selected nursing diagnoses and interventions for patients with dysrhythmias

7/28/2019 Selected Nursing Diagnoses and Interventions for Patients With Dysrhythmias

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Selected Nursing Diagnoses and Interventions forPatients with Dysrhythmias

Alteration in cardiac output (decreased): In the case of dysrhythmias,decreased cardiac output is due to changes in heart rate, rhythm andconduction. This ultimately effects the mechanical function of the heart.

Nursing Interventions:

Assess the patient for the underlying cause and contributingfactors.

Assess the patient for signs and symptoms of impending failure.

This includes physical assessment, review of lab values, patienthistory and invasive hemodynamic parameters if available. Correct the underlying cause. This may include reduction of pain

and anxiety, fluid restriction, fluid replacement, restricting activitiesthat precipitate dysrhythmias. (e.g.valsalva) or placing the patienton oxygen.

Maintain patency of all IV and other invasive lines. Provide psychosocial support for patient and family members. Promote adequate rest. Maintain appropriate nutritional and fluid balances.

Patient teaching: includes acute activities such as reporting chestpain or dyspnea and wellness teaching such as stop smoking,stress reduction, weight reduction, heart healthy diet, drugregimen, and relaxation. Other patient teaching activities includeteaching the patient home blood pressure, pulse and weightmonitoring.

Alteration in tissue perfusion (cardiopulmonary): Decreased tissueperfusion that is associated with dysrhythmias is probably due to decreasedcardiac output

Nursing Interventions:

Assess the patient for causative factors. In the case ofdysrhythmias, this would entail identifying the dysrhythmia anddetermining if it was causing a decrease in tissue perfusion.


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Assess the patient for alteration in mentation, vital signs, posturalblood pressure and signs of pulmonary emboli.

Assess baseline labs: ABGs, electrolytes, BUN/creatinine, cardiacprofile.

Document and report chest pain, noting precipitating factors. Encourage restful atmosphere. Teach patient to decrease cardiac workload. Administer cardiac medications. Teach patient to self administer medications. Discuss necessary lifestyle changes such as stop smoking, diet,

weight loss, appropriate exercises, and stress reduction. According to Beery (1998), nurses outside of critical care are being

asked to take care of patients with cardiac dysrhythmias. These nursesneed to have more than a basic understanding of the fundamentals ofcardiac monitoring, and dysrhythmia interpretation. It is essential thatinstitutions have emergency policies and procedures in place, alongwith a continuing competency education program and yearly refresherprograms. The programs should include validation of dysrhythmiainterpretation skills and problem solving of case studies.

Nurses have significant diagnostic influence in the areas of cardiacrhythm monitoring and dysrhythmia identification (Hebra, 1994). It isessential that nurses who care patients at risk for cardiac dysrhythmiashave a thorough understanding of accurate electrode placement. Theymust also use current principles when determining the optimal leads to

use in monitoring specific types of dysrhythmias. EKG monitoring is becoming more common in both inpatient and

outpatient care settings (Scrima, 1997). Nurses are asked to beresponsible for cardiac patients, including monitoring and interpretingcardiac dysrhythmias. They must develop critical thinking skills that helpthem evaluate the significance of these dysrhythmias. A thoroughunderstanding of cardiac anatomy, physiology and properties canprovide a framework for understanding and interpreting cardiac rhythms.

Critical care nurses also need to maintain and enhance EKG skills.Keller Buchanan, K. and Raines, D. (2005) published a qualitative study

of critical care nurses which indicated that the skills necessary torecognize and treat arrhythmias could be catagorized as basic,intermediate or advanced. Identification of specific arrhythmias includingheart block, aberrant conduction, and tachyarrhythmias varied acrosstraining and experience levels within the test sample.

Abnormal heart rhythms occur for several reasons.


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1. The vagal stimulation of the parasympathetic nervous system can causea decrease in the rate at the SA node and can also decrease theexcitability of the AV junction fibers. This causes a slowing of the heartrate, and in severe cases a complete blockage of the impulse throughthe AV junction.

2. Sympathetic stimulation also effects cardiac rhythm and conduction. Itincreases the rate at the SA node and increases the rate of conductionand excitability throughout the heart. It also increases the force ofmyocardial contraction. Subsequently, the overall workload on the heartis increased.

