Dysrhythmias EKG DANCEEKG DANCE-click here Abnormal cardiac rhythms are termed dysrhythmias. Prompt assessment of dysrhythmias and patient’s response.

Dysrhythmias

EKG DANCE-click here

Abnormal cardiac rhythms are termed dysrhythmias.

Prompt assessment of dysrhythmias and patient’s response to the rhythm is critical.

Dysrhythmias

EKG shows electrical activity of the heart.

Electrical precedes mechanical

(Without electricity…no pump!!)

Click here

How is the electricity generated?

By action potentials (click for animated visuals)

Na K pump (animation)

Calcium channelsDepolarization-contraction

Repolarization-

Think about this when administering cardiac meds…antidysrhytmics

*ECG wave forms- Produced by movement of charged ions across the semipermeable membranes of myocardial cells. Click here- YouTube- How Body Works-A Nerve Impulse

Understanding cardiac action potential & meds

Cardiac action potential of a fast-response Purkinje fiber. Arrows indicate the approximate time and direction of movement of each ion influencing membrane potential. Ca++ movement out of the cell is not well defined but is thought to occur during phase 4

Key Characteristics of Cardiac Cells Multimedia Tutorials*Great site

Cardiac cells- either contractile cells influencing pumping action or pacemaker cells influencing electrical activity of heart

AutomaticityExcitabilityConductivityContractility*Refractoriness

RelativeAbsolute

Each beat generated from same pacemaker - look identical.

Impulses from other cardiac cells = “ectopic” (PVC, PAC)

Electrical activity produces mechanical activity= waveforms

Refractory Period

Myocardial cells resistive to stimulation; **dysrhythmias triggered during relative refractory and absolute refractory periods

•Absolute refractory period: no depolarization can occur- from Q wave until middle of T wave•Relative refractory period: greater than normal stimulus needed for depolarization (contraction); goes through 2nd half T wave

Conduction System of the Heart

Fig. 32-4. A, Conduction system of the heart. AV, Atrioventricular; SA, sinoatrial. B, The normal electrocardiogram (ECG) pattern. The P wave represents depolarization of the atria. The QRS complex indicates depolarization of the ventricles. The T wave represents repolarization of the ventricles. The U wave, if present, may represent repolarization of the Purkinje fibers or it may be associated with hypokalemia. The PR, QRS, and QT intervals reflect the length of time it takes for the impulse to travel from one area of the heart to another.

Yellow = isoelectric phase.

Purple= "P"wave.

Purple and yellow split = "PR" interval

Red = "Q" wave; Light blue = “R" wave

Light green = "S" wave; Black = "ST" segment

Orange = "T" wave; Yellow again = isoelectric.

Dark blue ="U" wave (seldom seen)* risk for *hypokalemia, med effect, hypercalcemia, .

Intrinsic rates

SA node 60-100AV node 40-60Bundle of His; Left and Right Bundle Branch; Purkinge Fibers 15-40

EKG waveforms

P wave associated with atrial depolarization (stimulation)

QRS complex associated with ventricular depolarization (stimulation)

T wave associated with ventricular repolarization (recovery)

Atrial recovery wave hidden under QRS wave Stimulus causes atria to contract before ventricles Delay in spread of stimulus to ventricles allows time

for ventricles to fill and for atrial kick

Pacemakers other than *SA node

•Pacemaker from another site > lead to dysrhythmias; may be discharged in number of ways.

oSecondary pacemakers- may originate from AV node or His-Purkinje system.

oSecondary pacemakers can originate when they discharge more rapidly than normal pacemaker of SA node.

oTriggered beats (early or late) may come from ectopic focus (area outside normal conduction pathway) in atria, AV node, or ventricles.

How is rate controlled?Nervous System Control of Heart

Parasympathetic nervous system: when? Vagus nerve Dec. rate Slows impulse conductionDec. force of contraction

Sympathetic nervous system: when?Inc. rateInc. force of contraction

EKG graph paper

Horizontal measures timeVertical measures voltage

Helps to determine rateWidth of complexesDuration of complexes

Graphic tracing of electrical impulses produced by heart; waveforms of ECG represent activity of charged ions across membranes of myocardial cells.

