arrhythmias: by nancy jenkins. the ekg is the electrical activity of the heart. electrical precedes...
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Arrhythmias:
By Nancy Jenkins
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The EKG is the electrical activity of the heart.
Electrical precedes mechanical
(Without electricity, we have no pump!!)
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How is the electricity generated?
action potentials
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By action potentials Na K pump Calcium channels Depolarization Repolarization
YouTube - How the Body Works : A Nerve Impulse
ECG waveforms are produced by the movement of charged ions across the semipermeable membranes of myocardial cells.
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Na K pump
Animation: How the Sodium Potassium Pump Works
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Electrical systemMultimedia Tutorials
Each beat that is generated from the same pacemaker will look identical.
Impulses from other cardiac cells are called ectopic (PVC, PAC)
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This electrical activity produces mechanical activity that is seen as waveforms.
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Nervous System Control of the Heart
Parasympathetic nervous system: Vagus nerve Decreases rate Slows impulse conduction Decreases force of contraction
Sympathetic nervous system Increases rate Increases force of contraction
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Cardiac Cycle
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Yellow is the isoelectric phase. The purple is the "P"wave. The purple and yellow split is the "PR" interval. The red is the "Q" wave. The light blue is the "R" wave. The light green is the "S" wave. The black is the "ST" segment. The orange is the "T" wave. Yellow again is isoelectric. The dark blue is the "U" wave (seldom seen).
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Conduction system SA node 60-100 AV node 40-60 Bundle of His Left and Right Bundle Branch Purkinge Fibers 15-40
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Pacemakers other than SA node
A pacemaker from another site can lead to dysrhythmias and may be discharged in a number of ways.
o Secondary pacemakers may originate from the AV node or His-Purkinje system.
o Secondary pacemakers can originate when they discharge more rapidly than the normal pacemaker of the SA node.
o Triggered beats (early or late) may come from an ectopic focus (area outside the normal conduction pathway) in the atria, AV node, or ventricles.
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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
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EKG graph paper Horizontal measures time Vertical measures voltage Helps us determine rate Width of complexes Duration of complexes
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EKG graph paper
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Monitoring leads- based on 12 lead EKG Each lead has positive, negative and
ground electrode. Each lead looks at a different area of the
heart. This can be diagnostic in the case of an MI
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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
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(Grass under clouds, smoke above fire)
V1 is 2nd ICS right of sternum
Lead II R arm looking to LL positive
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Leads to monitor inEKG leads
Best- lead II and MCL or V1 leads- lead II easy to see Pwaves. MCL or V1 easy to see 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
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Cardiac cells are either contractile cells influencing the pumping action or pacemaker cells influencing the electrical activity of the heart
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4 Characteristics of Cardiac Cells
Automaticity Excitability Conductivity Contractility Refractoriness
Relative absolute
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Refractory Period
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Risk Factors for Arrhythmias Hypoxia Structural changes Electrolyte imbalances Central nervous system stimulation Medications Lifestyle behaviors
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Assessment Calculate rate
Big block Little block Number of R waves in 6 sec times 10
Calculate rhythm-reg or irreg Measure PR interval, <.20 QRS interval .06-.10 P to QRS relationship
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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
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Sinus Rhythm Normal P wave PR interval<.20 QRS.06-.10 T wave for every complex Rate is regular 60-100 Rate >100: Sinus Tachycardia
Causes-anxiety, hypoxia, shock, pain, caffeine, drugs Treatment-eliminate cause
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Sinus Tachycardia
Clinical significance Dizziness and hypotension due to
decreased CO Increased myocardial oxygen
consumption may lead to angina
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Rate<60: Sinus Bradycardia- relative-symptomatic, absolute-normal Cause-vagal stimulation, athlete, drugs
(Blockers and digoxin), head injuries, MI Watch for syncope Treatment- if symptomatic, atropine or pacer
brady heart song
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Sinus Bradycardia
Clinical significance Dependent on symptoms
Hypotension Pale, cool skin Weakness Angina Dizziness or syncope Confusion or disorientation Shortness of breath
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Sinus Arrhythmia (SA) Rate 60-100 Irregular rhythm- increases with
inspiration, decreases with expiration P, QRS,T wave normal Cause- children, drugs(MS04), MI Treatment- none
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Sinus Arrest See pauses May see ectopic beats(PAC’s PVC’s) do
not treat Cause MI Treatment
Atropine Isuprel Pacemaker
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Atrial Arrythmias Atria is the pacemaker Atrial rate contributes 25-30% of cardiac
reserve Serious in patients with MI- WHY?
