Dysrhythmias EKG DANCEEKG DANCE-click here EKG shows electrical activity of the heart. Electrical...

Dysrhythmias

EKG DANCE-click here

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

Electrical system

Multimedia Tutorials

Each beat that is generated from same pacemaker will look identical.

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

This electrical activity produces mechanical activity that is seen as waveforms

*Note pattern that occurs with atrial depolarization, re-polarization; ventricular depolarization, re-polarization

Cardiac Cycle

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

How is rate controlled?Nervous System Control of Heart

Parasympathetic nervous system: when? Vagus nerve Decreases rate Slows impulse conductionDecreases force of contraction

Sympathetic nervous system: when?Increases rateIncreases force of contraction

Pacemakers other than *SA node

•Pacemaker from another site can lead to dysrhythmias and may be discharged in a number of ways.

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

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

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

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

EKG graph paperHorizontal measures timeVertical measures voltage

Helps to determine rateWidth of complexesDuration of complexes

EKG graph paper

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)

Key Characteristics of Cardiac Cells

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

AutomaticityExcitabilityConductivityContractility*Refractoriness

RelativeAbsolute

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

Risk Factors for Dysrhythmia (Arrhythmia)

HypoxiaStructural changesElectrolyte imbalancesCentral nervous system stimulationMedicationsLifestyle behaviors

Assessment

Calculate rate (know how to do this)Big blockLittle blockNumber of R waves in 6 sec times 10

Calculate rhythm-reg or irregMeasure PR interval, <.20QRS interval .04.12P to QRS relationship

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

Therefore there are 300 lg boxes in 1 min.

Rate Calculation

Each small box represents 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.

Sinus Rhythm

Normal 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

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 an increase in rate of sinus node discharge.•Common dysrhythmia due to many things as exercise, fever, caffeine, anxiety, smoking, etc. •Treatment : address underlying cause and/or determining if it is even a problem (adenosine, beta blockers).

Sinus Tachycardia

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

Sinus Bradycardia- brady heart song Cause-vagal stimulation, athlete, drugs (Beta blockers; digoxin), head

injuries, MI 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 symptoms

Hypotension Pale, cool skinWeaknessAnginaDizziness or syncopeConfusion or disorientationShortness of breath

Treatment- if symptomatic, atropine or pacer

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

Sinus Dysrhythmias (Arrhythmia) (SA)

Rate 60-100Irregular rhythm- increases with

inspiration, decreases with expirationP, QRS,T wave normalCause- children, drugs (MS04), MITreatment- none

Sinus Arrest

See pausesMay see ectopic beats (PAC’s PVC’s) do

not treatCause MITreatment

AtropineIsuprelPacemaker

Atrial Dysrhythmias

Atria is the pacemakerAtrial rate contributes 25-30% of cardiac

reserveSerious in patients with MI- WHY?

Medications used to treat the atrial dysrhythmias (if patient symptomatic)CardizemDigoxinAmiodaroneTikosynVerapamil? Atropine

Think-rate too slow, too fast??

Premature Atrial Contraction (PAC’s)

P wave abnormally shapedPR interval shorterQRS normalCause-age, MI, CHF, stimulants, dig,

electrolyte imbalanceTreatment- watch for SVT, depends upon cause

Supraventricular Tachycardia (SVT)/PSVT (paroxysmal SVT)Rate- 150-250 (Very fast!)Atria is pacemaker (may not see p waves)Cause-SNS stimulation, MI, CHF,sepsis Treatment- adenosine, digoxin, cardizem or

verapamil (calcium channel blockers), inderal, tikosyn, Vagal stimulation

Atrial FlutterRate of atria is 250-300, vent rate variesRegular rhythmP waves saw tooth, ratio 2:1, 3:1, 4:1Flutter waves- No PR intervalCause-diseased heart, digTreatment- cardioversion, calcium channel

blockers and beta blockers, amiodorone, ablation, coumadin

3:1 flutter

Atrial Flutter

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

atrial “kick” can decrease CO and precipitate HF, angina

Risk for stroke due to risk of thrombus formation in the atria

Atrial Fibrillation-**most commonRate of atria 350-600- (disorganized rhythm)Ventricular response irregularNo P waves, “garbage baseline”Cause-#1 arrhythmia in elderly, heart disease- CAD,

rheumatic, CHF, alcohol

Complications- dec. CO and thrombi (stroke)

Treatment- *convert if possible); digoxin, calcium channel blockers, beta blockers, amiodorone, pronestyl, cardioversion (TEE ck for thrombus) Coumadin- ck PT and INR, ablation and Maze