Each small square box on the graph paper is equal to:

1. 0.06 sec.

2. 0.08 sec.

3. 0.04 sec.

4. 0.20 sec.

If you didn’t know, look at previous slide- 0.04

Cardiac Monitoring- based on 12 lead EKG

Each lead has positive, negative and ground electrode.

Each lead looks at different area of heart.*Can be diagnostic as in case of an MI

3 lead placement: Depolarization wave moving toward a positive lead will be upright. Depolarization wave moving toward a negative lead will inverted. Depolarization wave moving between negative and positive leads will have both upright and inverted components.

*Five lead placement allows viewing all leads within limits of monitor

Lead II positive R arm looking to LL neg

RNCEU’s

Leads to monitor EKG

Best- lead II and MCL or V1 leads- lead II easy to see P waves. MCL or V1 easy to view ventricular rhythms.

If impulse goes toward positive electrode complex is positively deflected or upright

If impulse goes away from positive electrode complex is negatively deflected or goes down form baseline

Five lead system- uses all leads shown: three lead system uses only black, white and red leads. Two lead telemetry systems use black and red leads- placement may change depending on what EKG lead (view) is required. Black and white leads are placed on shoulder area; green and red leads placed on lowest rib on both sides of torso, and brown lead (ground) is placed at 4th intercostal space, just to right of sternum. (follow guidelines of facility)

Lead Placement

Fig. 36-4. A, Lead placement for MCL, using a three-lead system. B, Lead placement for V1 or V6 using a five-lead system. C, Typical electrocardiogram tracing in lead MCL1. C, Chest; LA, left arm; LL, left leg; MCL, modified chest lead; RA, right arm; RL, right leg.

Risk Factors for Dysrhythmia (Arrhythmia)

HypoxiaStructural changesElectrolyte imbalancesCentral nervous system stimulationMedicationsLifestyle behaviors

Who is/are at Greatest Risk for Dysrhythmia? Patient(s) with1.COPD2.MI3.Valvular disease4.Colon resection

MI; valvular disease (best two answers- have high risk for hypoxia (MI) and structural chg with valvular)

Holter monitoring

Event recorder monitoring

Exercise treadmill testing

Signal-averaged ECG

Electrophysiologic study

Evaluation of Dysrhythmias

Count 1. Number of QRS complexes in 1 minute R-R intervals in 6 seconds; multiply by 10 2. Number of small squares between one R-R interval; divide this number into 1500 3. Number of large squares between one R-R interval; divide this number into 300

Calculate rate (*know how to do this)Big blockLittle blockNumber of R waves in 6

sec times 10Calculate rhythm-reg or

irregMeasure PR interval,

<0.20QRS interval .04- 0.12P to QRS relationship*Recognize artifact

1 lg box= .20 5 lg boxes =1 sec 30 lg boxes =6 secs

*Therefore 300 lg boxes in 1 min.

Rate Calculation

Each small box = 0.04 seconds on horizontal axis and 1 mm or 0.1 millivolt on vertical axis. PR interval-measured from beginning of P wave to beginning of QRS complex; QRS complex -measured from beginning of Q wave to end of S wave; QT interval -measured from beginning of Q wave to end of T wave; and TP interval- measured from end of T wave to beginning of next P wave.

If there are 10 small squares between 2 QRS waves, the rate would be:

2. 100

3. 150

4. 100

*Rate 150; 1500 / 10 = 150

Normal Sinus Rhythm

Follows normal conduction patternNormal P wavePR interval<.20QRS.04-.12T wave for every complexRate is regular 60-100*Rate >100: Sinus Tachycardia

Causes-anxiety, hypoxia, shock, pain, caffeine, drugsTreatment-eliminate cause

Sinus Bradycardia- brady heart song Normal in sleep; aerobically trained athlete Clinical assoc.: Response to carotid sinus massage; hypothermia; inc vagal

tone; adm. parasympathomimetic drugs (Beta blockers; digoxin), head injuries (inc ICP), inferior MI, hypothyroidism

