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Transcript of Wandering Atrial Pacemaker Multifocal Atrial Tachycardia Atrial Tachycardia Premature Atrial...
Wandering Atrial Pacemaker Multifocal Atrial Tachycardia Atrial Tachycardia Premature Atrial Contractions Paroxysmal Supraventricular
Tachycardia Atrial Flutter Atrial Fibrillation
NormalQRS
NormalPRI
Changes from beat to beat P Waves
VariesPacemaker Site
Slightly IrregularRhythm
Usually normalRate
Wandering Pacemaker
Rules of Interpretation
Wandering PacemakerEtiology
Transfer of pacemaker sites from the sinus node to other latent pacemaker sites in the atria and AV junction
A variant of sinus dysrhythmia, a normal phenomenon in the very young or the aged, Ischemic heart disease, atrial dilation
Clinical significance Usually has no detrimental effects Precursor of other atrial dysrhythmias such as
atrial fibrillation Treatment
If the patient is symptomatic, consider adenosine or verapamil
VariableQRS
Varies depending on source of impulse
PRI
Organized, nonsinus P waves; at least 3 formsP Waves
Ectopic sites in atriaPacemaker Site
IrregularRhythm
More than 100Rate
Multifocal Atrial Tachycardia
Rules of Interpretation
Multifocal Atrial TachycardiaEtiology
Often seen in acutely ill patients May result from pulmonary disease, metabolic
disorders, ischemic heart disease, or recent surgery
Clinical Significance Presence of multifocal atrial tachycardia often
indicates a serious underlying illnessTreatment
Treat the underlying illness
Usually normalQRS
Varies dependent on foci of impulse
PRI
Occurs earlier than expected
P Waves
Ectopic sites in atriaPacemaker Site
Usually regular except for the PAC
Rhythm
Depends on underlying rhythm
Rate
Premature Atrial Contractions
Rules of Interpretation
Premature Atrial ContractionsEtiology
Single electrical impulse originating outside the SA node
May result from use of caffeine, tobacco, or alcohol, sympathomimetic drugs, ischemic heart disease, hypoxia, or digitalis toxicity, or may be idiopathic
Clinical Significance None. Presence of PACs may be a precursor to
other atrial dysrhythmias.Treatment
None if asymptomatic. Treat symptomatic patients by administering high-flow, high-concentration oxygen and establishing IV access.
Usually normalQRS
Usually normalPRI
Often buried in preceding T wave
P Waves
Atrial (outside SA Node)
Pacemaker Site
RegularRhythm
150–250Rate
Paroxysmal Supraventricular Tachycardia
Rules of Interpretation
Paroxysmal Supraventricular TachycardiaEtiology
Rapid atrial depolarization overrides the SA node May be precipitated by stress, overexertion,
smoking, caffeineClinical Significance
May be tolerated well by healthy patients for short periods
Marked reduction in cardiac output can precipitate angina, hypotension, or congestive heart failure
Paroxysmal Supraventricular TachycardiaTreatment
Vagal Maneuvers Pharmacological Therapy
Adenosine Electrical Therapy
Consider if patient symptomatic with HR >150. Synchronized cardioversion starting at 50-100 J (or
biphasic equivalent
NormalQRS
Usually normalPRI
Difficult to seeP Waves
In the atriaPacemaker Site
RegularRhythm
150-250 bpmRate
Supraventricular Tachycardia
Rules of Interpretation
Supraventricular TachycardiaEtiology
Refers to tachycardias that originate above the ventricles
Use of caffeine, nicotine, or alcohol, cocaine sympathomimetic drugs, ischemic heart disease
Clinical Significance Rapid rates can cause a marked reduction in
cardiac output because of inadequate ventricular filling time
Treatment Manage with tachycardia algorithm
Click here to view the Tachycardia Management diagram.Reproduced with permission from “2005 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Care,” Circulation 2005, Volume 112, IV-70. © 2005 American Heart Association.
