Osvaldas Pranevicius

Cerebral venous steal: Blood flow diversion with increased tissue pressure

PURPOSE Flow in areas with increased tissue pressure is described by a Starling resistor and is determined by the inflow pressure (Pi), the external pressure (Pe), and the outflow or venous pressure (Pv). Flow is in Zone 1 at Pe >Pi >Pv, Zone 2 at Pi >Pe >Pv, and Zone 3 at Pi >Pv >Pe. A focal tissue pressure increase after stroke or trauma may lead to a transition from Zone 1 or 2 in the center to Zone 3 in the periphery. We hypothesize that the coexistence of different zones may lead to steal-like blood flow diversion in the perifocal area. CONCEPT We used a lumped-parameter model of two parallel Starling resistors with a common inflow. The first resistor, with higher Pe, represented the area with increased tissue pressure. The second resistor, with Pe′ = 0, represented the surrounding area. We evaluated the effects of venous pressure on the flow distribution between the two Starling resistors. RATIONALE The model demonstrated blood flow diversion toward the second Starling resistor with low external pressure. High inflow resistance facilitates this “steal.” Flow diversion is caused by effective outflow pressure differences for the Starling resistors (Pe for the first and Pv for the second). The venous pressure increase equilibrates the effective backpressure and decreases flow diversion. When the venous pressure equals the external tissue pressure, blood flow diversion (cerebral venous steal) is abolished. Although increased venous pressure causes global flow reduction, it may restore flow to more than 50% of baseline values in areas of increased tissue pressure. DISCUSSION Cerebral venous steal is a potential cause of secondary brain injury in areas of increased tissue pressure. It can be eliminated with increased venous pressure. Increased venous pressure may recruit the collapsed vascular network and correct perifocal perfusion maldistribution. This resembles how positive end expiratory pressure recruits collapsed airways and decreases the ventilation/perfusion mismatch.

Transition to Collateral Flow After Arterial Occlusion Predisposes to Cerebral Venous Steal

Background and Purpose— Stroke-related tissue pressure increase in the core and penumbra determines regional cerebral perfusion pressure (rCPP) defined as a difference between local inflow pressure and venous or tissue pressure, whichever is higher. We previously showed that venous pressure reduction below the pressure in the core causes blood flow diversion–cerebral venous steal. Now we investigated how transition to collateral circulation after complete arterial occlusion affects rCPP distribution. Methods— We modified parallel Starling resistor model to simulate transition to collateral inflow after complete main stem occlusion. We decreased venous pressure from the arterial pressure to zero and investigated how arterial and venous pressure elevation augments rCPP. Results— When core pressure exceeded venous, rCPP=inflow pressure in the core. Venous pressure decrease from arterial pressure to pressure in the core caused smaller inflow pressure to drop augmenting rCPP. Further drop of venous pressure decreased rCPP in the core but augmented rCPP in penumbra. After transition to collateral circulation, lowering venous pressure below pressure in the penumbra further decreased rCPP and collaterals themselves became a pathway for steal. Venous pressure level at which rCPP in the core becomes zero we termed the “point of no reflow.” Transition from direct to collateral circulation resulted in decreased inflow pressure, decreased rCPP, and a shift of point of no reflow to higher venous loading values. Arterial pressure augmentation increased rCPP, but only after venous pressure exceeded point of no reflow. Conclusions— In the presence of tissue pressure gradients, transition to collateral flow predisposes to venous steal (collateral failure), which may be reversed by venous pressure augmentation.

Application of Stochastic Automata Networks for Creation of Continuous Time Markov Chain Models of Voltage Gating of Gap Junction Channels

The primary goal of this work was to study advantages of numerical methods used for the creation of continuous time Markov chain models (CTMC) of voltage gating of gap junction (GJ) channels composed of connexin protein. This task was accomplished by describing gating of GJs using the formalism of the stochastic automata networks (SANs), which allowed for very efficient building and storing of infinitesimal generator of the CTMC that allowed to produce matrices of the models containing a distinct block structure. All of that allowed us to develop efficient numerical methods for a steady-state solution of CTMC models. This allowed us to accelerate CPU time, which is necessary to solve CTMC models, ~20 times.

Comment on: High stop-bang questionnaire scores predict intraoperative and early postoperative adverse events.

Dear Sir, With great interest, we read the article by Seet et al,(1) which delved into the ongoing controversy of how the risk of perioperative respiratory events is related to specific STOP-BANG scores. This controversy is fuelled by the belief that higher STOP-BANG scores translate to higher risks of OSA and hence, an increased incidence of postoperative complications.(2-4) Seet et al’s study also supports this belief; using logistic regression analysis, the authors analysed the cohort for the odds of adverse postoperative events occurring and found a statistically significant increase in the odds of an adverse event in patients with STOP-BANG scores of 2, 3, 4, 5 and ≥ 6. Moreover, they concluded that a STOP-BANG score ≥ 5 resulted in a five-fold increased odds ratio (OR) of adverse events and recommended that polysomnography be considered for these patients before elective surgery. However, upon reviewing the confidence intervals for the reported ORs, we noticed a significant overlap for most STOP-BANG score groups. Therefore, we re-analysed the study data with analysis of variance as well as performed a pairwise comparison between the groups using the Bonferroni correction. Our analysis showed that only two groups (that are separated by a STOP-BANG score of 3) have different risks for postoperative complications; adding points to the STOP-BANG score did not statistically alter the risk (Table I). Therefore, we suggest that a STOP-BANG score ≥ 3 should trigger an evaluation for sleep-disordered breathing. Table I Association of adverse events with STOP-BANG score (adapted from Seet et al).(1) Yours sincerely,

Clinical Assessment of Noninvasive Intracranial Pressure Absolute Value Measurement MethodAuthor ResponseAuthor Response

Ragauskas et al.1 demonstrated that when external pressure is applied, the orbit tends to equilibrate flow in the ipsilateral ophthalmic artery (OA) when its level approaches intracranial pressure (ICP). The authors detected this relationship by making the OA into a “natural pair of scales, in which the intracranial segment of the OA is compressed by extracranial pressure (Pe) applied to the orbit.”