEASES,
INFLAMMATORY DISEASES, HYPOTHYROIDISM,
HYPOTHERMIA, HYPOXIA, SURGICAL INJURY - EXTRINSIC CAUSES
- HYPERKALEMIA, DIGITALIS, CCB, BB, SYMPATHOLYTIC
AGENTS (CLONIDINE), CIMETIDINE, LITHIUM,
ACETYLCHOLINESTERASE INHIBITORS
SYMPTOMS
* FATIGUE, LIGHTHEADEDNESS, PALPITATIONS,
PRESYNCOPE, SYNCOPE, DYSPNEA WITH EXERTION, CHEST DISCOMFORT
SICK SINUS SYNDROME (AKA BRADY-
TACHY SYNDROME, SINUS NODE
DYSFUNCTION)
SSS treatment
- SYMPTOMATIC: PERMANENT PACEMAKER WITH
DUAL CHAMBER PACING - WITH BRADYCARDIA AND ALTERNATING VENTRICULAR TACHYCARDIA: PERMANENT PACEMAKER WITH AUTOMATIC IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR (AICD)
- ECTOPIC FOCI PACE THE HEART
- EXAMPLES
- PREMATURE ATRIAL CONTRACTIONS
- ATRIAL FIBRILLATION
- ATRIAL FLUTTER
- SUPRAVENTRICULAR TACHYCARDIA
- MULTIFOCAL ATRIAL TACHYCARDIA (MAT
atrial arrhythmias
- ECG MORPHOLOGY: IRREGULAR RHYTHM, P WAVE PRESENT/MAY
HAVE DIFFERENT MORPHOLOGY, PR INTERVAL DIFFERENT,
COMPENSATORY PAUSE FOLLOWS BEAT - PATHOPHYSIOLOGY
- EARLY IMPULSE GENERATED BY AN ECTOPIC FOCUS WITHIN THE
ATRIA - ETIOLOGIES
- IDIOPATHIC, ADRENERGIC EXCESS, SMOKING, ALCOHOL,
CAFFEINE, DECONGESTANTS, THEOPHYLLINE, ACUTE
MI/ISCHEMIA, MITRAL STENOSIS, MVP, HYPERTROPHIC
CARDIOMYOPATHY, COPD. - SYMPTOMS
- ASYMPTOMATIC
- PALPITATIONS OR SKIPPED BEATS
premature atrial complexes (PAC)
premature atrial complexes (PAC) treatment
- NO TREATMENT IF ASYMPTOMATIC
- IF SYMPTOMATIC: BETA BLOCKERS, STOP PRECIPITATING FACTORS
GENERAL CHARACTERISTICS
* IRREGULARLY IRREGULAR RHYTHM WITH NARROW QRS
* NO DISTINCT P-WAVE
* RR INTERVAL FOLLOWS NO DISTINCT PATTERN.
* ATRIAL RATE RANGES FROM 300 TO 600 BPM; VENTRICULAR RATE RANGES FROM 75 TO 175 BPM
* IF HR > 100, A FIB WITH RVR (RAPID VENTRICULAR RATE)
* MOST COMMON CHRONIC ARRHYTHMIA
- CLINICAL FEATURES
- FATIGUE AND EXERTIONAL DYSPNEA
- PALPITATIONS, DIZZINESS, ANGINA, SYNCOPE
- IRREGULARLY IRREGULAR PULSE
- REDUCED EXERCISE CAPACITY
- HYPOTENSION
- INSIDIOUS ONSET OF HEART FAILURE
- WEAKNESS
atrial fibrillation
- PATHOPHYSIOLOGY
- MULTIPLE ECTOPIC
ATRIAL FOCI FIRE SIMULTANEOUSLY IN A CHAOTIC PATTERN - RESULTING IN QUIVERING OF THE ATRIA
- IRREGULAR CONTRACTION OF
VENTRICLES - ETIOLOGIES/RISK FACTORS
- CARDIAC DISEASES
- CAD, MI, HTN, VALVULAR DISEASE, PERICARDITIS
- LUNG DISEASES
- COPD, PE
- HYPERTHYROIDISM
- SYSTEMIC ILLNESS
- SEPSIS, MALIGNANCY
- STRESS
- EXCESSIVE ALCOHOL INTAKE
- HYPERADRENERGIC STATE
- COCAINE USE, PHEOCHROMOCYTOMA
- EXTREMES OF ACTIVITY
A fib
what type of A fib terminates spontaneously or with intervention in < 7 days and recurrent episodes may occur
paroxysmal A fib
what A fib has continuous duration >7 days
persistant A fib
what A fib has continuous duration >12 months
longstanding persistant A fib
