Dysrhythmias Notes

8/2/2019 Dysrhythmias Notes

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DysrhythmiasDysrhythmiasD Abnormal cardiac rhythms are termed dysrhythmias.A Prompt assessment of dysrhythmias and the patients response tothe rhythm is critical.

Properties of Cardiac CellsProperties of Cardiac CellsP Automaticity happens on its ownh ExcitabilityE ConductivityC ContractilityStarts in SA node:AV node:Ventricles 20-40

P-wave: time it takes for impulse to go from SA node to AV nodeQRS: Down purkinje fibers

Conduction System of the HeartConduction System of the Heart

Nervous System Control of the HeartNervous System Control of the HeartAutonomic nervous system controls:A Rate of impulse formationR Speed of conductionS Strength of contractionSNervous System Control of the HeartNervous System Control of the HeartParasympathetic (rest and relax) nervous systemP Vagus nerveV Decreases rateD Slows impulse conductionS Decreases force of contractionSympathetic fight or flightnervous systemS Increases rateI Increases force of contractionIElectrocardiogram MonitoringElectrocardiogram Monitoringo Graphic tracing of electrical impulses produced by the heart

o Waveforms of ECG represent activity of charged ions across membranes

of myocardial cells.

12-Lead ECG12-Lead ECG


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12 recording leads1

Six leads (leads I, II, III, aVR, aVL, and aVF) measure electricalforces in the frontal plane.f

Six leads (V1V6) measure electrical forces in the horizontal plane(precordial leads).

P-wave atrial depolarizationQRS ventricle depolarizationT-wave - repolarization

Lead PlacementLead Placement

Depending on where the MI is you would choose the appropriate lead

Normal 12-Lead ECGNormal 12-Lead ECG

Lead PlacementLead Placement

ECG PaperECG PaperE

Rhythm strip provides documentation of patients rhythm.R

Allows for measurement of complexes and intervals

(1 mm going up (ST elevation), 0.04 for each little box going over toequal 0.20 for one square)

- know the 6-second interval

Assessment of Cardiac RhythmAssessment of Cardiac RhythmCalculating HRCalculating HRC

CountC

The number of QRS complexes in 1 minuteT

The R-R intervals in 6 seconds, and multiply by 10T

Number of small squares between one R-R interval, and divide thisnumber into 1500n

Number of large squares between one R-R interval, and divide this

number into 300

Assessment of Cardiac RhythmAssessment of Cardiac RhythmArtifact Artifact movement of the leadsmovement of the leadsTelemetry MonitoringTelemetry Monitoring


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1

HR and rhythm monitored from a distant siteH

Centralized monitoring systemC

Alarm system alerts when it detects dysrhythmias, ischemia, orinfarction.i

Evaluation of DysrhythmiasEvaluation of DysrhythmiasEHolter monitoring a pack and monitors all heart rate patterns over24/48 hour period.2

Event recorder monitoring they push a button during an event and itrecords it.r

Exercise treadmill testingE

Signal-averaged ECGS

Electrophysiologic studyE

Normal Electrical PatternNormal Electrical Pattern

(look in book)

PR - .12-.2 (can only come from sinus node if its .12)QRS - .04-.10 (.12) differs depending on book. Anything less than .12 really.Dont measure T-wave.

U wave = hypokalemia (a hump between T wave and next P wave)

St-elevation tells us MI or injurySt-depression tells us ischemia

Normal Sinus RhythmNormal Sinus Rhythm (from SA node)(

Sinus node fires 60 to 100 bpm.S

Follows normal conduction patternF

Sinus BradycardiaSinus BradycardiaS

Sinus node fires


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Clinical associationsC

Occurs in disease statesO

HypothyroidismH

Increased intracranial pressureIObstructive jaundiceO

Inferior wall MII

Sinus Bradycardia Sinus Bradycardia symptomatic observationssymptomatic observationss

Clinical significanceC

Dependent on symptomsD

HypotensionH

Pale, cool skinP

WeaknessW

AnginaADizziness or syncopeD

Confusion or disorientationC

Shortness of breathS


Treatment if symptomaticT

AtropineA

Pacemaker may be required.0 3 types of pacemakers? - External, transvenous, implantable3

Sinus TachycardiaSinus TachycardiaS

Discharge rate from the sinus node is increased and is >100 bpm.

