dysrhytmias & hemodynamic monitoring. cardiac rhythm monitoring 12 lead ecg telemetry halter...
TRANSCRIPT
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DYSRHYTMIAS& Hemodynamic Monitoring
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Cardiac Rhythm Monitoring 12 lead ECG Telemetry Halter monitor Bedside monitor
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Lead placement 12 lead
12 lead ECG
Diagnostic Structural
changes Ischemia Infarction Enlarged cardiac
chambers Electrolyte
imbalances Drug toxicity
Assessment of dysrhythmias
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Lead placement 5 lead
5 lead monitoring
Telemetry monitoring ICU Holter monitors Provides more views
in different leads
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Lead placement 3 lead Three Lead
Less lead views Simple monitoring Quick
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Patch Considerations
Properly prepare skin Clip excessive hair on
the chest wall with scissors
Gently rub the skin with dry gauze
If skin is oily, wipe with alcohol first
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Heart Anatomy& Conduction System
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Conduction System
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Properties of Cardiac Cells Automaticity
Ability to initiate an impulse spontaneously and continuously
Excitability
Ability to be electrically stimulated
Conductivity
Ability to transmit an impulse along membrane in an orderly
manner
Contractility
Ability to respond mechanically to an impulse
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Nervous System Control of the Heart
Autonomic nervous system
controls: Rate of impulse formation Speed of conduction Strength of contraction
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Nervous System Control of the Heart
Parasympathetic nervous system Vagus nerve Decreases rate Slows impulse conduction Decreases force of contraction
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Nervous System Control of the Heart
Sympathetic nervous system Increases rate Increases force of contraction
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Intrinsic Rates of the Conduction System
SA node 60-100
AV node 40-60
Bundle of His, Purkinje fibers 20-40
Ventricles <20
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P Wave Atrial depolarization Firing of SA node Should be upright
Normal duration 0.06-0.12 sec
Source of variation Disturbance in atria
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PR Interval
Impulse through atria to AV node, bundle of His
Measured from beginning of P wave to beginning of QRS complex
Normal duration 0.12-0.20 sec
Source of variation Short – impulse from AV
junction Longer – AV block
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QRS Interval Ventricular Depolarization Atrial repolarization
Hidden in wave Measured from the
beginning to end of QRS complex
Normal is not always a traditional wave form
Normal duration < 0.12 sec
Source of variation Disturbance in bundle
branches or in ventricles
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QRS variationsnot everyone has “normal” QRS
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ST Segment
Time between ventricular depolarization and repolarization
Should be flat (isoelectric) Look for elevation or
depression ST elevation – myocardial
injury ST depression – reciprocal
changes and ischemia Normal duration
0.12 sec Source of variation
Ischemia Injury infarction
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T Wave
Ventricular repolarization Should be upright Follows QRS complex Larger than a P wave Inversion indicates ischemia
to myocardium Normal duration
0.16 sec Sources of variation
Electrolyte imbalances Ischemia Infarction
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QT Interval Beginning of QRS complex to
end of T wave Represents time taken for
entire ventricular depolarization and repolarization
Normal duration 0.34-0.43 sec
Sources of variation Drugs Electrolyte imbalances Changes in heart rate – inverse
relationship
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U Wave
Sometimes seen after T wave
?? May be normal May indicate hypokalemia
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Rhythm interpretationA Systematic Approach
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Rules for Systematic Interpretation
If the rhythm doesn’t look right check your patient! Treat the patient not the monitor
Is the rhythm regular or irregular – R to R, then P to P
What is the heart rate Can you identify P waves Can you identify QRS complexes & T waves What is the ratio of P waves to QRS complexes What is the PR interval Anything else you notice that shouldn’t be there
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Calculating Heart RateRegular
Small blocks into 1500Large blocks into 300
Irregular = 6-second strip
Divide by 300 between waves
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Atrial Rhythms Rhythms that originate in the
atria
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Normal Sinus Rhythm
Follows normal conduction pattern Rate
60-100 P wave
Normal , one per QRS PR interval
Normal, consistent (0.12-0.20) QRS complex
Normal (<0.12)
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Sinus Bradycardia
ECG characteristics Rhythm
Regular, slow Rate
<60 P wave
Normal, one per QRS PR interval
0.12-0.20, consistent QRS complex
Normal, <0.12
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Sinus Bradycardia Clinical Associations
Normal in fit, athletic individuals Normal in sleep Increased vagal tone –e.g. vomiting Drugs
Beta blockers Calcium channel blockers
