Page 628 - Cardiac Nursing

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604 PA R T I V / Pathophysiology and Management of Heart Disease
surgery. Contributing factors of atrial fibrillation (AF) may in-
clude electrolyte or metabolic disturbances, increased circulating
catecholamines, volume overload, hypoxia, and myocardial is- A
chemia or MI. Although atrial tachyarrhythmias may occur any
time during the first few days to weeks after cardiac surgery, they
frequently peak around the second or third day postoperative.
Atrial fibrillation after cardiac surgery may be associated with im-
portant complications including stroke, renal dysfunction, and
38
prolonged hospitalization. Risk factors for postoperative AF in-
clude advanced age, history of congestive heart failure or AF, B
chronic obstructive lung disease, male sex, history of rheumatic
heart disease, prolonged aortic cross-clamp time, and bicaval can-
nulation. 39 The onset of tachyarrhythmias is often preceded by
frequent premature atrial contractions. Medications commonly
used to control the ventricular response in AF and flutter include
diltiazem (either intravenous drip or orally), digoxin, and - C
blockers (orally or by intravenous drip, such as esmolol). Medica- ■ Figure 25-4 Atrial electrocardiography is done by attaching limb
tions used to promote conversion of AF include procainamide, leads and V 1 in standard fashion and then attaching V 2 and V 3 di-
V
amiodarone, and sotalol. While multiple medications have been rectly to the atrial pacing wires with alligator clips. Simultaneous sur-
studied, -blockers have been the only medication consistently face lead and unipolar atrial lead ECG recordings are obtained. (A)
shown across clinical studies that reduce the frequency of postop- Lead V 1 is the surface or reference lead. There is no atrial enhance-
V
erative AF. 40 -Blockers should be considered early during the ment. (B, C) Leads V 2 and V 3 are unipolar atrial leads that accentu-
postoperative course, especially if the patient was on -blockers ate the atrial activity and demonstrate an atrial rate of approximately
preoperatively. Although -blockers, atrial pacing, antiarrhythmic 300 beats/min that was not apparent on the surface lead or standard
medications, or a combination of these therapies may reduce the 12-lead ECG.
incidence or duration of AF, optimal strategies are still being de-
fined. 41
Postoperative arrhythmia diagnosis and treatment is facilitated
by the presence of atrial epicardial pacemaker wires. Atrial activity or electrical conversion. If the AF is new in onset ( 1 year), the
is more pronounced when recorded in atrial ECGs than when patient may be successfully cardioverted by synchronized car-
recorded in a normal surface ECG (Fig. 25-4). When atrial activ- dioversion. If the patient has been in AF or flutter longer than
ity is accentuated, differentiation between supraventricular and 48 hours or the AF remains paroxysmal, it is desirable to antico-
ventricular arrhythmias, and AF and flutter is made easier. If the agulate for 3 to 4 weeks to prevent thromboembolism, and then
ventricular response to AF exceeds 110 beats/min, then the pa- have the patient return for elective cardioversion if they remain in
tient’s rate should be controlled. AF or flutter.
If pharmacologic modalities fail to convert the patient to a si- While premature ventricular contractions and nonsustained
nus rhythm, electrical therapies may be used. Atrial flutter may be runs of ventricular tachycardia may occur commonly after cardiac
converted using rapid atrial pacing. To perform rapid atrial pac- surgery, sustained ventricular tachycardia and ventricular fibrilla-
ing, both atrial epicardial wires are connected to the rapid atrial tion are rare but associated with a poor prognosis. 42 Premature
pacemaker. The pacemaker output is set between 10 and 20, and ventricular contractions and nonsustained runs of ventricular
the pacemaker rate is set approximately 20% faster than the exist- tachycardia should be treated with correction of electrolytes, re-
ing atrial rate (atrial rate can be determined on the atrial ECG). duction or elimination of arrhythmogenic drugs such as cate-
Rapid atrial pacing continues for 30 seconds or until the atrial cholamines, and ruled out for ischemia. Sustained ventricular
ECG complex changes from a negative to a positive deflection in tachycardia should be cardioverted and antiarrhythmic agents
lead II. Rapid atrial pacing is then abruptly discontinued, which such as amiodarone or lidocaine should be instituted. 42 Electro-
allows the atria to resume a normal sinus rhythm (Fig. 25-5). Pa- physiology studies and implantable defibrillators may be used in
tients with chronic AF may be refractory to either pharmacologic selected cases.
HEWLETT-PACKARD REORDER 40
■ Figure 25-5 Recording of a burst of rapid atrial pacing used to overdrive and convert this atrial flutter to
sinus rhythm. Arrows denote atrial pacing spikes.