Sinus tach TREAT THE CAUSE!!! (test)

Sinus TachycardiaSinus TachycardiaS


Associated with physiologic stressorsA

ExerciseE

PainPHypovolemiaH

Myocardial ischemiaM

Heart failureH

FeverF

Sinus TachycardiaSinus Tachycardia


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S


Dizziness and hypotension due to decreased CO due to less fillingin the left ventriclei

Increased myocardial oxygen consumption may lead to angina.I

Sinus TachycardiaSinus TachycardiaSTreatmentT

Determined by underlying causeD

-adrenergic blockers to reduce HR and myocardial oxygenconsumptionc

Antipyretics to treat feverA

Analgesics to treat painAA

Premature Atrial ContractionPremature Atrial Contractiono Contraction originating from ectopic focus in atrium in location other

than SA nodeo Travels across atria by abnormal pathway, creating distorted P wave

o May be stopped, delayed, or conducted normally at the AV nodeM

Premature Atrial ContractionPremature Atrial ContractionJust the p-wave is funky....the qrs complex is still the same.

Premature Atrial ContractionPremature Atrial ContractionP


Can result fromC

Emotional stressE

Use of caffeine, tobacco, alcoholUHypoxiaH

Electrolyte imbalancesE

COPDC

Valvular diseaseV



Isolated PACs are not significant in those with healthy hearts.I

In persons with heart disease, may be warning of more serious

dysrhythmiad


TreatmentT

Depends on symptomsD

-adrenergic blockers may be used to decrease PACs.-

Reduce or eliminate caffeine


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Paroxysmal Supraventricular Tachycardia (PSVT)Paroxysmal Supraventricular Tachycardia (PSVT)P

Originates in ectopic focus anywhere above bifurcation of bundle of HisO

Run of repeated premature beats is initiated and is usually a PAC.R

Paroxysmal refers to an abrupt onset and termination. (something stops

and starts on its own)

Superventricular above the level of the ventricle somewhere in the atriaS

Sinus tach we would see a P before every qrs, with PSVT there is notrue Pwavett

QRS complex stays normal. The rhythm starts in the atria....Q

The rate of PSVT is generally greater than 150T

Paroxysmal Supraventricular Tachycardia (PSVT)Paroxysmal Supraventricular Tachycardia (PSVT)P

Clinical associationsC In a normal heartI

OverexertionO

Emotional stressE

StimulantsS

Digitalis toxicityD

Rheumatic heart diseaseR

CADC

Cor pulmonaleC

Decreased pulse/pressure/etc....blood out to skinD

Paroxysmal Supraventricular Tachycardia (PSVT)Paroxysmal Supraventricular Tachycardia (PSVT)Clinical significanceC

Prolonged episode and HR >180 bpm may precipitate COP

PalpitationsP

HypotensionH

DyspneaD

AnginaParoxysmal Supraventricular Tachycardia (PSVT)Paroxysmal Supraventricular Tachycardia (PSVT)P

Treatmento Vagal maneuvers: Valsalva, coughing,Test: put face in a dish of

ice water.o IV adenosine push as fast as you possibly can (3-6 seconds)

o If vagal maneuvers and/or drug therapy is ineffective and/or

patient becomes hemodynamically unstable, DC cardioversion should be used.


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Atrial FlutterAtrial Fluttero Atrial tachydysrhythmia identified by recurring, regular, sawtooth-

shaped flutter waveso Originates from a single ectopic focus

o Not a normal PR interval.....if it was than itd be sinus.

o One spot in atria takes over as pacemaker in the heart

o You need to look at all 12 leads to diagnose somethingY

Atrial FlutterAtrial FlutterAtrial FlutterAtrial FlutterA

Clinical associations: Usually occurs withC

CADC

HypertensionH

Mitral valve disordersM

Pulmonary embolusP

Chronic lung diseaseC

CardiomyopathyC

HyperthyroidismH

Atrial FlutterAtrial FlutterA


High ventricular rates (>100) and loss of the atrial kick (which isabout 20% of cardiac output) can decrease CO and precipitate HF,

angina.aRisk for stroke due to risk of thrombus formation in the atriaR

With atrial flutter you lose part of your cardiac output****W

Anti-coagulant (long-term) Coumadin...measure PT and INR foreffectiveness

Atrial FlutterAtrial FlutterA

Treatmento Primary goal: Slow ventricular response by increasing AV block

o Drugs to slow HR: Calcium channel blockers, -adrenergic

blockerso Electrical cardioversion may be used to convert the atrial

flutter to sinus rhythm emergently and electively.Atrial FlutterAtrial FlutterA

TreatmentT

Primary goal is to slow ventricular response by increasing AVblock.

