Cardiac Dysrrhythmias

and Management

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ATRIAL DYSRHYTHMIAS
 Premature Atrial Contractions
 Atrial Tachycardia

 Wandering Atrial Pacemaker

 Atrial Flutter
 Atrial Fibrillation

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 ATRIAL DYSRRHYTHMIAS
1. ATRIAL FLUTTER
 Usually significant
 Rhythm: regular but
depend on conduction
ratio
 Dominant pacemaker:
atrial pacemakers
 R to R: variable

 Rate: 240-320 b/m 240-

320
 PR: can’t determine bpm
3
 QRS < .12
ATRIAL FLUTTER

• Atrial tachyarrhythmia identified by recurring, regular, saw tooth-

shaped flutter waves
• Associated with slower ventricular response
• AV may allow every 2nd, 3rd, or 4th atrial stimuli to reach the
ventricles resulting in 2:1, or 3:1, or 4:1 ratio flutter 4
ATRIAL FLUTTER
Clinical Associations Significance
Usually occurs with:  High ventricular rates with
 CAD

atrial flutter can decrease CO
Mitral valve disorders
 Pulmonary embolus
and cause serious consequences
 Chronic lung disease such as heart failure
 Cardiomyopathy  Risk for stroke because of risk
 Hyperthyroidism of thrombus formation in the
atria
 Coumadin used for atrial flutter
> 72h

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 ATRIAL FLUTTER
Treatment
 Primary goal is to slow ventricular response by
increasing AV block

 Electrical cardioversion may be used to convert atrial

flutter to sinus rhythm in emergency.

 Diltiazem,digoxin, and -adrenergic blockers used to

control ventricular rate.

 Interventional electrophysiological treatment.

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 ATRIAL FIBRILLATION

 Usually significant – 25% 

Cardiovascular output
 Rhythm: Irregularly
irregular
 Dominant pacemaker: atrial
 R to R: Irregularly irregular
 Rate: variable 300-600 bpm
 PR – fib absent
 QRS: < .12
300-600
bpm
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ATRIAL FIBRILLATION

• Total disorganization of atrial activity without effective atrial

contraction
• Chronic or intermittent
• No visible P wave
• P: QRS ratio: many:1
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ATRIAL FIBRILLATION
Clinical Associations Clinical Associations
 Underlying heart disease,  Thyrotoxicosis
such as rheumatic heart  Alcohol intoxication
disease  Caffeine use
 Pulmonary disease  Electrolyte disturbance
 CHF
 Congenital heart disease
 Open heart surgery

Significance
 Decrease in CO because of ineffective atrial contractions
and rapid ventricular response
 Thrombi may form in atria and may pass to brain,
causing stroke, HTN, structural heart disorders. 9
 Anticoagulation with Coumadin used to prevent stroke
ATRIAL FIBRILLATION
Treatment: same as in Atrial Flutter.

 Primary goal is to slow ventricular response by increasing AV block

 Electrical cardioversion may be used to convert atrial flutter to sinus rhythm in
emergency situation
 Diltiazem, digoxin, and -adrenergic blockers used to control ventricular rate
 Antiarrhythmic drugs used to convert atrial flutter to sinus rhythm or maintain
sinus rhythm (Ca++ Blockers, Ibutilide, ex: Amiadarone; 300 mg IV loading dose
and then 150 mg in 3.5 minutes)

 Ablation, Pacing, implanted cardioversion device (ICD) are other Rx options. 10

DYSRHYTHMIAS OF THE AV NODE
 Junctional escape rhythm
 Accelerated junctional rhythm and Junctional
tachycardia
 Premature junctional contractions

 Paroxysmal Supraventricular Tachycardia

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PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT)

 During an episode of SVT the heartbeat is not

controlled by SA node , another part of the heart
overrides this role with faster impulses .

 The source of the impulse is some where above

ventricles , but the impulse then spread to the ventricles
so the heart beats faster than normal .

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PAROXYSMAL SUPRAVENTRICULAR
TACHYCARDIA (PSVT)
 RATE: between (150 – 250) bpm .

 RHYTHM : regular .

 P WAVE : absent or fused with QRS or T wave .

 P-R INTERVAL : If P present, shortened .

 QRS COMPLEX : narrow < 0.06 second .

 T WAVE : peaked T wave .