Sinus node fires <60 bpm; Normal conduction; rhythm regular; P: QRS: 1:1; PR interval: 0:12 to .20 sec.; QRS complex: 0.04 to 0.12 sec

Clinical significance- Dependent on symptomsHypotension Pale, cool skinWeaknessAnginaDizziness or syncope; shortness of breathConfusion or disorientationShortness of breath

Treatment- if symptomatic, atropine or pacer

Treatment- if symptomatic, atropine or pacerSinus Bradycardia-

Patients with bradycardia are likely to display which of these symptoms:

1.Heart rate less than 602.Dizziness3.Hypertension4.Confusion

1. Heart rate less than 602. Dizziness3. Hypertension (all except)4. Confusion

Rhythm: RegularRate: Fast (>/= 100 bpm)P Waves: “Normal” and upright, one for each QRSPR Interval: “Normal” (0.12-0.20 seconds)QRS Complex: “Normal” (0.08-0.12 seconds)

•Due to inc. in rate of sinus node discharge (vagal inhibition).•Common dysrhythmia; many causes as exercise, fever, caffeine, anxiety, smoking, heart failure, hypovolemia, etc. •Treatment : address underlying cause and/or determine if it is even a problem (Meds-adenosine?, beta adrenergic blockers (dec. heart rate & myocardial oxygen consumption)*, antipyretics for fever); analgesic for pain

Sinus Tachycardia

Clinical significanceDizziness and hypotension due to decreased COInc. myocardial oxygen consumption may lead to angina

Name these rhythms & count rate!! (What you just covered)

Sinus Dysrhythmias (Arrhythmia) (SA)

Rate 60-100 Irregular rhythm- increases with inspiration, decreases with

expiration P, QRS,T wave normal Cause- children, drugs (Morphine sulphate), MI Treatment- none

Sinus Arrest•See pauses•May see ectopic beats (PAC’s PVC’s)*don’t treat•Due to MI•Treatment

AtropineIsoproterenol (Isuprel)Pacemaker

Isoproterenol-synthetic sympathomimetic amine

Atrial Dysrhythmias Atria is pacemakerAtrial rate contributes 25-30% of cardiac reserveSerious in patients with MI- WHY?

Medications - to treat atrial dysrhythmias (if patient symptomatic)

•Diltiazem (Cardizem) (Identify class)•Amiodarone (Cordarone) (Identify class)•Dofetilide (Tikosyn) (Identify class) Verapamil (Calan) (Identify class)Metoprololol (Lopressor) Identify class Digoxin (Lanoxin) Atropine

Think-rate too slow, too fast?? Ref to Tab. 36-9-next slide

Premature Atrial Contraction (PAC’s)P wave abnormally shaped-contraction originates

from ectopic focus in atrium other than SA Node

PR interval shorter-travels abnormal pathway (distorted “P” waves)

QRS normalCause-age, MI, CHF, stimulants, dig, electrolyte

imbalance; valvular disease; hypoxia

Treatment- remove stimulants; watch for SVT, depends upon cause; isolated not significant; B-adrenergic blockers

Supraventricular Tachycardia (SVT)/PSVT (paroxysmal SVT)Rate- 150-250 (Very fast!)Originates in ectopic focus above bifurcation of

bundle of His- atria=pacemaker (may not see p waves); *Paroxysmal = abrupt onset and termination

Cause-SNS stimulation, MI, CHF,sepsis

SVT/Paroxysmal Supraventricular Tachycardia (PSVT)

Clinical significance Prolonged episode and HR >180 bpm may

precipitate ↓ CO PalpitationsHypotensionDyspneaAngina

•Treatment- •Meds: adenosine, digoxin, diltiazem (Cardizem) or verapamil (calcium channel blockers), propranolol (inderal), dofetilide (Tikosyn)•Vagal stimulation

This YouTube site explains supraventriventricular tachycardias plus atrial flutter and atrial fibrillation- Click here to locate additional videos