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Medications used to treat the atrial rhythms Cardizem Digoxin Amiodarone Tikosyn Verapamil
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Premature Atrial Contraction (PAC’s)-ectopic P wave abnormally shaped PR interval shorter QRS normal Cause-age, MI, CHF, stimulants, dig,
electrolyte imbalance Treatment- remove stimulants and watch
for SVT
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Paroxysmal Supraventricular Tachycardia (PSVT) Rate is 150-300, regular, p often hidden Atria is pacemaker (may not see p waves) Cause-SNS stimulation, MI, CHF,sepsis Treatment- vagal stimulation, * adenosine,
digoxin, verapamil, inderal, cardizem,tikosyn, or cardioversion
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Paroxysmal Supraventricular Tachycardia (PSVT)
Clinical significance Prolonged episode and HR >180 bpm may
precipitate ↓ CO PalpitationsHypotensionDyspneaAngina
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Atrial Flutter Rate of atria is 250-300, vent rate varies Regular rhythm P waves saw tooth, ratio 2:1, 3:1, 4:1 Flutter waves- No PR interval Cause-diseased heart, dig Treatment- cardiovesion, calcium channel
blockers and beta blockers, amiodorone, ablation coumadin
3:1 flutter
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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
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Atrial Fibrillation-most common Rate of atria 350-600- (disorganized rhythm) Ventricular response irregular No P waves, “garbage baseline” Cause-#1 arrhythmia in elderly, heart disease- CAD,
rheumatic, CHF, alcohol Complications- dec. CO and thrombi (stroke) Treatment- start with digoxin, ca channel blockers, beta
blockers, amiodorone, pronestyl, cardioversion (TEE to see if clots before) Coumadin- check PT and INR, ablation and Maze
Thrombus formation, pulse deficit, AR>RR
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QuickTime™ and aYUV420 codec decompressor
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Atrial Fibrillation
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Atrial Fibrillation
Clinical significance Can result in decrease in CO due to
ineffective atrial contractions (loss of atrial kick) and rapid ventricular response
Thrombi may form in the atria as a result of blood stasis
Embolus may develop and travel to the brain, causing a stroke
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Arrhythmias of AV Node
AV Conduction Blocks
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First Degree AV Block Transmission through AV node delayed PR interval >.20 QRS normal and regular Cause-dig toxicity, MI, CAD vagal, and
blocker drugs Treatment- none but watch for further
blockage
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First-Degree AV Block
Clinical significance Usually asymptomatic May be a precursor to higher degrees of
AV block Treatment
Check medications Continue to monitor
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Second Degree AV Blockmore P’s than QRS’s A. Mobitz I (Wenckebach) YouTube - Diagnosis
Wenckebach PR progressively longer then drops QRS Cause- MI, drug toxicity Treatment- watch for type II and 3rd degree
B. MobitzII More P’s but skips QRS in regular pattern 2:1,3:1,
4:1(QRS usually greater than .12-BBB) Constant PR interval- can be normal or prolonged Treatment-Pacemaker Occurs in HIS bundle with bundle branch block
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Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)
Clinical significance Usually a result of myocardial ischemia
or infarction Almost always transient and well
tolerated May be a warning signal of a more
serious AV conduction disturbance
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Second-Degree AV Block, Type 2 (Mobitz II)
Clinical significance Often 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
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3rd Degree AV Block Atria and ventricles beat independently Atrial rate- 60-100 Slow ventricular rate 20-40 No PR interval Wide or normal QRS (depends on where block is) Cause- severe heart disease, blockers elderly, MI Complications- dec. CO, ischemia, HF, shock,
and syncope Treatment- atropine, pacemaker
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Third-Degree AV Heart Block (Complete Heart Block)
Clinical significance Decreased CO with subsequent
ischemia, HF, and shock Syncope may result from severe
bradycardia or even periods of asystole
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3rd Degree
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Bundle Branch Blocks Left BBB Right BBB QRS.12 or greater Rabbit ears- RR’ No change in rhythm
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Right Bundle Branch Block
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Junctional Rhythm AV node is pacemaker- slow rhythm (40-60) but
very regular impulse goes to atria from AV node- backward)
P wave patterns Absent P wave precedes QRS inverted in II, III, and AVF P wave hidden in QRS P wave follows QRS
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Cont. PR interval
