فشار خون بعد از عمل جراحی و افزایش فشار دی اکسید کربن
ساعت ۱٢:٠٥ ‎ب.ظ روز ۱۳۸٩/٥/٦   کلمات کلیدی: hypertension ،hypoventilation

این مطلب درباره فشار خون بعد از عمل و رابطه آن با هیپر کاپنی است :


Remember that Postoperative Hypertension can be a Result of Increased PCO2

Melvin K. Richardson MD

Postoperative hypertension is common and can be difficult to manage. When other vital signs are normal, including normal pulse oximetry and normal respiratory rate, it is common to assume that the hypertension is due to poorly treated pain and should be treated with opioids. This may be a dangerous approach.

Hypoventilation is a not uncommon postoperative occurrence. Frequent causes of hypoventilation include residual effects of inhaled anesthetics and opioids, as well as persistent neuromuscular blockade, suboptimal ventilation due to pain or surgical site factors, and coexisting chronic obstructive pulmonary disease (COPD). As hypoventilation worsens, it can lead to carbon dioxide retention and hypercarbia. As hypercarbia worsens, direct cardiac and vascular depression occurs, and in order to compensate for this depression, hypercarbia can also stimulate catecholamine release. There is a linear correlation between increases in PaCO2 and increases in heart rate and cardiac output. The overall effect of the catecholamine release is hypertension, along with increased pulse pressure, stroke volume, myocardial contractility, and heart rate. Treating hypertension with opioids, therefore, may worsen the situation, as opioids may lead to further hypoventilation, hypercarbia, hypertension, and eventually respiratory insufficiency or failure.

What not to Do

It cannot be overly stressed that the O2 saturation on the pulse oximeter is not an adequate measure of ventilatory status. While the pulse oximeter is considered the standard of care in the postoperative setting and is able to noninvasively measure peripheral oxygen saturation, it is an estimate only of arterial oxygenation. This is a nonlinear relationship, and as illustrated in the oxyhemoglobin dissociation curve, an oxygen saturation of 90% to 100% can reflect an extremely wide range of values for the PaO2, from 60 mm Hg to >100 mm Hg. The pulse oximeter is therefore a poor indicator of ventilatory status, as it can be misleading about the PaO2 value and can be poorly reflective of the underlying respiratory effort, including the PaCO2. Further, as the PaCO2 increases, it shifts the oxyhemoglobin dissociation curve to the right, reflective of increased oxygen unloading. In managing

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a postoperative patient with hypertension, therefore, it is important to assess the full clinical picture for other signs of respiratory depression, including dyspnea, shallow respirations, use of respiratory muscles, paradoxical motions of the chest and abdomen, cyanosis, and obtundation, to determine adequacy of ventilation, likelihood of hypoventilation/hypercarbia, and the full differential for the hypertension.

Suggested Readings

Dubbink DA. Physiologic Effects of Hyper- and Hypocarbia. In Faust RJ, ed. Anesthesiology Review. 3rd ed. Philadelphia: Churchill Livingstone, 2002:26–27.

Wilson WC and Benum of JL. Respiratory Physiology and Respiratory Function during Anesthesia. In Miller RD, ed. Anesthesia. 6th ed. Philadelphia: Churchill Livingstone, 2005:679–722.

Brian JE. Carbon dioxide and the cerebral circulation. Anesthesiology