الفهرس 
DEFINITIONS AND EPIDEMIOLOGYOnly 14 pages are availabe for public view
 |  | from | 137 |  |  |
| | | from | 137 | | |
Abstract
S
epsis and septic shock are serious, often life threatening medical conditions where insufficient blood flow reaches the body tissues. As the blood is the body’s carrier of oxygen and nutrients, this lead to a deficiency of these essential inputs to life, blood entrance to the tissues causes perfusion and if this process not accruing properly causes a hypoperfusional state. The significant economic and mortality impact of severe sepsis. And septic shock has often resulted in some controversy concerning optimal support. The results of many controlled clinical trials are valuable to clinicians since septic shock has a reported mortality rate of 40-70% and currently there are no convincing data supporting the use of one vasopressor strategy over another effective cardiovascular support plays an essential role in the management of patients with septic shock.
Oxygen delivery must be maintained above critical threshold, and arterial blood pressure must exceed a level that all our appropriate distribution of cardiac output for adequate regional perfusion. Combination of catecholamines, including norepinephrine and epinephrine, dopamine, dobutamine and vasopressin, are currently used to achieve these goals. So the current study was designed to compare the effect of low dose. Vasopressin versus norepinephrine in the maintenance of hemodynamic stability and adequate end organ perfusion in patients with sepsis and septic shock.
In this clinical trial, 40 patients were randomly allocated into two equal groups (n=20) using closed envelope technique.
Group I: Patients received standard treatment of sepsis plus vasopressin infusion.
Group II: Patients received standard treatment of sepsis plus norepinephrine infusion.
We used fixed volume infusion for both groups for 24 hours.
All patients received standardized supportive care including (volume infusion, O2 supply, antibiotics and drainage of infected sites were carried out).
All patients in the two groups were assessed and monitored for: cerebral blood flow at baseline and after 24 hours from vasopressor infusion, haemodynamics MAP and HR, CUP, RR T0-T4, laboratory investigation (blood urea – S. creatinine – bilirubin, total direct, AST-ALT, CBC, arterial blood gas and signs of cutaneous ischaemia.
Regarding the heart rate in group I were comparable to those in group II during T1 and T4, however heart rate during T3 and T4 were higher in group I compared those in group II. Regarding the central venous pressure and respiratory rate were comparable during the first 24 hours.
MAP values measured during T1-T4 were significantly higher compared to baseline among both groups. MAP in group I was significantly lower compared to group II. Regarding the cerebral blood flow in group I it had significant decrease after 24 hours compared to baseline values. However in group II it had decreased after 24 hrs, although such changes was statistically non-significant, laboratory data and parameters obtained from arterial blood gas analysis at baseline and after 24 hours from vasopressor infusion were comparable among both groups.
None of the patients among both groups did demonstrate any signs of cutaneous ischemia due to vasopressor infusion.