3. A small area of the heart can become more excitable than normal,which causes abnormal heart beats called ectopy. Ectopic foci areusually caused by an irritable area in the heart. This irritability can becaused by ischemia, stimulants such as nicotine and caffeine, lack ofsleep or anxiety (Guyton, 1982).

4. Aberrant conduction pathways can cause arrhythmias by providing analternate route for the wave of depolarization. Normally, atrial andventricular tissues are isolated by nonconductive fat and connectivetissue. Aberrant pathways form a short circuit bridge across thenonconductive tissue. Hence, tissue can be depolarized prematurely orout of sync.

5. Inherited or acquired channelopathy can predispose an individual todangerous arrhythmias, notably torsades de pointes. Faulty ionchannels may result in prolonged repolarization, lengthening the QT

interval. The heart is most vulnerable during repolarization.Channelopathies can be due to "leaky" or slow closing sodiumchannels, ineffective potassium channels or drugs and toxins which canaffect the transport of ions across these channels.

EKG paper is a grid where time is measured along the horizontal axis.

Each small square is 1 mm in length and represents 0.04 seconds. Each larger square is 5 mm in length and represents 0.2 seconds.

Voltage is measured along the vertical axis.

10 mm is equal to 1mV in voltage. The diagram below illustrates the configuration of EKG graph paper and

where to measure the components of the EKG wave form


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P wave

Indicates atrial depolarization, or contraction of the atrium. Normal duration is not longer than 0.11 seconds (less than 3 small

squares) Amplitude (height) is no more than 3 mm No notching or peaking

QRS complex

Indicates ventricular depolarization, or contraction of the ventricles. Normally not longer than .10 seconds in duration Amplitude is not less than 5 mm in lead II or 9 mm in V3 and V4 R waves are deflected positively and the Q and S waves are negative

T wave

Indicates ventricular repolarization Not more that 5 mm in amplitude in standard leads and 10 mm in

precordial leads Rounded and asymmetrical


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ST segment

Indicates early ventricular repolarization Normally not depressed more than 0.5 mm May be elevated slightly in some leads (no more than 1 mm)

PR interval

Indicates AV conduction time Duration time is 0.12 to 0.20 seconds

QT interval

Measured from the Q to the end of the T. Represents ventricular depolarization and

repolarization (sodium influx and potassium efflux) V3, V4 or lead II optimize the T-wave. QT usually less than half the R-R interval

(0.32-0.40 seconds when rate is 65-90/minute)

QT varies with rate. Correct for rate by dividing QT by the square root ofthe RR interval.

o http://www.qtsyndrome.ch/qtc.htmlo Normal corrected is < 0.46 for women and < 0.45 for men.

Prolonged QT may be inherited or acquired(predisposes to long QT syndrome andtorsades de pointe)

o

Inherited - defective sodium or potassium channelso Acquired - drugs, electrolyte imbalance or MI

Atleast, 50 drugs known to affect QT (including: quinidine,amiodarone and dofetilide)

Electrode Placement and Lead Selection

Properelectrode placement is essential in order to acquire accurate EKG strips. Most

EKG monitor manufacturers have a set of placement guidelines specific to their

products.

The following are some general guidelines.

Skin preparation:

Shave hair away from electrode placement site.

Rub site briskly with alcohol pad.
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Rub site with 2x2 gauze.

Place electrode. Be sure that the electrode has adequate gel and is not

dry.

3 lead placement:

o Depolarization wave moving toward a positive lead will be upright.

o Depolarization wave moving toward a negative lead will inverted.

o Depolarization wave moving between negative and positive leads will

have both upright and inverted components.

Five lead placement allows viewing of all leads within the limits of the

monitor.

Lead selection

Lead II is the same as standard lead two as seen in a 12 lead EKG.

o It is the most common monitoring lead.

o It is not the optimal monitoring lead.

V1 lead is the best lead to view ventricular activity and differentiate between

right and left bundle branch blocks.


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o The only way to view V1 is with a five lead system.

o Therefore, MCL1 was designed to overcome the inconvenience of a five

lead system and provide all the advantages of V1 viewing.

Trouble shooting and tips

Change the electrodes everyday.

Make sure all electrical patient care equipment is grounded. Be sure all the lead cables are intact. Some manufacturers require changing the

cables periodically.

