Horacio Adrogué

Acid-Base Disorders and Their Treatment

Acid-base disorders and their treatment , Acid-base disorders and their treatment , کتابخانه مرکزی دانشگاه علوم پزشکی تهران

Cross-talk between two organs: how the kidney responds to disruption of acid-base balance by the lung.

Hypoventilation increases PaCO2 (hypercapnia) and initiates the acid-base disorder known as respiratory acidosis. Hyperventilation decreases PaCO2 (hypocapnia) and initiates the acid-base disorder known as respiratory alkalosis. The impact on acidity of these primary changes in PaCO2 is ameliorated by secondary, directional changes in plasma bicarbonate concentration that occur in two stages. Acutely, modest changes in plasma bicarbonate originate from titration of the body’s nonbicarbonate buffers. In chronic hypercapnia and hypocapnia, larger changes in plasma bicarbonate occur that reflect adjustments in renal acidification mechanisms. As a result, the amelioration of systemic acidity is more pronounced in the chronic forms of the respiratory acid-base disorders.

Assessing Acid-Base Status in Circulatory Failure. Differences Between Arterial and Central Venous Blood

To assess arteriovenous differences in acid-base status, we measured the pH and partial pressure of carbon dioxide (PCO2) in blood drawn simultaneously from the arterial and central venous circulations in 26 patients with normal cardiac output, 36 patients with moderate and 5 patients with severe circulatory failure, and 38 patients with cardiac or cardiorespiratory arrest. The patients with normal cardiac output had the expected arteriovenous differences: venous pH was lower by 0.03 unit, and venous PCO2 was higher by 0.8 kPa (5.7 mm Hg). These differences widened only slightly in those with moderate cardiac failure. Additional simultaneous determinations in mixed venous blood from pulmonary arterial catheters were nearly identical to those in central venous blood. In the five hypotensive patients with severe circulatory failure there were substantial differences between the mean arterial and central venous pH (7.31 vs. 7.21) and PCO2 (5.8 vs. 9.0 kPa [44 vs. 68 mm Hg]). Large arteriovenous differences were present during cardiac arrest in patients whose ventilation was mechanically sustained, whether sodium bicarbonate had been administered (pH, 7.27 vs. 7.07; PCO2, 5.8 vs. 8.6 kPa [44 vs. 65 mm Hg]) or not (pH, 7.36 vs. 7.01; PCO2, 3.7 vs. 10.2 kPa [28 vs. 76 mm Hg]). By contrast, in patients with cardiorespiratory arrest, large arteriovenous differences were noted only when sodium bicarbonate had been given (pH, 7.24 vs. 7.01; PCO2, 9.5 vs. 16.9 kPa [71 vs. 127 mm Hg]). We conclude that both arterial and central venous blood samples are needed to assess acid-base status in patients with critical hemodynamic compromise. Although information about arterial blood gases is needed to assess pulmonary gas exchange, in the presence of severe hypoperfusion, the hypercapnia and acidemia at the level of the tissues are detected better in central venous blood.