o Antidysrhythmia drugs (e.g., amiodarone, propafenone) to


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convert atrial flutter to sinus rhythm or to maintain sinus rhythmo Radiofrequency catheter ablation can be curative therapy

for atrial flutter.f

Atrial FibrillationAtrial FibrillationA

Total disorganization of atrial electrical activity due to multiple ectopicfoci, resulting in loss of effective atrial contractionf

Most common dysrhythmiaM

Prevalence increases with age.P

Atrial FibrillationAtrial FibrillationHALLMARK: You have an irregular heart rate, a normal QRS (arising aboveatria), no discernable P-waves....so rhythm is being generated from multiplespots in atria, they all look different....1 out of every 10/15 will get throughwith no pattern. Heart rate is irregular.

The faster the heart rate the more problems with filling they have.


Clinical associations: Usually occurs with underlying heart diseaseC


CADC

CardiomyopathyC

HFH

PericarditisP

Anyone in long-term afib needs to be on anticoagulant!!

IF someone is in afib for more than 48 hours they need to be onanticoagulant for 3 weeks or so before cardiovesion so you dont throwa clot!


Clinical associations: Often acutely caused byC

ThyrotoxicosisT

Alcohol intoxicationA

Caffeine useC

Electrolyte disturbanceE

Cardiac surgeryAtrial FibrillationAtrial FibrillationA


Can result in decrease in CO due to ineffective atrial contractions(loss of atrial kick) and rapid ventricular response(

Thrombi may form in the atria as a result of blood stasis.


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T

Embolus may develop and travel to the brain, causing a stroke.

Atrial FibrillationAtrial FibrillationATreatmentT

GoalsG

Decrease ventricular rateD

Prevent embolic strokeP

Drugs for rate control: Digoxin, -adrenergic blockers, calciumchannel blockersc

Long-term anticoagulation: CoumadinL

Class of drug?C

Monitoring?M

New drugsAtrial FibrillationAtrial FibrillationA

TreatmentT

For some patients, conversion to sinus rhythm may be considered.

Antidysrhythmic drugs used for conversion: Amiodarone,A

DC cardioversion may be used to convert atrial fibrillation tonormal sinus rhythm.


TreatmentT

If patient has been in atrial fibrillation for >48 hours,anticoagulation therapy with warfarin (Coumadin) is

recommended for 3 to 4 weeks before cardioversion and for 4 to 6weeks after successful cardioversion.


TreatmentT

Radiofrequency catheter ablationR

Junctional DysrhythmiasJunctional DysrhythmiasJ

Dysrhythmia that originates in area of AV nodeD

SA node has failed to fire, or impulse has been blocked at the AV node.S

Junctional DysrhythmiasJunctional Dysrhythmias< .12....bc if it came from sinus node, the fastest it can get there it .12seconds, if its less than that it didnt come from the sinus node.

Rate between 40-60 and there is no PWAVE.

Junctional DysrhythmiasJunctional DysrhythmiasJ

Clinical associations


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C

CADC

HFH

CardiomyopathyC


Inferior MII

Rheumatic heart diseaseRDrugs: Digoxin, amphetamines, caffeine, nicotineD

Junctional DysrhythmiaJunctional DysrhythmiaJ


Serves as safety mechanism when SA node has not been effectiveS

Escape rhythms should not be suppressed. (bc the primary onehas failed......would be wiping out our safety net)h

If rhythms are rapid, may result in reduction of CO and HFI

Junctional DysrhythmiasJunctional DysrhythmiasJTreatmentT

If symptomatic, atropineI

Accelerated junctional rhythm and junctional tachycardia causedby digoxin toxicity; digoxin is heldb

First-Degree AV BlockFirst-Degree AV BlockF

Every impulse is conducted to the ventricles, but duration of AVconduction is prolonged.

When the PR is greater than .20 and everything else is normal. It got hung upin the AV node.


Clinical associations: Usually occurs withC

MI (especially in inferior wall MI, prone to heart blocks, need closemonitoring)m

CADC

Rheumatic feverR

HyperthyroidismH

Vagal stimulationV

Drugs: Digoxin, -adrenergic blockers, calcium channel blockers,flecainidef



Usually asymptomaticU

May be a precursor to higher degrees of AV block


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M

TreatmentT

Check medications.C

Continue to monitor.

