Post cardiac arrest syndrome is associated with high morbidity and mortality, which is related not only to a poor neurological outcome but also to respiratory and cardiovascular dysfunctions. The control of gas exchange, and in particular oxygenation and carbon dioxide levels, is fundamental in mechanically ventilated patients after resuscitation, as arterial blood gases derangement might have important effects on the cerebral blood flow and systemic physiology.In particular, the pathophysiological role of carbon dioxide (CO2) levels is strongly underestimated, as its alterations quickly affect also the changes of intracellular pH, and consequently influence metabolic energy and oxygen demand. Hypo/hypercapnia, as well as mechanical ventilation during and after resuscitation, can affect CO2 levels and trigger a dangerous pathophysiological vicious circle related to the relationship between pH, cellular demand, and catecholamine levels. The developing hypocapnia can nullify the beneficial effects of the hypothermia. The aim of this review was to describe the pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest.According to our findings, the optimal ventilator strategies in post cardiac arrest patients are not fully understood, and oxygen and carbon dioxide targets should take in consideration a complex pattern of pathophysiological factors. Further studies are warranted to define the optimal settings of mechanical ventilation in patients after cardiac arrest.
The role of hyperventilation -hypocapnia in the pathomechanism of panic disorder O papel da hiperventilação -a hipocapnia no patomecanismo do distúrbio de pânico A b s t r a c t Objective: The authors present a profile of panic disorder based on and generalized from the effects of acute and chronic hyperventilation that are characteristic of the respiratory panic disorder subtype. The review presented attempts to integrate three premises: hyperventilation is a physiological response to hypercapnia; hyperventilation can induce panic attacks; chronic hyperventilation is a protective mechanism against panic attacks. Method: A selective review of the literature was made using the Medline database. Reports of the interrelationships among panic disorder, hyperventilation, acidosis, and alkalosis, as well as catecholamine release and sensitivity, were selected. The findings were structured into an integrated model. Discussion: The panic attacks experienced by individuals with panic disorder develop on the basis of metabolic acidosis, which is a compensatory response to chronic hyperventilation. The attacks are triggered by a sudden increase in (pCO 2 ) when the latent (metabolic) acidosis manifests as hypercapnic acidosis. The acidotic condition induces catecholamine release. Sympathicotonia cannot arise during the hypercapnic phase, since low pH decreases catecholamine sensitivity. Catecholamines can provoke panic when hyperventilation causes the hypercapnia to switch to hypocapnic alkalosis (overcompensation) and catecholamine sensitivity begins to increase. Conclusion: Therapeutic approaches should address long-term regulation of the respiratory pattern and elimination of metabolic acidosis.Descriptors: Acidosis; Catecholamines; Hyperventilation; Hypocapnia; Panic disorder Resumo Objetivo: Os autores apresentam um modelo de transtorno do pânico que se baseia nos efeitos da hiperventilação aguda e crônica, característicos do subtipo respiratório de transtorno do pânico. O modelo é generalizado a partir desses efeitos. Ele integra três características da hiperventilação: a hiperventilação é uma resposta fisiológica à hipercapnia; a hiperventilação pode induzir ataques de pânico; a hiperventilação crônica representa um mecanismo protetor contra os ataques de pânico. Método: Revisão seletiva da literatura a partir da base de dados Medline. Foram selecionados relatos referentes à inter-relação entre transtorno do pânico, hiperventilação, acidose, alcalose, liberação de catecolaminas e sensibilidade a catecolaminas, sendo os achados estruturados de modo a formar um modelo integrado. Discussão: Os ataques de pânico do transtorno do pânico desenvolvem-se com base numa acidose metabólica, que é uma resposta compensatória à hiperventilação crônica. Os ataques são desencadeados por um súbito aumento da pressão parcial de dióxido de carbono (pCO 2 ), quando a acidose (metabólica) latente se manifesta pela acidose hipercápnica. A condição acidótica induz liberação de catecolaminas. A simpaticotonia não pode manifestar-se durante...
Insulin is one of the most important of anabolic hormones. Type 2 Diabetes (T2D) is characterized by persistent, stealth catabolism, as well as impaired glucose and phosphate uptake. The phosphate transporting capability of insulin has been known for a long time, although it has been studied mainly since the 21 st century. According to the logic of the Momentary Intracellular Ion-Pattern Signaling, insulin should increase of HPO 4 2in the cytosol -and does it, indeed. (It is not clear that this is a one-or multistep membrane-transport phenomenon.) Insulin does not only stimulate the transport of phosphate (Pi) into the cytosol but alkalinizes it, as well. Cytoplasmic alkalinization is a vital process by insulin, which mechanism has not been studied in detail. Insulin is one of the most important players in the regulation of intracellular pH, which, together with phosphate transport, is crucial for maintaining its anti-catabolic effect. Acidotic cytoplasm of the pancreas beta-cells increases while alkalotic decreases insulin secretion, which may be a feedback mechanism.All insulin-mediated vital anabolic processes use energy derived from ATP. The impaired mitochondrial ATP production capability is a consequence of insulin resistance, which develops during the early stage of Metabolic Syndrome, and can persist for decades without a manifest of T2D. Decreased ATP productivity is compensated by increased lipid availability. T2D develops when high triglyceride availability cannot compensate for insulin resistance and reduced ATP production. The guiding principle is that mitochondria have to provide near-normal ATP content at all costs in the cytoplasm of the cells; otherwise, the cells will be severely ill or killed.Catabolism rises to increase ATP production. The liberated amino acids allow gluconeogenesis to proceed and raise serum glucose levels. Pathophysiologically, both hyperglycemia and increased food uptake have compensatory roles in ATP production, though many vicious circles are generated.
According to the hypothesis of the author, the Metabolic Syndrome and Type 2 Diabetes are mainly consequences of chronic lowgrade hypercapnia and related intracellular acidosis. The altered pCO 2 status changes the Intracellular Ion-Pattern and, consequently, the metabolism. The author has developed a recovery strategy based on his metabolic model, experiences, and data of literature. The primary goal is to increase the minute-ventilation to achieve low-grade hypocapnia (~ 35 mmHg on average) and to maintain it in the long run. As a consequence of the decreased pCO 2 level-according to the hypothesis-an intracellular alkaline pH develops and results in increased metabolism, ATP production, and consequently, phosphate, Mg 2+ , K + , and Zn 2+ influx into the cytosol. Serum Ca 2+ levels may also decrease due to increased calcium and phosphate uptake into the 'hungry bones.' It is expected that both the carbohydrates and fats will be burned more intensively in mitochondria, which would also mean a decrease in insulin resistance, serum glucose, and lipid levels. The essence of the method is that regular daily administration of monobasic phosphate (H 2 PO 4-) salts as fixed acids can increase respiratory minute volume and decrease the pCO 2 level. It is advised to give these salts routinely in doses below the Recommended Dietary Allowance. After achieving the desired pCO 2 level, it is advocated that an acidotic H 2 PO 4-/ HPO 4 2salt mixture be titrated to maintain the low-grade hypocapnia. Preferably, the cations are provided by combinations of Mg 2+ , K + , and Ca 2+. The amounts of ions to be administered can be determined by monitoring serum electrolytes. According to the hypothesis, this method could be particularly useful in diseases where elevated levels of pCO 2 play a pathophysiological role. The author also proposes an improved method of Sodi-Pallarés; alternatively, it can be an infusion containing the combination of phosphate buffer, K + , Mg 2+ , Zn 2+ , and (possibly) other 'cytoplasm-builder' nutrients plus glucose and insulin. Theoretically, it could improve the metabolism of the chronically ill or insulin-resistant patients.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.