A Window in the Heart Is Sometimes a Good Start: It’s Not Always Sepsis

Cardiac tamponade is a life-threatening compression of the heart caused by abnormal accumulation of pericardial fluid. Important elements affecting its disposition and treatment are the rate of fluid accumulation relative to pericardial stretch and the effectiveness of compensatory mechanisms before critical hemodynamic compromise occurs. It is a clinical diagnosis and waiting for the threshold of steep rise in cardiac transmural pressure to critical levels may lead to catastrophic outcomes which is why early drainage has to be strongly considered in suspected cases.

Modulation of p66Shc impairs cerebrovascular myogenic tone in low renin but not low nitric oxide models of systemic hypertension

Cerebral blood flow and perfusion are tightly maintained through autoregulation despite changes in transmural pressure. Oxidative stress impairs cerebral blood flow, precipitating cerebrovascular events. Phosphorylation of the adaptor protein p66Shc increases mitochondrial-derived oxidative stress. The effect of p66Shc gain or loss of function in non-hypertensive rats is unclear. We hypothesized that p66Shc gain of function would impair autoregulation of cerebral microcirculation under physiological and pathological conditions. Three previously established transgenic (salt-sensitive background; SS) p66Shc rats were utilized, p66-Del/SS (express p66Shc with a 9-amino acid deletion), p66Shc-KO/SS (frameshift premature termination codon), and p66Shc-S36A/SS (substitution of Ser36Ala). The p66Shc-Del were also bred on Sprague-Dawley backgrounds (p66-Del/SD), and a subset was exposed to a hypertensive stimulus (L-NAME) for 4 weeks. Active and passive diameters to increasing transmural pressure were measured and myogenic tone was calculated. Myogenic responses to increasing pressure were impaired in p66Shc-Del/SS rats relative to WT/SS and knock-in substitution of S36A (P<0.05). p66-Del/SD rats did not demonstrate changes in active/passive diameters or myogenic tone relative to WT/SD, but did demonstrate attenuated passive diameter responses to higher transmural pressure relative to p66-Del/SS. 4 weeks of a hypertensive stimulus (L-NAME) did not alter active or passive diameter responses to increasing transmural pressure (P=0.86-0.99), but increased myogenic responses relative to p66-Del/SD (P<0.05). Collectively, we demonstrate the functional impact of modulation of p66Shc within the cerebral circulation and demonstrate that the genetic background of p66Shc rats largely drives changes in cerebrovascular function.

Differential responsiveness of glabrous and non-glabrous skin to local transmural pressure elevations; the impact of 5 weeks of iterative local pressure loading

We examined the in vivo pressure-flow relationship in human cutaneous vessels during acute and repeated elevations of local transmural pressure. In 10 healthy men, red blood cell flux was monitored simultaneously on the non-glabrous skin of the forearm and the glabrous skin of a finger during a vascular pressure provocation, wherein the blood vessels of an arm were exposed to a wide range of stepwise increasing distending pressures. Forearm skin blood flux was relatively stable at slight and moderate elevations of distending pressure, whereas it increased ~3-4-fold at the highest levels (P = 0.004). Finger blood flux on the contrary, dropped promptly and consistently throughout the provocation (P < 0.001). Eight of the subjects repeated the provocation trial after a 5-week pressure-training regimen, during which the vasculature in one arm was exposed intermittently (40 min, 3 times･week-1) to increased transmural pressure (from +65 mmHg week-1 to +105 mmHg week-5). The training regimen diminished the pressure-induced increase in forearm blood flux by ~34% (P = 0.02), whereas it inhibited the reduction in finger blood flux (P < 0.001) in response to slight and moderate distending pressure elevations. The present findings demonstrate that, during local pressure perturbations, the cutaneous autoregulatory function is accentuated in glabrous compared to in the non-glabrous skin regions. Prolonged intermittent regional exposures to augmented intravascular pressure blunt the responsiveness of the glabrous skin, but enhance arteriolar pressure resistance in the non-glabrous skin.

Biophysical Conceptual Doxastic Errors in Arterial Hypertension in Surgical and Medical Management, in the Frame of Navier Stokes Equations

Multiple tragic biophysical errors in relation to hypertension in surgery and medicine, constitute conceptual atrocities: 1) Many physicians believe that perfusion decays with the fourth power of the radius, which is the result of a doxastic misunderstanding of the Poiseuille equation. These phenomena are even more transcendent in the case of surgical situations when the homeostatic metastability is more critical and with less margin to be compensated. 2) Furthermore, when seen the occlusion of an artery, frequently, instead of measuring the radius, they measure the apparent cross-sectional area. 3) By reducing the driving pressure with antihypertensive drugs, we are decreasing axial pressure in the flow and consequently the perfusion. 4) The sphygmomanometer measures transmural pressure and not driving pressure which is what produces perfusion. 5) The main hemodynamic cause of damage is not transmural hypertension but Laplacian tension. 6) The damage to the arteries does not depend on transmural pressure but on the energy density per time, in units of Joules per cubic meter per second, or Watts per cubic meter. 7) Hypertension, ceteris parivus, increases perfusion. 8) The baroreceptors do not respond to transmural pressure but to Laplacian arterial tension. 9) The brain and the heart have self-regulation of their perfusion, but vasodilators increase perfusion in other tissues, reducing cerebral and coronary perfusion due to the stolen effect. 10). Strictly, all gradients constitute potential energy, as happens in the instances of the concentration gradients, temperature gradients, pressure gradients, and electrical gradients. 11) The derivative of pressure with respect to time, that is the change in pressure due to change in time, is the derivative of the work per volume per time (change in work density due to time), that is, power density. 12) What determines the perfusion is the axial gradient, not of pressure but energy. 13) Hyperbolically if we consider taking the pressure of a pachyderm, we would obtain readings significantly higher. 14) Pressure is, in reality, energy density, which means, energy per infinitesimal unit of volume. 15) The venous return consists of the blood flow returning to the right heart. Because the input of the right side must equal its output, then in the steady-state situation, the cardiac outputs of the right and left sides are essentially equal. Consequently, the systemic venous return matches the systemic cardiac output. The venous return should be equal to or less than the cardiac output. The heart, as a pump, cannot expel a volume that has not been received; notwithstanding, in the case of valve regurgitation, the heart can expel a fraction of the venous return twice. The clinical physician should ask himself or herself: Is the preload volume in the EDV or the pressure at the time of the EDV which has been diminished before starting the isovolumic contraction?