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
ECG Changes Associated with Acute Coronary Syndrome (ACS)
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
ECG Changes Associated with Acute Coronary Syndrome (ACS)
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Fig. 36-29 A
ECG Changes Associated with Acute Coronary Syndrome (ACS)
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Fig. 36-29 B
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
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
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.
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.