Early and late hemodynamic consequences of group B beta streptococcal sepsis in piglets: effects on systemic, pulmonary, and mesenteric circulations.
We have modified our previously described experimental model of neonatal sepsis using group B beta hemolytic streptococci (GBS) in piglets and report here early and late hemodynamic responses to GBS infusion in the systemic, pulmonary, and mesenteric circulations. Piglets were anesthetized, intubated, and ventilated. Aortic blood pressure (AOP), pulmonary artery pressure (PAP), central venous pressure (CVP), left atrial pressure (LAP), cardiac index (CI), mesenteric blood flow index (MBFI), and heart rate (HR) were measured directly. Systemic vascular resistance index (SVRI), pulmonary vascular resistance index (PVRI), mesenteric vascular resistance index (MVRI), and stroke volume index (SVI) were calculated. Sepsis was induced by continuous IV infusion of live GBS beginning at 0.5 X 10(7) organisms/kg/min. LAP was held constant throughout the sepsis protocol. PAP and PVRI were the most sensitive hemodynamic indices of early GBS sepsis, rising to greater than two times baseline levels within 11 min of the onset of bacteremia (approximately 1.0 X 10(8) cumulative organisms/kg). In contrast, AOP was unaffected during the first 83 min of GBS sepsis (approximately 25 X 10(8) organisms/kg) but fell from 84 to 47 mmHg in the final 31 min of the experiment. Both CI and MBFI fell monotonically as a function of cumulative GBS dose, reaching 72% and 64% of baseline at 55 min (approximately 12.5 X 10(8) organisms/kg) and 40% and 34% of baseline by 3 hr of sepsis (approximately 125 X 10(8) organisms/kg), respectively. At every GBS dose, the fall in CI was entirely accounted for by a reduction in SVI. SVRI, MVRI, and PVRI were elevated at all times during GBS sepsis. Despite a 34% reduction in systemic oxygen delivery during the first 83 min of GBS infusion (approximately 25 X 10(8) organisms/kg), arterial pH and base excess did not change significantly. Thereafter, pH fell monotonically reflecting the progressive development of metabolic acidosis.
D000138:Acidosis / Q000209:etiology; D000818:Animals; D000831:Animals, Newborn; D004195:Disease Models, Animal; D006439:Hemodynamics; D006976:Hypertension, Pulmonary / Q000209:etiology; D011652:Pulmonary Circulation; D012772:Shock, Septic / Q000503:physiopathology*; D013152:Splanchnic Circulation; D013290:Streptococcal Infections / Q000503:physiopathology*; D013292:Streptococcus agalactiae; D013552:Swine; D013997:Time Factors