Usually normalQRS
Usually normalPRI
F waves are present
P Waves
Atrial (outside SA node)
Pacemaker Site
Usually regularRhythm
Atrial rate 250–350Ventricular rate variesRate
Atrial Flutter
Rules of Interpretation
Atrial FlutterEtiology
Results when the AV node cannot conduct all the impulses Impulses may be conducted in fixed or variable
ratios Usually associated with organic disease such as
congestive heart failure (rarely seen with MI)Clinical Significance
Generally well tolerated Rapid ventricular rates may compromise cardiac
output and result in symptoms May occur in conjunction with atrial fibrillation
Atrial FlutterTreatment
Electrical Therapy Consider if ventricular rate >150 and symptomatic Synchronized cardioversion starting at 100 J
Pharmacological Therapy Diltiazem or beta blockers Do not use a calcium channel and beta blockers
concomitantly
NormalQRS
NonePRI
None discernibleP Waves
Atrial (outside SA Node)Pacemaker Site
Irregularly irregularRhythm
Atrial rate 350–750Ventricular rate variesRate
Atrial Fibrillation
Rules of Interpretation
Atrial FibrillationEtiology
Results from multiple ectopic foci; AV conduction is random and highly variable
Often associated with underlying heart diseaseClinical Significance
Atria fail to contract effectively, reducing cardiac output
Well tolerated with normal ventricular rates High or low ventricular rates can result in cardiac
compromise
Atrial FibrillationTreatment
Electrical Therapy Consider if ventricular rate >150 and symptomatic Synchronized cardioversion starting at 100 J
Pharmacological Therapy Diltiazem or beta blockers
AV junction serves two important physiological purposes:Slows the impulse between the atria and
the ventricles Backup pacemaker if the SA node or cells
higher in the conductive system fail to fire
AV BlocksLocations
At the AV node At the Bundle of His Below the Bundle of
HisClassifications
First-Degree AV block Type I Second-Degree
AV block Type II Second-Degree
AV block Third-Degree AV block
Usually <0.12 seconds
QRS
>0.20 SecondsPRI
NormalP Waves
SA node or atrialPacemaker Site
Usually regularRhythm
Depends on underlying rhythm
Rate
First-Degree AV Block
Rules of Interpretation
First-Degree AV BlockEtiology
Delay in the conjunction of an impulse through the AV node
May occur in healthy hearts, but often indicative of ischemia at the AV junction
Clinical Significance Usually not significant, but new onset may
precede a more advanced blockTreatment
Generally, none required other than observation Avoid drugs that may further slow AV conduction
Usually <0.12 secondsQRS
Increases until QRS is dropped, then repeatsPRI
Normal, some P waves not followed by QRSP Waves
SA node or atrialPacemaker Site
Atrial, regular; ventricular, irregular
Rhythm
Atrial, normal; ventricular, normal to
slowRate
Type I Second-Degree AV Block
Rules of Interpretation
Type I Second-Degree AV BlockEtiology
Also called Mobitz I, or Wenckebach Delay increases until an impulse is blocked Indicative of ischemia at the AV junction
Clinical Significance Frequently dropped beats can result in cardiac
compromiseTreatment
Generally, none required other than observation Avoid drugs that may further slow AV conduction Treat symptomatic bradycardia
Normal or >0.12 secondsQRS
Constant for conducted beats, may be >0.21 secondsPRI
Normal, some P waves not followed by QRSP Waves
SA node or atrialPacemaker Site
May be regular or irregular
Rhythm
Atrial, normal; ventricular, slow
Rate
Type II Second-Degree AV Block
Rules of Interpretation
Type II Second-Degree AV BlockEtiology
Also called Mobitz II or infranodal Intermittent block of impulses Usually associated with MI or septal necrosis
Clinical Significance May compromise cardiac output and is indicative
of MI Often develops into full AV blocks
Treatment Avoid drugs that may further slow AV conduction Treat symptomatic bradycardia
