Small volumes (4-6 mL/kg) of 7.5% hypertonic saline solution (HTS) are reported to be effective for resuscitation from circulatory shock. When infused rapidly into either hypovolemic or normovolemic subjects, HTS can cause an immediate and severe hypotension before cardiovascular improvement. In the present study, we examined the hypothesis that the early hypotension produced by HTS was mediated by an acute and transient depression of cardiac contractility. Left ventricular pressure and wall motions were measured simultaneously in 10 anesthetized dogs for the assessment of cardiac contractility. Infusion of HTS at 3 mL/kg in 1 min significantly decreased mean arterial blood pressure by 49%, from 95 ± 4 to 51 ± 5 mm Hg (P < 0.05, mean ± SEM) at 45 s after the onset of infusion. This initial decrease in arterial blood pressure was abrupt and transient (106 ± 9 s). Concomitantly, cardiac output and coronary blood flow increased significantly from 2.8 ± 1.0 to 3.9 ± 1.1 L/min and from 23.7 ± 5.3 to 49.8 ± 4.7 mL/min, respectively. Although heart rate remained constant, systolic shortenings of left ventricular diameter and wall thickness increased from 5.6% ± 0.5% to 7.8% ± 0.5% and from 13.9% ± 0.6% to 15.1% ± 1.2%, respectively, indicating an improvement in cardiac contractility. This was confirmed by subsequent analysis of the left ventricular end-systolic pressure-diameter relationship. Systemic and pulmonary vascular resistance decreased by 60% and 27%, respectively. Despite an initial period of hypotension after rapid infusion of HTS, mean arterial blood pressure, cardiac output, and contractility were all significantly increased at 5 min after HTS infusion. The results show that acute hypotension caused by rapid infusion of HTS was not mediated by cardiac depression but by a decrease in total peripheral resistance.
|Original language||English (US)|
|Number of pages||6|
|Journal||Anesthesia and analgesia|
|State||Published - Jan 1 1991|
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine