ch 36 powerpoint lewis medsurg

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Dysrhythmias

Chapter 36

Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

Properties of Cardiac Cells

• Automaticity

• Excitability

• Conductivity

• Contractility

Copyright © 2014 by Mosby an imprint of Elsevier Inc

Conduction System of the Heart


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Nervous System Control of Heart

• Autonomic nervous system controls

• Parasympathetic nervous system

• Decreases rate of SA node

• Slows impulse conduction of AV node

• Sympathetic nervous system

• Increases rate of SA node

• Increases impulse conduction of AV node

• Increases cardiac contractility


Dysrhythmias

• Disorder of impulse formation, conduction of impulses, or both

• SA node normal pacemaker of heart (60–100 beats/minute)

• Secondary pacemakers

• AV node (40–60 beats/minute)

• His‐Purkinje fibers (20–40 beats/minute)


Electrocardiogram Monitoring

• Graphic tracing of electrical impulses produced by heart

• Waveforms of ECG represent activity of charged ions across membranes of myocardial cells


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Electrocardiogram Monitoring



12‐Lead ECG


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Case Study

• S.D. is a 45‐year‐old woman who comes to the ED complaining of sudden onset of palpitations and shortness of breath.

• Standard protocol requires you to obtain a 12‐lead ECG and attach S.D. to the cardiac monitor for continuous monitoring.

iStockphoto/Thinkstock


Case Study

• Describe the appropriate location to apply the leads for both the 5‐lead cardiac monitor as well as the 12‐ lead ECG.



Lead Placement


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Lead Placement


ECG Time and Voltage


Calculating HR

• Count

• Number of QRS complexes in 1 minute

• R‐R intervals in 6 seconds, and multiply by 10

• Number of small squares between one R‐R interval, and divide this number into 1500

• Number of large squares between one R‐R interval, and divide this number into 300


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Assessment of Cardiac Rhythm


Patient Preparation

• Clip excessive hair on chest wall

• Rub skin with dry gauze

• May need to use alcohol for oily skin

• Apply electrode pad


Artifact


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Telemetry Monitoring

• Observation of HR and rhythm at a distant site

• Two types

• Centralized monitoring system

• Advanced alarm system alerts when it detects dysrhythmias, ischemia, or infarction



• Interpret the rhythm AND evaluate the clinical status of the patient

• Is the patient hemodynamically stable?

• Determine cause of dysrhythmia

• Treat the patient, not the monitor!


Case Study

• The UAP obtains the 12‐lead ECG recording for S.D. while you print out a rhythm strip from the cardiac monitor.

• Describe the method you would use to assess S.D.’s rhythm strip.



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1. P wave

2. Atrial rate and rhythm

3. P‐R interval

4. Ventricular rate and rhythm

5. QRS complex

6. ST segment

7. Q‐T interval

8. T wave


Normal Sinus Rhythm

• Sinus node fires 60–100 beats/minute

• Follows normal conduction pattern



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Sinus Bradycardia



Sinus Bradycardia

• Normal rhythm in aerobically trained athletes and during sleep

• Can occur in response to parasympathetic nerve stimulation and certain drugs

• Also associated with some disease states


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Sinus Bradycardia

• Manifestations• Hypotension

• Pale, cool skin

• Weakness

• Angina

• Dizziness or syncope

• Confusion or disorientation

• Shortness of breath


Sinus Bradycardia

• Treatment

• Atropine

• Pacemaker

• Stop offending drugs


A patient’s cardiac rhythm is sinus bradycardia with a heart rate of 34 beats/minute. If the bradycardia is symptomatic, the nurse would expect the patient to exhibit

a. Palpitations.

b. Hypertension.

c. Warm, flushed skin.

d. Shortness of breath.