what A fib is joint decision between patient and clinician not to pursue rhythm control treatment
permanent A fib
what a fib is in the absence of rheumatic mitral stenosis, a mechanical or bio prosthetic heart valve, or mitral valve repair
nonvalvular A fib
A fib complicaitons
- STROKE
- LEFT ATRIAL THROMBI
- PERIPHERAL EMBOLIZATION
- HEART FAILURE
- LOSS OF AV SYNCHRONY
- INCREASED HEART RATE
- CARDIAC ISCHEMIA
- INCREASED HEART RATE
- INCREASED MORTALITY
what is the A fib stroke risk and what medication is given
- SCORE > 2 IN MEN OR >3 IN
WOMEN: ORAL
ANTICOAGULATION (OAC) IS
RECOMMENDED (WARFARIN
V DOAC) - CONSIDER OAC IF 1 IN MEN
AND 2 IN WOMEN - NO OAC IF A FIB WITH
SCORE OF 0 - NO NEED FOR ASPRIN
(ANTIPLATELET) UNLESS
PATIENT HAS CHD
(CONGENITAL HEART
DISEASE) OR PERIPHERAL
VASCULAR DISEASE
HAS BLED SCORE
- A SCORE OF 0-1 GENERALLY
INDICATES A LOW BLEEDING
RISK. - A SCORE OF 2 MAY SUGGEST A
MODERATE BLEEDING RISK. - A SCORE OF 3 OR HIGHER IS
CONSIDERED HIGH BLEEDING
RISK, PROMPTING CLOSER
MONITORING AND POTENTIAL
ADJUSTMENTS TO MEDICATION
OR LIFESTYLE FACTORS
A FIB treatment
- rate control
- reversion to sinus rhythm
- maintenance of sinus rhythm
- prevention of embolization
BACKGROUND TREATMENT
REGARDLESS IF RHYTHM CONTROL IS EVENTUALLY PURSUED AND MAY BE CONSIDERED PRIMARY
TREATMENT IN PATIENTS WITH MINIMAL TO NO SYMPTOMS RELATED TO LONG STANDING A FIB
RATE CONTROL
AN INDIVIDUALIZED DECISION
* CARDIOVERSION FIRST LINE IF NEW ONSET WITH
IDENTIFIABLE CAUSE OR IF REMAIN SYMPTOMATIC
DESPITE RATE CONTROL
* A FIB >48 HOURS/UNKNOWN, PATIENT MUST HAVE 3
WEEKS OF ANTICOAGULATION OR EXCLUSION OF
THROMBUS VIA TEE PRE-CONVERSION WITH
ANTICOAGULATION CONTINUED FOR 4 WEEKS AFTER
rhythm control
A FIB indications for hospitalization
- ACTIVE ISCHEMIA
- HEART FAILURE
- HYPOTENSION
- DIFFICULT RATE CONTROL
- EVIDENCE OF ORGAN HYPOPERFUSION
- CONFUSION
- ACUTE RENAL INJURY
ACUTE A. FIB
UNSTABLE PATIENT treatment
- IV HEPARIN
- IV RATE CONTROL
- BETA BLOCKER
- CALCIUM CHANNEL BLOCK
- DC CARDIOVERSION
- 120-200 JOULES
new onset atrial fibrillation stable patient treatment
look for and treat underlying cause
potentially reversible:
- hyperthyroidism
- hypoxemia (PE)
- cardiac ischemia
indications for rhythm control (instead of long term rate control)
- hemodynamic instability
- failure of rate control
- first episode
- younger patient
- CHF
- potentially reversible cause
DC cardio version advantages for rhythm control
- higher success rates
- adverse effects of anti-arrhythmic drugs
- there is a need for prolonged telemetric monitoring with pharmacologic cardioversion
- patient compliance
choice of anticoagulation for stroke prophylaxis
WARFARIN
