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The European Respiratory Journal Jun 2022Pulmonary arterial hypertension (PAH) is a rare dyspnoea-fatigue syndrome caused by a progressive increase in pulmonary vascular resistance and eventual right... (Review)
Review
Pulmonary arterial hypertension (PAH) is a rare dyspnoea-fatigue syndrome caused by a progressive increase in pulmonary vascular resistance and eventual right ventricular (RV) failure. In spite of extensive pulmonary vascular remodelling, lung function in PAH is generally well preserved, with hyperventilation and increased physiological dead space, but minimal changes in lung mechanics and only mild to moderate hypoxaemia and hypocapnia. Hypoxaemia is mainly caused by a low mixed venous oxygen tension from a decreased cardiac output. Hypocapnia is mainly caused by an increased chemosensitivity. Exercise limitation in PAH is cardiovascular rather than ventilatory or muscular. The extent of pulmonary vascular disease in PAH is defined by multipoint pulmonary vascular pressure-flow relationships with a correction for haematocrit. Pulsatile pulmonary vascular pressure-flow relationships in PAH allow for the assessment of RV hydraulic load. This analysis is possible either in the frequency domain or in the time domain. The RV in PAH adapts to increased afterload by an increased contractility to preserve its coupling to the pulmonary circulation. When this homeometric mechanism is exhausted, the RV dilates to preserve flow output by an additional heterometric mechanism. Right heart failure is then diagnosed by imaging of increased right heart dimensions and clinical systemic congestion signs and symptoms. The coupling of the RV to the pulmonary circulation is assessed by the ratio of end-systolic to arterial elastances, but these measurements are difficult. Simplified estimates of RV-pulmonary artery coupling can be obtained by magnetic resonance or echocardiographic imaging of ejection fraction.
Topics: Familial Primary Pulmonary Hypertension; Heart Failure; Humans; Hypertension, Pulmonary; Hypocapnia; Hypoxia; Pulmonary Arterial Hypertension; Pulmonary Artery; Ventricular Dysfunction, Right; Ventricular Function, Right
PubMed: 34737219
DOI: 10.1183/13993003.02334-2021 -
Sleep Mar 2023Central sleep apnea is not a single disorder; it can present as an isolated disorder or as a part of other clinical syndromes. In some conditions, such as heart failure,... (Review)
Review
Central sleep apnea is not a single disorder; it can present as an isolated disorder or as a part of other clinical syndromes. In some conditions, such as heart failure, central apneic events are due to transient inhibition of ventilatory motor output during sleep, owing to the overlapping influences of sleep and hypocapnia. Specifically, the sleep state is associated with removal of wakefulness drive to breathe; thus, rendering ventilatory motor output dependent on the metabolic ventilatory control system, principally PaCO2. Accordingly, central apnea occurs when PaCO2 is reduced below the "apneic threshold". Our understanding of the pathophysiology of central sleep apnea has evolved appreciably over the past decade; accordingly, in disorders such as heart failure, central apnea is viewed as a form of breathing instability, manifesting as recurrent cycles of apnea/hypopnea, alternating with hyperpnea. In other words, ventilatory control operates as a negative-feedback closed-loop system to maintain homeostasis of blood gas tensions within a relatively narrow physiologic range, principally PaCO2. Therefore, many authors have adopted the engineering concept of "loop gain" (LG) as a measure of ventilatory instability and susceptibility to central apnea. Increased LG promotes breathing instabilities in a number of medical disorders. In some other conditions, such as with use of opioids, central apnea occurs due to inhibition of rhythm generation within the brainstem. This review will address the pathogenesis, pathophysiologic classification, and the multitude of clinical conditions that are associated with central apnea, and highlight areas of uncertainty.
Topics: Humans; Sleep Apnea, Central; Hypocapnia; Respiration; Sleep; Heart Failure
PubMed: 35551411
DOI: 10.1093/sleep/zsac113 -
Archivos Argentinos de Pediatria Oct 2020Cerebral edema (CE) is the most severe complication of diabetic ketoacidosis (DKA) in children. There is no accurate knowledge of CE pathogenesis and its onset has been...
INTRODUCTION
Cerebral edema (CE) is the most severe complication of diabetic ketoacidosis (DKA) in children. There is no accurate knowledge of CE pathogenesis and its onset has been related to intravenous rehydration therapy during the initial treatment.
OBJECTIVES
To estimate the prevalence of CE among DKA patients treated at Hospital General de Niños Pedro de Elizalde with intravenous rehydration and analyze potential risk factors for the development of CE.
MATERIALS AND METHODS
Cross-sectional prevalence study and exploratory analysis to compare clinical and laboratory characteristics between patients with and without CE. Patients aged 1-18 years hospitalized with the diagnosis of DKA between January 1st, 2005 and December 31st, 2014 were included.
RESULTS
A total of 693 DKA events from 561 medical records were analyzed. Ten patients had evidence of CE (1.44 %; 95 % confidence interval: 0.8-2.6). Patients with CE had higher serum urea levels (p < 0.001), lower carbon dioxide pressure (p < 0.001), and lower serum sodium levels (p < 0.001) than those without CE.