Atrial FlutterRate of atria is 250-300, vent rate variesRegular rhythmP waves saw tooth, ratio 2:1, 3:1, 4:1Flutter waves-*Originate from single ectopic

focus; No PR intervalCause-diseased heart (mitral valve), PE, chronic lung;

hyperthyroidism, drugs as dig, quinidine, epinephrine

3:1 flutter

Video Atrial flutter

Atrial Flutter

Clinical significance High ventricular rates (>100) and loss of the atrial

“kick” can dec. CO and precipitate HF, angina

Risk for stroke due to risk of thrombus formation in atria

Treatment- *Goal slow ventricular resopnse Cardioversion

Calcium channel blockers and beta blockers, amiodorone (What classes?)

Ablation

, warfarin (Coumadin)

Atrial Fibrillation-**most commonRate of atria 350-600- (total disorganized rhythm);

*multiple ectopic foci > loss effective atrial contractionVentricular response irregularNo P waves, “garbage baseline”Cause-#1 arrhythmia in elderly, heart disease- CAD,

rheumatic heart disease, HF, cardiomyopathy, caffeine, alcohol, etc.

Complications- dec. CO due to loss atrial kick and rapid ventricular response; thrombi (stroke) from blood stasis

Treatment-Goal dec. ventricular rate; pvt stroke; *convert if possible);

Meds: digoxin, calcium channel blockers, beta adrenergic blockers, amiodorone, cardioversion (TEE ck for thrombus) warfarin - ck PT and INR,

*ablation, Maze procedure (involves open heart) or Mini Maze (modified)

Atrial FibrillationRsult in dec. in CO due to ineffective atrial

contractions (loss of atrial kick) and rapid ventricular response

Thrombi may form in atria as a result of blood stasis

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

*Thrombus formation, pulse deficit

Click to view You Tube video on Abalation for Atrial fibrillation!

Dysrhythmias- AV Node

AV Conduction Blocks

Junctional RhythmDysrhythmia that originates in area of AV node AV node is pacemaker- slow rhythm (40-60) but

regular impulse goes to atria from AV node- backward); SA node failed to fire or impulse delayed or blocked at AV node

P wave patternsAbsent or hidden; Short < .0.12 or negative or PR

interval; P wave precedes QRS inverted in II, III, and AVF or P wave hidden in QRS or P wave follows QRS

QRS normalOften no treatment

Junctional Dysrhythmias

Clinical significance Serves as safety mechanism when SA node has not been

effectiveEscape rhythms should not be suppressed.If rhythms rapid >result in reduction of CO and HF

Treatment If symptomatic, atropineAccelerated junctional rhythm and junctional tachycardia

caused by digoxin toxicity; digoxin is held -Adrenergic blockers, calcium channel blockers, and

amiodarone for rate control for junctional tachycardia not caused by digoxin toxicity

DC cardioversion is contraindicated

Junctional Dysrhythmia

First Degree AV Block

Transmission through AV node delayedPR interval >0.20QRS normal and regular Cause-dig toxicity, MI, CAD, vagal

stimulation; hyperthyroidism, beta- adrenergic drugs; calcium channel blockers, flecainaide drugs

Treatment- none but watch for further blockage

Clinical significanceUsually asymptomaticMay be a precursor to higher degrees of AV

Treatment Check medications. Continue to monitor.

First-Degree AV Block

Characteristics of 1st degree block include ?

1. Regular rhythm

2. Long PR interval

3. More P’s than QRS’s

4. Rate less than 100

1. Regular rhythm2. Long PR interval3. More P’s than

QRS’s4. Rate less than 100

Second Degree AV Blockmore P’s than QRS’s

A. Mobitz I (Wenckebach) YouTube - Diagnosis WenckebachPR progressively longer then drops QRS due to prolonged

AV conduction; atrial impulse non-conducted and a QRS complex is blocked

Cause- MI, drug toxicityTreatment- watch for type II and 3rd degree

B. Mobitz II More P’s but skips QRS in regular pattern 2:1,3:1, 4:1Constant PR intervalTreatment-Pacemaker

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

Clinical significance/associationsUsually result of myocardial ischemia or infarctionAlmost always transient; well toleratedMay be a warning signal of more serious AV

conduction disturbance Drugs: Digoxin, -adrenergic blockersAssociated with CAD and other diseases that can

slow AV conduction

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

Clinical significanceOften progresses to third-degree AV block ;

associated with poor prognosisReduced HR often results in dec. CO with

subsequent hypotension and myocardial ischemia

Fig. 36-16. Heart block. C, Second-degree AV block, type II, with constant PR intervals and variable blocked QRS complexes.

