Journal articles on the topic 'Hypercapnia – Pathophysiology'
To see the other types of publications on this topic, follow the link: Hypercapnia – Pathophysiology.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Hypercapnia – Pathophysiology.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Marcus, Carole L., Janita Lutz, John L. Carroll, and Owen Bamford. "Arousal and ventilatory responses during sleep in children with obstructive sleep apnea." Journal of Applied Physiology 84, no. 6 (June 1, 1998): 1926–36. http://dx.doi.org/10.1152/jappl.1998.84.6.1926.
Full textAbstract:
Abnormal central regulation of upper airway muscles may contribute to the pathophysiology of the childhood obstructive sleep apnea syndrome (OSAS). We hypothesized that this was secondary to global abnormalities of ventilatory control during sleep. We therefore compared the response to chemical stimuli during sleep between prepubertal children with OSAS and controls. Patients with OSAS aroused at a higher[Formula: see text] (58 ± 2 vs. 60 ± 5 Torr, P < 0.05); those with the highest apnea index had the highest arousal threshold ( r = 0.52, P < 0.05). The hypercapnic arousal threshold decreased after treatment. For all subjects, hypoxia was a poor stimulus to arousal, whereas hypercapnia and, particularly, hypoxic hypercapnia were potent stimuli to arousal. Hypercapnia resulted in decreased airway obstruction in OSAS. Ventilatory responses were similar between patients with OSAS and controls; however, the sample size was small. We conclude that children with OSAS have slightly blunted arousal responses to hypercapnia. However, the overall ventilatory and arousal responses are normal in children with OSAS, indicating that a global deficit in respiratory drive is not a major factor in the etiology of childhood OSAS. Nevertheless, subtle abnormalities in ventilatory control may exist.
2
Deacon, Naomi L., R. Doug McEvoy, Daniel L. Stadler, and Peter G. Catcheside. "Intermittent hypercapnic hypoxia during sleep does not induce ventilatory long-term facilitation in healthy males." Journal of Applied Physiology 123, no. 3 (September 1, 2017): 534–43. http://dx.doi.org/10.1152/japplphysiol.01005.2016.
Full textAbstract:
Intermittent hypoxia-induced ventilatory neuroplasticity is likely important in obstructive sleep apnea pathophysiology. Although concomitant CO2levels and arousal state critically influence neuroplastic effects of intermittent hypoxia, no studies have investigated intermittent hypercapnic hypoxia effects during sleep in humans. Thus the purpose of this study was to investigate if intermittent hypercapnic hypoxia during sleep induces neuroplasticity (ventilatory long-term facilitation and increased chemoreflex responsiveness) in humans. Twelve healthy males were exposed to intermittent hypercapnic hypoxia (24 × 30 s episodes of 3% CO2and 3.0 ± 0.2% O2) and intermittent medical air during sleep after 2 wk washout period in a randomized crossover study design. Minute ventilation, end-tidal CO2, O2saturation, breath timing, upper airway resistance, and genioglossal and diaphragm electromyograms were examined during 10 min of stable stage 2 sleep preceding gas exposure, during gas and intervening room air periods, and throughout 1 h of room air recovery. There were no significant differences between conditions across time to indicate long-term facilitation of ventilation, genioglossal or diaphragm electromyogram activity, and no change in ventilatory response from the first to last gas exposure to suggest any change in chemoreflex responsiveness. These findings contrast with previous intermittent hypoxia studies without intermittent hypercapnia and suggest that the more relevant gas disturbance stimulus of concomitant intermittent hypercapnia frequently occurring in sleep apnea influences acute neuroplastic effects of intermittent hypoxia. These findings highlight the need for further studies of intermittent hypercapnic hypoxia during sleep to clarify the role of ventilatory neuroplasticity in the pathophysiology of sleep apnea.NEW & NOTEWORTHY Both arousal state and concomitant CO2levels are known modulators of the effects of intermittent hypoxia on ventilatory neuroplasticity. This is the first study to investigate the effects of combined intermittent hypercapnic hypoxia during sleep in humans. The lack of neuroplastic effects suggests a need for further studies more closely replicating obstructive sleep apnea to determine the pathophysiological relevance of intermittent hypoxia-induced ventilatory neuroplasticity.
3
Goossens, Liesbet, Nicole Leibold, Ronald Peeters, Gabriel Esquivel, Inge Knuts, Walter Backes, Machteld Marcelis, Paul Hofman, Eric Griez, and Koen Schruers. "Brainstem response to hypercapnia: A symptom provocation study into the pathophysiology of panic disorder." Journal of Psychopharmacology 28, no. 5 (March 19, 2014): 449–56. http://dx.doi.org/10.1177/0269881114527363.
Full text
4
Mukhlis, Mokhammad, and Arief Bakhtiar. "Obstructive Sleep Apneu (OSA), Obesitas Hypoventilation Syndrome (OHS) dan Gagal Napas." Jurnal Respirasi 1, no. 3 (April 1, 2019): 94. http://dx.doi.org/10.20473/jr.v1-i.3.2015.94-102.
Full textAbstract:
Background: Obstructive sleep apnea (OSA) is a state of the occurrence of upper airway obstruction periodically during sleep that causes breathing to stop intermittently, either complete (apnea) or partial (hipopnea). Obesity hypoventilation syndrome (OHS) is generally defined as a combination of obesity (BMI ≥ 30 kg / mc) with arterial hypercapnia while awake (PaCO2 > 45 mmHg) in the absence of other causes of hypoventilation. Purpose: In order for the pulomonologis can understand the pathogenesis and pathophysiology of OSA and its complications. Literature review: Several studies have been expressed about the link between OSA, OHS with respiratory failure disease. Pathophysiology of OSA, OHS in respiratory failure were difficult to detect, can cause respiratory failure disease management becomes less effective. Conclusion: A good understanding can help with the diagnosis and management of the appropriate conduct to prevent complications of respiratory failure associated with OSA.
5
Bykov, Yu V., and V. A. Baturin. "Pathophysiological Mechanisms of Cerebral Edema in Diabetic Ketoacidosis in Pediatric Practice." Medicina 9, no. 1 (2021): 116–27. http://dx.doi.org/10.29234/2308-9113-2021-9-1-116-127.