Consider transcutaneous pacing Atropine
Normal or >0.12 secondsQRS
Constant for conducted beats, may be >0.21 secondsPRI
2 P waves for each QRSP Waves
SA node or atrialPacemaker Site
RegularRhythm
Atrial, normal; ventricular, slow
Rate
2:1 AV Block
Rules of Interpretation
2:1 AV BlockEtiology
Second degree AV block where there are two P waves for each QRS
Associated with acute myocardial infarction and septal necrosis
Clinical significance Can compromise cardiac output Can develop into full AV block
Treatment Prepare for transcutaneous pacing Atropine
0.12 seconds or greaterQRS
No relationship to QRSPRI
Normal, with no correlation to QRS
P Waves
SA node and AV junction or ventricle
Pacemaker Site
Both atrial and ventricular are regularRhythm
Atrial, normal; ventricular, 40–60
Rate
Third-Degree AV Block
Rules of Interpretation
Third-Degree AV Block (Complete Heart Block)Etiology
Absence of conduction between the atria and the ventricles
Results from AMI, digitalis toxicity, or degeneration of the conductive system
Clinical Significance Severely compromised cardiac output
Treatment Transcutaneous pacing for acutely symptomatic
patients Treat symptomatic bradycardia Avoid drugs that may further slow AV conduction
DysrhythmiasPremature junctional contractions Junctional escape complexes and rhythm Junctional bradycardiaAccelerated junctional rhythm
Characteristics of all junctional rhythms Inverted P Waves in Lead IIPRI of <0.12 SecondsNormal QRS Complex Duration
Usually normalQRS
Normal if P occurs before QRS
PRI
Inverted, may occur after QRS
P Waves
Ectopic focus in the AV junction
Pacemaker Site
Depends on underlying rhythm
Rhythm
Depends on underlying rhythm
Rate
Rules of InterpretationPremature Junctional Contractions
Premature Junctional ContractionsEtiology
Single electrical impulse originating in the AV node May occur with use of caffeine, tobacco, alcohol,
sympathomimetic drugs, ischemic heart disease, hypoxia, or digitalis toxicity, or may be idiopathic
Clinical Significance Limited, frequent PJCs may be precursor to other
junctional dysrhythmiasTreatment
None usually required
Usually normalQRS
Normal if P occurs before QRS
PRI
Inverted, may occur after QRS
P Waves
AV junctionPacemaker Site
Irregular in single occurrence, regular
in escape rhythmRhythm
40–60Rate
Junctional Escape Complexes and Rhythms
Rules of Interpretation
Junctional Escape Complexes and RhythmsEtiology
Results when the AV node becomes the pacemaker Results from increased vagal tone, pathologically
slow SA discharges, or heart blockClinical Significance
Slow rate may decrease cardiac output, precipitating angina and other problems
Treatment None if the patient remains asymptomatic Treat symptomatic episodes with atropine or pacing
Usually normal, may be greater than 0.12
QRS
Normal if P occurs before QRS
PRI
Inverted, may occur after QRS
P Waves
AV junctionPacemaker Site
Irregular in single occurrence, regular in
escape rhythmRhythm
Less than 40Rate
Junctional Bradycardia
Rules of Interpretation
Junctional BradycardiaEtiology
Junctional dysrhythmia with a heart rate less than the intrinsic rate of the AV node
Increased vagal tone, pathological slow SA node discharge, heart block, intrinsic disease
Clinical Significance Decreased cardiac output
Treatment Prepare for transcutaneous pacing Consider Atropine
NormalQRS
Normal if P occurs before QRS
PRI
Inverted, may occur after QRS
P Waves
AV junctionPacemaker Site
RegularRhythm
60–100Rate
Accelerated Junctional Rhythm
Rules of Interpretation
Accelerated Junctional RhythmEtiology
Results from increased automaticity in the AV junction
Often occurs due to ischemia of the AV junctionClinical Significance
Usually well tolerated, but monitor for other dysrhythmias
Treatment None generally required in the prehospital
setting
NormalQRS
Normal if P occurs before QRS
PRI
Inverted, may occur after QRS
P Waves