Audience Response Question


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Sinus Tachycardia



Sinus Tachycardia

• Caused by vagal inhibition or sympathetic stimulation

• Associated with physiologic and psychologic stressors

• Drugs can increase rate


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Sinus Tachycardia

• Manifestations

• Dizziness

• Dyspnea

• Hypotension

• Angina in patients with CAD


Sinus Tachycardia

• Treatment

• Guided by cause (e.g., treat pain)

• Vagal maneuver

• β‐adrenergic blockers


Premature Atrial Contraction


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• Contraction originating from ectopic focus in atrium in location other than SA node

• Travels across atria by abnormal pathway, creating distorted P wave

• May be stopped, delayed, or conducted normally at the AV node



• Causes• Stress• Fatigue• Caffeine• Tobacco• Alcohol• Hypoxia• Electrolyte imbalance• Disease states



• Manifestations

• Palpitations

• Heart “skips a beat”

• Treatment

• Monitor for more serious dysrhythmias

• Withhold sources of stimulation

• β‐adrenergic blockers


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Paroxysmal Supraventricular Tachycardia (PSVT)




• Reentrant phenomenon: PAC triggers a run of repeated premature beats

• Paroxysmal refers to an abrupt onset and termination

• Associated with overexertion, stress, deep inspiration, stimulants, disease, digitalis toxicity


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• Manifestations• HR is 150–220 beats/minute (add for clarification)

• HR > 180 leads to decreased cardiac output and stroke volume

• Hypotension

• Dyspnea

• Angina


• Treatment

• Vagal stimulation

• IV adenosine

• IV β‐adrenergic blockers

• Calcium channel blockers

• Amiodarone

• DC cardioversion


Atrial Flutter


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Atrial Flutter

• Typically associated with disease

• Symptoms result from high ventricular rate and loss of atrial “kick” →decreased CO → heart failure

• Increases risk of stroke


Atrial Flutter

• Treatment

• Pharmacologic agent

• Electrical cardioversion

• Radiofrequency ablation


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Case Study

• S.D.’s ECG reveals atrial fibrillation with a rapid ventricular response (HR = 168).

• Describe what S.D.’s rhythm would look like.

• What might be the cause of this dysrhythmia for S.D.?



Atrial Fibrillation


Atrial Fibrillation

• Paroxysmal or persistent

• Most common dysrhythmia

• Prevalence increases with age

• Usually occurs in patients with underlying heart disease

• Can also occur with other disease states


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Case Study

• S.D.’s blood pressure is 94/58 with HR of 168.

• What treatment might you expect the health care provider to initially order for S.D.’s atrial fibrillation?




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Atrial Fibrillation

• As with atrial flutter – causes a decrease in CO and an increased risk of stroke


Atrial Fibrillation

• Treatment• Drugs to control ventricular rate and/or convert to sinus rhythm (amiodarone and ibutilide most common)

• Electrical cardioversion

• Anticoagulation

• Radiofrequency ablation

• Maze procedure with cryoablation


Junctional Dysrhythmias

• Dysrhythmias that originate in area of AV node

• SA node has failed to fire, or impulse has been blocked at the AV node

• AV node becomes pacer—retrograde transmission of impulse to atria

• Abnormal P wave; normal QRS

• Associated with disease, certain drugs


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Junctional Dysrhythmias


Junctional Dysrhythmia

• Serves as safety mechanism—do not suppress

• If rhythms are rapid, may result in reduction of CO

• Treat if patient is symptomatic • Atropine for escape rhythm

• Correct cause

• Drugs to reduce rate if tachycardia


First‐Degree AV Block


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First‐Degree AV Block

• Associated with disease states and certain drugs

• Typically not serious

• Patients asymptomatic

• No treatment

• Monitor for changes in heart rhythm


Second‐Degree AV Block, Type 1 (Mobitz I, Wenckebach)


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Second‐Degree AV Block, Type 1 (Mobitz I, Wenckebach)

• May result from drugs or CAD

• Typically associated with ischemia

• Usually transient and well tolerated

• Treat if symptomatic

• Atropine

• Pacemaker

• If asymptomatic, monitor closely


Second‐Degree AV Block, Type 2 (Mobitz II)


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Second‐Degree AV Block, Type 2 (Mobitz II)

• Associated with heart disease and drug toxicity

• Often progressive and results in decreased CO

• Treat with pacemaker


Third‐Degree AV Heart Block (Complete Heart Block)