Full textAbstract:
Diabetic ketoacidosis is a frequent complication of type 1 diabetes mellitus in children and adolescents. One of the leading causes of death in this pathology is cerebral edema. This complication is often asymptomatic, which makes it difficult to diagnose. The main risk factors for cerebral edema in children include the true factors (low partial pressure of carbon dioxide, high blood urea nitrogen, concomitant psychiatric pathology, etc.) and iatrogenic factors (large volume of infusion therapy, rapid decrease in blood glucose levels, administration of bicarbonate, etc.). The pathophysiology of this complication is not yet fully understood. The main pathophysiological elements of cerebral edema in children with DKA include the disruption of blood-brain barrier permeability, edema of brain cells, and dysfunction of cell membranes. Important roles are also played by hypercapnia and reduction of osmotic pressure. Based on the character of pathophysiologic changes, cerebral edema in children and adolescents with DKA is subdivided into vasogenic and cytotoxic. Gaining a better understanding of the pathophysiological mechanisms of this complication will increase the quality of care provided in pediatric practice.
6
Bykov, Yu V., and V. A. Baturin. "Pathophysiological Mechanisms of Cerebral Edema in Diabetic Ketoacidosis in Pediatric Practice." Medicina 9, no. 4 (2021): 54–65. http://dx.doi.org/10.29234/2308-9113-2021-9-4-54-65.
Full textAbstract:
Diabetic ketoacidosis is a frequent complication of type 1 diabetes mellitus in children and adolescents. One of the leading causes of death in this pathology is cerebral edema. This complication is often asymptomatic, which makes it difficult to diagnose. The main risk factors for cerebral edema in children include the true factors (low partial pressure of carbon dioxide, high blood urea nitrogen, concomitant psychiatric pathology, etc.) and iatrogenic factors (large volume of infusion therapy, rapid decrease in blood glucose levels, administration of bicarbonate, etc.). The pathophysiology of this complication is not yet fully understood. The main pathophysiological elements of cerebral edema in children with DKA include the disruption of blood-brain barrier permeability, edema of brain cells, and dysfunction of cell membranes. Important roles are also played by hypercapnia and reduction of osmotic pressure. Based on the character of pathophysiologic changes, cerebral edema in children and adolescents with DKA is subdivided into vasogenic and cytotoxic. Gaining a better understanding of the pathophysiological mechanisms of this complication will increase the quality of care provided in pediatric practice.
7
Totaro, R., C. Marini, G. De Matteis, M. Di Napoil, and A. Carolei. "Cerebrovascular Reactivity in Migraine During Headache-Free Intervals." Cephalalgia 17, no. 3 (May 1997): 191–94. http://dx.doi.org/10.1046/j.1468-2982.1997.1703191.x.
Full textAbstract:
Alterations of intracranial vessel tone have been implicated in the pathophysiology of migraine. The cerebrovascular reactivity was measured by means of transcranial Doppler in 60 migraine patients with ( n = 30) or without aura ( n = 30) during the headache-free interval and in 30 healthy controls. The vasomotor response was evaluated during hypercapnia induced by inhalation of a mixture of CO2 5% and O2 95% and during hypocapnia obtained after voluntary hyperventilation. To improve the power of the study in detecting possible abnormalities of cerebrovascular reactivity, two different measures were performed at 1 week intervals in migraine patients and controls. Reactivity index values during CO2 inhalation were significantly different ( p=0.01) among the three groups during the first and second measurements; in particular, lower values were found in patients suffering from migraine without aura with respect to controls ( p<0.05, Scheffe's test). Values of reactivity index obtained following induction of hypocapnia did not differ between migraine patients and controls (all p values >0.05). Our data suggest a reduced vasodilatory response to hypercapnia of cerebral arterioles in patients suffering from migraine without aura with respect to controls that might be related to baseline arteriolar vasodilation.
8
Levitzky, Michael G. "Using the pathophysiology of obstructive sleep apnea to teach cardiopulmonary integration." Advances in Physiology Education 32, no. 3 (September 2008): 196–202. http://dx.doi.org/10.1152/advan.90137.2008.
Full textAbstract:
Obstructive sleep apnea (OSA) is a common disorder of upper airway obstruction during sleep. The effects of intermittent upper airway obstruction include alveolar hypoventilation, altered arterial blood gases and acid-base status, and stimulation of the arterial chemoreceptors, which leads to frequent arousals. These arousals disturb sleep architecture and cause hypersomnolence. Chronic intermittent alveolar and systemic arterial hypoxia-hypercapnia can cause pulmonary and systemic hypertension, with effects on the right and left ventricles, and even the renal system. The pathophysiology of OSA can therefore be used to review and integrate many topics in pulmonary and cardiovascular physiology in the context of problem-based learning, a guided discussion, or a formal lecture. The discussion begins with a case scenario, followed by a definition of the disorder, the common symptoms and signs of OSA, and a description of an apneic event. These are related to the physiology of the upper airway in OSA, normal alterations in the respiratory system during sleep, the effects of apnea on gas exchange and arterial blood gases, and the cardiovascular consequences of alterations in alveolar and systemic arterial Po2 and Pco2. The treatment of OSA, particularly how the use of continuous positive airway pressure relates to the pathophysiology of the disorder, is discussed briefly.
9
Slobod, Douglas, Anna Damia, Marco Leali, Elena Spinelli, and Tommaso Mauri. "Pathophysiology and Clinical Meaning of Ventilation-Perfusion Mismatch in the Acute Respiratory Distress Syndrome." Biology 12, no. 1 (December 30, 2022): 67. http://dx.doi.org/10.3390/biology12010067.
Full textAbstract:
Acute respiratory distress syndrome (ARDS) remains an important clinical challenge with a mortality rate of 35–45%. It is being increasingly demonstrated that the improvement of outcomes requires a tailored, individualized approach to therapy, guided by a detailed understanding of each patient’s pathophysiology. In patients with ARDS, disturbances in the physiological matching of alveolar ventilation (V) and pulmonary perfusion (Q) (V/Q mismatch) are a hallmark derangement. The perfusion of collapsed or consolidated lung units gives rise to intrapulmonary shunting and arterial hypoxemia, whereas the ventilation of non-perfused lung zones increases physiological dead-space, which potentially necessitates increased ventilation to avoid hypercapnia. Beyond its impact on gas exchange, V/Q mismatch is a predictor of adverse outcomes in patients with ARDS; more recently, its role in ventilation-induced lung injury and worsening lung edema has been described. Innovations in bedside imaging technologies such as electrical impedance tomography readily allow clinicians to determine the regional distributions of V and Q, as well as the adequacy of their matching, providing new insights into the phenotyping, prognostication, and clinical management of patients with ARDS. The purpose of this review is to discuss the pathophysiology, identification, consequences, and treatment of V/Q mismatch in the setting of ARDS, employing experimental data from clinical and preclinical studies as support.
10
Mingbunjerdsuk, Prompan, Noah Andrews, Lu Wang, Loutfi Aboussouan, Reena Mehra, Madeleine Grigg-Damberger, and Nancy Foldvary-Schaefer. "802 Seizure-Associated Central Respiratory Events: What’s Sleep Go To Do With It?" Sleep 44, Supplement_2 (May 1, 2021): A312. http://dx.doi.org/10.1093/sleep/zsab072.799.
