Page 557 - Cardiac Nursing

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C HAP TE R 22 / Acute Coronary Syndromes 533

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Nursing Care Plan 22-1 (c (continued) ) )
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NURSING INTERVENTIONS RATIONALE
7. Observe, document, and report the following hemodynam- 7. Investigative reports suggest that these hemodynamic cri-
ic patterns: teria may be indicative of RV infarction.
a. RA pressure 10 mm Hg and RA:PAWP ratio of 0.8
b. RA waveform: prominent y descent that is at least as
great as the x descent
c. RV waveform: diastolic dip-plateau pattern (“square-
root sign”)
d. Cardiac index 2.2 L/min/m 2
Nursing Goal 2 ➧ To eliminate the signs of RV dysfunction secondary to RV infarction.
Outcome Criteria ➧ During hospitalization, the following signs are observed and documented: SBP 90 mm Hg
PAWP of 15–20 mm Hg
Urine output at least 0.5 mL/kg/h or 4 mL/kg/8h
Cardiac index 2.2 L/min/m 2
Skin pink, warm, dry
Mentation unchanged
NURSING INTERVENTIONS RATIONALE
1. Infuse IV fluid bolus per physician protocol to attain a 1. Initial rapid volume expansion increases RV end-diastolic
PAWP of 15–20 mm Hg. volume, which may optimize contractility of a diastolic
noncompliant RV.
2. Administer positive inotropic agents such as dobutamine 2. Dobutamine (2–20 g/kg/min) and dopamine (2–10
or dopamine per physician protocol. Monitor heart rate g/kg/min) directly stimulate -adrenergic myocardial
and rhythm for development of tachycardia or tach- receptors, resulting in increased contractility and cardiac
yarrhythmias. output. Although dobutamine is less arrhythmogenic than
dopamine, both agents may precipitate tachycardia and
tachyarrhythmias, resulting in decreased diastolic filling
and reduced cardiac output.
3. Administer peripheral vasodilators such as nitroprusside 3. These agents decrease RV and LV afterload, thereby
or hydralazine per physician protocol. Monitor pulmonary enhancing RV and LV stroke volume. Hydralazine may be
and systemic vascular resistance at least every hour. preferable because it selectively vasodilates arterioles and
should not decrease preload. Pulmonary and systemic vas-
cular resistance parameters are necessary to optimize pre-
load and afterload.
4. When pacing therapy is indicated, institute atrial or atri- 4. Preservation of atrioventricular synchronous contraction
oventricular sequential method per physician protocol. maximizes contractility and cardiac output.
5. Avoid administration of drugs and performance of maneu- 5. Filling of the left ventricle is dependent on distention of
vers that decrease preload: the right ventricle. These actions decrease preload, there-
a. Diuretics by reducing stretch of the RV myocardial fibers and fur-
b. Venodilators (NTG, morphine) ther compromising the ability of the noncompliant cham-
c. Sitting up in bed ber to propel blood forward. Reduced cardiac output
d. Valsalva maneuver results.
*Contributed by Sherri Del Bene and Anne Vaughan.

acute inferior or posterior LV infarction. A right precordial ECG with RV infarction and the systematic and continual assessment
should be obtained for any patient with evidence of an inferior of these features as well as the evaluation of the patient’s re-
MI. Initial clues to the development of RV dysfunction may be sponse to therapy.
subtle. In addition, the low cardiac output syndrome may be Patients with RV infarction experience similar alterations in
thought secondary to primary LV dysfunction. The major dif- functional health status as those with LV infarction. Nursing
ferences between the low cardiac output state of predominant Care Plan 22-1 encompasses altered health patterns of patients
RV and LV infarction are listed in Table 22-6. Critical care with MI. In the setting of RV infarction, however, decreased
nurses can facilitate the diagnosis and appropriate management cardiac output is a potential nursing problem that requires
of patients with RV infarction through awareness of the usual a different approach in terms of detection, assessment, and
clinical features and electrocardiographic changes associated treatment.