Be sure the patient's skin is clean and dry.

Make sure the leads are connected tightly to the electrodes.

Patient movement frequently causes interference. For example, the action of

brushing teeth may cause interference that mimicsV-tach.

Sinus Arrhythmia
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Rate 45-100/bpm

P wave sinusQRS normal

Conduction normal

Rhythm regularly irregular

The rate usually increases with inspiration and decreases withexpiration.

This rhythm is most commonly seen with breathing due to fluctuations inparasympathetic vagal tone. During inspiration stretch receptors in the

lungs stimulate the cardioinhibitory centers in the medulla via fibers inthe vagus nerve.

The non respiratory form is present in diseased hearts and sometimesconfused withsinus arrest(also known as "sinus pause").

Treatment is not usually required unless symptomatic bradycardia ispresent.

Sinoatrial Block
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Rate normal or bradycardia

P wave those present are normal

QRS normal

Conduction normal

Rhythm basic rhythm is regular*.

*In a type I SA block, the P-P interval shortens until one P wave isdropped.

*In a type II SA block, the P-P intervals are an exact multiple of thesinus cycle, and are regular before and after the dropped P wave.

This usually occurs transiently and produces no symptoms. It may occurin healthy patients with increased vagal tone. It may also be found with

CAD, inferior MI, and digitalis toxicity.

Junctional Tachycardia


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Rate faster than 60/bpm

P wave as with junctional rhythm.

QRSnormal or widened with

aberrant ventricular conduction.

ConductionP-R interval usually < .12seconds if present

Rhythm usually regular

The clinical significance of this rhythm depends upon the basic rhythm disturbance. If

the ventricular rate is rapid, cardiac output may decrease.

Treatment includes:

finding and correcting the underlying cause, vagal maneuvers,

verapamil, and

cardioversion.

Second Degree AV Block (Mobitz type I,Wenkebach)

[Image]

Rate variable

P wave normal morphology withconstant P-P interval

QRS normal

Conduction

the P-R interval is

progressively longer until one P

wave is blocked; the cycle

begins again following the
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blocked P wave.

Rhythm irregular

Second degree AV block type I occurs in the AV node above the Bundle

of His. It is often transient and may be due to acute inferior MI or digitalis

toxicity. Treatment is usually not indicated as this rhythm usually produces no

symptoms.

Second Degree AV Block (Mobitz type II)

Rate variable

P wavenormal with constant P-P

intervals

QRS

usually widened because this is

usually associated with a

bundle branch block.

Conduction

P-R interval may be normal or

prolonged, but it is constant

until one P wave is not

conducted to the ventricles.

Rhythmusually regular when AV

conduction ratios are constant

This block usually occurs below the Bundle of His and may progressinto a higher degree block.

It can occur after an acute anterior MI due to damage in the bifurcationor the bundle branches.

It is more serious than the type I block. Treatment is usually artificial pacing.


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Third Degree AV Block or Complete AV Block

Rate

atrial rate is usually normal;

ventricular rate is usually less

than 70/bpm. The atrial rate is

always faster than the

ventricular rate.

P wave

normal with constant P-P

intervals, but not "married" to

the QRS complexes.

QRS

may be normal or widened

depending on where the escape

pacemaker is located in the

conduction system

Conduction

atrial and ventricular activities

are unrelated due to the

complete blocking of the atrial

impulses to the ventricles.

Rhythm irregular

Complete block of the atrial impulses occurs at the A-V junction, commonbundle or bilateral bundle branches.

Another pacemaker distal to the block takes over in order to activate theventricles or ventricular standstill will occur.


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May be caused by:

digitalis toxicity acute infection MI and degeneration of the conductive tissue.

Treatment modalities include:

external pacing and atropine for acute, symptomatic episodes and permanent pacing for chronic complete heart block.

Torsade de Pointes

Rateusually between 150 to

220/bpm,

P wave obscured if present

QRS wide and bizarre morphology

Conduction as with PVCs

Rhythm Irregular

Paroxysmalstarting and stopping suddenly

Hallmark of this rhythm is the upward and downward deflection of the QRScomplexes around the baseline. The term Torsade de Pointes means"twisting about the points."