CONCLUSION
The prevalence of CE among DKA patients was 1.44 %, smaller than that reported in our country (1.8 %). The risk factors at admission associated with CE development were high serum urea levels, hyponatremia, and hypocapnia.
Topics: Adolescent; Argentina; Brain Edema; Child; Child, Preschool; Cross-Sectional Studies; Diabetic Ketoacidosis; Female; Fluid Therapy; Humans; Hypocapnia; Hyponatremia; Infant; Male; Prevalence; Risk Factors; Urea
PubMed: 32924396
DOI: 10.5546/aap.2020.eng.332 -
British Journal of Anaesthesia Feb 2023Previous studies indicated an association between impaired cerebral perfusion and post-procedural neurological disorders. We investigated whether intra-procedural...
BACKGROUND
Previous studies indicated an association between impaired cerebral perfusion and post-procedural neurological disorders. We investigated whether intra-procedural hypoxaemia or hypocapnia are associated with delirium after surgery.
METHODS
Inpatients ≥60 yr of age undergoing anaesthesia for surgical or interventional procedures between 2009 and 2020 at an academic healthcare network in the USA (Massachusetts) were included in this hospital registry study. The primary exposure was intra-procedural hypoxaemia, defined as peripheral oxygen saturation <90% for >2 cohering min. The co-primary exposure was hypocapnia during general anaesthesia, defined as end-tidal carbon dioxide pressure ≤25 mm Hg for >5 cohering min. The primary outcome was delirium within 7 days after surgery.
RESULTS
Of 71 717 included patients, 1702 (2.4%) developed postoperative delirium, and hypoxaemia was detected in 2532 (3.5%). Of 42 894 patients undergoing general anaesthesia, 532 (1.2%) experienced hypocapnia. The occurrence of either hypoxaemia (adjusted odds ratio [OR]=1.71; 95% confidence interval [CI], 1.40-2.07; P<0.001) or hypocapnia (OR=1.77; 95% CI, 1.30-2.41; P<0.001) was associated with a higher risk of delirium within 7 days. Both associations were dependent on the magnitude, and increased with event duration (OR=1.03; 95% CI, 1.02-1.04; P<0.001 and OR=1.01; 95% CI, 1.00-1.01; P=0.005, for each minute increase in the longest continuous episode, respectively). There was no association between occurrence of hypercapnia and postoperative delirium (OR=1.24; 95% CI, 0.90-1.71; P=0.181).
CONCLUSIONS
Intra-procedural hypoxaemia and hypocapnia were dose-dependently associated with a higher risk of postoperative delirium. These findings support maintaining normal gas exchange to avoid postoperative neurological disorders.
Topics: Humans; Aged; Emergence Delirium; Hypocapnia; Postoperative Complications; Hypoxia; Nervous System Diseases
PubMed: 36192221
DOI: 10.1016/j.bja.2022.08.032 -
Critical Care (London, England) 2010Carbon dioxide is a waste product of aerobic cellular respiration in all aerobic life forms. PaCO2 represents the balance between the carbon dioxide produced and that... (Review)
Review
Carbon dioxide is a waste product of aerobic cellular respiration in all aerobic life forms. PaCO2 represents the balance between the carbon dioxide produced and that eliminated. Hypocapnia remains a common - and generally underappreciated - component of many disease states, including early asthma, high-altitude pulmonary edema, and acute lung injury. Induction of hypocapnia remains a common, if controversial, practice in both adults and children with acute brain injury. In contrast, hypercapnia has traditionally been avoided in order to keep parameters normal. More recently, advances in our understanding of the role of excessive tidal volume has prompted clinicians to use ventilation strategies that result in hypercapnia. Consequently, hypercapnia has become increasingly prevalent in the critically ill patient. Hypercapnia may play a beneficial role in the pathogenesis of inflammation and tissue injury, but may hinder the host response to sepsis and reduce repair. In contrast, hypocapnia may be a pathogenic entity in the setting of critical illness. The present paper reviews the current clinical status of low and high PaCO2 in the critically ill patient, discusses the insights gained to date from studies of carbon dioxide, identifies key concerns regarding hypocapnia and hypercapnia, and considers the potential clinical implications for the management of patients with acute lung injury.
Topics: Carbon Dioxide; Critical Illness; Humans; Hypocapnia
PubMed: 20497620
DOI: 10.1186/cc8926 -
Journal of Applied Physiology... Apr 2014This review summarizes evidence in humans for an association between hyperventilation (HV)-induced hypocapnia and a reduction in cerebral perfusion leading to syncope... (Review)
Review
This review summarizes evidence in humans for an association between hyperventilation (HV)-induced hypocapnia and a reduction in cerebral perfusion leading to syncope defined as transient loss of consciousness (TLOC). The cerebral vasculature is sensitive to changes in both the arterial carbon dioxide (PaCO2) and oxygen (PaO2) partial pressures so that hypercapnia/hypoxia increases and hypocapnia/hyperoxia reduces global cerebral blood flow. Cerebral hypoperfusion and TLOC have been associated with hypocapnia related to HV. Notwithstanding pronounced cerebrovascular effects of PaCO2 the contribution of a low PaCO2 to the early postural reduction in middle cerebral artery blood velocity is transient. HV together with postural stress does not reduce cerebral perfusion to such an extent that TLOC develops. However when HV is combined with cardiovascular stressors like cold immersion or reduced cardiac output brain perfusion becomes jeopardized. Whether, in patients with cardiovascular disease and/or defect, cerebral blood flow cerebral control HV-induced hypocapnia elicits cerebral hypoperfusion, leading to TLOC, remains to be established.