Clinical associations

Rheumatic heart disease

Anterior MI

Digitalis toxicityTreatment

If symptomatic (e.g., hypotension, angina) before permanent pacemaker can be inserted, temporary transvenous or transcutaneous pacemaker

Permanent pacemaker

Mobitz type 1 or Wenchebach has a constant PR interval.

1. True

2. False

Answer: False-Mobitz I (Wenckebach)-PR progressively longer then drops QRS

3rd Degree AV BlockAtria and ventricles beat independently (ventricular

rhythm is “escape” rhythmAtrial rate- 60-100Slow ventricular rate 20-40No PR intervalWide or normal QRS (depends on where block is)Cause- severe heart disease, systemic diseases; meds

as digoxin, beta-adrenergic blockers, calcium channels blockers

Complications- dec. CO, ischemia, HF, shock, bradycardia, syncope, possible asystole

Third-Degree AV Heart Block (Complete Heart Block)

Fig. 36-16. D, Third-degree AV block. Note that there is no relationship between P waves and QRS complexes.

TreatmentIf symptomatic, transcutaneous pacemaker until

a temporary transvenous pacemaker can be insertedDrugs (e.g., atropine, epinephrine): Temporary

measure to increase HR and support BP until temporary pacing is initiated

Permanent pacemaker as soon as possible

Third-Degree AV Heart Block (Complete Heart Block)

Bundle Branch Blocks *not in text- & no test items but to

understand concept

Left BBBRight BBBQRS.12 or greaterRabbit ears- RR’No change in rhythm

Normal bundle conduction

Right Bundle Branch Block

Ventricular ArrythmiasMost serious

Easy to recognize

Premature Ventricular Contractions (PVC’s)-ectopic

QRS wide and bizarre No P wavesT opposite deflection of PVCCause- 90% with MI, stimulants, dig,

electrolyte imbalanceTreatment- O2, lidocaine, procainamide

(Pronestyl), *amiodarone, *abalationNo longer prophylactic

Premature Ventricular Contractions

Fig. 36-17. Various forms of premature ventricular contractions (PVCs). Note: Recorded from lead II.

Multifocal- from more than one foci

Bigeminy- every other beat is a PVC

trigeminy- every third beat is a PVC

Couplet- 2 PVC’s in a row

Premature Ventricular ContractionsClinical significance

In normal heart, usually benignIn heart disease, PVCs may dec. CO and

precipitate angina and HF **Patient’s response to PVCs must be

monitored PVCs often do not generate a sufficient

ventricular contraction to result in a peripheral pulse

**Apical-radial pulse rate- assess to determine if pulse deficit exists

Premature Ventricular Contractions

Clinical significance**Ventricular irritability > Ventricular

Fibrillation . May occur

After lysis of coronary artery clot with thrombolytic therapy in acute MI—reperfusion dysrhythmias

Following plaque reduction after percutaneous coronary intervention

Treat if:

>5 PVC’s a minuteRuns of PVC’sMulti focal PVC’s“R on T”

What is this?