Full textAbstract:
Abstract Introduction Seizure-related respiratory dysfunction has been reported in patients with epilepsy(PWE) on scalp EEG. We assessed this in Stereo-EEG(SEEG) recordings in patients with pharmacoresistant focal epilepsy. Methods PWE undergoing SEEG wore temperature/pressure-based airflow,RIP belts, SpO2, and EtCO2/TcpCO2. Interpretable recordings required SpO2 and at least one airflow and effort channel. Respiratory events including apneas, hypopneas(3%) and central pauses (5 to<10sec). Respiratory events, respiratory rate(RR), SpO2 nadir, total desaturation time, Peak EtCO2/TcpCO2, and hypercapnia duration were analyzed surrounding seizures. Frequency and duration of central events were compared in sleep-onset and awake seizures. Linear mixed-effects models evaluated relationships between respiratory variables and the frequency and duration of central events associated with seizures and compared respiratory variables between seizures with and without events. Results 44 seizures were recorded in 23 patients. Seizures were focal-onset in 79.5%(n=35), GTC in 20.5%(9). Respiratory events accompanied 61.4%(27) of the seizures with median duration/seizure duration of 0.40(IQR: 0.27, 0.61). Of the 47 respiratory events, 42 were central events, and 66.6%(28) were central apneas. Respiratory events occurred during the seizure in 73.8%, postictal in 26.2%; median SpO2 nadir was 90%(77.0, 93.0), total desaturation duration 104.3(50.3, 195.0)sec, peak TcpCO2 41.3(38.7, 44.8) mmHg, hypercapnia duration 157.6(51.0, 367.9) sec, and ictal-postictal RR change 3.3 ± 4.0bpm. For every 1 sec duration increase in central event duration, there was a significant increase in peak TcpCO2 0.35(95%CI [0.09,0.62],p=0.015) and TcpCO2 change 0.25(95%CI [0.02,0.49],p=0.037). Presence of central events were associated with increased peak TcpCO2(9.82[3.77,15.9], p=0.006). Seizures with central events trended greater changes in RR, SpO2, and EtCO2/TcpCO2, desaturation and hypercapnia time, with negative changes in SpO2 nadir. No significant difference on central event frequency was found between sleep-onset and awake seizures. Conclusion Central events including apneas and pauses are common in focal seizures arising from sleep and wake and are associated with hypercapnia. In addition to the significant association between TcpCO2 and the frequency and duration of central events, there is a positive trend of association of other respiratory dysfunction parameters. These findings suggest that central events may lead to a cascade of respiratory disturbance that may participate in the pathophysiology of sudden unexplained death in epilepsy. Support (if any):
11
Athayde, Rodolfo Augusto Bacelar de, José Ricardo Bandeira de Oliveira Filho, Geraldo Lorenzi Filho, and Pedro Rodrigues Genta. "Obesity hypoventilation syndrome: a current review." Jornal Brasileiro de Pneumologia 44, no. 6 (December 2018): 510–18. http://dx.doi.org/10.1590/s1806-37562017000000332.
Full textAbstract:
ABSTRACT Obesity hypoventilation syndrome (OHS) is defined as the presence of obesity (body mass index ≥ 30 kg/m²) and daytime arterial hypercapnia (PaCO2 ≥ 45 mmHg) in the absence of other causes of hypoventilation. OHS is often overlooked and confused with other conditions associated with hypoventilation, particularly COPD. The recognition of OHS is important because of its high prevalence and the fact that, if left untreated, it is associated with high morbidity and mortality. In the present review, we address recent advances in the pathophysiology and management of OHS, the usefulness of determination of venous bicarbonate in screening for OHS, and diagnostic criteria for OHS that eliminate the need for polysomnography. In addition, we review advances in the treatment of OHS, including behavioral measures, and recent studies comparing the efficacy of continuous positive airway pressure with that of noninvasive ventilation.
12
Cappadona, Francesca, Elisa Costa, Laura Mallia, Filippo Sangregorio, Lorenzo Nescis, Valentina Zanetti, Elisa Russo, Stefania Bianzina, Francesca Viazzi, and Pasquale Esposito. "Extracorporeal Carbon Dioxide Removal: From Pathophysiology to Clinical Applications; Focus on Combined Continuous Renal Replacement Therapy." Biomedicines 11, no. 1 (January 5, 2023): 142. http://dx.doi.org/10.3390/biomedicines11010142.
Full textAbstract:
Lung-protective ventilation (LPV) with low tidal volumes can significantly increase the survival of patients with acute respiratory distress syndrome (ARDS) by limiting ventilator-induced lung injuries. However, one of the main concerns regarding the use of LPV is the risk of developing hypercapnia and respiratory acidosis, which may limit the clinical application of this strategy. This is the reason why different extracorporeal CO2 removal (ECCO2R) techniques and devices have been developed. They include low-flow or high-flow systems that may be performed with dedicated platforms or, alternatively, combined with continuous renal replacement therapy (CRRT). ECCO2R has demonstrated effectiveness in controlling PaCO2 levels, thus allowing LPV in patients with ARDS from different causes, including those affected by Coronavirus disease 2019 (COVID-19). Similarly, the suitability and safety of combined ECCO2R and CRRT (ECCO2R–CRRT), which provides CO2 removal and kidney support simultaneously, have been reported in both retrospective and prospective studies. However, due to the complexity of ARDS patients and the limitations of current evidence, the actual impact of ECCO2R on patient outcome still remains to be defined. In this review, we discuss the main principles of ECCO2R and its clinical application in ARDS patients, in particular looking at clinical experiences of combined ECCO2R–CRRT treatments.
13
Marion, Tara L., and Wanda T. Bradshaw. "Congenital Central Hypoventilation Syndrome and the PHOX2B Gene Mutation." Neonatal Network 30, no. 6 (2011): 397–401. http://dx.doi.org/10.1891/0730-0832.30.6.397.
Full textAbstract:
Congenital central hypoventilation syndrome (CCHS) is a rare syndrome of dysfunction of the autonomic nervous system characterized by a decreased response to hypercarbia. It is a disorder in which affected individuals fail to breathe during sleep despite progressive hypercapnia and hypoxia. Infants simply fall asleep and quit breathing. They are found by their parents or caregivers blue and lifeless. CCHS is an autosomal dominant disease. It has been linked with tumors of neural crest origin, segmental aganglionosis of the colon, and diffuse autonomic dysregulation but can occur alone. Discovery of the genetic link between the paired-like homeobox 2B (PHOX2B) genetic mutations and CCHS represents a breakthrough in the diagnosis of CCHS, association of mutated alleles with disease severity, and clues to the pathophysiology responsible for the disorder. Early genetic screening and intervention can provide the families of these infants with hope for achieving a normal life.