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Third‐Degree AV Heart Block (Complete Heart Block)

• Associated with severe heart disease, some systemic diseases, certain drugs

• Usually results in decreased CO

• Can lead to syncope, HF, shock

• Treat with pacemaker

• Drugs to increase heart rate if needed while awaiting pacing


Premature Ventricular Contractions


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• Associated with stimulants, electrolyte imbalances, hypoxia, heart disease

• Not harmful with normal heart but CO reduction, angina, and HF in diseased heart

• Assess apical‐radial pulse deficit


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• Treatment

• Correct cause

• Antidysrhythmics


A patient has a diagnosis of acute myocardial infarction, and his cardiac rhythm is sinus bradycardia with 6 to 8 premature ventricular contractions (PVCs) per minute. The pattern that the nurse recognizes as the most characteristic of PVCs is

a. An irregular rhythm.

b. An inverted T wave.

c. A wide, distorted QRS complex.

d. An increasingly long P‐R interval.



Ventricular Tachycardia


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• Ectopic foci take over as pacemaker

• Monomorphic, polymorphic, sustained, and nonsustained

• Considered life‐threatening because of decreased CO and the possibility of deterioration to ventricular fibrillation


Ventricular TachycardiaTorsades de Pointes


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• Associated with heart disease, electrolyte imbalances, drugs, CNS disorder

• Can be stable (patient has a pulse) or unstable (pulseless)

• Sustained VT causes severe decrease in CO

• Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest



• Precipitating causes must be identified and treated (e.g., hypoxia)

• VT with pulse (stable) treated with antidysrhythmics or cardioversion

• Pulseless VT treated with CPR and rapid defibrillation


Accelerated Idioventricular Rhythm (AIVR)

• Develops when the intrinsic pacemaker rate (SA node or AV node) becomes less than that of ventricular ectopic pacemaker

• Rate is between 40 and 100 beats/minute

• Atropine if patient symptomatic

• Temporary pacing

• Do not suppress rhythm


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Ventricular Fibrillation



Ventricular Fibrillation

• Associated with MI, ischemia, disease states, procedures

• Unresponsive, pulseless, and apneic

• If not treated rapidly, death will result

• Treat with immediate CPR and ACLS

• Defibrillation

• Drug therapy (epinephrine, vasopressin)


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A patient in the coronary care unit develops ventricular fibrillation. The first action the nurse should take is to

a. Perform defibrillation.

b. Initiate cardiopulmonary resuscitation.

c. Prepare for synchronized cardioversion.

d. Administer IV antidysrhythmic drugs per protocol.



Asystole

• Represents total absence of ventricular electrical activity

• No ventricular contraction

• Patient unresponsive, pulseless, apneic

• Must assess in more than one lead



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Asystole

• Usually result of advanced cardiac disease, severe conduction disturbance, or end‐stage HF

• Treat with immediate CPR and ACLS measures• Epinephrine and/or vasopressin

• Intubation

• Poor prognosis


Pulseless Electrical Activity

• Electrical activity can be observed on the ECG, but no mechanical activity of the ventricles is evident, and the patient has no pulse

• Prognosis is poor unless underlying cause quickly identified and treated



• Hypovolemia

• Hypoxia

• Hydrogen ion (acidosis)

• Hyper‐/hypokalemia

• Hypoglycemia

• Hypothermia

• Toxins

• Tamponade (cardiac)

• Thrombosis (MI and pulmonary)

• Tension pneumothorax

• Trauma

Hs and Ts Pneumonic

Copyright© 2014 byMosby an imprint of Elsevier Inc

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• Treatment

• CPR followed by intubation and IV epinephrine

• Treatment is directed toward correction of the underlying cause


Sudden Cardiac Death (SCD)