Absent or hidden Short <.12 Negative or RP interval
QRS normal No treatment
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Ventricular ArrythmiasMost serious
Easy to recognize
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Premature Ventricular Contractions (PVC’s)-ectopic QRS wide and bizarre No P waves T opposite deflection of PVC Cause- 90% with MI, stimulants, dig,
electrolyte imbalance Treatment- O2, lidocaine,
pronestyl,amiodarone No longer prophylactic
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Premature Ventricular Contractions
Clinical significance In normal heart, usually benign In 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
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Premature Ventricular Contractions
Clinical significance Represents ventricular irritability May occur
After lysis of a coronary artery clot with thrombolytic therapy in acute MI—reperfusion dysrhythmias
Following plaque reduction after percutaneous coronary intervention
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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
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Treat if: >5 PVC’s a minute Runs of PVC’s Multi focal PVC’s R on T
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Ventricular Tachycardia (VT) Ventricular rate 150-250, regular or irregular No P waves QRS>.12 Can be stable- pulse or unstable –no pulse Cause- electrolyte imbalance, MI, CAD, dig Life- threatening, dec. CO, watch for V-fib Treatment- same as for PVC’s and defibrillate for
sustained
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Ventricular Tachycardia Clinical significance
VT 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
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Ventricular Tachycardia
Clinical significance Treatment for VT must be rapid May recur if prophylactic treatment is
not initiated Ventricular fibrillation may develop
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VT- Torsades de PointesFrench for twisting of the points
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Ventricular Fibrillation Garbage baseline-quivering No P’s No QRS’s No CO Cause-MI, CAD, CMP, shock, K+,
hypoxia, acidosis, and drugs Treatment- code situation, ACLS, CPR,
**defibrillate
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Diagnostic Tests Telemetry- 5 lead( lead II and V1) 12 lead EKG Holter monitor- pt. keeps a diary Event monitoring- pt. records only when
having the event Exercise stress test Electrophysiology studies- induce
arrhythmias under controlled situation
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Nursing Assessment Apical rate and rhythm Apical/radial deficit Blood pressure Skin Urine output Signs of decreased
cardiac output
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Nursing Diagnoses Decreased cardiac output Decreased tissue perfusion Activity intolerance Anxiety and Fear Knowledge deficit
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Goals
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Medications Classified by effect on action potential Class I- fast Na blocking agents-ventricular
Quinidine, Pronestyl, Norpace,Lidocaine, Rhythmol Class II-beta blockers (esmolol, atenolol, inderal)
SVT,Afib,flutter Class III- K blocking (amiodorone, tikosyn,
sotalol)both atrial and ventricular Class IV- Ca, channel blockers (verapamil
cardiazem)SVT,Afib,flutter Other- adenosine, dig, atropine, covert, magnesium
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Antiarrhythmics
Remembering 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
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Comfort Measures Rest O2 Relieve fear and anxiety- valium
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Invasive procedures Defibrillation
Emergency- start at 200 watt/sec, go to 400 Safety precautions AED’s now
Synchronized Cardioversion- for vent. or SVT Can be planned- if stable Get permit Start at 50 watt/sec Awake, give O2 and sedation Have to synchronize with rhythm
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Implanted Cardiac Defibrillator (ICD) Senses rate and width of QRS Goes off 3 times, then have to be reset Combined with pacemaker- overdrive pacing
or backup pacing
ICD resources
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Implantable Cardioverter- Defibrillator (ICD)
Fig. 36-22
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
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My journey started july 13th 2008. Went to doctor thinking i had bronchitis. 2 days later went in because i got awoken during the night not being able to breath. dr thought i had gone into pnemonia, gave chest xray,18th go back tells me i have congestive heart failure, starts me on water pills and something else has me scheduled for an echo on monday, wait 2 days calls and wants me to come in on friday and wants a
