Arrhythmias:
By Nancy Jenkins
The EKG is the electrical activity of the heart.
Electrical precedes mechanical
(Without electricity, we have no
pump!!)
How is the electricity generated?
By action potentials- Na, K and Ca very important for this
Na K pump
Calcium channels
Depolarization
Repolarization
Na K pump
Electrical system
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
Conduction system
SA node 60-100
AV node 40-60
Bundle of His
Left and Right Bundle Branch
Purkinge Fibers 15-40
How is the rate controlled?
Nervous System Control of the Heart
Parasympathetic nervous system:when? Vagus nerve
Decreases rate
Slows impulse conduction
Decreases force of contraction
Sympathetic nervous system: when?
Increases rate
Increases force of contraction
Pacemakers other than SA node
EKG graph paper
Horizontal measures time
Vertical measures voltage
Helps us determine rate
Width of complexes
Duration of complexes
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
Leads to monitor in
EKG leads
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
Relative
absolute
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 .06-.10
P to QRS relationship
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
Sinus Tachycardia
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
Treatment- if symptomatic, atropine or pacer
Sinus Bradycardia
Clinical significance
Dependent on symptoms
Hypotension
Pale, cool skin
Weakness
Angina
Dizziness or syncope
Confusion or disorientation
Shortness of breath
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
Isuprel
Pacemaker
Atrial Arrythmias
Atria is the pacemaker
Atrial rate contributes 25-30% of cardiac reserve
Serious in patients with MI- WHY?
Medications used to treat the atrial rhythms
Cardizem
Digoxin
Amiodarone
Tikosyn
Verapamil
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 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
Paroxysmal Supraventricular Tachycardia (PSVT)
Clinical significance
Prolonged episode and HR >180 bpm may precipitate ↓ CO
Palpitations
Hypotension
Dyspnea
Angina
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- cardioversion, calcium channel blockers and beta blockers, amiodorone,
ablation coumadin
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
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
Atrial Fibrillation
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
Arrhythmias of AV Node
AV Conduction Blocks
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
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 Block
more P’s than QRS’s
A. Mobitz I (Wenckebach) YouTube - Diagnosis Wenckebach
PR progressively longer then drops QRS
Cause- MI, drug toxicity
rd
Treatment- watch for type II and 3 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
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
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
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
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 (patient may
present with history of fall)
3rd Degree
Bundle Branch Blocks
Left BBB
Right BBB
QRS.12 or greater
Rabbit ears- RR’
No change in rhythm
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 Arrythmias
Most serious
Easy to recognize
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
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

Treat if:
>5 PVC’s a minute
Runs of PVC’s
Multi focal PVC’s
R on T
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
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
VT- Torsades de Pointes
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
Complications of Arrhythmias
Hypotension
Tissue ischemia
Thrombi- low dose heparin, or ASA
Heart failure
Shock
Death
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
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
Comfort Measures
Rest
O2
Relieve fear and anxiety- valium
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
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 back up pacing
Implantable Cardioverter- Defibrillator (ICD)
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-http://en.wikipedia.org/wiki/Artificial_pacemaker
Pacemakers
Ablation
Done in special cardiac procedures lab
Use a laser to burn abnormal pathway
3 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)
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)
Infarction/Necrosis
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)
ECG Changes Associated with Acute Coronary Syndrome (ACS)
ECG Changes Associated with Acute Coronary Syndrome (ACS)
Syncope
Brief lapse in consciousness
CausesVasovagal
Cardiac dysrhythmias
Other- hypoglycemia, seizure, hypertrophic cardiomyopathy
1-year mortality rate as high as 30% for syncope from cardiovascular cause
QuizzesDiscussionQuestions
Casestudies
Video acting out rhythms
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
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.
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.