Respiratory Depression After Sufentanil

Similar to all potent narcotic analgesics, sufentanil dose-proportionally depresses respiratory drive and the responsiveness of the respiratory center to an elevated paCO2-level. In addition it inhibits centers in the pons and the medulla, which regulate respiratory rate and tidal volume. Besides its direct effect on the respiratory center, indirectly sufentanil also affects ventilation via an increase in muscular rigidity, which reduces the compliance of the thoracic cage, resulting in

Table 111-13. Comparative pharmacokinetic data of various opioids [70, 72, 88]

Pharmacokinetics

Sufentanil

Fentanyl

Alfentanil

Morphine

Remifentanil

Non-ionized portion

20

8.5

89

23

> 50

(%)

Octanol/water- partition

1727

816

129

1.4

17.9

coeff.

Protein bound (%)

92.5

84.4

92.1

60

70

Distribution volume

2.9

4.0

0.86

3.2

32.8

(L/kg)

Elimination half-time

164

219

94

177

9.1

(ti/2E; mm)

Plasma clearance

12.7

13.0

6.4

114.7

an obstruction to gas exchange. In contrast to fentanyl, however, the respiratory depressive effect is less and of shorter duration, while analgesia is still maintained [108, 112]. Such dissimilarity may be due to a selective affinity to alternative opioid sub-receptor sites termed and ^2 respectively [113].

Following the injection of sufentanil the following sequence of effects on spontaneous respiration can be observed:

1. First there is a reduction respiratory rate (bradypnea) with a compensatory increase in tidal volume.

2. This is followed by a phase where only intense stimuli (nociceptive, acoustic) are able to induce a spontaneous respiratory drive.

3. Thereafter the patient "forgets" to breathe, and he will only take deep breaths on command.

4. At the end there is total apnea where the patient has to be ventilated artificially. Any co-administration of sufentanil with a volatile anesthetic, a barbiturate, a benzodiazepine, a neuroleptic, a hypnotic, an antidepressive agent (MAO-inhibitors), the administration of lithium, or the concomitant use of a cytostatic will result in a poten-tiation of respiratory depression. Patients with a low protein level, patients with a pre-existing pulmonary disease, or patients who present an alkalosis, a prolongation of sufentanil-related respiratory depression has to be anticipated [114]. Similarly as with any other opioid, respiratory impairment can successfully be reversed with a selective antagonist (naloxone, nalmefene) or a mixed narcotic analgesic such as

Figure 111-36. Difference in steepness of slope of tidal volume to increasing inspiratory concentrations of CO2 following equianalgesic doses of fentanyl and sufentanil respectively. Note, the faster recovery of the respiratory center response to CO2 after sufentanil (Adapted from [111])

1200

800 600

o 400

8 Sufentanil

8 Sufentanil

Control 5 min post 1 min post 10 min post induction L&I L&I

Figure III-37. Relative changes of power in the delta-band of the EEG to control, reflecting a more pronounced hypnosedative effect of sufentanil when compared to fentanyl in patients undergoing open-heart surgery, where the opioid was used for induction of anesthesia (Adapted from [119])

nalbuphine. However, it has to be recognized that the duration of action of sufentanil tends to be longer than the antagonist. This is why, after initial recovery of respiration, there is a rebound of a depressed spontaneous respiration. Therefore, after an initial return of normal ventilation the patient still has to be supervised in order to detect any deterioration of respiratory drive.

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