AV junctionPacemaker Site
RegularRhythm
60-100Rate
Accelerated Junctional Rhythm
Rules of Interpretation
Accelerated Junctional RhythmEtiology
Results from increased automaticity in the AV junction
Ischemia of the AV junction Clinical Significance
Patient should be monitored for other dysrhythmias Treatment
Prehospital treatment generally is unnecessary
Ventricular escape complexes and rhythms
Accelerated idioventricular rhythm
Premature ventricular contraction
Ventricular tachycardia
Torsades de pointes
Ventricular fibrillation
Asystole Artificial
pacemaker rhythm
>0.12 seconds, bizarreQRS
NonePRI
NoneP Waves
VentriclePacemaker Site
Escape complex, irregular;escape rhythm, RegularRhythm
15–40Rate
Ventricular Escape Complexesand Rhythms
Rules of Interpretation
Ventricular Escape Complexes and RhythmsEtiology
Safety mechanism to prevent cardiac standstill Results from failure of other foci or high-degree
AV blockClinical Significance
Decreased cardiac output, possibly to life-threatening levels
Treatment For perfusing rhythms, administer atropine
and/or TCP For nonperfusing rhythms, follow pulseless
electrical activity (PEA) protocols
>0.12 seconds, bizarre
QRS
NonePRI
NoneP Waves
VentriclePacemaker Site
Escape complex, irregular;escape rhythm, RegularRhythm
60-100Rate
Accelerated Idioventricular Rhythm
Rules of Interpretation
Accelerated Idioventricular RhythmEtiology
A subtype of ventricular escape rhythm that frequently occurs with MI
Ventricular escape rhythm with a rate of 60–110Clinical Significance
May cause decreased cardiac output if the rate slows
Treatment Does not usually require treatment unless the
patient becomes hemodynamically unstable Primary goal is to treat the underlying MI
>0.12 seconds, bizarreQRS
NonePRI
NoneP Waves
VentriclePacemaker Site
Interrupts regular underlying rhythm
Rhythm
Underlying rhythmRate
Premature Ventricular Contractions
Rules of Interpretation
Premature Ventricular Contractions Etiology
Single ectopic impulse resulting from an irritable focus in either ventricle
Myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid-base disturbances, electrolyte imbalances, or as a normal variation of the ECG
May occur in patterns Bigeminy, trigeminy, or quadrigeminy Couplets and triplets
Premature Ventricular ContractionsClinical Significance
Malignant PVCs More than 6/minute, R on T phenomenon, couplets
or runs of ventricular tachycardia, multifocal PVCs, or PVCs associated with chest pain
Ventricles do not adequately fill, causing decreased cardiac output
Premature Ventricular ContractionsTreatment
Nonmalignant PVCs do not usually require treatment in patients without a cardiac history
Cardiac patient with nonmalignant PVCs Administer oxygen and establish IV access
Malignant PVCs: Lidocaine 1.0 –1.5 mg/kg IV bolus Repeat doses of 0.5-0.75 mg/kg to max dose of 3.0
mg/kg If PVCs are suppressed, administer lidocaine drip 2–
4 mg/min Reduce the dose in patients with decreased output
or decreased hepatic function and patients >70 years old
>0.12 seconds, bizarre
QRS
NonePRI
If present, not associated with
QRSP Waves
VentriclePacemaker Site
Usually regularRhythm
100–250Rate
Ventricular Tachycardia
Rules of Interpretation
Ventricular TachycardiaEtiology
3 or more ventricular complexes in succession at a rate of >100
Causes include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid-base disturbances, or electrolyte imbalances
VT may appear monomorphic or polymorphic Torsade’s De Pointes
Clinical Significance Decreased cardiac output, possibly to life-
threatening levels May deteriorate into ventricular fibrillation
Click here to view an animation on dysrhythmia.
Click here to view the Tachycardia Management diagram.Reproduced with permission from “2005 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Care,” Circulation 2005, Volume 112, IV-70. © 2005 American Heart Association.