*Thrombus formation, pulse deficit, AR>RR

Atrial FibrillationCan 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

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

*Thrombus formation, pulse deficit

Video here

Dysrhythmias- AV Node

AV Conduction Blocks

Junctional RhythmAV node is pacemaker- slow rhythm (40-60) but

very regular impulse goes to atria from AV node- backward)

P wave patternsAbsent or hiddenShort < .0.12 or negative or RP intervalP wave precedes QRS inverted in II, III, and AVFP wave hidden in QRSP wave follows QRS

QRS normalOften no treatment

First Degree AV BlockTransmission through AV node delayedPR interval >.20QRS normal and regular Cause-dig toxicity, MI, CAD, vagal, and

blocker drugsTreatment- none but watch for further

blockage

Second Degree AV Blockmore P’s than QRS’sA. Mobitz I (Wenckebach)

YouTube - Diagnosis WenckebachPR progressively longer then drops QRSCause- 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 significanceUsually a result of myocardial ischemia

or infarctionAlmost always transient and well

toleratedMay be a warning signal of a more

serious AV conduction disturbance

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

Clinical significanceOften progresses to third-degree AV

block and is associated with a poor prognosis

Reduced HR often results in decreased CO with subsequent hypotension and myocardial ischemia

3rd Degree AV BlockAtria and ventricles beat independentlyAtrial rate- 60-100Slow ventricular rate 20-40No PR intervalWide or normal QRS (depends on where block is)Cause- severe heart disease, blockers elderly, MIComplications- dec. CO, ischemia, HF, shock, syncopeTreatment- atropine, pacemaker

Third-Degree AV Heart Block (Complete Heart Block)

Clinical significanceDecreased CO with subsequent ischemia,

HF, and shockSyncope may result from severe

bradycardia or even periods of asystole (patient may present with history of fall)

Bundle Branch Blocks *not in text- understand

concept

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

Normal bundle conduction

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, pronestyl,

*amiodarone, *abalationNo longer prophylactic

Premature Ventricular ContractionsClinical significance

In normal heart, usually benignIn heart disease, PVCs may decrease 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 should be assessed to determine if pulse deficit exists

Premature Ventricular Contractions

Clinical significanceRepresents ventricular irritability > VF . May occur

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

Following plaque reduction after percutaneous coronary intervention

PVC’s-unifocal

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

PVC’s multi-focal

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 decrease in CO

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

Ventricular Tachycardia

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

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

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

Complications of Arrhythmias

HypotensionTissue ischemiaThrombi- low dose heparin, or ASAHeart failureShockDeath

Diagnostic Tests

Telemetry- 5 lead (lead II and V1)12 lead EKGHolter or event monitoringExercise stress testElectrophysiology studies- induce

arrhythmias under controlled situation

EKG changes in an acute MI

Not linked…but watch EKG changes in evolving MI

Nursing Assessment

Apical rate and rhythmApical/radial deficitBlood pressureSkinUrine outputSigns of decreased

cardiac output

Nursing Diagnoses

Decreased cardiac outputDecreased tissue perfusionActivity intoleranceAnxiety and FearKnowledge deficit

Goals-

MedicationsClassified 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

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

(correct electrolytes)

AntiarrhythmicsRemembering that of all anti-arrhythmics "some block potassium channels" can help you: 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- valium

Invasive procedures-

DefibrillationEmergency- start at 200 watt/sec, go to 400Safety precautionsAED’s now

Synchronized Cardioversion- vent tachycardia or SVT or a- fib, flutter to convertUsually plannedGet permitStart at 50 watt/secAwake, give O2 and sedationHave to synchronize with rhythm

cardioversion

Implanted Cardiac Defibrillator (AICD)Senses rate and width of QRSGoes off 3 times, then have to be resetSome combined with pacemaker

PacemakerPermanent- battery under skinTemporary- battery outside bodyTypes

TransvenousEpicardial- bypass surgeryTranscutaneous- emergency

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

rateReview classifications- (Wikipedia)

Pacemaker resources

Pacemaker Problems:

•Failure to sense

•Failure to capture

Ablation

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

View video

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; will be seen in leads that face the 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)

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

ECG Changes Associated with Acute Coronary Syndrome (ACS)

Injury/InfarctionST 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


Infarction/NecrosisNote: 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

EKG changes in an acute MI

Syncope

Brief lapse in consciousnessCausesVasovagal

Cardiac dysrhythmiasOther- hypoglycemia, seizure, hypertrophic

cardiomyopathy1-year mortality rate as high as 30% for

syncope from cardiovascular cause

QuizzesDiscussionQuestions

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

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.

Prioritization question

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.

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