• Death from a cardiac cause

• Majority of SCDs result from ventricular dysrhythmias

• Ventricular tachycardia

• Ventricular fibrillation


Prodysrhythmia

• Life‐threatening dysrhythmias caused by antidysrhythmia drugs

• Severe LV dysfunction increases risk

• Digoxin and class IA, IC, and III antidysrhythmia drugs

• Most susceptible first few days of drug therapy


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Defibrillation

• Treatment of choice for VF and pulseless VT

• Most effective when completed within 2 minutes of dysrhythmia onset

• Passage of DC electrical shock through the heart to depolarize cells of myocardium

• Allows SA node to resume pacemaker role


Defibrillation

• Monophasic defibrillators deliver energy in one direction

• Biphasic defibrillators deliver energy in two directions

• Use lower energies

• Fewer postshock ECG abnormalities


Defibrillation


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Defibrillation

• Output is measured in joules or watts per second

• Recommended energy for initial shocks in defibrillation

• Biphasic: 120 to 200 joules

• Monophasic: 360 joules

• Immediate CPR after first shock


Defibrillation


Defibrillation

1. Start CPR while obtaining and setting up defibrillator

2. Turn on and select energy3. Make sure sync button is turned off4. Apply gel pads5. Charge6. Position paddles firmly on chest7. Ensure “All clear”!!!!!8. Deliver charge


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Case Study

• S.D. was admitted to the telemetry unit and an IV amiodarone drip was started.

• The purpose of the drug was to convert her atrial fibrillation to normal sinus rhythm.



Case Study

• Although her heart rate has decreased to 108 beats/minute, she remains in atrial fibrillation 24 hours later.

• A cardiologist was consulted and electrical cardioversion is planned.



Case Study

• What would you teach S.D. about the scheduled procedure?

• What are three differences between defibrillation and cardioversion?



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Synchronized Cardioversion

• Choice of therapy for ventricular ( VT with a pulse) or supraventricular tachydysrhythmias

• Synchronized circuit delivers a countershock on the R wave of the QRS complex of the ECG


Synchronized Cardioversion

• Procedure similar to defibrillation except sync button turned ON

• If patient stable, sedate prior

• Initial energy lower • 70–75 joules (biphasic)

• 100 joules (monophasic)

• If patient becomes pulseless, turn sync button off and defibrillate


Implantable Cardioverter‐Defibrillator (ICD)

• Appropriate for patients who• Have survived SCD

• Have spontaneous sustained VT

• Have syncope with inducible ventricular tachycardia/fibrillation during EPS

• Are at high risk for future life‐threatening dysrhythmias

• Decreases mortality


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• Consists of a lead system placed via subclavian vein to the endocardium

• Battery‐powered pulse generator is implanted subcutaneously

• Sensing system monitors HR and rhythm – delivering 25 joules or less to heart when detects lethal dysrhythmia





• Includes antitachycardia and antibradycardia pacemakers

• Overdrive pacing for tachycardias

• Backup pacing for bradycardias

• Preprocedure and postprocedure care same as pacemaker


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• Variety of emotions are possible

• Fear of body image change

• Fear of recurrent dysrhythmias

• Expectation of pain with ICD discharge

• Anxiety about going home

• Participation in an ICD support group should be encouraged



1. Follow‐up appointments

2. Incision care

3. Arm restrictions

4. Sexual activity

5. Driving

6. Avoid direct blows

7. Avoid large magnets, MRI

Patient and Caregiver Teaching



8. Air travel

9. Avoid antitheft devices

10. What to do if ICD fires

11. Medic Alert ID

12. ICD identification card

13. Caregivers to learn CPR



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Pacemakers

• Used to pace the heart when the normal conduction pathway is damaged

• Pacing circuit consists of• Programmable pulse generator (power source)

• One or more conducting (pacing) leads to myocardium


Pacemaker Spike


Pacemakers

• Pace atrium and/or one or both of ventricles

• Most pace on demand, firing only when HR drops below preset rate• Sensing device inhibits pacemaker when HR adequate

• Pacing device triggers when no QRS complexes within set time frame


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Pacemakers

• Antitachycardia pacing: delivery of a stimulus to the ventricle to terminate tachydysrhythmias

• Overdrive pacing: pacing the atrium at rates of 200–500 impulses/minute to terminate atrial tachycardias