Hypothyroidism MI Increased intracranial pressure Hypoglycemia
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Sinus Bradycardia Clinical significance
Dependent on patient tolerance Symptomatic
Pale Cool skin Hypotension Weakness Angina Dizziness Syncope Confusion or disorientation SOB
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Sinus Bradycardia Treatment
Atropine Pacemaker Treat underlying cause
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Sinus Tachycardia
ECG characteristics Rhythm
Regular, fast Rate
100-200 P wave
Normal, one for every QRS PR interval
0.12-0.20, consistent QRS complex
Normal, <0.12
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Sinus Tachycardia Clinical Associations
Exercise Anxiety, pain, fear Hypotension Hyperthyroidism Hypovolemia Anemia Hypoxia Hypoglycemia MI Heart failure
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Sinus Tachycardia
Clinical Associations (cont’d) Drugs
Epinephrine Norepinephrine Atropine Caffeine Theophylline Nifedipine Hydralazine Sudafed
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Sinus Tachycardia Clinical significance
Dependent on tolerance Symptoms
Dizziness Dyspnea Hypotension Angina
Treatment Treat underlying cause Vagal maneuvers Beta blockers
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Sinus Arrhythmia
ECG characteristics Rhythm
Irregular, but with a pattern Speeds up with respiration
Rate 60-100
P wave normal
PR interval normal
QRS complex normal
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Sinus Arrhythmia Clinical Associations Clinical significance Treatment
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Atrial Fibrillation
ECG characteristics Rhythm
irregular Rate
Atrial 350-600, irregular Ventricular - < & > 100 – irregular
P wave Irregular, chaotic
PR interval Not measurable
QRS complex normal
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Atrial Fibrillation Clinical Associations
CAD Rheumatic heart disease cardiomyopathy Hypertensive heart disease Heart failure Pericarditis Thyrotoxicosis Alcohol intoxication Caffeine Electrolyte disturbances Stress Cardiac surgery
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Atrial Fibrillation Clinical significance
Most common, clinically significant dysrhythmia Decreased cardiac output Thrombus formation Stroke
Accounts for as many as 20% of all strokes Treatment
Calcium channel blockers Beta blockers Digoxin Amiodarone Cardioversion Anticoagulation therapy
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Atrial Flutter
ECG characteristics Rhythm
May be regular or irregular Rate
Atrial – 200-350 and regular Ventricular - < & > 100 – regular or irregular
P wave Flutter waves – sawtoothed More than QRS complexes – may be in a ratio
PR interval Not measurable
QRS complex Normal
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Atrial Flutter Clinical Associations
CAD HTN Mitral valve disorders PE’s Chronic lung disease Cor pulmonale Cardiomyopathy Hyperthyroidism Digoxin Quinidine Epinephrine
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Atrial Flutter Clinical significance
Decrease cardiac output Heart failure Increased risk of stroke
Treatment Slow ventricular response by increasing AV
block Calcium channel blockers Beta blockers Cardioversion Amiodarone Rhythmol Ablation
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Supraventricular Tachycardia
ECG characteristics Rhythm
Regular Rate
150-220 P wave
Difficult to determine – may be hidden Abnormal
PR interval Normal or shortened
QRS complex Normal
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Supraventricular Tachycardia Clinical Associations
Overexertion Emotional stress Deep inspiration Caffeine Tobacco Rheumatic heart disease Digitalis toxicity CAD Cor pulmonale
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Supraventricular Tachycardia Clinical significance
Prolonged episodes may precipitate decreased cardiac output
Symptoms Hypotension Dyspnea Angina
Treatment Vagal stimulation
Valsalva maneuver Drugs
Adenosine Beta blockers Calcium channel blockers
Cardioversion
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Asystole
There is no electrical activity in the heart during asystole, therefore there will only be a flat line on the rhythm strip
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Asystole Clinical Associations
Advanced cardiac disease Severe cardiac conduction system disturbance End stage heart failure
Clinical significance Prolonged arrest, may not be resuscitated
Treatment CPR with ACLS Epinephrine Atropine Intubation Transcutaneous temporary pacemaker
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Premature Beats
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Premature Atrial Contractions (PAC’s)
Beats occur early in the cycle and there is no compensatory pause ECG characteristics
Rhythm irregular
Rate Dependent on underlying rhythm
P wave Abnormal shape
PR interval Normal Will be different than underlying rhythm
QRS complex Normal
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Premature Atrial Contractions (PAC’s) Clinical Associations
Can occur normally Emotional stress Physical fatigue Alcohol Caffeine Tobacco CHF Ischemia COPD Hypoxia Hyperthyroidism CAD
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Premature Atrial Contractions (PAC’s)
Clinical significance In healthy hearts, not significant Symptoms
Heart “skipped” beat Palpitations
May be early indication of more serious dysrhythmias
Treatment Reduce stimulants Beta blockers
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Premature Ventricular Contractions (PVC’s)
Beat early in cycle with compensatory pause ECG characteristics
Rhythm irregular
Rate Dependent on underlying rhythm