14
Sitompul, Harles, and Aura Ihsaniar. "Obesity Hypoventilation Syndrome." Journal of Anesthesiology and Clinical Research 3, no. 1 (July 6, 2022): 284–91. http://dx.doi.org/10.37275/jacr.v3i1.206.
Full textAbstract:
Obesity Hypoventilation Syndrome or commonly abbreviated as OHS, is a respiratory disorder that often occurs in patients characterized by decreased oxygen levels and increased carbon dioxide in the blood. Based on the criteria of the World Health Organization (WHO), the definition of obesity is if the BMI is equal to or greater than 30 kg/m2. The classification of obesity is BMI 30-34.9 kg/m2, 35-39.9 kg/m2 and > 40 kg/m2. The pathophysiology of OHS is still not fully known with certainty. Severe obesity causes an increase in the burden on the respiratory system, weakness of the respiratory muscles, leptin resistance, and respiratory disturbances during sleep, causing a decrease in the sensitivity of the ventilation center response, which can lead to hypoventilation and hypercapnia. Basically, there are six points of OHS management, including a weight loss program, oxygen therapy, positive pressure ventilation, pharmacotherapy, tracheostomy, and management of OHS complications.
15
Gupta, Anju, Yamini Dudeja, Rashmi Ramachandran, and Rajeshwari Subramaniam. "Anaesthetic considerations in a child with methylmalonic acidemia and its literature review." BMJ Case Reports 13, no. 12 (December 2020): e237270. http://dx.doi.org/10.1136/bcr-2020-237270.
Full textAbstract:
Methyl malonyl coenzyme A mutase deficiency is a rare autosomal inherited inborn error in branched-chain amino acid metabolism characterised by the accumulation of methylmalonic acids. There is relative paucity of literature regarding anaesthetic management of these children presenting for incidental major abdominal surgery. Preoperative management includes goal-directed correction of dehydration, metabolic acidosis and hyperammonemia. Anaesthetic goals include avoidance of factors that can trigger metabolic crisis like hypercapnia, hypothermia, hypoxia, surgical stress, hypovolaemia, hypotension and so on. Herein, we are reporting the anaesthetic management of a 17-month-old child with methylmalonic acidemia (MMA) posted for a major upper abdominal surgery for excision of an adrenal mass, which was incidentally diagnosed during admission for an episode of metabolic crisis. We aim to highlight the specific nuances of pathophysiology of the disease, preoperative optimisation, anaesthetic considerations, role of advanced monitoring and regional anaesthesia and current literature on the management of patients with MMA.
16
Merle, Evan, Saad Zaatari, Rory Spiegel, and Mabrouk Bahloul. "Is It the pH That Matters? Challenging the Pathophysiology of Acidemia in a Case of Severe Hypercapnia Secondary to Intraoperative CO2 Insufflation." Case Reports in Critical Care 2020 (September 27, 2020): 1–4. http://dx.doi.org/10.1155/2020/1898759.
Full textAbstract:
Background. Acidemia has been long thought to lead to hemodynamic compromise. While some literature to date challenges this idea, there is no consensus on this topic. Case Summary. To our knowledge, this is the most severe case of hypercapnia and acidosis due to carbon dioxide (CO2) insufflation during laparoscopy reported in the literature. Remarkably, this patient remained hemodynamically normal despite having a blood pH below 6.81. This prompts a wider discussion about the effects of blood pH on human physiology. Most patients who present acidotic are critically ill and have confounding underlying metabolic or respiratory pathophysiology driving their illness. In this case, the patient experienced no respiratory insult leading to an increase in blood CO2 but rather had CO2 iatrogenically introduced into the circulatory system, effectively detaching the deleterious effects of CO2 from the respiratory pathologies that so often cause its accumulation. Conclusion. This raises the question, in patients with severe acidosis and hemodynamic compromise, is acidosis a symptom of the underlying process, or is the acidosis itself causing harm?
17
Tigyi, G., L. Hong, M. Yakubu, H. Parfenova, M. Shibata, and C. W. Leffler. "Lysophosphatidic acid alters cerebrovascular reactivity in piglets." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 5 (May 1, 1995): H2048—H2055. http://dx.doi.org/10.1152/ajpheart.1995.268.5.h2048.
Full textAbstract:
Effects of the lipid mediator lysophosphatidic acid (LPA) were studied on the cerebral circulation of newborn pigs using closed cranial windows. Topical application of synthetic LPA caused dose-dependent vasoconstriction and inhibited vasodilation to hypercapnia and isoproterenol. These vasodilators elicited a rise in the adenosine 3',5'-cyclic monophosphate (cAMP) content of the cerebrospinal fluid, which was inhibited dose dependently by LPA. Pertussis toxin (1 microgram/ml) completely abolished LPA-induced vasoconstriction and the altered vascular reactivity, and LPA no longer decreased cAMP. Electrophysiological recording of currents evoked by LPA-like lipids in Xenopus oocytes showed that cerebrospinal fluid is normally devoid of LPA-like factors. In contrast, the amount of LPA-like factors generated 4 days after intrathecal injection of autologous blood was in the range of 1-10 microM LPA equivalents. The data indicate that LPA-like bioactive mediators were generated in an intracranial hematoma model and that these phospholipids might play a role in the pathophysiology of altered vascular reactivity often found in posthemorrhagic conditions and could also contribute to the development of posthemorrhagic vasoconstriction.
18
Koketsu, Naoki, Michael A. Moskowitz, Hermes A. Kontos, Masayuki Yokota, and Takeo Shimizu. "Chronic Parasympathetic Sectioning Decreases Regional Cerebral Blood Flow during Hemorrhagic Hypotension and Increases Infarct Size after Middle Cerebral Artery Occlusion in Spontaneously Hypertensive Rats." Journal of Cerebral Blood Flow & Metabolism 12, no. 4 (July 1992): 613–20. http://dx.doi.org/10.1038/jcbfm.1992.85.