* FOR PTS WITH MECHANICAL VALVES, MITRAL VALVULAR DISEASE, OR VENTRICULAR ASSIST DEVICE
* INR RANGE IS 2-3 FOR WARFARIN
* HIGHER RISK OF BLEEDING AND INTRACRANIAL BLEEDS
* ACUTE WARFARIN-ASSOCIATED BLEEDING
* TREAT WITH FRESH FROZEN PLASMA OR PROTHROMBIN COMPLEX CONCENTRATE
DIRECT ORAL ANTICOAGULANTS (DOACS)
* FACTOR XA INHIBITORS
* APIXABAN, RIVAROXABAN, EDOXABAN
* NO MONITORING NECESSARY
* NO APPROVED REVERSAL AGENT
DIRECT THROMBIN INHIBITORS
* DABIGATRAN
* HAS A REVERSAL AGENT:
IDARUCIZUMAB
- ATRIAL RHYTHM
CHARACTERIZED BY - RAPID, REGULAR ATRIAL
DEPOLARIZATIONS - ATRIAL RATE OF 250 TO
300 BPM - LONG REFRACTORY PERIOD
IN THE AV NODE ALLOWS - ONE OF EVERY TWO OR
THREE WAVES TO
CONDUCT TO THE
VENTRICLES
ATRIAL FLUTTER
ETIOLOGIES
* HEART DISEASES
* HEART FAILURE (MC), RHEUMATIC HEART DISEASE, CAD
* LUNG DISEASES
* COPD, HYPOXIA, PE
* ATRIAL SEPTAL DEFECT
* SIMILAR RISK FACTORS TO A FIB
SYMPTOMS
* PALPITATIONS, TACHYCARDIA, FATIGUE, WEAKNESS,
DYSPNEA, PRESYNCOPE, HYPOTENSION, ANGINA, REDUCED
EXERCISE CAPACITY
DIAGNOSIS
* ECG
* SHOWS SAW-TOOTH BASELINE, WITH QRS COMPLEX
APPEARING AFTER EVERY SECOND OR THIRD TOOTH (P
WAVE)
* BEST SEEN IN INFERIOR LEADS II, III, & AVF
atrial flutter
atrial flutter treatment
- SIMILAR TO A FIB
- ATRIAL FLUTTER ABLATION IS MORE
SUCCESSFUL AND CAN BE USED TO AVOID LONG- TERM ANTICOAGULATION IF RISK FACTORS ARE PRESENT - GENERALLY, DIGOXIN NOT USED IN ATRIAL FLUTTER
- CARDIOVERSION
- DC 50 – 100 JOULES
- PHARMACOLOGIC CONVERSION NOT PREFERRED
- IBUTILIDE 60% EFFECTIVE (DRUG OF CHOICE)
- RISK OF TORSADES DE POINTES AND QT PROLONGATION
what are the 2 causes of atrioventricular reciprocating/reentrant tachycardia (AVRT)
- AV NODAL REENRANT TACHYCARDIA: 60% OF SVT CASES.
RENTRY WITHIN THE AV NODE - AV RECIPROCATING TACHYCARDIA AVRT: 30% OF SVT
CASES. USES AN ACCESSORY PATHWAY FOR REENTRY
INTO THE RIGHT ATRIUM
- REGULAR ATRIAL RHYTHM
- REGULAR, NARROW QRS
- HEART RATE > 100 BPM
- AV CONDUCTION IS USUALLY
1:1 - USUALLY PAROXYSMAL AND
SELF-LIMITING - P WAVES HARD TO DISCERN
- HIDDEN OR BEHIND QRS
CAUSES:
* ISCHEMIC HEART DISEASE, DIGOXIN TOXICITY, A FLUTTER WITH
RVR, EXCESSIVE CAFFEINE/ALCOHOL USE
* MOST COMMON AMONG YOUNG FEMALES
SYMPTOMS
* PALPITATIONS, CHEST DISCOMFORT, DYSPNEA,
LIGHTHEADEDNESS, DIAPHORESIS, NAUSEA, SYNCOPE,
PRESYNCOPE
DIAGNOSIS
* ECG
supra ventricular tachycardia (SVT)
SVT Treatment for stable and unstable
UNSTABLE
* DIRECT CURRENT CARDIOVERSION
STABLE
* NARROW COMPLEX: VAGAL MANEUVERS, ADENOSINE
(FIRST-LINE MEDICAL TX), BETA-BLOCKERS, CCB
- PREMATURE VENTRICULAR
EXCITATION CAUSED BY AN
ACCESSORY CONDUCTION
PATHWAY - CONGENITAL; 3-4% FAMILIAL
- MAY LEAD TO PAROXYSMAL
TACHYCARDIA - DIAGNOSIS:
- ECG: SHORT PR INTERVAL AND
DELTA WAVE
wolff-parkinson white (WPW syndrome)
