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The patient with acute respiratory problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
During acute exacerbations, the increased work of breathing with inevitable fatigue can result in poor ventilatory drive. The consequence of this is a falling PaO2 and a rising PaCO2. However, it is important to remember that someone living with COPD may have adjusted to living with chronic hypoxaemia and hypercapnia – this individual’s ‘normal’ state. Arterial blood gasses (discussed in more detail later in the chapter), in those who have adjusted to chronic hypoxaemia and hypercapnia, will reveal smaller reductions in pH in relation to raised PaCO2 levels. The metabolic component of the blood gas will reveal an elevation in the levels of the buffer bicarbonate (HCO3-), secondary to the renal compensation response of bicarbonate reabsorption. During acute episodes, great skill is needed in reducing PaCO2 levels without over-correction of PaO2 oxygen levels. Non-invasive ventilatory support, in the form of bilevel positive airway pressure ventilation (BiPAP) and careful oxygen titration aims to achieve this. This is discussed later in this chapter.
Control of Ventilation
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
In chronic lung conditions with elevated arterial , the ventilatory response to carbon dioxide is lost by resetting of the central chemoreceptors by correction of the CSF hydrogen ion concentration by uptake of bicarbonate ions. In addition, renal compensation reduces the effect of elevated carbon dioxide on the peripheral chemoreceptors. Ventilation is then controlled by arterial , not .
Clinical Chemistry
Published in Paul Bentley, Ben Lovell, Memorizing Medicine, 2019
Acidosis has two types of 1° cause, each being compensated by the other system: Respiratory: PaCO2 ↑, due to ventilation ↓ → renal compensation, via HCO3– resorption, and acid and NH4+ excretionMetabolic: HCO3– ↓ due to acid gain (high anion gap) or HCO3– loss (low anion gap) →respiratory compensation, by PaCO2 ↓
Calcium and pH value might predict persistent renal failure in acute pancreatitis in the early phase
Published in Current Medical Research and Opinion, 2022
Xuanfu Chen, Meng Jin, Yi Li, Yamin Lai, Xiaoyin Bai, Hong Yang, Hong Lv, Jiaming Qian
The two parameters were simple, quantitative and easy to obtain. However, their mechanisms of predicting renal injury are likely multifactorial. With respect to pH, on the one hand, some AP patients lost intravascular blood volume due to severe response to pancreatic injury, which led to a decrease of the renal perfusion and then caused renal failure. On the other hand, a complex inflammatory network combined with (peri)pancreatic necrosis influenced the severity of the renal failure, and the latter exacerbated the development of pancreatitis3. The acid–base balance was maintained by pulmonary excretion of carbon dioxide, metabolic utilization of organic acids and renal excretion of nonvolatile acids. Respiratory compensation in metabolic acidosis or alkalosis was a rapid response. For instance, the reaction of metabolic acidosis began within 30 min14 and was completed within 12–24 h. If the respiratory disorder persisted for more than minutes to hours, the kidneys responded by producing more significant changes in serum HCO3. As it always took hours for patients to reach the hospital, the pH was regulated by renal compensation. So we could conclude that a lower pH level on admission indicated impaired renal compensatory function and was more likely to be associated with PRF. Previous research has found that lower arterial pH on admission could better predict an adverse outcome in patients with AP15. Meanwhile, lower blood pH suggests higher mortality, elevated severity scores and longer hospital stay in AP patients, which is similar to our results16.
Advances in the available non-biological pharmacotherapy prevention and treatment of acute mountain sickness and high altitude cerebral and pulmonary oedema
Published in Expert Opinion on Pharmacotherapy, 2018
K.E. Joyce, S.J.E. Lucas, C.H.E. Imray, G.M Balanos, A. D. Wright
The hypobaric hypoxic conditions at altitude elicit distinct temporary and reversible physiologic responses in lowlanders who have spent a few hours to days at high altitude (generally over 3000 m). These responses are predominantly attributed to hypoxemia [3,4]. The initial physiologic acclimatization is hyperventilation, which negates reductions in the partial pressure of oxygen (PO2) but also results in a greater loss of carbon dioxide (CO2) (hypocapnia) and subsequent respiratory alkalosis [5]. This respiratory alkalosis elicits a renal compensation response by which the kidneys increase bicarbonate (HCO3−) excretion and increase hydrogen (H+) retention, resulting in a secondary metabolic acidosis and a mild diuretic effect [6,7]. Hypoxia also elicits an increase in sympathetic tone, an increase in blood pressure (BP), and an elevation in resting heart rate [8]. The magnitude of the response to hypoxia varies considerably between individuals [9].
FFNT25 ameliorates unilateral ureteral obstruction-induced renal fibrosis
Published in Renal Failure, 2019
Wen Li, Yue Lu, Yan Lou, Shiyue Zhao, Wenpeng Cui, Yangwei Wang, Manyu Luo, Jing Sun, Lining Miao
We used UUO to induce renal fibrosis in our study. We found that UUO significantly decreased left/right KW ratio, which was reversed by FFNT25 treatment (Table 3). While renal function indicators, such as serum Cr, urine Cr, and urine NAG, were not affected by UUO, we concluded that these indices also estimated the function of the contralateral non-obstructed kidney in the UUO model, which suggests that there is renal compensation. We observed no obvious side effects (e.g., diarrhea) of FFNT25. These results indicate that FFNT25 could be used to alleviate interstitial edema in renal fibrosis.