Page 486 - Clinical Application of Mechanical Ventilation

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nervous system activity, clinically significant episodes of hypotension, bradycardia,
Adverse reactions of and sinus arrest are potential adverse reactions of this drug. Hypotension or brady-
dexmedetomidine (Precedex)
include hypotension, brady- cardia may be more pronounced in patients with hypovolemia, diabetes mellitus,
cardia, and sinus arrest. chronic hypertension, and in elderly patients. On occasion, transient hypertension
may develop. For these reasons, cautions should be exercised when administering
this drug to patients with advanced heart block or severe left ventricular dysfunction
(Precedex, 2012). In some children, transient neurological abnormalities (i.e., de-
creased verbal communication, facial drooping, and unilateral pupil dilation) have
been observed upon discontinuation of the medication (Honey et al., 2010).
Clinical Considerations. Due to the known pharmacological effects of dexmedeto-
midine, patients receiving this drug should be monitored continuously for signs
of cardiovascular instability. If persistent or severe hypotension and bradycardia
occur, the infusion should be decreased or discontinued. Mild hypotension from
this drug may be managed by increasing the rate of intravenous fluid, elevating the
lower extremities, and using vasopressors (rtlist, 2012).

Nitric Oxide

Nitric oxide is endogenously synthesized in vascular endothelium from the amino
nitric oxide: Inhaled nitric oxide
(iNO) therapy has been used to acid L-arginine (Palmer et al., 1987). After being released from the endothelium,
treat persistent pulmonary hyper- nitric oxide diffuses into vascular smooth muscle cells where it stimulates produc-
tension and hypoxemic respiratory
failure of the newborn, respiratory tion of 3′5′-cyclic guanosine monophosphate (cGMP). cGMP decreases the con-
distress syndrome and hypoxemic centration of calcium in the muscle, resulting in vasodilatation. Because nitric
respiratory failure of older infants
and children, and acute respiratory oxide is extremely labile (rapidly inactivated by hemoglobin) it causes only local
distress syndrome in adults.
regulation of endothelial tone without systemic hypotensive effects.
Indications. Inhaled nitric oxide (iNO) therapy has been used as a treatment or sup-
portive modality for a variety of clinical conditions. Some of these conditions in-
clude persistent pulmonary hypertension and hypoxemic respiratory failure of the
newborn (Abman & Kinsella, 1999), respiratory distress syndrome and hypoxemic
respiratory failure of older infants and children (Dobyns et al., 1999), and acute
respiratory distress syndrome (Burke-Martindale, 1998). In addition, iNO therapy
has been effective in increasing pulmonary blood flow and oxygenation and improv-
ing systemic cardiopulmonary hemodynamics in infants (Ochikubo et al., 1997).

Mechanism of Action. Inhaled nitric oxide produces local vasodilation of vascular
Inhaled nitric oxide smooth muscles. Because the gas is delivered to alveolar units still presumably par-
produces local vasodilation of
vascular smooth muscles. ticipating in gas exchange, these alveolar capillary units are preferentially vasodilated,
diverting blood from hypoxic capillary beds with high vascular resistance (Stamler
et al., 1992). The net physiologic results are reduction of pulmonary vascular resis-

Pulmonary vasodila- tance, reversal of hypoxic pulmonary vasoconstriction in unobstructed airway (im-
tion may reduce pulmonary provement of V/Q matching), and improvement of oxygenation (Figure 13-8).
vascular resistance, correct
V/Q mismatch, and improve Adverse Effects. Adverse effects of iNO therapy are dependent on the dosage and
oxygenation.
concentration of inhaled NO. When combined with oxygen, NO is converted to
nitrogen dioxide (NO ). NO levels of higher than 10 ppm can cause cell damage,
2
2
hemorrhage, pulmonary edema, and death. However, at therapeutic dosages

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