wolff-parkinson white (WPW syndrome) TREATMENT
- RADIOFREQUENCY ABLATION OF
ONE ARM OF THE REENTRANT
LOOP - MEDICAL OPTION:
PROCAINAMIDE OR IBUTILIDE - AVOID DRUGS THAT ACT ON
THE AV NODE
- ATRIAL TACHYCARDIA
- 3 OR MORE DISTINCT P WAVES (DIFFERENT
ORIGINS) - VARIABLE PR INTERVAL
- IRREGULAR RHYTHM
- RATE IS > 100 BPM
- SIMILAR TO WANDERING ATRIAL
PACEMAKER; EXCEPT HR IS 60 TO 100 BPM
CAUSES
* COPD, PE
* ISCHEMIC HEART DISEASE, VALVULAR DISEASE,
CHF
* HYPOKALEMIA, HYPOMAGNESEMIA
* THEOPHYLLINE, CHRONIC DISEASE, SEPSIS
multifocal atrial tachycardia (MAT)
MAT treatment
- TREAT UNDERLYING CONDITIONS, IMPROVE OXYGENATION AND VENTILATION
- PRESERVED LV FUNCTION
- CCB, BB, DIGOXIN, ADENOSINE, IV FLECAINIDE, IV
PROPAFENONE - LV FUNCTION NOT PRESERVED
- DIGOXIN, DILTIAZEM, AMIODARONE
- interruption of normal impulse form sa node to av node (AV node dysfunction)
- first degree AV block
- second degree AV block (mobitz type 1 (wenckebach) and mobitz type 2
- third degree AV block
atrioventricular conduction blocks
- ECG MORPHOLOGY
- PR INTERVAL IS PROLONGED AND CONSTANT
(> 0.20) - A QRS FOLLOWS A P-WAVE
- DELAY IS USUALLY IN THE AV NODE
- CAUSES: UNDERLYING STRUCTURAL
ABNORMALITIES, INCREASE IN VAGAL TONE,
DIGOXIN, BB, VERAPAMIL, DILTIAZEM,
SARCOIDOSIS, LYME CARDITIS - SYMPTOMS: USUALLY NONE
first degree AV block
first degree AV block treament
OBSERVATION, NO SPECIFIC
TREATMENT
- NOT ALL ATRIAL IMPULSES ARE CONDUCTED TO THE
VENTRICLES - SOME P WAVES ARE NOT FOLLOWED BY QRS
COMPLEXES (DROPPED QRS) - TWO TYPES
- MOBITZ TYPE I (WENCKEBACH)
- MOBITZ TYPE II
second degree AV block
- INTERRUPTION IN AV NODE
CONDUCTION IN WHICH PROGRESSIVE
PR INTERVAL PROLONGATION
PRECEDES A NON-CONDUCTED P-WAVE - SYMPTOMS:
- RARELY PRODUCES SYMPTOMS
- BRADYCARDIA, FATIGUE,
LIGHTHEADEDNESS,
DYSPNEA. - RARELY PROGRESSES TO
THIRD DEGREE AV BLOCK
mobitz type 1 (wenckebach)
mobitz type 1 (wenckebach) treatment
- ASYMPTOMATIC: OBSERVATION,
CARDIAC CONSULT - SYMPTOMATIC: ATROPINE,
EPINEPHRINE, W/WOUT
PACEMAKER
AV conduction interruption resulting in intermittent
atrial conduction to the ventricles
Often in regular pattern
PR remains unchanged prior to a non-conducted p-wave
Site of block is within the his-purkinje system
Often progresses to third degree av block
- SYMPTOMS: FATIGUE,
DYSPNEA, CHEST PAIN,
PRESYNCOPE, SYNCOPE,
SUDDEN CARDIAC ARREST
mobitz type 2
mobitz type 2 treatment
- IF SYMPTOMATIC GIVE
ATROPINE AND/OROR
TEMPORARY PACING - PERMANENT PACEMAKER IF
NOT RESOLVED
- NO ATRIAL IMPULSES REACH THE VENTRICLES
- ECG MORPHOLOGY
- P-WAVES AND QRS ACTIVITY ARE INDEPENDENT
OF EACH OTHER - CONSTANT P-P INTERVAL
- CONSTANT R-R INTERVAL
- ATRIAL RATE > VENTRICULAR RATE
- NO ASSOCIATION BETWEEN P WAVES AND QRS
COMPLEX - SYMPTOMS: FATIGUE,