P wave No P wave with premature beat
PR interval none
QRS complex Wide bizarre, >0.12
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Premature Ventricular Contractions (PVC’s) Bigeminy
Every other beat is a PVC Trigeminy
Every third beat is a PVC Unifocal
All PVC’s from same source Look alike
Multifocal Different sources of beat Beats look different
Couplet Two in a row Runs will turn into V-tach
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Premature Ventricular Contractions (PVC’s)
Clinical Associations Caffeine Alcohol Nicotine Aminophylline Epinephrine Digoxin Electrolyte imbalances Hypoxia Fever Exercise Emotional stress MI Mitral valve prolapse Heart failure CAD
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Premature Ventricular Contractions (PVC’s) Clinical significance
Usually benign May precipitate
Decreased cardiac output Angina Heart failure
Assess apical-radial pulse rate Treatment
Treat underlying cause Beta blockers Procainamide Amiodarone Lidocaine
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Premature Junctional Contractions (PJC’s)
Beat occurs early in cycle and no compensatory pause ECG characteristics
Rhythm Irregular
Rate Dependent on underlying rhythm
P wave May or may not be present – if present will be inverted
PR interval Different from underlying rhythm if there at all
QRS complex normal
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Premature Junctional Contractions (PJC’s) Clinical significance &Treatment
Similar to PAC’s
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Junctional Rhythms Originate below atria and above
ventricles
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Junctional Rhythm
ECG characteristics Rhythm
regular Rate
40-60 P wave
Inverted, may be hidden in QRS complex PR interval
Shortened or missing QRS complex
normal
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Accelerated Junctional Rhythm & Junctional Tachycardia
ECG characteristics Rhythm
regular Rate
60-180 P wave
Inverted, may be hidden in QRS complex PR interval
Shortened or missing QRS complex
normal
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Junctional Dysrhythmias Clinical Associations
CAD Heart failure Cardiomyopathy Electrolyte imbalances Inferior MI Rheumatic heart disease Digoxin Amphetamines Caffeine Nicotine
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Junctional Dysrhythmias Clinical significance
Occur when the SA node has not been effective
If increases to junctional tachycardia patient may become hemodynamically unstable
Treatment Dependent on tolerance Atropine Beta blockers Calcium channel blockers Amiodarone
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Ventricular Rhythms Originate in the ventricles
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Idioventricular Rhythm
ECG characteristics Rhythm
Regular Rate
20-40 P wave
none PR interval
absent QRS complex
Wide, bizarre >0.20
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Ventricular Tachycardia
ECG characteristics Rhythm
Regular R to R Rate
Ventricular rate 150-250 P wave
none PR interval
none QRS complex
Wide, bizarre, > 0.12
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Ventricular Tachycardia Run of three or more PVC’s Clinical Associations
MI CAD Significant electrolyte imbalances Cardiomyopathy Mitral valve prolapse Long QT syndrome Drug toxicity CNS disorders
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Ventricular Tachycardia Clinical significance
Stable – patient has a pulse Unstable – no pulse Decreased cardiac output Hypotension Pulmonary edema Decreased cerebral blood flow Cardio-pulmonary arrest
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Ventricular Tachycardia Treatment
Treat quickly Identify and treat underlying causes Procainamide Sotalol Amiodarone Lidocaine Beta blockers Magnesium Dilantin Cardioversion CPR & ACLS
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Ventricular Fibrillation
ECG characteristics Rhythm
No rhythm present Rate
No rate P wave
No P waves PR interval
none QRS complex
none
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Ventricular Fibrillation Clinical associations
Acute MI Myocardial ischemia Heart failure Cardiomyopathy Cardiac catheterization Cardiac pacing Accidental electric shock Hyperkalemia Hypoxemia Acidosis Drug toxicity
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Ventricular Fibrillation Clinical significance
Symptoms Unresponsive Pulseless Apneic state
If not treated rapidly, patient will die Treatment
Immediate CPR & ACLS Immediate defibrillation
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Ventricular Standstill
ECG characteristics Rhythm
Regular p waves Rate
Atria 60-80 P wave
normal PR interval
none QRS complex
none
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Heart Blocks
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First Degree AV Block
ECG characteristics Rhythm
Regular Rate
Normal P wave
Normal PR interval
>0.20 QRS complex
normal
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First Degree AV Block Clinical Association
MI CAD Rheumatic fever Hyperthyroidism Vagal stimulation Digoxin Beta blockers Calcium channel blockers
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First Degree AV Block Clinical significance
Usually not serious Can be a precursor for higher degrees of AV
block Patients are asymptomatic
Treatment No treatment unless caused by medications Monitor patient for increase in block
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Second Degree AV Block – Type I
Also called Mobitz I or Wenckebach ECG characteristics
Rhythm Irregular
Rate Atrial – normal and regular Ventricular – slightly higher than atrial rate
P wave More p waves than QRS complexes
