Abstract
Considering maternal mortality in state-of-the-art clinics and sophisticated methods of treatment and diagnosis, the human factor of the doctor and the available methods of treatment and diagnosis remained a priority in reducing and even eliminating obstetric mortality. The of success since the last century as in this century of which we described in this work, as in many other previously published works, and represented at international congresses in the Republic of Moldova, Romania, Spain, the Netherlands, Russia and others, where decrease in the increased marker of tissue hypoxia pCO2> (AV-gap) in microcirculatory-mitochondrial distress syndrome in critical obstetrics is achieved by complex methods of recruiting microcirculatory-mitochondrial distress syndrome, contributed to the absence of maternal mortality over 40 years of work in critical obstetrics is presented as a brilliant proof of an affordable model in any medical institution that finds itself next to a dying woman in labor.
Highlights
Obstetric mortality was absent, for more than 40 years of emergency anaesthesiology and resuscitation in Moldova, Central Asia and Russia, and on-air ambulance, with critical [1,2,3,4] situations in obstetrics
In the presence of a normal HR, hyper- and normovolemia (↑ECBV, ↑ BP) with an increased pre- and post-load, selectively justified themselves, nitrates and α-β-adreno blockers (Labetalol), which by establishing peripheral vasodilation with in arterioles and venules anti-hypertensive effects, have a beneficial effect on the cardiac output fraction and HR. In this direction proved that the combined use of α-vasopressor on the background of the N-cholinergic ganglion blockade, ganglion blockade without hypotension is established, at which a different pharmacological effect occurs, a new, not present in their isolated application, since post-capillary venules increase their susceptibility to the vasopressor and thereby support the macrocirculation, while decentralizing it, which optimizes vascular systemic perfusion pressure (SPP) ∆VP in which the microcirculation improves, mainly, increased susceptibility to adrenomimetic - pre, postsynaptic, etc, metabolic capillary sphincters, close the shunting through capillary anastomoses
The pressure / volume loop of the trachea is considered, which are presented in 4 types, which means that the more the loop surface is expanded, the more the respiratory pattern, as well as the definition of the dynamic ( Cdyn.) and statistical (Cst.) compliance confirming damage to the respiratory organs aggravating mitochondrial collapse (MC) microcirculatory-mitochondrial distress syndrome (MMDs) and RMM in such cases are supplemented with MOST therapy in the Extracorporeal Life Support Organization, ELSO with active detoxification methods: 1) Alveolar recruitment with respiratory support in special modes of ventilation, mainly APRV, with permissive hypercapnia at normal pH; 2) Recruitment of microcirculatory – mitochondrial, RMM, with support for optimal SPP
Summary
For more than 40 years of emergency anaesthesiology and resuscitation in Moldova, Central Asia and Russia, and on-air ambulance, with critical [1,2,3,4] situations in obstetrics. Recruitment of microcirculatory – mitochondrial (RMM) had the goal of optimizing vascular volume pressure compliance (∆VP) of microcirculatory perfusion of space: capillary ↔ cell ↔ mitochondria, with accelerated venous return and elimination of CO2 and other endogenous toxic substances (ETS) with energy-resuscitation of mitochondrial collapse (MC) [5,6,7]. Recruitment of microcirculatory – mitochondrial reduces, microcirculatory-mitochondrial distress syndrome (MMDs) and syndrome of multi-organ dysfunction (MODs), by decentralizing macro-circulation, as a result, systemic perfusion pressure (SPP), is stabilized representing the difference between mean arterial pressure (MAP), and capillary resistance pressure, CRP, which adequately perfused the microcirculatory space of capillary ↔ cell ↔ mitochondria, thanks to adequate vascular compliance ∆VP with an accelerated speed of delivery and return of blood flow, which directly leads to a decrease in tissue hypoxia marker pCO2 (AV gap ) and, respectively, decrease MMDs, MODs and many other endogenous toxic substances. Demonstrating eu-ergic mitochondria with the normalization of mitochondrial Ca++ uniporter - channel and mitochondrial permeability pore transition, which productively inactivate the toxic forms of oxygen, Reactive oxygen species, ROS and Reactive nitrogen species, RNS
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