Full textAbstract:
Regional cerebral blood flow (rCBF) during controlled hemorrhagic hypotension (140–20 mm Hg) was assessed 10–14 days after chronic unilateral sectioning of parasympathetic and/or sensory fibers innervating pial vessels in spontaneously hypertensive rats (SHR). rCBF was measured in the cortical barrel fields bilaterally by laser Doppler blood flowmetry. Immunohistochemistry of middle cerebral artery (MCA) whole mount preparations was used to verify the surgical lesion. During hemorrhagic hypotension, rCBF was equivalent on the two sides in shams, after selective sensory denervation, or in parasympathetically sectioned animals exhibiting small decreases (≤30%) in immunoreactive vasoactive intestinal peptide (VIP)-containing fibers. After chronic parasympathetic denervation, decreases in perfusion pressure were accompanied by greater reductions in rCBF on the lesioned side; changes in vascular resistance were also attenuated on that side. The rCBF response to hypercapnia (Paco2 50 mm Hg), however, was symmetrical and robust. To examine the effects of impaired neurogenic vasodilation on the pathophysiology of cerebral ischemia, infarct size was measured 24 h following tandem MCA occlusion in denervated animals. Infarction volume was larger after selective parasympathetic sectioning (sham, 156 ± 27 vs. 196 ± 32 mm3, respectively) but only in those denervated animals demonstrating ≥40% decrease in immunoreactive VIP-containing fibers within the ipsilateral MCA. Lower than expected blood flow/perfusion pressure in the cortex distal to an occluded blood vessel may relate the observed blood flow responses to the occurrence of larger cortical infarcts in parasympathetically denervated animals. If true, the findings suggest a novel role for neurogenic vasodilation in the pathophysiology of cerebral ischemia and in rCBF regulation within the peri-infarction zone.
19
Segers, J., A. Hadzic, S. Van Boxstael, I. Van Herreweghe, and O. De Fré. "Management of Acute Respiratory Distress Syndrome in COVID-19 Patients." Acta Anaesthesiologica Belgica 73, no. 1 (March 2022): 5–14. http://dx.doi.org/10.56126/73.1.02.
Full textAbstract:
Acute respiratory distress syndrome (ARDS) is a life-threatening condition characterized by an acute, diffuse inflammation leading to pulmonary edema and hypoxemia. The pathophysiology of the lung failure in COVID- 19 ARDS is a combination of the viral infection and the immune response of the host. ARDS due to COVID-19 appears to be similar to the non-COVID-19 ARDS, with exception of hypercoagulability. The mortality due to ARDS remains high and the treatment focuses on supportive measures, such as lung-protective ventilation strategy with small tidal volumes, low driving pressures and PEEP-titration, early consideration of prone positioning and a restrictive fluid management. Oxygen should be titrated, and permissive hypercapnia might be necessary to achieve lung-protective ventilation. The use of extracorporeal membrane oxygenation (ECMO) in COVID-19 ARDS is restricted as a rescue therapy in patients who remain hypoxemic. ECMO should be reserved to experienced ECMO centers. Prophylactic anticoagulant therapy is indicated to reduce the formation of thrombi in the microcirculation of organs, especially in the pulmonary microvasculature. Steroids may reduce the host’s immune response and improve mortality in patients requiring oxygen supplementation or invasive ventilation.
20
Moreton, Fiona C., Breda Cullen, Christian Delles, Celestine Santosh, Rosario L. Gonzalez, Krishna Dani, and Keith W. Muir. "Vasoreactivity in CADASIL: Comparison to structural MRI and neuropsychology." Journal of Cerebral Blood Flow & Metabolism 38, no. 6 (May 24, 2017): 1085–95. http://dx.doi.org/10.1177/0271678x17710375.
Full textAbstract:
Impaired cerebrovascular reactivity precedes histological and clinical evidence of CADASIL in animal models. We aimed to more fully characterise peripheral and cerebral vascular function and reactivity in a cohort of adult CADASIL patients, and explore the associations of these with conventional clinical, imaging and neuropsychological measures. A total of 22 adults with CADASIL gave informed consent to participate in an exploratory study of vascular function in CADASIL. Clinical assessment, comprehensive vascular assessment, MRI and neuropsychological testing were conducted. We measured cerebral vasoreactivity with transcranial Doppler and arterial spin labelling MRI with hypercapnia challenge. Number and volume of lacunes, subcortical hyperintensity volume, microbleeds and normalised brain volume were assessed on MRI. Analysis was exploratory and examined the associations between different markers. Cerebrovascular reactivity measured by ASL correlated with peripheral vasoreactivity measured by flow mediated dilatation. Subjects with ≥5 lacunes were older, with higher carotid intima-media thickness and had impaired cerebral and peripheral vasoreactivity. Subjects with depressive symptoms, disability or delayed processing speed also showed a trend to impaired vasoreactivity. Impaired vasoreactivity and vascular dysfunction may play a significant role in the pathophysiology of CADASIL, and vascular assessments may be useful biomarkers of severity in both longitudinal and clinical trials.
21
Nelson, R. J., S. Perry, A. C. R. Burns, J. Roberts, and J. D. Pickard. "The Effects of Hyponatraemia and Subarachnoid Haemorrhage on the Cerebral Vasomotor Responses of the Rabbit." Journal of Cerebral Blood Flow & Metabolism 11, no. 4 (July 1991): 661–66. http://dx.doi.org/10.1038/jcbfm.1991.118.
Full textAbstract:
Impairment of cerebral autoregulation and development of hyponatraemia are both implicated in the pathogenesis of delayed cerebral ischaemia and infarction following subarachnoid haemorrhage (SAH) but the pathophysiology and interactions involved are not fully understood. We have studied the effects of hyponatraemia and SAH on the cerebral vasomotor responses of the rabbit. Cerebrovascular reactivity to hypercapnia and cerebral autoregulation to trimetaphan-induced hypotension were determined in normal and hyponatraemic rabbits before and 6 days after experimental SAH produced by two intracisternal injections of autologous blood. Hyponatraemia (mean plasma sodium of 119 m M) was induced gradually over 48 h by administration of Desmopressin and intraperitoneal 5% dextrose. Sham animals received normal saline. The cerebrovascular reactivity (% change ±SD in cortical CBF/mm Hg PaCO2, measured by hydrogen clearance) of hyponatraemic (4.8 ± 3.0%) and SAH (1.3 ± 2.0%) animals was significantly less ( p < 0.05) than control (11.6 ± 4.0%) and sham (8 ± 2.0%) animals, whereas the reactivity of hyponatraemic-SAH animals was preserved (9.8 ± 6.0%). Hyponatraemia and SAH alone each significantly impaired CBF autoregulation but their combined effects were not additive. Systemic hyponatraemia impairs normal cerebral vasomotor responses but does not augment the effects of experimental SAH in the rabbit.
22
Burgess, Keith R., Samuel J. E. Lucas, Katie M. E. Burgess, Kate E. Sprecher, Joseph Donnelly, Aparna S. Basnet, Michael M. Tymko, et al. "Increasing cerebral blood flow reduces the severity of central sleep apnea at high altitude." Journal of Applied Physiology 124, no. 5 (May 1, 2018): 1341–48. http://dx.doi.org/10.1152/japplphysiol.00799.2017.
