arrhythmias by laurie dickson with thanks to nancy jenkins

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

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



Fig. 36-29 A


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


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



Fig. 36-29 B



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

arrhythmias by laurie dickson with thanks to nancy jenkins

Documents

lead ekg

mi slide

depolarization wave

ll positive slide

r wave

negative lead

atrial kick slide

ekg graph paper slide