arrhythmias by laurie dickson with thanks to nancy jenkins
TRANSCRIPT
Arrhythmias
By Laurie DicksonWith thanks to Nancy Jenkins
The EKG is the electrical activity of the heart.
Electrical precedes mechanical
(Without electricity, we have no pump!!)
By action potentials
Na K pump Calcium channels Depolarization Repolarization
YouTube - Action Potenital
ECG waveforms are produced by the movement of charged ions across the semipermeable membranes of myocardial cells.
Animation: How the Sodium Potassium Pump Works
Electrical System Each beat that is generated from the 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.
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
Cardiac Cycle
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)..
Conduction system SA node 60-100 AV node 40-60 Bundle of His Left and Right Bundle Branch Purkinge Fibers 20-40
Pacemakers other than SA nodeA 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.
EKG waveforms
P wave = Atrial depolarization (stimulation) QRS = Ventricular depolarization (stimulation) T wave = 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 paper Horizontal measures time Vertical measures voltage Helps us determine rate Width of complexes Duration of complexes
EKG graph paper
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
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
(Grass under clouds, smoke above fire)
V1 is 2nd ICS right of sternum
Lead II R arm looking to LL positive
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
Cardiac cells are either contractile cells influencing the pumping action or pacemaker cells influencing the electrical activity of the heart
4 Characteristics of Cardiac Cells
Automaticity Excitability Conductivity Contractility
Refractoriness- Refractory period Absolute/ Relative/ Full
Refractory Period
Risk Factors for Arrhythmias Hypoxia Structural changes Electrolyte imbalances Central nervous system stimulation Medications Lifestyle behaviors
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 .04-.12 P 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
Sinus Rhythm Normal P wave- 0.06-0.12 sec PR interval – 0.12-0.20 QRS- 0.04-0.12 T wave for every complex- 0.16 Rate is regular 60-100
Sinus Tachycardia
Rate >100: Sinus Tachycardia Causes-anxiety, hypoxia, shock, pain,
caffeine, drugs Treatment-eliminate cause
Clinical significance Dizziness and hypotension due to decreased
CO Increased myocardial oxygen consumption
may lead to angina
Rate<60: Sinus Bradycardia- relative-symptomatic, absolute-normal Cause-vagal stimulation, athlete, drugs
(Blockers and digoxin), head injuries, MI Watch for syncope
brady heart song
Sinus Bradycardia
Clinical significance-Dependent on symptoms Hypotension , Weakness Pale, cool skin Angina, Shortness of breath Dizziness or syncope Confusion or disorientation
Treatment- if symptomatic, atropine or pace maker
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
Sinus Arrest See pauses May see ectopic beats(PAC’s PVC’s) do
not treat Cause MI Treatment
atropine Pacemaker
Medications used to treat the atrial rhythms diltiazem (Cardizem) digoxin (Lanoxin) amiodarone (Cordarone) dofetilide (Tikosyn) verapamil (Calan, Calan SR, Covera-HS,
Isoptin SR, Verelan, Verelan PM, Isoptin, Isoptin I.V.)
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
Paroxysmal Supraventricular Tachycardia (PSVT) Rate is 100-300, regular, p often hidden Ectopic foci in atrium above bundle of HIS Cause-SNS stimulation, MI, CHF,sepsis
Paroxysmal Supraventricular Tachycardia (PSVT)
Clinical significance -Prolonged episode and HR >180 bpm may precipitate ↓ CO
Palpitations, Hypotension, Dyspnea, Angina
Treatment- Vagal stimulation * adenosine, B blockers, Calcium channel
blockers, digoxin, amiodarone. Cardioversion
Atrial Flutter Rate of atria is 250-300, vent rate varies Regular rhythm P waves saw tooth, one ectopi focus AV block in ratio 2:1, 3:1, 4:1 Flutter waves- No PR interval Cause-diseased heart, drugs (digoxin)
3:1 flutter
Atrial Flutter Clinical significance
High ventricular rates (>100) + loss of the atrial “kick” can decrease CO, precipitate HF, angina
Risk for stroke due to risk of thrombus formation in the atria
Treatment- Calcium channel blockers, Beta blockers
amiodarone, Cardioversion
Ablation
warfarin (Coumadin)
Atrial Fibrillation-most common Rate of atria 350-600- (disorganized rhythm) Ventricular response irregular No P waves, “garbage baseline” PR cannot measure QRS- normal
Cause-#1 arrhythmia in elderly, heart disease- CAD, rheumatic, CHF, alcohol
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, travel to the brain, causing a stroke
Complications- dec. CO and thrombi (stroke risk increases x5)
Atrial Fibrillation-most common Treatment-
digoxin, Ca channel blockers, Beta blockers
amiodorone, procainamaide (Pronestyl)
Cardioversion – warfarin + TEE
Ablation, Maze
QuickTime™ and aYUV420 codec decompressor
are needed to see this picture.