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Consider it V-tach if it doesnt respond to antiarrythmic therapy or treatments

Caused by:

drugs which lengthen the QT interval such as quinidine electrolyte imbalances, particularly hypokalemia myocardial ischemia

Treatment:

Synchronized cardioversion is indicated when the patient is unstable. IV magnesium IV Potassium to correct an electrolyte imbalance Overdrive pacing

Ventricular Tachycardia

Rate

usually between 100 to

220/bpm, but can be as rapid as

250/bpm

P wave

obscured if present and are

unrelated to the QRS

complexes.

QRS wide and bizarre morphology

Conduction as with PVCs

Rhythmthree or more ventricular beats

in a row; may be regular or
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irregular.

Ventricular tachycardia almost always occurs in diseased hearts.

Some common causes are:

CAD acute MI digitalis toxicity CHF ventricular aneurysms.

Patients are often symptomatic with this dysrhythmia.

Ventricular tachycardia can quickly deteriorate into ventricular fibrillation.

Electrical countershock is the intervention of choice if the patient issymptomatic and rapidly deteriorating.

Some pharmacological interventions include amiodarone and lidocaine.

Premature Ventricular Contractions

Rate variable

P waveusually obscured by the QRS,

PST or T wave of the PVC

QRSwide > 0.12 seconds;

morphology is bizarre with the


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ST segment and the T wave

opposite in polarity. May be

multifocal and exhibit different

morphologies.

Conduction

the impulse originates belowthe branching portion of the

Bundle of His; full

compensatory pause is

characteristic.

Rhythm

irregular. PVC's may occur in

singles, couplets or triplets; or

in bigeminy, trigeminy or

quadrigeminy.

PVCs can occur in healthy hearts. For example, an increase in circulatingcatecholamines can cause PVCs. They also occur in diseased hearts andfrom drug (such as digitalis) toxicities.

Treatment is required if they are:

associated with an acute MI, occur as couplets, bigeminy or trigeminy, are multifocal, or are frequent (>6/min).

Interventions include:

lidocaine, pronestyl, or quinidine.

Premature Atrial Contractions


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Rate normal or accelerated

P wave

usually have a differentmorphology than sinus P waves

because they originate from an

ectopic pacemaker

QRS normal

Conduction

normal, however the ectopic

beats may have a different P-R

interval.

Rhythm

PAC's occur early in the cycle

and they usually do not have acomplete compensatory pause.

PAC's occur normally in a non diseased heart.

However, if they occur frequently, they may lead to a more serious atrialdysrhythmias.

They can also result from CHF, ischemia and COPD.

Paroxysmal Atrial Tachycardia


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Rate

atrial 160-250/min: may

conduct to ventricles 1:1, or

2:1, 3:1, 4:1 into the presence

of a block.

P wavemorphology usually varies

from sinus

QRS

normal (unless associated with

aberrant ventricular

conduction).

Conduction

P-R interval depends on the

status of AV conduction tissue

and atrial rate: may be normal,

abnormal, or not measurable.

PAT also known as Paroxysmal Supraventricular Tachycardia (PSVT) mayoccur in the normal as well as diseased heart.

It is a common complication of Wolfe-Parkinson-White syndrome. Formore on WPW, click here.

This rhythm is often transient and usually requires no treatment.

However, it can usually be terminated with vagal maneuvers. Digoxin, antiarrhythmics, adenosine and cardioversion may be used.

Frequent symptomatic episodes may require surgical intervention. When anaccessory conduction pathway can be demonstrated, interventional surgery toablate the accessory conduction pathway can be curative.Click here for amore complete description of the PSVT mechanism.
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Atrial Flutter

Rate

atrial 250-350/min; ventricular

conduction depends on the

capability of the AV junction

(usually rate of 150-175 bpm).

P wavenot present; usually a "saw

tooth" pattern is present.

QRS normal

Conduction2:1 atrial to ventricular most

common.

Rhythm

usually regular, but can be

irregular if the AV block

varies.

Atrial flutter almost always occurs in diseased hearts. It frequently precipitatesCHF.

The treatment depends on the level of hemodynamic compromise.

Cardioversion, vagal maneuvers and verapamil are used when promptrate reduction is needed. Otherwise, digoxin and other antiarrhythmic drugs can be used.

selected nursing diagnoses and interventions for patients with dysrhythmias

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