Full textAbstract:
Earlier studies have indicated an important role for cerebral blood flow in the pathophysiology of central sleep apnea (CSA) at high altitude, but were not decisive. To test the hypothesis that pharmacologically altering cerebral blood flow (CBF) without altering arterial blood gas (ABGs) values would alter the severity of CSA at high altitude, we studied 11 healthy volunteers (8M, 3F; 31 ± 7 yr) in a randomized placebo-controlled single-blind study at 5,050 m in Nepal. CBF was increased by intravenous (iv) acetazolamide (Az; 10 mg/kg) plus intravenous dobutamine (Dob) infusion (2–5 μg·kg−1·min−1) and reduced by oral indomethacin (Indo; 100 mg). ABG samples were collected and ventilatory responses to hypercapnia (HCVR) and hypoxia (HVR) were measured by rebreathing and steady-state techniques before and after drug/placebo. Duplex ultrasound of blood flow in the internal carotid and vertebral arteries was used to measure global CBF. The initial 3–4 h of sleep were recorded by full polysomnography. Intravenous Az + Dob increased global CBF by 37 ± 15% compared with placebo ( P < 0.001), whereas it was reduced by 21 ± 8% by oral Indo ( P < 0.001). ABGs and HVR were unchanged in both interventions. HCVR was reduced by 28% ± 43% ( P = 0.1) during intravenous Az ± Dob administration and was elevated by 23% ± 30% ( P = 0.05) by Indo. During intravenous Az + Dob, the CSA index fell from 140 ± 45 (control night) to 48 ± 37 events/h of sleep ( P < 0.001). Oral Indo had no significant effect on CSA. We conclude that increasing cerebral blood flow reduced the severity of CSA at high altitude; the likely mechanism is via a reduction in the background stimulation of central chemoreceptors.NEW & NOTEWORTHY This work is significant because it shows convincingly for the first time in healthy volunteers that increasing cerebral blood flow will reduce the severity of central sleep apnea in a high-altitude model, without the potentially confounding effects of altering partial pressure of arterial carbon dioxide or the ventilatory response to hypoxia. The proposed mechanism of action is that of increasing the removal of locally produced CO2from the central chemoreceptors, causing the reduction in hypercapnic ventilatory response, hence reducing loop gain.
23
Hosford, Patrick S., Natalia Ninkina, Vladimir L. Buchman, Jeffrey C. Smith, Nephtali Marina, and Shahriar SheikhBahaei. "Synuclein Deficiency Results in Age-Related Respiratory and Cardiovascular Dysfunctions in Mice." Brain Sciences 10, no. 9 (August 24, 2020): 583. http://dx.doi.org/10.3390/brainsci10090583.
Full textAbstract:
Synuclein (α, β, and γ) proteins are highly expressed in presynaptic terminals, and significant data exist supporting their role in regulating neurotransmitter release. Targeting the gene encoding α-synuclein is the basis of many animal models of Parkinson’s disease (PD). However, the physiological role of this family of proteins in not well understood and could be especially relevant as interfering with accumulation of α-synuclein level has therapeutic potential in limiting PD progression. The long-term effects of their removal are unknown and given the complex pathophysiology of PD, could exacerbate other clinical features of the disease, for example dysautonomia. In the present study, we sought to characterize the autonomic phenotypes of mice lacking all synucleins (α, β, and γ; αβγ−/−) in order to better understand the role of synuclein-family proteins in autonomic function. We probed respiratory and cardiovascular reflexes in conscious and anesthetized, young (4 months) and aged (18–20 months) αβγ−/− male mice. Aged mice displayed impaired respiratory responses to both hypoxia and hypercapnia when breathing activities were recorded in conscious animals using whole-body plethysmography. These animals were also found to be hypertensive from conscious blood pressure recordings, to have reduced pressor baroreflex gain under anesthesia, and showed reduced termination of both pressor and depressor reflexes. The present data demonstrate the importance of synuclein in the normal function of respiratory and cardiovascular reflexes during aging.
24
Bisogni, Valeria, Giuseppe Maiolino, Giulio Ceolotto, Martino F. Pengo, Rosario Marchese Ragona, Carlo Artusi, Laura Brugnolo, et al. "Design of a study to investigate the mechanisms of obstructive sleep apnoea by means of drug-induced sleep endoscopy." Clinical Chemistry and Laboratory Medicine (CCLM) 57, no. 9 (August 27, 2019): 1406–13. http://dx.doi.org/10.1515/cclm-2019-0113.
Full textAbstract:
Abstract Background Obstructive sleep apnoea (OSA) is an independent risk factor of hypertension and cardiovascular diseases. Recurrent episodes of upper airways collapse during sleep causing blood oxygen desaturation, hypercapnia, and micro-arousals, are known to activate the sympathetic nervous system (SNS). However, whether changes in the renin-angiotensin-aldosterone system and endothelial activation also occur remains contentious. Methods Based on routine use of drug-induced sleep endoscopy (DISE) for the work-up of OSA patients in our centre, we designed a prospective study to investigate the haemodynamic and humoral changes occurring during the apnoeic episodes reproduced in vivo in the course of DISE. Specifically, plasma aldosterone concentration and renin activity, C-terminal fragment of proendothelin-1, as a marker of endothelial damage, and free plasma catecholamines, will be measured at fixed times during DISE. The activity of catechol-O-methyltransferase (COMT), a key catecholamine-inactivating enzyme that has been scantly investigated thus far owing to the lack of commercially available kits, will be also determined by a newly developed high performance liquid chromatography method, which is herein described. Results and conclusions The aim of this study is to provide novel information on the haemodynamic, hormonal, and SNS changes, and also on COMT activity modification concomitantly occurring during apnoea, thus contributing substantively to the understanding of the pathophysiology of OSA.
25
Halimi, Radian Ahmad, and Dewi Yulianti Bisri. "Manajemen Pasien Stroke Perdarahan Spontan dengan Komorbid Penyakit Paru Obstruktif Kronik yang Terjadi Bronkhospasme Intraoperasi." Jurnal Neuroanestesi Indonesia 8, no. 2 (June 25, 2019): 105–11. http://dx.doi.org/10.24244/jni.v8i2.222.