Second-Degree AV Block, Type 1 (Mobitz I,Second-Degree AV Block, Type 1 (Mobitz I, WenckebachWenckebach))o Gradual lengthening of the PR interval due to prolonged AV conduction

timeo Atrial impulse is nonconducted, and a QRS complex is blocked (missing).

o Usually block occurs at AV node, but can occur in His-Purkinje system

PR continues to get progressively longer....then all the sudden you have a PR

Pwave with no QRS.....it resets itself.P

Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)

Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)S


Drugs: Digoxin, -adrenergic blockersD

May be associated with CAD and other diseases that can slow AVconductionc

Inferior wall MI can be precursor of things to comeI



Usually a result of myocardial ischemia or infarctionU

Almost always transient and well toleratedA

May be a warning signal of a more serious AV conductiondisturbanced


TreatmentT

If symptomatic, atropine or a temporary pacemakerI

If asymptomatic, monitor with a transcutaneous pacemaker onstandbys

Symptomatic bradycardia is more likely with one or more of thefollowing: Hypotension, HF, shock.f

Second-Degree AV Block, Type 2 (Mobitz II)Second-Degree AV Block, Type 2 (Mobitz II)S

Some P waves are not conducted, PR stays the same but a dropped QRS


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Underlying rhythm is usually regularU

(more Ps than QRSs)(

PR remains constantP

P to P is regularP

PR interval for the P waves that are conducted are consistentP

Second-Degree AV Block, Type 2 (Mobitz II)Second-Degree AV Block, Type 2 (Mobitz II)

Second-Degree AV Block, Type 2 (Mobitz II)Second-Degree AV Block, Type 2 (Mobitz II)S



CADC

Anterior MIA

Digitalis toxicitySecond-Degree AV Block, Type 2 (Mobitz II)Second-Degree AV Block, Type 2 (Mobitz II)S


Often progresses to third-degree AV block and is associated with apoor prognosisp

Reduced HR often results in decreased CO with subsequent

hypotension and myocardial ischemia.Second-Degree AV Block, Type 2 (Mobitz II)Second-Degree AV Block, Type 2 (Mobitz II)S

TreatmentT

If symptomatic (e.g., hypotension, angina) before permanentpacemaker can be inserted, temporary transvenous ortranscutaneous pacemakert

Permanent pacemakerP

Atropine and pacemaker = treatmentA

Third-Degree AV Heart Block (Third-Degree AV Heart Block (CompleteComplete Heart Block)Heart Block)

Form of AV dissociation in which no impulses from the atria areconducted to the ventriclesc

Atria are stimulated and contract independently of the ventricles.A

NO regular PR intervalN

Ventricular rhythm is an escape rhythm.V

Ectopic pacemaker may be above or below the bifurcation ofthe bundle of His.

NO connection between atrial and ventricular beats.


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No relationship between PWaves and QRSThey are all marching to their own beat, irregular

Side note: Ventricular inherent rate : 20-40 bpm

Third-Degree AV Heart Block (Complete Heart Block)Third-Degree AV Heart Block (Complete Heart Block)Third-Degree AV Heart Block (Complete Heart Block)Third-Degree AV Heart Block (Complete Heart Block)T


Severe heart disease: CAD, MI, myocarditis, cardiomyopathyS

Systemic diseases: Amyloidosis, sclerodermaS

Drugs: Digoxin, -adrenergic blockers, calcium channel blockersAs a general rule Atropine only works temporarily. They will need aAs a general rule Atropine only works temporarily. They will need apacemaker.pacemaker.

Third-Degree AV Heart Block (Complete Heart Block)Third-Degree AV Heart Block (Complete Heart Block)T


Decreased CO with subsequent ischemia, HF, and shockD

Syncope may result from severe bradycardia or even periods ofasystole.a

Third-Degree AV Heart Block (Complete Heart Block)Third-Degree AV Heart Block (Complete Heart Block)T

TreatmentT

If symptomatic, transcutaneous pacemaker until a temporarytransvenous pacemaker can be insertedt