Atrial Fibrillation
Arrhythmias of AV Node
AV Conduction Blocks
First Degree AV Block Transmission through AV node delayed PR interval >.20 QRS normal and regular Cause- digoxin toxicity, MI, CAD, vagal,
and blocker drugs
First-Degree AV Block
Clinical significance Usually asymptomatic May be a precursor to higher degrees of
AV block Treatment
Check medications Continue to monitor
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
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 Occurs in HIS bundle with bundle branch block
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
Treatment- watch for type II and 3rd degree
If symptomatic- atropine, pacer
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
Treatment- pacemaker
3rd Degree AV Block Atria and ventricles beat independently
Atrial rate- 60-100 Slow ventricular rate 20-40 P normal No PR interval- no relationship with QRS Wide or normal QRS (depends on where block is)
Cause- severe heart disease, blockers, elderly, MI Complications- dec. CO, ischemia, HF, shock,
and syncope
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
Treatment- atropine, pacemaker
3rd Degree
Bundle Branch Blocks Left BBB Right BBB QRS.12 or greater Rabbit ears- RR’ No change in rhythm
Right Bundle Branch Block
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
.
Cont. PR interval
Absent or hidden Short <.12 Negative or RP interval
QRS normal No treatment
Ventricular ArrythmiasMost serious
Easy to recognize
Premature Ventricular Contractions (PVC’s)-ectopic No P waves QRS wide and bizarre T opposite deflection of PVC Cause- 90% with MI, stimulants, digoxin,
electrolyte imbalance
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
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
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 minute Runs of PVC’s Multi focal PVC’s R on T Treatment- based on cause
O2, lidocaine, procainamide, amiodarone
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, digoxin Life- threatening, decreased CO, watch for V-fib
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
Ventricular Tachycardia
Clinical significance Treatment for VT must be rapid May recur if prophylactic treatment is
not initiated Ventricular fibrillation may develop
Treatment- same as for PVC’s and defibrillate for sustained
VT- Torsades de PointesFrench for twisting of the points
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
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
Nursing Assessment Apical rate and rhythm Apical/radial deficit Blood pressure Skin Urine output Signs of decreased
cardiac output
Nursing Diagnoses Decreased cardiac output Decreased tissue perfusion Activity intolerance Anxiety and Fear Knowledge deficit
Goals Maintain stable signs of effective cardiac output
and tissue perfusion Achieve a realistic program of activity that
balances physical activity with energy conserving activities
Report decreased anxiety and increased sense of self-control
Describe risk factors, the disease process, and treatment regimen
Medications Classified by effect on action potential
Class I- fast Na blocking agents-ventricular quinidine, procainamide, lidocaine, disopyramide phosphate (Norpace), propafenone
(Rhythmol)
Class II- beta blockers SVT,Afib,flutter esmolol, atenolol (Tenormin), propranolol(Inderal)
Medications Class III- K blocking
both atrial and ventricular amiodarone, dofetilide, sotalol
Class IV- Ca, channel blockers SVT,Afib,flutter verapamil, diltiazem
Other- adenosine, digoxin, atropine, magnesium
Antiarrhythmics
Remembering that of all anti-arrhythmics "some block potassium channels" can help you:
Class I "Some" = Sodium Class II "Block" = Beta blockers Class III "Potassium" = Potassium channel blockers Class IV "Channels" = Calcium channel blockers
Comfort Measures Rest O2 Relieve fear and anxiety-
diazapam (Valium)
Invasive procedures Defibrillation
Emergency- start at 200 watt/sec, go to 400 Safety precautions AED safety AED’s now AED 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
cardioversion
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
Implantable Cardioverter- Defibrillator (ICD)
Fig. 36-22
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
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
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
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 Classifications
pacemaker classification
Pacemaker Problems:
Failure to sense
Failure to capture
Ablation Done in special cardiac procedures lab Use a laser to burn abnormal pathway radiofrequency ablation
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)
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)
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
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
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 B
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
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.
Syncope Brief lapse in consciousness accompanied
by a loss of tone (fainting) Causes
Cardiovascular Vasovagal, Cardiac dysrhythmias, hypertrophic
cardiomyopathy , PE
Noncardiovascular hypoglycemia, seizure, hysteria, TIA
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
Complications of Arrhythmias Hypotension Tissue ischemia Thrombi- low dose heparin, or ASA Heart failure Shock Death
Prioritization QuestionA 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
Prioritization questionA 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.
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.
Video Acting Out Rhythms mad german doctor dances to heart
rhythms Practice-http://www.skillstat.com/Flash/
ECG_Sim_2004.html Casestudies QuizzesDiscussionQuestions