Hemodynamic Effects of Bolus of Ketamine Versus Fentanyl in Patients With Septic Shock

Not Applicable

Completed

Brief Summary: Ketamine is a commonly used drug for sedation and induction of anesthesia in patients with shock and/or cardiac dysfunction. Ketamine is characterized by its cardiovascular stimulatory effect due to increase release of endogenous catecholamines. On the other hand, laboratory data on the isolated human myofibers suggest that ketamine had a direct myocardial depressive effect; accordingly, many experts believe that ketamine might have a negative hemodynamic effect in catecholamine depleted patients such as critically ill patients. In critically ill patients, there are contradicting results for the effect of ketamine on the hemodynamic profile and there is paucity of clinical data about the effect of ketamine on cardiac contractility and cardiac output (CO). Cardiac output is the primary determinant of global oxygen delivery to organs and maintaining stable CO in critically ill patients is at most importance to avoid further organ damage in such patients.

Therefore, this study is designed to evaluate the effect a single bolus of ketamine on CO in patients with septic shock in comparison to fentanyl bolus.

Detailed Description: Patients meeting the inclusion criteria will receive the study drug according to the randomization, if a bolus of sedation is required for resuming sedation after sedation vacation. All patients will be monitored by 5-lead electrocardiogram, pulse oximetry, and noninvasive blood pressure.

Hypotension defined as mean arterial pressure \< 65 mmHg and will be managed by increasing the norepinephrine infusion rate by 20%.

Bedside echocardiography will be used to measure the cardiac output by an experienced physician who is not aware of the nature of the study drug. The left ventricular outflow diameter (LVOT) will be measured in the parasternal long-axis view. Then velocity time integral (VTI) will be measured from the apical five-chamber view. The average of three VTI readings will be calculated.

The cardiac output will be calculated by the equation:

CO = π X (LVOT diameter/2) X VTI X heart rate Delta CO% will be calculated as percentage of change at each time point in relation to the baseline measurement the CO, heart rate, mean blood pressure will be measured before drug administration and at 3, 6, 10 and 15 min after drug administration

Recruitment & Eligibility

Inclusion Criteria

Exclusion Criteria

Hemodynamic instability (MAP <65 mmHg) despite appropriate volume replacement and vasopressor therapy
Noradrenaline infusion rate <0.05 mcg/kg/min
Poor cardiac window on the ultrasound.
Known allergy to study drugs
Neurocritical patients with signs of increased intracranial tension

Arm && Interventions

Group	Intervention	Description
Ketamine group	Ketamine	bolus of sedation for resuming sedation after sedation vacation
Fentanyl group	Fentanyl	bolus of sedation for resuming sedation after sedation vacation

Primary Outcome Measures

Name	Time	Method
6-minutes Delta CO%	at 6 minutes after drug administration	percentage of change at 6 min after drug administration in relation to the baseline measurement

Secondary Outcome Measures

Name	Time	Method
Delta CO%	3, 6, 10 and 15 minutes after drug administration	percentage of change at each time point after drug administration in relation to the baseline measurement
heart rate	3, 6, 10 and 15 minutes after drug administration	beat per minute
mean blood pressure	3, 6, 10 and 15 minutes after drug administration	mmHg
norepinephrine dose	3, 6, 10 and 15 minutes after drug administration	mcg/kg/min

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