Torsades de pointes Polymorphic VTUse of certain
antidysrhythmic drugs
Exacerbated by coadministration of antihistamines, azole antifungal agents and macrolide
Torsades de pointesTypically occurs in nonsustained bursts
Prolonged QT interval during “breaks” QRS rates from 166–300 RR interval highly variable
Treatment Do not treat as standard VT Administer magnesium sulfate 1–2 g diluted in
100 ml D5W over 1–2 minutes Overdrive pacing
NoneQRS
NonePRI
Usually absentP Waves
Numerous ventricular foci
Pacemaker Site
No organized rhythm
Rhythm
No organized rhythm
Rate
Ventricular Fibrillation
Rules of Interpretation
Ventricular FibrillationEtiology
Wide variety of causes, often resulting from advanced coronary artery disease
Clinical Significance Lethal dysrhythmia with no cardiac output and
no organized electrical pattern
Ventricular FibrillationTreatment
Initiate CPR Defibrillate with 360 J (or biphasic equivalent) Control the airway and establish IV access Administer epinephrine 1:10,000 every 3–5
minutes Consider 40 IU Vasopressin IV (one time only)
Consider second-line drugs Amiodarone Lidocaine
Provide continuous compressions
AbsentQRS
AbsentPRI
AbsentP Waves
No Electrical Activity
Pacemaker Site
No Electrical Activity
Rhythm
No Electrical Activity
Rate
Asystole
Rules of Interpretation
AsystoleEtiology
Primary event in cardiac arrest, resulting from massive myocardial infarction, ischemia, and necrosis
Final outcome of ventricular fibrillationClinical Significance
Asystole results in cardiac arrest Poor prognosis for resuscitation
AsystoleTreatment
Administer CPR and manage the airway Treat for ventricular fibrillation if there is any
doubt about the underlying rhythm Administer medications:
Epinephrine and Atropine
Click here to view the Pulseless Arrest diagram.Reproduced with permission from “2005 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Care,” Circulation 2005, Volume 112, IV-59. © 2005 American Heart Association.
>0.12 seconds, bizarre
QRS
If present, variesPRI
None produced by ventricular pacemakers;
pacemaker spikeP Waves
Depends upon electrode placement
Pacemaker Site
May be regular or irregular
Rhythm
Varies with
pacemakerRate
Artificial Pacemaker
Rules of Interpretation
Artificial Pacemaker RhythmEtiology
Single vs. dual chamber pacemakers Fixed-rate vs. demand pacemakers
Clinical Significance Used in patients with a chronic high-grade heart
block, sick sinus syndrome, or severe symptomatic bradycardia
Artificial Pacemaker RhythmProblems with Pacemakers
Battery failure “Runaway” pacers Displaced leads
Management Considerations Identify patients with pacemakers Treat the patient
Use of a Magnet
CharacteristicsElectrical impulses are present, but with
no accompanying mechanical contractions of the heart
Treat the patient, not the monitor Causes
Hypovolemia, cardiac tamponade, tension pneumothorax, hypoxemia, acidosis, massive pulmonary embolism, ventricular wall rupture
TreatmentPrompt recognition and early treatmentEpinephrine 1 mg every 3–5 minutesTreat underlying cause of PEA
Categories of Conductive DisordersAtrioventricular BlocksDisturbances of Ventricular ConductionPre-excitation Syndromes
Disturbances of Ventricular ConductionAberrant Conduction
A single supraventricular beat conducted through the ventricles in a delayed manner
Bundle Branch Block All supraventricular beats are conducted through
the ventricles in a delayed manner Causes
Ischemia or necrosis of a bundle branch PAC or PJC that reaches one of the bundle
branches in a refractory periodDifferentiation of SVT and Wide-Complex
Tachycardias
Pre-excitation SyndromesExcitation by an
impulse that bypasses the AV node Creates Delta wave slur
Wolff-Parkinson-White (WPW) syndrome Conduction from the
atria to the ventricles is abnormal
Associated with tachydysrhythmias
Wolfe-Parkinson-White Syndrome
HypokalemiaNormal potassium
levels are 3.5–-5.0 mEg/L
Flattened T waves Prominent U waves
HyperkalemiaTall Ts
Suspect in patients with a history of renal failure
HypocalcemiaCan be caused by
the use of diuretics and certain endocrine conditions
Prolongs ST segment
HypercalcemiaCan be caused by
adrenal insufficiency, hyperparathyroidism, kidney failure, or malignancies
Shortens ST segment
Digitalis useSagging or
scooping of the ST segment
Prolonged PR interval
HypothermiaOsborn wave
(“J” wave)T wave
inversion, sinus bradycardia, atrial fibrillation or flutter, AV blocks, PVCs, VF, asystole
Cardiovascular Anatomy Cardiovascular Physiology Electrocardiographic Monitoring Dysrhythmias