Drugs (e.g., atropine)D

Temporary measure to increase HR and support BP until

temporary pacing is initiatedtPermanent pacemaker as soon as possibleP

Premature Ventricular ContractionsPremature Ventricular Contractionso Contraction originating in ectopic focus of the ventricles

o Premature occurrence of a wide and distorted QRS complex

o Multifocal, unifocal, ventricular bigeminy, ventricular trigeminy, couples,

triplets, R-on-T phenomenao Big, Fat, and Funny

Premature Ventricular ContractionsPremature Ventricular ContractionsTend to tell us the ventricles are irritated which can lead to bad things tocome, vtach and vfib.Because the ventricles beat so fast they dont have time to fill, decreasedcardiac output

Premature Ventricular ContractionsPremature Ventricular ContractionsP

Clinical associations


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C

Stimulants: Caffeine, alcohol, nicotine, aminophylline, epinephrine,isoproterenoli

DigoxinD


HypoxiaH

FeverFDisease states: MI, mitral valve prolapse, HF, CAD



In normal heart, usually benignI

In heart disease, PVCs may decrease CO and precipitate anginaand HF.a

Monitor patients response to PVCsM

PVCs often do not generate a sufficient ventricularcontraction to result in a peripheral pulse.c

Assess apical-radial pulse rate to determine if pulse deficitexists.e


Clinical significanceCRepresents ventricular irritabilityR

May occurM

After lysis of a coronary artery clot with thrombolytic therapyin acute MIreperfusion dysrhythmiasi

Following plaque reduction after percutaneous coronaryintervention


TreatmentT

Based on cause of PVCsB

Oxygen therapy for hypoxiaOElectrolyte replacementE

Drugs: -adrenergic blockers, procainamide, amiodarone,lidocainel

Ventricular TachycardiaVentricular TachycardiaV

Run of three or more PVCs

Monomorphic, polymorphic, sustained, and nonsustained


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Considered life-threatening because of decreased CO and the possibilityof deterioration to ventricular fibrillation

ABCs!Check pulse, open airway, CPR until crash cart comes...

Cardiovert!Want to shock them out of it!

Ventricular TachycardiaVentricular Tachycardia

If they dont have a pulse defibIf they do synchronized cardiovert



MIM

CADC


CardiomyopathyC

Mitral valve prolapseM

Long QT syndromeLDigitalis toxicityD

Central nervous system disordersC



VT can be stable (patient has a pulse) or unstable (patient ispulseless).p

Sustained VT: Severe decrease in COS

HypotensionH

Pulmonary edemaP

Decreased cerebral blood flowD

Cardiopulmonary arrest

Drugs: (know for sim-lab for CODE)AmiodaroneEpinephrineAtropine


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M



Treatment for VT must be rapid.T

May recur if prophylactic treatment is not initiatedM

Ventricular fibrillation may develop.Ventricular TachycardiaVentricular TachycardiaV

TreatmentT

VT without a pulse is a life-threatening situation.V

Cardiopulmonary resuscitation (CPR) and rapid defibrillationC

Epinephrine if defibrillation is unsuccessfulVentricular FibrillationVentricular FibrillationV

Severe derangement of the heart rhythm characterized on ECG byirregular undulations of varying contour and amplitudei

No effective contraction or CO occurs.

Ventricular FibrillationVentricular FibrillationVentricular FibrillationVentricular FibrillationV


Acute MI, CAD, cardiomyopathyA

May occur during cardiac pacing or cardiac catheterizationM

May occur with coronary reperfusion after fibrinolytic therapyVentricular FibrillationVentricular FibrillationV


Unresponsive, pulseless, and apneic stateU

If not treated rapidly, death will result.Ventricular FibrillationVentricular FibrillationV

TreatmentT

Immediate initiation of CPR and advanced cardiac life support(ACLS) measures with the use of defibrillation and definitive drugtherapyt

Asystole -Asystole - the worst thingt

Represents total absence of ventricular electrical activityR

No ventricular contraction (CO) occurs because depolarization does notoccur.

AsystoleAsystoleAClinical associationsC

Advanced cardiac diseaseA

Severe cardiac conduction system disturbanceS

End-stage HFAsystoleAsystoleA

Clinical significance


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C

Unresponsive, pulseless, and apneic stateU

Prognosis for asystole is extremely poor.AsystoleAsystoleA

TreatmentT

CPR with initiation of ACLS measures (e.g., intubation,

transcutaneous pacing, IV therapy with epinephrine and atropine))

Pulseless Electrical ActivityPulseless Electrical ActivityP

Electrical activity can be observed on the ECG, but no mechanical activityof the ventricles is evident, and the patient has no pulse.

o Rhythm but no pulse pt wont last long. Can be deceiving bc if youre

looking at a rhythm however, the patient could be dead. There is usually acause.