DYSPNEA, CHEST PAIN,
PRESYNCOPE, SYNCOPE,
SUDDEN CARDIAC ARREST
third degree AV block
third degree AV block treatment
TREATMENT: TEMPORARY
PACING
* DEFINITIVE TX: PERMANENT
PACEMAKER
EKG shows wide complex (>0.12sec) QRS
BBB
- CAUSES: COMMON IN
PEOPLE WITHOUT
STRUCTURAL DEFECTS;
VALVULAR DISEASE, ATRIAL
SEPTAL DEFECT
RBBB
- ADVANCED CORONARY
HEART DISEASE (NEW
LBBB SEEN IN ACUTE MI) - LONGSTANDING HTN
(LVH) - AORTIC VALVE DISEASE
- CARDIOMYOPATHY
LBBBB
- depolarization of right ventricle is delayed
ECG criteria:
1. QRS duration greater than 120 milliseconds
2. rsR “bunny ear” pattern in the anterior precordial leads (V1-V3)
3. slurred S waves in leads 1, aVL, and V5 and V6
RBBB
- depolarization of left ventricle is delayed
ECG criteria:
- QRS duration greater than 120 milliseconds
- absence of Q wave in leads 1, V5, V6
- broad notched or slurred R wave in leads 1, aVL, V5, V6
- ST and T wave displacement opposite the the major deflection of the QRS complex
LBBB
- WIDE COMPLEX RHYTHM
ORIGINATING FROM
BELOW THE AV NODE - PREMATURE VENTRICULAR
COMPLEXES - VENTRICULAR TACHYCARDIA
- TORSADES DE POINTES
- VENTRICULAR FIBRILLATION
ventricular arrhythmias
- IMPULSE GENERATED FROM A FOCUS ON
THE VENTRICLE, WHICH SPREADS TO THE
REST OF THE VENTRICLE - UNIFOCAL PVCS
- FROM ONE ORIGIN
- ALL PVCS HAVE THE SAME MORPHOLOGY
- MULTIFOCAL PVCS
- FROM DIFFERENT ORIGIN
- HAVE DIFFERENT MORPHOLOGIES
CAUSES:
* HYPOXIA, ELECTROLYTE ABNORMALITIES,
STIMULANTS, CAFFEINE, MEDICATIONS, AND
STRUCTURAL HEART DISEASE
SYMPTOMS
* ASYMPTOMATIC
* PALPITATIONS, HEART “POUNDS, STOPS, OR TURNS OVER
premature ventricular complexes
3 or more consecutive PVCs
non sustained VTach
PVCs treatment
- ASYMPTOMATIC NO TX
- TREAT UNDERLYING CAUSE; REMOVE
PRECIPITATING FACTOR - BB: SYMPTOMATIC OR WITH HIGH PVC BURDEN IN
A PT WITH CHF - CATHETER ABLATION: HIGH PVC BURDEN IN A CHF
PT
- THREE OR MORE PVCS IN A ROW
WITH A HEART RATE OF 100 – 250
BPM - WIDE QRS COMPLEXES
- P-WAVES ARE DISSOCIATED OR
ABSENT - ORIGINATES BELOW THE BUNDLE
OF HIS - CAUSES:
- CAD WITH PRIOR MI (MC)
- ACTIVE ISCHEMIA,
HYPOTENSION,
CARDIOMYOPATHIES,
VENTRICULAR SCAR TISSUE,
CONGENITAL DEFECTS, LONG
QT SYNDROME, DRUG
TOXICITY. - ASYMPTOMATIC IF RATE IS SLOW
- PALPITATIONS, DYSPNEA, LIGHTHEADEDNESS,
ANGINA, IMPAIRED CONSCIOUSNESS, SYNCOPE
OR PRESYNCOPE - MAY PRESENT WITH SUDDEN CARDIAC DEATH
- SIGNS OF CARDIOGENIC SHOCK MAY BE PRESENT
- DIAGNOSIS
- ECG: WIDE AND BIZARRE QRS COMPLEXES
- QRS COMPLEXES MAY BE MONO- OR POLYMORPHIC
- UNLIKE SVT, VT DOES NOT RESPOND TO VAGAL MANEUVERS OR ADENOSINE
ventricular tachycardia (V tach)
- Lasts longer than 30 seconds and is
symptomatic - Associated with hypotension
- Can progress to ventricular fibrillation.
