Dysrhytmias

Most result from:

Abnormalities in IMPULSE FORMATION

Disturbances in IMPULSE CONDUCTION

Or a combination of both

other examples:

Scarred pathways, Hx of ischemic disease, some drugs, caff. & alcohol, hyperthyroidism, acute MI, hypertensive heart disease, CAD, mitral conditions.

TACHYDYSRHYTMIAS

HR >100 beats/min

serious hemodynamic consequence in a person w/CAD.

Normal ECG pattern, but rate is faster.

TACHYDSYRHYTHMIAS

continued...

THREE CONSEQUENCES:

1) Shorten DIASTOLIC time (shorten/decreased cornary perfusion/myocardium perfusion)

2) Intially increase CARDIAC OUTPUT and B/P

3) Increases WORK of heart

*Pt may have Angina, depends on underlying health of heart.

BRADYDYSRHYTHMIAS

HR <60

DIASTOLE may be prolonged overfilling & increasing PRELOAD.

CORONARY PERFUSION pressure may decrease if HR is too slow, results in aa decreased CARDIAC OUTPUT & decreased B/P.

Myocardial O2 demand is reduced

*Can lead to MI

TYPES OF DYSRTHYMIAS

*SINUS BRADYCARDIA

TAHCYCARDIA

ARRHYTMIA

*ATRIAL DYSRHYTNMIAS= Premature atrial contraction, Paroxysmal atrial tahcycardia, Atrial flutter, Atrial fibrillation

*VENTRICULAR DYSRHYTHMIAS= Premature ventricular contraction, Ventricular tachycardia, ventricular fibrillation, Idioventricular rhythm, Ventricular Asystole.

CODUCTION ABNORMAILITIES

AV BLOCKS:

First degree AV BLOCK= may not have s/sx

Second degree AV BLOCK: Type 1 & 2

*Type 1= P wave normal, gets longer, have P wave..NO QRS complex.

*Type 2= P wave fairly reg., P wave may not result in QRS.

Third degree AV BLOCK

DYSRHYTMIA ANALYSIS

Origin of beat

Mechanism of CONDUCTION= atrial/junctional

Rate

Effect on CARDIAC OUTPUT

Clinical manifestations

Clinical Implications

Comorbidities?

HX of client, is this new?

IS client taking Herbal supplements?

How is it effecting the client?

NSG assessment

of

DYSRHYTMIAS

Assess:

LOC & VS

Listen to heart sounds

obs. skin color= are they gray, cool, cyanotic?

Obs. for edema

LS=crackles?

Obs. for diaphoresis

Is there a decrease in C.O.?

INTERVENTIONS:

Control ventricular rate

Improve CARDAIC OUTPUT

ATRIAL FIBRILLATION

Conditions contributing to the RISK OF A-FIB:

Cardiac surgery

Hyperthyroidism

Long standing hypertension

Ishemic heart disease

Rheumatic heart disease

Tahcy-brady syndrome

Holiday heart syndrome= increased alcohol

Electrolyte imbalances

COPD, PE= can worsen A-Fib

A-Fib=

Blood is not flowing smoothly b/c of blockage

Look for CVA & PE

RVR= RAPID VENTRICULAR RESPONSE-

More dangerous b/c ventricles are trying to keep up.

NSG assessment

of

A-FIb

Assess for:

S/SX of heart failure

decreased B/P, increased HR, increased RR= can change CARDIAC OUTPUT due to pump.

Client may feel impending doom

Client may be lightheaded

Client may expereince butterflies in chest

A-Fib

Possible S/SX

Palpitations

Dyspnea

Light headedness

Syncope

Chest pain

Chest pressure

Change in LOC

A-Fib TX

Relieve HYPOXIA= monitor O2 sat, put O2 on.

ANTICOAGULANT TX= 24-48hrs increased risk for clots INR b/t 2-3

CARDIOVERSION= (unless anticoagulated)

Pharmacologic

Electrical

*A-Fib= ECG-there will be no P WAVE*

MAZZ PROCEDURE:

Pathways all over heart in circles, surgery can correct flow & pathways by making small incisions in the heart pathways that cause scarring, altering the heart pathways.

TEACHING

for

A-Fib

Teach client:

How to check pulse

S/SX of chest pain, light headedness

If on diuretics: effects of low K+ & leg cramps

certain DRUGS toxicity=

ex. Digoxin-

If toxicity occurs client may see halo, N/V/D, fatigue

PREMATURE

VENTRICULAR
CONTRACTON

(PVC)

Possible client presentation:

Temp 98.4

HR 96 (may be increased)

RR 28 (increased)

B/P 110/56 (normal)

Normal Labs except=

K+  3.2 mEq/L

Chloride 93 mEq/L

Diaphoretic, cool

Complaint of substernal pressure

*Caused by=

Ishemia- increased work of heart (exercise, fever), fires by itself.

EFFECTS ON CARDIAC OUTPUT

S/SX of altered/effected C.O.:

Decrease in LOC

Tired/lethargic

Cyanotic

Can have a increase in HR & a derease in B/P

NSG assessment/interventions

of

Effects/alterations

on

CARDIAC OUTPUT

NSG:

Assess for PAIN

Administer approx. meds.

Monitor VS

Decrease C.O.

HX of client:

-Meds.

-Caff. use

-Alcohol use

-Smoking

TX

of

PREMATURE

VENTRICULAR
CONTRACTION

(PVC)

Eliminate underlying cause if possible

Eval severity of prob.

Medication TX:

Antidysrhythmic medications

EX. Lidocaine

Give Na+ Blocker

*How does it interfere w/client's activities?

DYSRHYTHMIAS:

Elderly Considerations

SPECIAL NSG CONSIDERATIONS:

Eval for presence of hemodynamic deterioration

Asses for Angina, hypotension, heart failure, dereased cerebral & renal function

Considere cause of dysrhytmias

Instruct to AVOID- alcohol

smoking

Caff.

Teach client to assess pulse & have reg. B/P checks