Full textAbstract:
Stroke perdarahan spontan dan penyakit paru obstruktif kronik (chronic obstructive pulmonary disease/COPD) merupakan dua penyakit yang memiliki angka morbiditas dan mortalitas yang paling tinggi di dunia. Kondisi COPD akan meningkatkan resiko terjadinya stroke, selain itu dapat mengakibatkan terjadinya hipoksemia dan hiperkapnia. Seorang pria berusia 62 tahun datang ke unit gawat darurat karena mengalami penurunan kesadaran dan tidak dapat menggerakkan anggota tubuh sebelah kiri sejak 1 hari, pasien memiliki riwayat hipertensi namun tidak rutin meminum obat, pasien memiliki riwayat sering sesak, dan berdasarkan pemeriksaan fisik didapatkan kondisi barrel chest. Berdasarkan pemeriksaan CT-scan kepala didapatkan perdarahan intrakranial spontan pada basal ganglia sinistra. Pasien dilakukan tindakan kraniotomi evakuasi, namun 2 jam setelah dilakukan induksi anestesi terjadi kondisi desaturasi, hiperkapnia, peningkatan tekanan jalan nafas, dan ditemukan wheezing pada kedua lapang paru, kemudian diberikan terapi farmakologis dan non farmakologis untuk mengatasi kondisi bronkospasme. Pascabedah dilakukan pemanjangan ventilasi mekanik hingga pasien memenuhi kriteria untuk dilakukan ekstubasi. Penanganan pasien stroke dengan komorbid COPD membutuhkan pemahaman yang lebih mendalam mengenai interaksi otak dengan fungsi pernafasan akibat perubahan fisiologi dan patofisiologi pasien COPD. Management of Spontaneous Intracranial haemorhage with Comorbids Chronic Obstructive Pulmonary Disease Occurring Intraoperative BronchospasmAbstractStroke and chronic obstructive pulmonary disease (COPD) are the two diseases that have the highest morbidity and mortality rates in the world. COPD conditions will increase the risk of stroke, but it can lead to hypoxemia and hypercapnia. A 62-year-old man came to the emergency room because of a decreased consciousness and was unable to move the left limb since 1 day, the patient had a history of hypertension but did not regularly take medication, the patient had a history of frequent tightness, and based on physical examination was obtained barrel chest condition. Based on a head CT scan, spontaneous intracranial hemorrhage occurs in the left basal ganglia. Evacuation craniotomy was performed, but 2 hours after anesthesia induction occurred conditions of desaturation, hypercapnia, increased airway pressure, and wheezing was found in both lung fields, then given pharmacological and non-pharmacological therapy to overcome the condition of bronchospasm. After surgery, lengthening of mechanical ventilation is done until the patient meets the criteria for extubation. The treatment of stroke patients with co-morbid COPD requires a deeper understanding of brain interactions with respiratory function due to changes in physiology and pathophysiology of COPD patients.
26
Nur, Erfan, Yu-Sok Kim, Jasper Truijen, Eduard J. van Beers, Shyrin C. A. T. Davis, Dees P. Brandjes, Bart J. Biemond, and Johannes J. van Lieshout. "Cerebrovascular reserve capacity is impaired in patients with sickle cell disease." Blood 114, no. 16 (October 15, 2009): 3473–78. http://dx.doi.org/10.1182/blood-2009-05-223859.
Full textAbstract:
Abstract Sickle cell disease (SCD) is associated with a high incidence of ischemic stroke. SCD is characterized by hemolytic anemia, resulting in reduced nitric oxide-bioavailability, and by impaired cerebrovascular hemodynamics. Cerebrovascular CO2 responsiveness is nitric oxide dependent and has been related to an increased stroke risk in microvascular diseases. We questioned whether cerebrovascular CO2 responsiveness is impaired in SCD and related to hemolytic anemia. Transcranial Doppler-determined mean cerebral blood flow velocity (Vmean), near-infrared spectroscopy-determined cerebral oxygenation, and end-tidal CO2 tension were monitored during normocapnia and hypercapnia in 23 patients and 16 control subjects. Cerebrovascular CO2 responsiveness was quantified as Δ% Vmean and Δμmol/L cerebral oxyhemoglobin, deoxyhemoglobin, and total hemoglobin per mm Hg change in end-tidal CO2 tension. Both ways of measurements revealed lower cerebrovascular CO2 responsiveness in SCD patients versus controls (Vmean, 3.7, 3.1-4.7 vs 5.9, 4.6-6.7 Δ% Vmean per mm Hg, P < .001; oxyhemoglobin, 0.36, 0.14-0.82 vs 0.78, 0.61-1.22 Δμmol/L per mm Hg, P = .025; deoxyhemoglobin, 0.35, 0.14-0.67 vs 0.58, 0.41-0.86 Δμmol/L per mm Hg, P = .033; total-hemoglobin, 0.13, 0.02-0.18 vs 0.23, 0.13-0.38 Δμmol/L per mm Hg, P = .038). Cerebrovascular CO2 responsiveness was not related to markers of hemolytic anemia. In SCD patients, impaired cerebrovascular CO2 responsiveness reflects reduced cerebrovascular reserve capacity, which may play a role in pathophysiology of stroke.
27
Satrio Putra, Eka, Retno Suryandari, Purwoko Purwoko, and Ardana Tri Arianto. "Pengelolaan Neuroanestesi pada Pasien dengan Pentalogy of Fallot." Jurnal Neuroanestesi Indonesia 9, no. 2 (October 17, 2020): 168–72. http://dx.doi.org/10.24244/jni.v9i3.273.
Full textAbstract:
Pentalogy of Fallot (POF) is a rare type of cyanotic congenital heart defect with high risk of having cerebral abscesses as one of its complications. Cerebral abscesses are often found in cyanotic heart disease due to chronic hypoxia and hyperviscosity reduced microcirculatory flow to the brain. We report a 6-year-old boy, 14 kg body weight with multiple brain abscesses accompanied by Pentalogy of Fallot (POF) who undergone a craniotomy to evacuate the abscess. Preoperative physical examination found GCS E4V5M6, other vital signs within normal limits, preductal oxygen saturation 88%, post ductal oxygen saturation in supine position 84%. The I-II heart sounds are regular with grade 3 systolic murmur in the left parasternal third intercostal space and clubbing finger was found. The laboratory shows a hemoglobin value of 14.4gr%, hematocrit of 43%, leukocytosis 13,200/mm³. The goal of anesthesia in cyanotic heart disease is to maintain cardiac output by stabilize heart rate, contractility as well as preload, prevent the increase of PVR:SVR ratio and avoid hypercyanotic due to sudden increase in systemic oxygen demand. The choice of anesthetic agent must be based on the patient's physiology. Adequate rehydration before induction and use of mannitol diuretics can be considered to reduce hyperviscosity that decrease oxygen delivery to the brain. Increased intracranial pressure from ketamine can be reduced by hyperventilation, in conjunction to benzodiazepines and prevention of hypercapnia. Therefore, monitoring end tidal CO2 (ETCO2) needs to be done. This case report delineating the perioperative management of a 6 years old boy with POF underwent evacuation of cerebral abscesses, will highlight the importance of understanding the pathophysiology of POF and neuroanesthesia techniques in order to receive a good outcome.