- Hence, can be life-threatening.
sustained V tach
- Brief, self-limiting runs of v. tach
- Usually, asymptomatic
- In the presence of cad or lv dysfunction, it can
be an independent risk factor for sudden death - Hence, pts with nonsustained v. tach should
be thoroughly evaluated for cad and lv dysfunction
non sustained V tach
V tach treatment
- NONSUSTAINED V. TACH
- ASYMPTOMATIC: NO TX; TREAT UNDERLYING CAUSE
- SYMPTOMATIC: BB (METOPROLOL, CARVEDILOL); CCB
(VERAPAMIL, DILTIAZEM); ANTIARRHYTHMIC DRUGS
(AMIODARONE); RADIOFREQUENCY ABLATION - SUSTAINED V. TACH
- IDEALLY, ALL PTS WITH SUSTAINED V. TACH SHOULD HAVE
IMPLANTABLE CARDIOVERTER DEFIBRILLATOR - TO PREVENT SUDDEN CARDIAC DEATH
- MILD SYMPTOMS AND HEMODYNAMICALLY STABLE: IV
AMIODARONE - HEMODYNAMICALLY UNSTABLE
- IMMEDIATE SYNCHRONOUS DC CARDIOVERSION
- FOLLOWED BY IV AMIODARONE TO MAINTAIN SINUS
RHYTHM
- A TYPE OF POLYMORPHIC V. TACH
- REGULAR VENTRICULAR RHYTHM WITH A RATE
OF > 100 BPM - “TWISTING OF POINTS”
- usually occurs in patients with QT prolongation
- usually terminates spontaneously
- most patients experience multiple episodes of the arrhythmia
- potentially degenerating to ventricular fibrillation and sudden cardiac death
torsades de pointes
torsades de pointe treatment
- cardioversion
- IV magnesium
- discontinue all drugs that prolong QT interval
- correct all risk factors for QT prolongation
- QUIVERING OF THE VENTRICLES DUE TO
ACTIVATION OF MULTIPLE VENTRICULAR FOCI - NO CARDIAC OUTPUT
- USUALLY BEGINS AS V. TACH
- FATAL IF UNTREATED DUE TO CARDIAC ARREST
- RATE IS > 300 BPM
- CAUSES: ISCHEMIC HEART DISEASE (MC),
ANTIARRHYTHMIC DRUGS THAT CAUSE TORSADES
DE POINTES, A FIB WITH RVR IN PTS WITH WPW. - CLINICAL FEATURES: CANNOT MEASURE BP, ABSENT
PULSE AND HEART SOUNDS - PATIENT IS UNCONSCIOUS
- LEADS TO SUDDEN CARDIAC DEATH IF UNTREATED
- DIAGNOSIS:
- ECG: NO ATRIAL P WAVES; NO QRS; IRREGULAR
RHYTHM
ventricular fibrillation (V fib)
treatment of V fib
THIS IS CONSIDERED A
MEDICAL EMERGENCY
* REQUIRING IMMEDIATE DC
DEFIBRILLATION AND CPR
* INITIATE DC DEFIBRILLATION
IMMEDIATELY; IF EQUIPMENT IS NOT
READY, START CPR UNTIL IT IS
* GIVE UP TO THREE SEQUENTIAL SHOCKS TO ESTABLISH ANOTHER RHYTHM; ASSESS RHYTHM BETWEEN EACH SHOCK
IF V. FIB PERSISTS
* CONTINUE CPR
* INTUBATION IF NECESSARY
* IV EPINEPHRINE
* INCREASES MYOCARDIAL AND CEREBRAL BLOOD FLOW
* REDUCES THE DEFIBRILLATION THRESHOLD
OTHER OPTION
* FOR REFRACTORY V. FIB
* IV AMIODARONE FOLLOWED BY DEFIBRILLATION
* LIDOCAINE, MAGNESIUM, AND PROCAINAMIDE ARE SECOND-
LINE AGENTS
IF CARDIOVERSION IS SUCCESSFUL
* MAINTAIN CONTINUOUS IV INFUSION OF AMIODARONE (OR ANY
EFFECTIVE ANTIARRHYTHMIC DRUG)
* IMPLANTABLE DEFIBRILLATORS: FOR PTS AT RISK OF V. FIB
* LONG-TERM AMIODARONE THERAPY IS AN ALTERNATIVE