PR interval Progressing lengths until drops QRS
QRS complex Normal and then one dropped
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Second Degree AV Block – Type I Clinical Association
Digoxin Beta blockers CAD
Clinical significance Myocardial ischemia or infarction Generally transient and well tolerate May be warning sign for a more serious AV
disturbance Treatment
Symptomatic Atropine Temporary pacemaker
Asymptomatic Closely monitored Transcutaneous pacer on standby
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Second Degree AV Block – Type II
Also called Mobitz II ECG characteristics
Rhythm Irregular Regular if consistent conduction ratio
Rate Atrial – normal and regular Ventricular – slower, regular or irregular
P wave More p waves than QRS complexes, stated in a ratio
PR interval Normal or prolonged
QRS complex Preceded by two or more P waves
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Second Degree AV Block – Type II Clinical Association
Rheumatic heart disease CAD Anterior MI Drug toxicity
Clinical significance Often progresses to third degree AV block Poor prognosis Decreased cardiac output Hypotension Myocardial ischemia
Treatment Permanent pacemaker
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Third Degree AV Block
ECG characteristics Rhythm
R-R regular P-P regular
Rate Atrial 60-100 Ventricular 20-60, dependent on focus
P wave Normal, more P waves than QRS complexes
PR interval No relationship between P waves and QRS complexes
QRS complex Dependent on focus
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Third Degree AV Block Clinical Association
Severe heart disease CAD MI Myocarditis Cardiomyopathy
Amyloidosis Scleroderma Digoxin Beta blockers Calcium channel blockers
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Third Degree AV Block Clinical significance
Reduced cardiac output Ischemia Heart failure Shock Syncope possible periods of asystole
Treatment Pacemaker Atropine Epinephrine Dopamine Calcium chloride
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Bundle Branch Blocks
ECG characteristics QRS complex
Wide, bizarre
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Bundle Branch Blocks Clinical significance Treatment
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• http://www.skillstat.com/Flash/ECG_Sim_2004.html
• http://www.nobelprize.org/educational/medicine/ecg/index.html
• http://www.iphoneappsplus.com/medical/instant-ecg--an-electrocardiogram-rhythms-interpretation-guide/index.htm
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Defibrillation & Cardioversion
Including pacemakers and implanted cardioverter defibrillator
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Lifepak
Can be used as defibrillator, monitor, or transcutaneous pacer
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Defibrillation The use of a carefully controlled electric shock,
administered either through a device on the exterior of the chest wall or directly to the exposed heart muscle, to restart or normalize heart rhythms.
Most effective method of terminating V-Fib and pulseless V-Tach
Deliver energy using a monophasic or biphasic waveform Monophasic defibrillators deliver energy in one
direction. Biphasic defibrillators deliver energy in two
directions. Deliver successful shocks at lower energiesFewer post shock ECG abnormalities
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Defibrillation Output is measured in joules or watts
per second. Recommended energy for initial shocks
in defibrillation Biphasic defibrillators: First and
successive shocks: 150 to 200 joules Monophasic defibrillators: Initial shock at
360 joules
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Defibrillation
Indications Pulseless v-tach V-fib Always done as emergent
Contraindications Multifocal atrial tachycardia Digitalis toxicity
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Cardioversion Restoration of normal heart rhythm: the
use of an electric shock to convert a dangerously rapid, fluttering, and ineffective heartbeat to its normal rhythm Synchronized circuit delivers a counter
shock on the R wave of the QRS Synchronizer switch must be turned
ON
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Cardioversion Indications
A-fib If unstable or new witnessed onset – may do
without anticoagulation but preferred method is with anticoagulation three weeks prior
TEE to rule out blood clots A-flutter (if unstable)
Anticoagulation therapy Stable V-tach (with pulse)
If patient does not respond to medications Contraindications
Digitalis toxicity associated tachycardia
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Defibrillation & Cardioversion Nursing Considerations
IV access Airway management equipment Sedative drugs Monitor Be aware of possible implanted devices Firm pressure when discharging
Decrease chance for arcing and burns Clear of patient and bed
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Defibrillation & Cardioversion Complications
Hypoxia or hypoventilation from sedation Burns
Mostly superficial some deep tissue Dysrhythmias
Premature beats V-fib
Hypotension Pulmonary edema Thromboembolization Myocardial necrosis r/t high energy discharge
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ICD’s & Pacemakers
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Implantable Cardioverter- Defibrillators (ICD’s)
A, The implantable cardioverter-defibrillator (ICD) pulse generator from Medtronic, Inc.B, The ICD is placed in a subcutaneous pocket over the pectoralis muscle. A single-lead system is placed transvenously from the pulse generator to the endocardium. The single lead detects dysrhythmias and delivers an electric shock to the heart muscle.