Topics: Age Factors; Blood Flow Velocity; Carbon Dioxide; Cerebrovascular Circulation; Chemoreceptor Cells; Humans; Hyperventilation; Hypocapnia; Middle Cerebral Artery; Oxygen; Syncope
PubMed: 24265279
DOI: 10.1152/japplphysiol.00637.2013 -
Minerva Anestesiologica Jan 2015The mortality of postcardiac arrest patients has gradually reduced in years but it still is as high as 50%, despite advancements in the diagnostic and therapeutic... (Review)
Review
The mortality of postcardiac arrest patients has gradually reduced in years but it still is as high as 50%, despite advancements in the diagnostic and therapeutic approaches, i.e. revascularization and therapeutic moderate hypothermia. However, recent evidence suggests that other therapeutic interventions aimed to minimize progressive deterioration of the brain and other organs function might be helpful to reduce in-hospital mortality and improve neurologic outcome as well as quality of life after cardiac arrest. In this article, we discuss the role of ventilator management on the prognosis after cardiac arrest. We performed a meta-analysis showing that in adult patients not only hypoxia but also hyperoxia was associated with higher in-hospital mortality, while hypercapnia and hypocapnia worse neurologic outcome. In pediatric patients, hypoxia and hyperoxia were not associated with higher in-hospital mortality, while hypocapnia and hypercabia with higher in-hospital mortality worse neurologic outcome. We propose a general bundle for ventilator treatment after cardiac arrest, including: 1) therapeutic hypothermia for 12-24 hours; 2) mean arterial pressure ≥65-75 mmHg; 3) PaO2 between 60-200 mmHg and PCO2 between 30 and 50 mmHg; 4) protective MV with tidal volume of 6-8 mL/kg and positive end expiratory pressure of between 5-10 cmH2O; 5) monitoring of respiratory mechanics, extravascular lung water, hemodynamics, non-invasive transcranial Doppler and intracranial pressure monitoring; and 6) others supportive care, i.e. blood sugar and seizures control.
Topics: Cardiopulmonary Resuscitation; Heart Arrest; Humans; Respiration, Artificial; Respiratory Mechanics
PubMed: 24642487
DOI: No ID Found -
Pediatric Research Apr 2022There is no consensus on the optimal pCO levels in the newborn. We reviewed the effects of hypercapnia and hypocapnia and existing carbon dioxide thresholds in neonates.... (Review)
Review
There is no consensus on the optimal pCO levels in the newborn. We reviewed the effects of hypercapnia and hypocapnia and existing carbon dioxide thresholds in neonates. A systematic review was conducted in accordance with the PRISMA statement and MOOSE guidelines. Two hundred and ninety-nine studies were screened and 37 studies included. Covidence online software was employed to streamline relevant articles. Hypocapnia was associated with predominantly neurological side effects while hypercapnia was linked with neurological, respiratory and gastrointestinal outcomes and Retinpathy of prematurity (ROP). Permissive hypercapnia did not decrease periventricular leukomalacia (PVL), ROP, hydrocephalus or air leaks. As safe pCO ranges were not explicitly concluded in the studies chosen, it was indirectly extrapolated with reference to pCO levels that were found to increase the risk of neonatal disease. Although PaCO ranges were reported from 2.6 to 8.7 kPa (19.5-64.3 mmHg) in both term and preterm infants, there are little data on the safety of these ranges. For permissive hypercapnia, parameters described for bronchopulmonary dysplasia (BPD; PaCO 6.0-7.3 kPa: 45.0-54.8 mmHg) and congenital diaphragmatic hernia (CDH; PaCO ≤ 8.7 kPa: ≤65.3 mmHg) were identified. Contradictory findings on the effectiveness of permissive hypercapnia highlight the need for further data on appropriate CO parameters and correlation with outcomes. IMPACT: There is no consensus on the optimal pCO levels in the newborn. There is no consensus on the effectiveness of permissive hypercapnia in neonates. A safe range of pCO of 5-7 kPa was inferred following systematic review.
Topics: Carbon Dioxide; Humans; Hypercapnia; Hypocapnia; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Respiration, Artificial
PubMed: 34230621
DOI: 10.1038/s41390-021-01473-y -
Journal of Applied Physiology... Jan 2023
PubMed: 36592407
DOI: 10.1152/japplphysiol.00699.2022