Ventricular Tachycardia (VT)

Ventricular rate 150-250, regular or irregularNo P wavesQRS>.12Can be stable- pulse or unstable –no pulseCause- electrolyte imbalance, MI, CAD, digLife- threatening, dec. CO, watch for V-fibTreatment- same as for PVC’s and defibrillate

for sustained (if not responsive)

Ventricular Tachycardia

Clinical significanceVT can be stable (patient has a pulse) or

unstable (patient is pulseless)Sustained VT: Severe dec. in CO

• Hypotension• Pulmonary edema• Decreased cerebral blood flow• Cardiopulmonary arrest

Clinical significanceTreatment for VT must be rapidMay recur if prophylactic treatment is

not initiated

Ventricular fibrillation may develop

Polymorphic Ventricular Tachycardia- Torsades de Pointes” (“twisting around a point”)

Rhythm: Well…irregular…but…Rate: 100-250 bpmP Waves: Usually not seen (buried in QRS if they exist)PR Interval: NoneQRS Complexes: Wide, distorted, bizarre, and “rhythmic” – getting smaller, then larger, then smaller, then…

AKA: “Torsades de Pointes” (“twisting around a point”)Usually caused by hypo/hyperkalemia, HYPOMAGNESEMIA, TCA OD, and some antidysrhythmic medications.

Treatment - includes treating cause(s), medications, and defibrillation or cardioversion.

VT- Torsades de Pointes

French for twisting of the points

Treatment Precipitating causes must be identified and treated (e.g., hypoxia). Monomorphic VT

Hemodynamically stable (e.g., + pulse) + preserved LV function: IV procainamide, sotalol, amiodarone, or lidocaine

Hemodynamically unstable or poor LV function: IV amiodarone or

lidocaine followed by cardioversion Polymorphic VT with a normal baseline QT interval: -adrenergic

blockers, lidocaine, amiodarone, procainamide, or sotalol; cardioversion used if drug therapy is ineffective.

Polymorphic VT with a prolonged baseline QT interval: IV magnesium, isoproterenol, phenytoin, lidocaine, or antitachycardia pacing; Drugs that prolong QT interval should be discontinued if rhythm is not converted, cardioversion may be needed.

Treatment VT without a pulse is a life-threatening

situation.

Cardiopulmonary resuscitation (CPR) and rapid defibrillation

• Epinephrine if defibrillation is unsuccessful

Ventricular FibrillationGarbage baseline-quiveringNo P’sNo QRS’sNo COCause-MI, CAD, CMP, shock, altered K+, hypoxia,

acidosis, and drugsTreatment- code situation, ACLS, CPR, **defibrillate

*cannot cardiovert…no rhythm to cardiovert

Clinical significanceUnresponsive, pulseless, and apneic statePrognosis for asystole is extremely poor.

TreatmentCPR with initiation of ACLS measures (e.g.,

intubation, transcutaneous pacing, IV therapy with epinephrine and atropine)

Asystole

Electrical activity can be observed on ECG, but no mechanical activity of ventricles is evident; patient has no pulse.

TreatmentCPR > intubation > IV epinephrineAtropine if ventricular rate is slow. Treatment directed toward correction of

underlying cause.

Pulseless Electrical Activity (PEA)

Death from a cardiac causeMajority of SCDs result from ventricular

dysrhythmias.Ventricular tachycardiaVentricular fibrillation

Sudden Cardiac Death (SCD)

Complications Dysrhythmias Hypotension Tissue ischemia Thrombi- low dose heparin, or ASA Heart failure Shock Death

•Telemetry- 5 lead (lead II and V1)•12 lead EKG•Holter or event monitoring•Exercise stress test•Electrophysiology studies- induce arrhythmias under controlled situation > Ablation to correct underlying problem .

Diagnostic Tests

Nursing Assessment

Apical rate and rhythmApical/radial deficitBlood pressureSkinUrine outputSigns of dec.

cardiac output

•Dec. cardiac output•Dec. tissue perfusion•Activity intolerance•Anxiety and Fear•Knowledge deficit

Nursing Diagnoses

Goals/Outcomes??