cardioligist to see me and the echo, go in tells me to go to a hospital north of us saying they have a room ready and will shedule a cath and the cardiolgist can reveiew the ecko. get up there doc reviews ecko, while nurses are hooking me up with ivs, dr comes in and says may have major heart damage but will wait until cath on monday. monday comes have cath a surgeon comes in with cardiolisgist telling us i have over half my heart damaged may need transplant, cardioligist says they would rather transport me to a major hospital that can handle transplant surgery if something goes wrong with bypass. ef is 15%. go to indianapolis by ambulance,
Journal of Patient Needing Heart Transplant
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i am in total shock by this point not being able to even comprehend what is going on 2 weeks from going from broncitis or so i thought to maybe haveing heart transplant. My wife god bless her is haveing her own stress out of her mind over this. get to indy tues and wed nuclear test, friday high risk bypass surgery. Now its 6 weeks after surgery have had another ecko ef went up a woping 5% now getting defibed tuesday, today is sunday and again my mind is wondering into the worst scenorios, it is gettting harder and harder to grasp this stuff. hopefully sites like this will help, letting blow off steam, and learning.dave
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Pacemaker Permanent- battery under skin Temporary- battery outside body Types
Transvenous Epicardial- bypass surgery Transcutaneous- emergency
Modes Asynchronous- at preset time without fail Synchronous or demand- when HR goes below set rate
Review classifications
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Pacemakers
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Fig. 36-27
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http://www.vmth.ucdavis.edu/cardio/cases/case14/pacemaker.htm
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Pacemaker Problems:
Failure to sense
Failure to capture
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Ablation Done in special cardiac procedures lab Use a laser to burn abnormal pathway
http://www.aboutatrialfibrillation.com/treated.html # cardioversion
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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
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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
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ECG Changes Associated with Acute Coronary Syndrome (ACS)
Injury/Infarction ST 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
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ECG Changes Associated with Acute Coronary Syndrome (ACS)
Injury/Infarction Note: 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
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EKG changes in an acute MI
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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
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ECG Changes Associated with Acute Coronary Syndrome (ACS)
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Fig. 36-30
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EKG CHANGES ASSOCIATED WITH ACUTE CORONARY SYNDROME The 12-lead ECG is the primary diagnostic tool used to evaluate patients presenting with ACS. There are definitive ECG changes that occur in response to ischemia, injury, or infarction of myocardial cells and will be seen in the leads that face the area of involvement. Typical ECG changes seen in myocardial ischemia include ST-segment depression and/or T wave inversion. The typical ECG change seen during myocardial injury is ST-segment elevation.
An ST-segment elevation and a pathologic Q wave may be seen on the ECG with myocardial infarction.
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Syncope Brief lapse in consciousness Causes
Vasovagal Cardiac dysrhythmias Other- hypoglycemia, seizure, hypertrophic
cardiomyopathy
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Syncope
Diagnostic studies Echocardiography EPS Head-upright tilt table testing Holter monitor Subcutaneously implanted loop recording
device 1-year mortality rate as high as 30% for
syncope from cardiovascular cause
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Complications of Arrhythmias Hypotension Tissue ischemia Thrombi- low dose heparin, or ASA Heart failure Shock Death
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QuizzesDiscussionQuestions
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Casestudies
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Video acting out rhythms
YouTube - Mad German Doctor Dances To Heart Rhythms
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rhythm practice/
Practice-http://www.skillstat.com/Flash/ECG_Sim_2004.html
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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 pulse C. Take the client’s blood pressure D. Have the client breathe deeply
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Prioritization question Cardiac rhythms are being observed for clients in the
CCU. Which client will need 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.
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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 joules B. Begin CPR C. Administer epinephrine 1 mg IV D.Intubate and manually ventilate.