 Cause and treatment:

1-
Normal adult, heart disease, catecholamines, and
electrolytes imbalance.

asymptomatic

 Vagal maneuverer

 >150 cardioversion, adenosine

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VENTRICULAR DYSRHYTHMIAS
 Premature ventricular contractions (PVC)
 Ventricular tachycardia
 Asystole
 Ventricular fibrillation

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 PREMATURE VENTRICULAR
CONTRACTIONS
 PVC or escape beat?
 Wide QRS, > .12
 Single, coupled, trigeminy,
quad?
Comp. pause
 Contraction originating in
ectopic focus of the ventricles
 Premature occurrence of QRS
complex
 Multifocal, unifocal, ventricular
bigeminy, ventricular trigeminy, 15
couples, and triplets
PREMATURE VENTRICULAR
CONTRACTIONS
Clinical Associations
 Stimulants

 Hypokalemia

 Exercise

 MI, ischemia

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 PVCS - MORE
 Tx depends
1. Quantity,
2. location,
3. Pt. clinical T
presentation,
underlying cause,
and if post arrest.
“Wide and bizarre”

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PVCs are warning signs, that something is wrong …..
 PREMATURE VENTRICULAR CONTRACTIONS

Significance
 Usually a benign finding in patient with a normal heart

 In heart disease, PVCs may reduce CO and precipitate angina

and heart failure
 In ischemic heart disease or acute MI, represents ventricular irritability

Treatment
 Assessment of hemodynamic status is important to determine if
drug therapy is indicated
 lidocaineor amiodarone (Drugs of choice)
 -adrenergic blockers, procainamide,
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 VENTRICULAR TACHYCARDIA

 Always significant
 Rate: 100-200

 Rhythm: regular

 R to R: regular

 P wave not seen or not

related to QRS
 PR: none

 QRS: > .12

 Dominant pacemaker:
ventricular pacers
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 VENTRICULAR TACHYCARDIA
 Run of three or more PVCs occurs
 Monomorphic, polymorphic, sustained, and nonsustained

 Considered life-threatening because of decreased CO

and the possibility of deterioration of ventricular
tachycardia to ventricular fibrillation

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VENTRICULAR TACHYCARDIA
Clinical Associations
• Associated with
• Acute MI
• Significant electrolyte imbalances
• Coronary reperfusion after
thrombolytic therapy
• CNS disorders
Significance
 Have been observed in patients
with no evidence of heart disease
 May cause severe decrease in CO
 Precursor to V-Fib
 Result may be pulmonary edema,
shock, and decreased blood flow
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to the brain
 VENTRICULAR TACHYCARDIA

Treatment

 If VT is monomorphic and patient is hemodynamically stable and has preserved left

ventricular function IV lidocaine, procainamide, or amiodarone is used

 Synchronized cardioversion is used when drug therapy is ineffective if the patient

is unstable

 Long-term: Implanted Cardioverter Device (ICD)

 Drugs prolonging QT should be discontinued

 Defibrillation may be needed

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 Ventricular tachycardia without a pulse is treated as ventricular fibrillation, rapid
defibrillation is attempted
ASYSTOLE

 Cardiac arrest pt.

 Rate: none

 Rhythm: absent

 PR: none

 QRS: none

 Dominant pacemaker: sinus

or atria
 Tx: BLS and ACLS

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VENTRICULAR FIBRILLATION

 Always significant – “dead

patient”
 Rate: more 300 ???
 Rhythm: none
 PR: none (fib. waves)
 QRS: none distinctive
 Dominant pacemaker:
ventricular 24
VENTRICULAR FIBRILLATION

Clinical Associations Significance

 Occurs in
 Results in
 Acute MI unconsciousness, absence
 Myocardial ischemia
of pulse, apnea, and
 Chronic diseases such as
seizures
CAD  If untreated, patient will die
 Electrical shock
 Hyperkalemia
 Drug toxicity Treatment
 Hypothermia  Immediate initiation of CPR
 May occur during and ACLS with use of drug
catheterization procedures or therapy and defibrillation
with coronary reperfusion
after thrombolytic therapy 25
ATRIOVENTRICULAR BLOCKS
 Four types of blocks exist :
 Firstdegree
 Second degree type I

 Second degree type II

 Third degree

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 CONDUCTION RHYTHM :
FIRST DEGREE AV BLOCK
 Can be significant, esp.
with previous MI
 Rate: usually 60-140
 Rhythm: regular
 PR: > .20
 R to R: regular
 QRS: < .12
 Dominant pacemaker:
sinus

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 FIRST-DEGREE AV BLOCK

Clinical Associations Significance

Usually occurs with:  May be a precursor to higher degree
 Chronic ischemic heart disease
of AV block
 Aging
 No treatment
 Valvular heart disease