InterventionsMedicationsPacemaker (Types)Mapping

AblationMaze & modified Maze

CPRCardioversionDefibrillation

Medications- review *Know your meds

Classified by effect on action potentialClass I- fast Na blocking agents-ventricular

Quinidine, Pronestyl, Norpace,Lidocaine, RhythmolClass II- beta blockers (esmolol, inderal) SVT,

Atrial fibrillation, Atrial flutterClass III- K blocking (sotalol, amiodorone)both

atrial and ventricularClass IV- Calcium channel blockers (verapamil,

diltiazem(cardiazem) for SVT, Afib, atrial flutterOther- adenosine, dig, atropine, magnesium

(correct electrolytes)

AntiarrhythmicsRemember-phrase “Some Block Potassium Channels”

Class I "Some" = S = Sodium Class II "Block" = B =Beta blockers Class III "Potassium" = Potassium channel blockers Class IV "Channels" = C =Calcium channel blockers

Comfort Measures Rest- dec. cardiac demands; careful monitoring!!O2IV access; Select appropriate therapyRelieve fear and anxiety- Diazepam (valium)

Defibrillation Most effective method of terminating VF and pulseless VT Passage of DC electrical shock through heart to depolarize cells of

myocardium to allow SA node to resume the role of pacemaker 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

Safety precautions** After initial shock, chest compressions (CPR) should be started AED’s

Fig. 36-20. Paddle placement and current flow in monophasic defibrillation (A) and biphasic defibrillation (B).

Fig. 36-21. LifePak contains monitor, defibrillator, & transcutaneous pacemaker.

Synchronized Cardioversion-

Choice of therapy for hemodynamically unstable ventricular or supraventricular tachydysrhythmias

Synchronized circuit delivers countershock on R wave of QRS complex of ECG.

Synchronizer switch must be turned ON.

Use for Ventricular Tachycardia, SVT or a- fib, flutter to convert Usually planned Get permit Start at 50 watt/sec Awake, give O2 and sedation Have to synchronize with rhythm

http://www.dearnurses.net/

cardioversion

To defibrillate a rhythm, it needs to be synchronized to the QRS? True or False? False! No QRS to

synchronize with!!

Appropriate for patients who have

survived SCD

spontaneous sustained VT

syncope with inducible ventricular tachycardia/fibrillation during EPS

at high risk for future life-threatening dysrhythmias Consists of lead system placed via subclavian vein to endocardium Battery-powered pulse generator is implanted subcutaneously. Equipped with antitachycardia and antibradycardia pacemakers.

Initiate overdrive pacing of supraventricular and ventricular tachycardias; Provide backup pacing for bradydysrhythmias that may occur after defibrillation discharges

Implantable Cardioverter-Defibrillator (ICD)

Implanted Cardiac Defibrillator (ICD) Senses rate and width of QRS Goes off 3 times, then have to be reset Some combined with pacemaker If fires- seek medical attention! Teaching critical!

Pacemaker

Used to pace heart when normal conduction pathway damaged or diseased Pacing circuit consists of a power source, one or more

conducting (pacing) leads, and myocardium. Permanent- battery under skinTemporary- battery outside bodyTypes

TransvenousEpicardial- bypass surgeryTranscutaneous- emergency

ModesAsynchronous- at preset time without failSynchronous or demand- when HR goes below set rate

Review classifications- (Wikipedia)

Pacemaker resources

View Pacemaker insertion

Transcutaneous- emergency

Temporary Transvenous Pacemaker

Fig. 36-26. Temporary transvenous pacemaker catheter insertion. A single lead is positioned in the right ventricle through either the basilic or jugular vein.

Pacemaker Spike

Fig. 36-23. Ventricular capture (depolarization) secondary to signal (pacemaker spike) from pacemaker lead in the right ventricle.

Antibradycardia pacing Antitachycardia pacing: Delivery of a stimulus to the ventricle to

terminate tachydysrhythmias 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 cardiac cycle by pacing both ventricles Pacemaker Problems (next slide) Teaching critical (text table 36-11)

Pacemakers

Pacemaker Problems:

•Failure to sense

•Failure to capture

Electrode-tipped ablation catheter “burns” accessory pathways or ectopic sites in atria, AV node, and ventricles. Nonpharmacologic treatment for

AV nodal reentrant tachycardiaReentrant tachycardia related to accessory bypass

tractsControl of ventricular response of certain

tachydysrhythmias Done in special cardiac procedures labUse a laser to burn abnormal pathway

Radiofrequency Catheter Ablation Therapy

View video

EKG changes in an acute MI

EKG CHANGES ASSOCIATED WITH ACUTE CORONARY SYNDROME 12-lead ECG - primary diagnostic tool used to evaluate patients presenting with ACS. Definitive ECG changes occur in response to ischemia, injury, or infarction of myocardial cells; seen in leads that face area of involvement. Typical ECG changes seen in myocardial ischemia include ST-segment depression and/or T wave inversion. Typical ECG change seen during myocardial injury is ST-segment elevation.