Clinical associations/causesc

HypovolemiaH

Hypoxia treat with oxygen, find out why (pneumo, flail chest?)t

Metabolic acidosis cause? bicarbc

Hyperkalemia or hypokalemiaH

HypothermiaHHAVE TO FIX THE CAUSE OR IT WONT RESOLVE.H


TreatmentT

CPR followed by intubation and IV epinephrineC

Atropine is used if the ventricular rate is slow.A

Treatment is directed toward correction of the underlying cause.T

Sudden Cardiac Death (SCD)Sudden Cardiac Death (SCD)S

Death from a cardiac causeDMajority of SCDs result from ventricular dysrhythmias.M

Ventricular tachycardiaV

Ventricular fibrillationDefibrillationDefibrillationD

Most effective method of terminating VF and pulseless VTM

Passage of DC electrical shock through the heart to depolarize the cellsof the myocardium to allow the SA node to resume the role of pacemaker


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DefibrillationDefibrillationD

Deliver energy using a monophasic or biphasic waveformD

Monophasic defibrillators deliver energy in one direction. Biphasicdefibrillators deliver energy in two directions. use less jules bc it

goes one direction/less energy which causes fewer problemsafterwards with akg rhythms. (about 60 jules)a

(uses less energy)

Deliver successful shocks at lower energies and with fewerpostshock ECG abnormalities

DefibrillationDefibrillationDefibrillationDefibrillationD

Output is measured in joules or watts per second.O

Recommended energy for initial shocks in defibrillationR

Biphasic defibrillators: First and successive shocks: 150 to 200joulesj

Monophasic defibrillators: Initial shock at 360 joulesM

After shock, check pulse and start CPR if indicated

Testing: Check pulse, then CPRT

DefibrillationDefibrillation

Synchronized CardioversionSynchronized CardioversionS

Choice of therapy for hemodynamically unstable ventricular orsupraventricular tachydysrhythmiass

Synchronized circuit delivers a countershock on the R wave of theQRS complex of the ECG. Dont want on T wave bc it could sendthem into vfib.t

Synchronizer switch must be turned ON.S

Implantable Cardioverter-Defibrillator (ICD)Implantable Cardioverter-Defibrillator (ICD)I

Appropriate for patients whoA

Have survived SCDH

Have spontaneous sustained VTH

Have syncope with inducible ventricular tachycardia/fibrillationduring EPSd

Are at high risk for future life-threatening dysrhythmiasA

EFs less than 25/30 are candidates bc at high risk for suddencardiac deathc


Consists of a lead system placed via subclavian vein to the endocardiumC

Battery-powered pulse generator is implanted subcutaneously.


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B


ICD sensing system monitors the HR and rhythm and identifies VT or VF.I

Approximately 25 seconds after detecting VT or VF, ICD delivers


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PacemakersPacemakersP

Permanent pacemaker: Implanted totally within the bodyP

Cardiac resynchronization therapy (CRT): Pacing technique thatresynchronizes the cardiac cycle by pacing both ventriclesr

PacemakerPacemakerPacemakersPacemakersP

Temporary pacemaker: Power source outside the bodyT

TransvenousT

Epicardial on the surface of the hearto

Transcutaneous on the skin/patcho

Temporary PacemakerTemporary Pacemaker

Temporary Transvenous PacemakerTemporary Transvenous PacemakerPacemakersPacemakersP

Pacemaker malfunctionP

Failure to sense : Failure to recognize spontaneous atrial orventricular activity and pacemaker fires inappropriatelyv

Lead damage, battery failure, dislodgement of the electrode

Not sensing the underlying rhythm and firing inappropriately.Failure to capture: sensing but not firing....

