Peripheral Perfusion Index Predicts Hypotension during Fluid Withdrawal by Continuous Veno-Venous Hemofiltration in Critically Ill Patients

Aim: Peripheral perfusion may predict harmful hypovolemic hypotension during fluid withdrawal by continuous veno-venous hemofiltration (CVVH) in critically ill patients with acute kidney injury. Methods: Twenty-three critically ill AKI patients were subjected to progressive fluid withdrawal. Systemic hemodynamics and peripheral perfusion index (PPI) by pulse oximetry, forearm-to-fingertip skin temperature gradient (Tskin-diff) and tissue oxygen saturation (StO2, near infra-red spectroscopy) were measured. Results: Most hemodynamic values decreased with fluid withdrawal, particularly in the hypotensive group, except for stroke volume (SV) and cardiac output, which decreased to a great extent in the non-hypotensive patients. Increases in systemic vascular resistance (SVR) were less in hypotension. Baseline pulse pressure and PPI were lower in hypotensive (n = 10) than non-hypotensive patients and subsequent PPI values paralleled SV decreases. A baseline PPI ≤0.82 AU predicted hypotension with a sensitivity of 70%, and a specificity of 92% (AUC 0.80 ± 0.11, p = 0.004). Conclusion: Progressive fluid withdrawal during CVVH is poorly tolerated in patients with less increases in SVR. The occurrence of hypotension can be predicted by low baseline PPI.

Effects of Anemia and Hypotension on Porcine Optic Nerve Blood Flow and Oxygen Delivery

Background Perioperative ischemic optic neuropathy occurs after major surgical procedures, which are often associated with hypotension, anemia, or venous congestion. However, the effects of these conditions on optic nerve (ON) blood flow are unknown and cannot be studied adequately in humans. Methods Farm-raised pigs were anesthetized with isoflurane, kept normocapnic and normothermic, and subjected to conditions of euvolemic or hypovolemic hypotension (mean arterial pressure 50-55 mm Hg), anemia (hematocrit 17%), venous congestion, and combinations thereof. Control animals were kept euvolemic and normotensive for the entire experiment. Fluorescent microspheres were used to measure cerebral blood flow (CBF) and ON blood flow at baseline and after experimental conditions, and to calculate oxygen delivery (DO2). Results No significant changes in CBF or ON blood flow or DO2 occurred with euvolemic hypotension (n = 5), compared with controls (n = 12). Hypovolemic hypotension (n = 4) resulted in stable CBF and cerebral DO2, but significant reductions in ON DO2 (P = 0.032). The significant increase in CBF associated with anemia (n = 6) resulted in stable cerebral DO2. In contrast, ON blood flow did not significantly change with anemia, with (n = 5) or without (n = 6) euvolemic hypotension, resulting in significant reductions in ON DO2 (P < 0.01). Conclusion Compensatory mechanisms for porcine CBF maintain stable DO2 under specified conditions of hypotension or anemia, whereas ON compensatory mechanisms were unable to maintain blood flow and to preserve DO2. The authors conclude that the porcine ON is more susceptible to physiologic perturbations than the brain.

Effects of arterial hypotension on microvascular oxygen exchange in contracting skeletal muscle

In healthy animals under normotensive conditions (N), contracting skeletal muscle perfusion is regulated to maintain microvascular O2 pressures (Pmv[Formula: see text]) at levels commensurate with O2 demands. Hypovolemic hypotension (H) impairs muscle contractile function; we tested whether this condition would alter the matching of O2 delivery (Q̇o2) to O2 utilization (V̇o2), as determined by Pmv[Formula: see text] at the onset ofmuscle contractions. Pmv[Formula: see text] in the spinotrapezius muscles of seven female Sprague-Dawley rats (280 ± 6 g) was measured every 2 s across the transition from rest to 1-Hz twitch contractions. Measurements were made under N (mean arterial pressure, 97 ± 4 mmHg) and H (induced by arterial section; mean arterial pressure, 58 ± 3 mmHg, P < 0.05) conditions; Pmv[Formula: see text] profiles were modeled using a multicomponent exponential fitted with independent time delays. Hypotension reduced muscle blood flow at rest (24 ± 8 vs. 6 ± 1 ml−1·min−1·100 g−1 for N and H, respectively; P < 0.05) and during contractions (74 ± 20 vs. 22 ± 4 ml−1·min−1·100 g−1 for N and H, respectively; P < 0.05). H significantly decreased resting Pmv[Formula: see text] and steady-state contracting Pmv[Formula: see text](19.4 ± 2.4 vs. 8.7 ± 1.6 Torr for N and H, respectively, P < 0.05). At the onset of contractions, H reduced the time delay (11.8 ± 1.7 vs. 5.9 ± 0.9 s for N andH, respectively, P < 0.05) before the fall in Pmv[Formula: see text] and accelerated therate of Pmv[Formula: see text] decrease (time constant, 12.6 ± 1.4 vs. 7.3 ± 0.9 s for N and H, respectively, P < 0.05). Muscle V̇o2 was reduced by 71% at rest and 64% with contractions in H vs. N, and O2 extraction during H averaged 78% at rest and 94% during contractions vs. 51 and 78% in N. These results demonstrate that H constrains the increase of skeletal muscle Q̇o2 relative to that of V̇o2 at the onset of contractions,leading to a decreased Pmv[Formula: see text]. According to Fick's law, this scenario will decrease blood-myocyte O2 flux, thereby slowing V̇o2 kinetics and exacerbating the O2 deficit generated at exercise onset.

Staphylococcus aureus Induces Release of Bradykinin in Human Plasma

ABSTRACT Staphylococcus aureus is a prominent human pathogen. Here we report that intact S. aureus bacteria activate the contact system in human plasma in vitro, resulting in a massive release of the potent proinflammatory and vasoactive peptide bradykinin. In contrast, no such effect was recorded withStreptococcus pneumoniae. In the activation of the contact system, blood coagulation factor XII and plasma kallikrein play central roles, and a specific inhibitor of these serine proteinases inhibited the release of bradykinin by S. aureus in human plasma. Furthermore, fragments of the cofactor H-kininogen of the contact system efficiently blocked bradykinin release. The results suggest that activation of the contact system at the surface ofS. aureus and the subsequent release of bradykinin could contribute to the hypovolemic hypotension seen in patients with severeS. aureus sepsis. The data also suggest that the contact system could be used as a target in the treatment of S. aureus infections.