ST-segment elevation and a pathologic Q wave may be seen on ECG with myocardial infarction.

3 ECG Changes Associated with Acute Coronary Syndrome (ACS)> STEMI

Ischemia ST segment depression and/or T wave inversion

ST segment depression- significant if at least 1 mm (one small box) below isoelectric line

Injury/Infarction ST segment elevation is significant if >1 mm above isoelectric line

If treatment is prompt & effective, may avoid infarction

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

Infarction/Necrosis Note: physiologic Q wave is first negative deflection following P wave

Small and narrow (<0.04 second in duration)

*Pathologic Q wave- deep and >0.03 second in duration

ECG Changes Associated with Acute Coronary Syndrome (ACS)

Typical EKG changes associated with an MI include:

1. Long PR interval

2. Q waves

3. ST segment elevation

4. T wave inversion1. Long PR interval2. Q waves

(Pathological)3. ST segment

elevation4. T wave inversion

Syncope

Brief lapse in consciousnessCausesVasovagal

Cardiac dysrhythmiasOther- hypoglycemia, seizure, hypertrophic

cardiomyopathy1-year mortality rate as high as 30% for

syncope from cardiovascular cause

Casestudies

Practice!

Prioritization Question

A client with atrial fibrillation is ambulating in the hall on the coronary step-down unit and suddenly tells you, “I feel really dizzy.” which action should you take first?

A. Help the client sit down.B. Check the client’s apical pulseC. Take the client’s blood pressureD. Have the client breathe deeply

Prioritization Question

A client with atrial fibrillation is ambulating in the hall on the coronary step-down unit and suddenly tells you, “I feel really dizzy.” which action should you take first?

A. Help the client sit down.B. Check the client’s apical pulseC. Take the client’s blood pressureD. Have the client breathe deeply

Prioritization question

Cardiac rhythms are being observed for clients in the CCU. Which client needs immediate intervention? A client:

A. admitted with heart failure who has atrial fibrillation with a rate of 88 while at rest.

B. with a newly implanted demand ventricular pacemaker, who has occasional periods of sinus rhythm, rate 90-100.

C. who has just arrived on the unit with an acute MI and has sinus rhythm, rate 76, with frequent PVC’s.

D. who recently started taking atenolol (Tenormin)) and has a first-degree heart block rate 58.

Cardiac rhythms are being observed for clients in the CCU. Which client needs immediate intervention? A client:

A. admitted with heart failure who has atrial fibrillation with a rate of 88 while at rest.

B. with a newly implanted demand ventricular pacemaker, who has occasional periods of sinus rhythm, rate 90-100.

C. who has just arrived on the unit with an acute MI and has sinus rhythm, rate 76, with frequent PVC’s.

D. who recently started taking atenolol (Tenormin)) and has a first-degree heart block rate 58.

A diagnosis of ventricular fibrillation is identified for an unresponsive 50 year old client who has just arrived in the ED. Which action should be taken first?

A. Defibrillate at 200 joulesB. Begin CPRC. Administer epinephrine 1 mg IVD. Intubate and manually ventilate.

Prioritization questions

A diagnosis of ventricular fibrillation is identified for an unresponsive 50 year old client who has just arrived in the ED. Which action should be taken first?

A. Defibrillate at 200 joulesB. Begin CPRC. Administer epinephrine 1 mg IVD. Intubate and manually ventilate.

Dysrhythmias EKG DANCEEKG DANCE-click here Abnormal cardiac rhythms are termed dysrhythmias. Prompt assessment of dysrhythmias and patient’s response.

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