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Transcript of Dysrhythmias EKG DANCEEKG DANCE-click here Abnormal cardiac rhythms are termed dysrhythmias. Prompt...
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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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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
Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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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
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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
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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:
1. 75
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
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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
block
Treatment Check medications. Continue to monitor.
First-Degree AV Block
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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
Second-Degree AV Block, Type 2 (Mobitz II)
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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
CAD
Anterior MI
Digitalis toxicityTreatment
If symptomatic (e.g., hypotension, angina) before permanent pacemaker can be inserted, temporary transvenous or transcutaneous pacemaker
Permanent pacemaker
Second-Degree AV Block, Type 2 (Mobitz II)
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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)
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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)
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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
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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
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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
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
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.
Ventricular Tachycardia
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Treatment VT without a pulse is a life-threatening
situation.
Cardiopulmonary resuscitation (CPR) and rapid defibrillation
• Epinephrine if defibrillation is unsuccessful
Ventricular Tachycardia
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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
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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)
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Death from a cardiac causeMajority of SCDs result from ventricular
dysrhythmias.Ventricular tachycardiaVentricular fibrillation
Sudden Cardiac Death (SCD)
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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)
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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
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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
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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
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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
96
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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.
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 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.