PacemakersPacemakersP

Pacemaker malfunctionP

Failure to capture: Electrical charge to myocardium is insufficientto produce atrial or ventricular contractiont

Lead damage, battery failure, dislodgement of the electrode,fibrosis at the electrode tipf

Patient education cant lift arm above shoulder for 6 weeks its allimportant

Know ST-depression: ischemiaST-elevation: MI

Know Tombstone Ts.K

ECG Changes Associated With Acute Coronary Syndrome (ACS)ECG Changes Associated With Acute Coronary Syndrome (ACS)


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m

Definitive ECG changes occur in response to ischemia, injury, orinfarction of myocardial cells.i

Changes seen in the leads that face the area of involvementC

Definitive ECG ChangesDefinitive ECG Changes

ECG Changes Associated With Acute Coronary Syndrome (ACS)ECG Changes Associated With Acute Coronary Syndrome (ACS)EIschemiaI

ST segment depression and/or T wave inversionS

ST segment depression is significant if it is at least 1 mm (onesmall box) below the isoelectric line.s

Changes Associated With MIChanges Associated With MIECG Changes Associated With Acute Coronary Syndrome (ACS)ECG Changes Associated With Acute Coronary Syndrome (ACS)E

IschemiaI

Changes occur in response to the electrical disturbance inmyocardial cells due to inadequate supply of oxygen.m

Once treated (adequate blood flow is restored), ECG changesresolve and ECG returns to baseline.

ECG Changes Associated With Acute Coronary Syndrome (ACS)ECG Changes Associated With Acute Coronary Syndrome (ACS)E

InjuryI

ST segment elevation is significant if >1 mm above the isoelectricline.l

If treatment is prompt and effective, may avoid infarctionI

If serum cardiac markers are present, an ST-segment-elevation myocardial infarction (STEMI) has occurred.

Changes Associated With InjuryChanges Associated With InjuryECG Changes Associated With Acute Coronary Syndrome (ACS)ECG Changes Associated With Acute Coronary Syndrome (ACS)E

InfarctionI

Physiologic Q wave is the first negative deflection following the Pwave.w

Small and narrow (0.03 second in duration.

Changes Associated With InfarctionChanges Associated With InfarctionECG Changes Associated With Acute Coronary Syndrome (ACS)ECG Changes Associated With Acute Coronary Syndrome (ACS)E

InfarctionI

Pathologic Q wave indicates that at least half the thickness of theheart wall is involved.h

Referred to as a Q wave MIR

Pathologic Q wave may be present indefinitely.P

T wave inversion related to infarction occurs within hours and may


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persist for months.ECG Finding With Anterolateral Wall MIECG Finding With Anterolateral Wall MISyncopeSyncopeS

Brief lapse in consciousness accompanied by a loss in postural tone(fainting)(

Cardiovascular causesCCardioneurogenic syncope or vasovagal syncope (e.g., carotidsinus sensitivity)s

Primary cardiac dysrhythmias (e.g., tachycardias, bradycardias)SyncopeSyncopeS

Noncardiovascular causesN

HypoglycemiaH

HysteriaH

Unwitnessed seizureU

StrokeS

Vertebrobasilar transient ischemic attackSyncopeSyncopeS

Diagnostic studiesD

EchocardiographyE

EPSE

Head-upright tilt table testingH

Holter monitorH

Event monitor/loop recorder

A patient in the coronary care unit develops ventricular fibrillation. The firstaction the nurse should take is to:

1. Perform defibrillation.2. Initiate cardiopulmonary resuscitation.3. Prepare for synchronized cardioversion.4. Administer IV antidysrhythmic drugs per protocol.

A patient has a diagnosis of acute myocardial infarction, and his cardiacrhythm is sinus bradycardia with six to eight premature ventricularcontractions (PVCs) per minute. The pattern that the nurse recognizes as themost characteristic of PVCs is:

1. An irregular rhythm.2. An inverted T wave.3. A wide, distorted QRS complex.4. An increasingly long PR interval.

A patients cardiac rhythm is sinus bradycardia with a heart rate of 34beats/minute. If the bradycardia is symptomatic, the nurse would expect the


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patient to exhibit:

1. Palpitations.2. Hypertension.3. Warm, flushed skin.

4. Shortness of breath.

Case StudyCase StudyC

45-year-old woman enters the ED complaining of sudden onset ofpalpitations and shortness of breath.p

ECG reveals atrial fibrillation with a rapid ventricular response (HR =168).

Case StudyCase StudyCShe has no previous history of cardiac problems.S

An emergent cardioversion is planned.Discussion QuestionsDiscussion QuestionsD

What are some teaching points before the procedure?W

What treatments are available if the procedure is unsuccessful?

Discussion QuestionsDiscussion QuestionsD

What risks does sustained atrial fibrillation pose, and how can thisinformation be helpful in ensuring compliance?

Dysrhythmias Notes

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