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SECOND DEGREE BLOCK:
MOBITZ I (WENCKEBACH)
 Usually significant: esp. if
bradycardic
 Rate: variable
 Rhythm: variable, progressive
PR ratio, dropped QRS
 PR: gradual lengthening
 R to R: gradual increase,
dropped QRS
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 QRS: usually < .12
SECOND-DEGREE AV BLOCK, TYPE 1

Clinical Associations Significance

 May result from drugs
such as digoxin or -
adrenergic blockers
 Associated with
ischemic cardiac
disease and other
diseases slowing AV
conduction
Treatment
 If symptomatic, drugs are stopped that cause this disturbance
 Usually a result of
myocardial ischemia on
an inferior MI
 May be warning signal of
impending significant AV
conduction disturbance

 If asymptomatic, rhythm closely observed with 30

transcutaneous pacemaker on standby
SECOND DEGREE BLOCK:
MOBITZ TYPE II
 Usually significant: high degree AV
block, may progress to 3rd degree block
 Rate: variable 60-100
 Rhythm: regular, depends on ratio
 PR: consistent .12-.20, except when there
is a dropped QRS
 R to R: usually regular, depends on ratio
 QRS: usually > .12

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 SECOND-DEGREE AV BLOCK, TYPE 2

Clinical Associations
 Associated with rheumatic heart disease, CAD, acute
anterior MI, and digitalis toxicity
Significance
 Often progresses to third-degree and is associated with poor
prognosis
 May result in decreased CO with subsequent hypotension
and myocardial ischemia
Treatment
 Before the insertion of a permanent pacemaker may involve
use of temporary transvenous or transcutaneous pacemaker
 Temporary drug measures (Atropine or isoproterenol) to
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increase HR until pacemaker is available
THIRD DEGREE HEART BLOCK
COMPLETE HEART BLOCK
 Significant/serious

 Rate: slow (30-40)

 Rhythm: regular
 R to R & P to P: regular

 P-wave: more than one P per QRS; no

relation to QRS

 PR: varies in length

 QRS: > .12 usually (vent)

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 THIRD-DEGREE AV HEART BLOCK
 Complete heart block
 no impulses from atria are conducted to ventricles
 P waves have no association with QRS complexes

 Ventricular rhythm is escape rhythm, and ectopic pacemaker

may be above or below bifurcation of His bundle

Clinical Associations
 Calcification or fibrosis of conduction system
 CAD
 MI
 Cardiomyopathy
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THIRD-DEGREE AV HEART BLOCK

Significance
 Almost always results in reduced CO with subsequent ischemia
and heart failure
 Syncope may result from severe bradycardia or periods of asystole

Treatment

 Temporary transvenous or transcutaneous pacemaker may be used on an emergency basis in

a patient with acute MI

 Drugs used to temporarily increase HR and support blood pressure before permanent 35

pacemaker insertion
MEDICAL MANAGEMENT
 Pharmacological management
 Antidysrhythmic drugs
 Class I (Quinidine, Procainamide)
 Class II (Lidocaine, Phenytoin)

 Class III (Propafenone)

 Class IV (Verapamil, Diltiazem)

 Class V: (Adenosine, Digoxin)

 Nursing responsibilities in regard to Medications:

 Baseline data (VS, ECG wave, rate and rhythm)
 Assess medication regimen to identify drugs that interfere

with antidysrhythmic medications.

 Observe for drug toxicity

 Monitor ECG

 Client and family teaching

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MEDICAL MANAGEMENT CONTINUED

 Counter shock
 Synchronized Cardioversion
 Defibrillation
 Electrical current (shock) of pre-set voltage to the heart
 Causes the myocardium to completely repolarize (that will produce

transient asystole!!!)
 Allows the heart’s intrinsic pacemaker gain control

 ONLY used for Ventricular Fibrillation and for PULSELESS AND

UNCONSCIOUS PATIENT’S
 Follow ACLS protocol and only specially trained personnel may

perform the procedure

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NURSING PROCESS:
THE PATIENT WITH A DYSRHYTHMIA
Nursing diagnoses:
Based on assessment data, major nursing diagnoses of the
patient may include:
• Decreased cardiac output
• Anxiety related to fear of the unknown
• Deficient knowledge about the dysrhythmia and its treatment
Planning and Goals
 Decreasing the incidence of the dysrhythmia (by decreasing
contributory factors) to maintain cardiac output, minimizing
anxiety, and acquiring knowledge about the dysrhythmia and
its treatment. 38