Pacemaker


Pacemakers

• Cardiac resynchronization therapy (CRT)

• Resynchronizes the cardiac cycle by pacing both ventricles

• Biventricular pacing

• Used to treat patients with heart failure

• Can be combined with ICD for maximum therapy


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Temporary Pacemakers

• Power source outside the body

• Transvenous

• Epicardial

• Transcutaneous


Temporary Transvenous Pacemaker


Epicardial Pacing

• Leads placed on epicardium during heart surgery

• Passed through chest wall and attached to external power source as needed


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Transcutaneous Pacing

• For emergent pacing needs

• Noninvasive

• Bridge until transvenous pacer can be inserted

• Use lowest current that will “capture”

• Patient may need analgesia/sedation


Transcutaneous Pacing

Fig 10‐9. Anterioposterior placement of adhesive electrode pads for defibrillation or transcutaneous pacing. From: Sole et al. Introduction to Critical Care Nursing, 5th Edition. W.B. Saunders


Temporary Pacemaker


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Pacemakers

• ECG monitoring for malfunction

• Failure to sense

• Causes inappropriate firing

• Failure to capture

• Lack of pacing when needed leads to bradycardia or asystole


Pacemakers

• Monitor for other complications

• Infection

• Hematoma formation

• Pneumothorax

• Atrial or ventricular septum perforation

• Lead misplacement


Pacemakers

• Postprocedure care

• OOB once stable

• Limit arm and shoulder activity

• Monitor insertion site for bleeding and infection

• Patient teaching important


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Pacemakers

• Follow‐up appointments for pacemaker function checks

• Incision care

• Arm restrictions

• Avoid direct blows

• Avoid high‐output generator

• No MRIs unless pacer approved

• Microwaves OK

• Avoid antitheft devices

• Air travel

• Monitor pulse

• Pacemaker ID card

• Medic Alert ID


Copyright© 2014 byMosby an imprint of Elsevier Inc

Radiofrequency Catheter Ablation Therapy

• Electrode‐tipped ablation catheter “burns” accessory pathways or ectopic sites in the atria, AV node, and ventricles

• Nonpharmacologic treatment of choice for several atrial dysrhythmias

• Postcare similar to cardiac catheterization


Case Study

• S.D.’s electrical cardioversion was successful.

• S.D.’s sinus rhythm has remained stable for 24 hours and she is ready to go home.



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Case Study

• As you enter her room to provide discharge teaching, she tells you she is experiencing some chest “heaviness and tightness right under her breast bone.”



Case Study

• You ask the UAP to obtain a 12‐lead ECG while you notify S.D.’s health care provider.

• What specific ECG change will you be looking for to determine if S.D.’s chest pain is related to cardiac ischemia? Injury? Infarction?



ECG Changes Associated With Acute Coronary Syndrome (ACS)


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• 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

• Changes reverse when adequate blood flow is restored to myocardium


Changes Associated With Myocardial Ischemia



• Injury

• ST‐segment elevation occurs

• Significant if >1 mm above the isoelectric line

• If treatment is prompt and effective, may avoid or limit infarction

• Absence of serum cardiac markers confirms no infarction


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Changes Associated With Injury



• Infarction

• 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


Changes Associated With Infarction


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ECG Finding With Anterolateral Wall MI


Syncope

• Brief lapse in consciousness accompanied by a loss in postural tone (fainting)

• Noncardiovascular causes

• Stress

• Hypoglycemia

• Dehydration

• Stroke

• Seizure


Syncope

• Cardiovascular causes • Cardioneurogenic or “vasovagal” syncope

• Carotid sinus sensitivity

• Dysrhythmias (tachycardias, bradycardias)

• Prosthetic valve malfunction

• Pulmonary emboli

• HF


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Syncope

• Diagnostic studies• Echocardiography

• Stress test

• EPS

• Head‐up, tilt test • To assess for cardioneurogenic syncope• Abnormal response to position change causes paradoxic vasodilation and bradycardia (vasovagal response)


ch 36 powerpoint lewis medsurg

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