Abstract
BackgroundSepsis is a common fatal complication of an infection. As part of the host response, sympathetic stimulation can result in many serious complications such as septic myocardial depression and metabolic, hematological, and immunological dysfunction. Treatment with beta blockers may reduce this pathophysiological response to infection, but the clinical outcomes are not clear.ResultsOur study showed a significant difference as regards decrease in heart rate in group B with P value < 0.001 compared to group A, besides a reduction in 28-day mortality (P value 0.0385) and ICU stay (P value < 0.001) in group B compared to group A.ConclusionThis study supports the role of intravenous beta blockers in sepsis patients by decreasing heart rate without affecting the hemodynamics, in addition to decreasing 28-day mortality and ICU stay.
Highlights
Sepsis is a common fatal complication of an infection
There was no significant difference between the two groups regarding age, sex (Table 1), and admission hemodynamic and inflammatory variables (Table 2), mean arterial pressure (Table 3 and Fig. 1), central venous pressure (Table 4 and Fig. 2), central venous oxygen saturation measured from the central venous line sample (Table 5 and Fig. 3), serum lactate (Table 6 and Fig. 4), and APACHE Acute Physiology and Chronic Health Evaluation (II) score (Table 2) and Sequential Organ Failure Assessment Score (SOFA) score (Table 7 and Fig. 5) during the first week
Heart rate showed a significant reduction in group B compared to group A in days 1–6 (P value < 0.001) (Table 8 and Fig. 6)
Summary
Sepsis is a common fatal complication of an infection. As part of the host response, sympathetic stimulation can result in many serious complications such as septic myocardial depression and metabolic, hematological, and immunological dysfunction. Septic shock can be diagnosed by a clinical evidence of sepsis with persisting hypotension that needs vasopressors to keep mean arterial blood pressure (MAP) more than or equal to 65 mmHg in addition to a serum lactate level more than 2 mmol/L not responding to proper volume resuscitation. This raises the hospital mortality to be more than 40% (Shankar-Hari et al 2016). The attacking pathogens interact with the patient’s immune system initiating a downstream inflammatory sequence including the release This pathophysiological process can cause multi-organ failure, and further clinical deterioration occurs due to a global imbalance between systemic oxygen supply and demand. This imbalance is due to the excessive release of catecholamine that causes sepsis-induced myocardial dysfunction, decreasing left ventricular ejection fraction followed by vasodilation, altered vascular permeability, myocardial depression, and failure of the coagulation cascade (Kenney and Ganta 2014)
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