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Indications for ICD
Spontaneous sustained v-tach Syncope with inducible v-tach/v-fib
during EP study At high risk for future life-threatening
dysrhythmias (cardiomyopathy) Have survived cardiac arrest
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ICD’s Consists of a lead system placed via
subclavian vein to the endocardium Battery-powered pulse generator is
implanted subcutaneously ICD sensing system monitors the HR and
rhythm and identifies VT or VF.
Approximately 25 seconds after detecting VT or VF, ICD delivers <25 joules.
If first shock is unsuccessful, ICD recycles and delivers successive shocks
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ICD’S ICDs are equipped with anti-tachycardia
and anti-bradycardia pacemakers. Initiate overdrive pacing of
supraventricular and ventricular tachycardias
Provide backup pacing for brady dysrhythmias that may occur after defibrillation discharges
Education is extremely important Participation in an ICD support group
should be encouraged
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A, A dual-chamber rate-responsive pacemaker from Medtronic, Inc., is designed to treat patients with chronic heart problems in which the heart beats too slowly to adequately support the body's circulation needs.B, Pacing leads in both the atrium and ventricle enable a dual-chamber pacemaker to sense and pace in both heart chambers.
Pacemakers
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Pacemakers Used to pace the heart when the normal
conduction pathway is damaged or diseased Pacing circuit consists of a power source,
one or more conducting (pacing) leads, and the myocardium
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Pacemaker types Permanent
Single chamber Dual chamber
Temporary Transcutaneous Transvenous epicardial
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Indications for permanent pacemakers
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Indications for a temporary pacemaker
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Pacemakers Anti-bradycardia pacing Anti-tachycardia pacing: Delivery of a
stimulus to the ventricle to terminate tachy-dysrhythmias
Overdrive pacing: Pacing the atrium at rates of 200 to 500 impulses per minute to terminate atrial tachycardias
Permanent pacemaker: Implanted totally within the body
Cardiac resynchronization therapy (CRT): Pacing technique that resynchronizes the cardiac cycle by pacing both ventricles
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Temporary pacemakers Temporary pacemaker: Power source
outside the body Transvenous
Leads threaded through veins to right atrium or ventricle
Epicardial Placed during cardiac surgery – leads are
passed through the chest wall and can be attached to an external power source
Transcutaneous Placed one lead on top of chest and one lead
posterior
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ICD’s & Pacemakers Complications
Infection Hematoma formation at sites of insertion Pneumothorax Failure to sense or capture Perforation of atrial or ventricular septum
by the pacing lead Corrosion of leads Battery depletion
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ECG Changes Associated with ACS
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ECG changes in ACS Ischemia
ST segment depression and/or T wave inversion
ST segment depression is significant if it is at least 1 mm (one small box) below the isoelectric line.
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ECG changes in ACS
Changes occur in response to the electrical disturbance in myocardial cells due to inadequate supply of oxygen.
Once treated (adequate blood flow is restored), ECG changes resolve and ECG returns to baseline
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ECG changes in ACS Injury
ST segment elevation is significant if >1 mm above the isoelectric line. If treatment is prompt and effective, may avoid
infarction If serum cardiac markers are present, an ST-segment-
elevation myocardial infarction (STEMI) has occurred.
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ECG changes in ACS Infarction
Physiologic Q wave is the first negative deflection following the P wave. Small and narrow (<0.04 second in
duration) Pathologic Q wave is deep and >0.03
second in duration
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ECG changes in ACS Infarction
Pathologic Q wave indicates that at least half the thickness of the heart wall is involved. Referred to as a Q wave MI Pathologic Q wave may be present
indefinitely. T wave inversion related to infarction
occurs within hours and may persist for months