28
Saigal, Anita, Amar J. Shah, and Swapna Mandal. "Acute hypercapnic respiratory failure and its management on the acute medical take." British Journal of Hospital Medicine 82, no. 10 (October 2, 2021): 1–12. http://dx.doi.org/10.12968/hmed.2021.0251.
Full textAbstract:
Acute hypercapnic respiratory failure accounts for 50 000 hospital admissions each year in the UK. This article discusses the pathophysiology and common causes of acute hypercapnic respiratory failure, and provides practical considerations for patient management in acute medical settings. Non-invasive ventilation for persistent acute hypercapnic respiratory failure is widely recognised to improve patient outcomes and reduce mortality. National audits highlight a need to improve patients' overall care and outcomes through appropriate patient selection and treatment initiation. Multidisciplinary involvement is essential, as this underpins inpatient care and follow up after hospital discharge. New non-invasive ventilation modalities may offer better patient comfort and compensate better for sleep-related changes in respiratory mechanics. Emerging therapies, such as nasal high flow, may offer an alternative treatment approach in those who cannot tolerate non-invasive ventilation, but more research is required to completely understand its effectiveness in treating acute hypercapnic respiratory failure.
29
Saigal, Anita, Amar J. Shah, and Swapna Mandal. "Acute hypercapnic respiratory failure and its management on the acute medical take." British Journal of Hospital Medicine 82, no. 10 (October 2, 2021): 1–12. http://dx.doi.org/10.12968/hmed.2021.0251.
Full textAbstract:
Acute hypercapnic respiratory failure accounts for 50 000 hospital admissions each year in the UK. This article discusses the pathophysiology and common causes of acute hypercapnic respiratory failure, and provides practical considerations for patient management in acute medical settings. Non-invasive ventilation for persistent acute hypercapnic respiratory failure is widely recognised to improve patient outcomes and reduce mortality. National audits highlight a need to improve patients' overall care and outcomes through appropriate patient selection and treatment initiation. Multidisciplinary involvement is essential, as this underpins inpatient care and follow up after hospital discharge. New non-invasive ventilation modalities may offer better patient comfort and compensate better for sleep-related changes in respiratory mechanics. Emerging therapies, such as nasal high flow, may offer an alternative treatment approach in those who cannot tolerate non-invasive ventilation, but more research is required to completely understand its effectiveness in treating acute hypercapnic respiratory failure.
30
Prohovnik, Isak, Anne Hurlet-Jensen, Robert Adams, Darryl De Vivo, and Steven G. Pavlakis. "Hemodynamic Etiology of Elevated Flow Velocity and Stroke in Sickle-Cell Disease." Journal of Cerebral Blood Flow & Metabolism 29, no. 4 (February 11, 2009): 803–10. http://dx.doi.org/10.1038/jcbfm.2009.6.
Full textAbstract:
Elevation of blood flow velocity in the large cerebral vessels is known to be of substantial pathophysiologic and prognostic significance in sickle-cell disease (SCD). Its precise cause is not established, but the two obvious proximal mechanisms are obstructive vascular stenosis and hemodynamic dilatation. Here we revisit this distinction by analyzing cerebrovascular reserve capacity. Forty-two patients with SCD underwent measurements of global cerebral blood flow in grey matter by the 133Xe inhalation method during normocapnia and hypercapnia to quantify cerebrovascular reactivity. Cerebral blood flow was significantly higher in SCD patients (120±31 ml/100 g/min) than in controls (76±20 ml/100 g/min). Reactivity was significantly lower in SCD patients (1.06±1.92 versus 2.16±1.15%/mm Hg). Stepwise multiple regressions within the SCD sample determined that normocapnic cerebral blood flow was largely predicted by hematocrit ( r =–0.59; P > 0.0001), whereas hypercapnic reactivity was only predicted by normocapnic flow across all subjects ( r =–0.52; P > 0.0001). None of the controls, but 24% of the SCD patients showed ‘steal’ (negative reactivity, χ2 = 6.05; P > 0.02). This impairment of vasodilatory capacity, occurring at perfusion levels above 150 ml/100 g/min, may reflect intrinsic limitations of the human cerebrovascular system and can explain both the elevated blood flow velocities and the high risk of stroke observed in such patients.
31
Lenz, Christian, Annette Rebel, Enrico Bucci, Klaus van Ackern, Wolfgang Kuschinsky, and Klaus F. Waschke. "Lack of Hypercapnic Increase in Cerebral Blood Flow at High Blood Viscosity in Conscious Blood-exchanged Rats." Anesthesiology 95, no. 2 (August 1, 2001): 408–15. http://dx.doi.org/10.1097/00000542-200108000-00024.
Full textAbstract:
Background The hypothesis of a compensatory dilation of cerebral vessels to maintain cerebral blood flow at a high blood viscosity was tested during hypercapnia in the study after replacement of blood by hemoglobin solutions of defined viscosities. If compensatory vasodilation exists at normocapnia at a high blood viscosity, vasodilatory mechanisms may be exhausted when hypercapnia is added, resulting in a lack of increase in cerebral blood flow at hypercapnia. Methods In conscious rats, blood was replaced by ultrapurified cross-linked hemoglobin solutions that had defined and shear rate-independent low or high viscosities (low- and high-viscosity groups). Blood viscosity differed threefold between both groups (1.2 vs. 3.6 mP x s). Thereafter, rats inhaled either a normal or an increased concentration of carbon dioxide in air. Cerebral blood flow was determined by the iodo[14C]antipyrine method. Results During normocapnia, global and local cerebral blood flows did not differ between both groups. With increasing degrees of hypercapnia, global and local cerebral blood flows were gradually elevated in the low-viscosity group (2.8 ml x mmHg(-1) CO2 x 100 g(-1) x min(-1)), whereas they remained unchanged in the high-viscosity group. Conclusions Changes in blood viscosity do not result in changes of cerebral blood flow as long as cerebral vessels can compensate for these changes by vasodilation or vasoconstriction. However, such vascular compensatory adjustments may be exhausted in their response to further pathophysiologic conditions in blood vessels that have already been dilated or constricted as a result of changes in blood viscosity.
32
Arens, R., D. Gozal, K. J. Omlin, F. R. Livingston, J. Liu, T. G. Keens, and S. L. Ward. "Hypoxic and hypercapnic ventilatory responses in Prader-Willi syndrome." Journal of Applied Physiology 77, no. 5 (November 1, 1994): 2224–30. http://dx.doi.org/10.1152/jappl.1994.77.5.2224.
Full textAbstract:
Abnormalities of ventilatory control may play a significant role in the pathophysiology of sleep-disordered breathing in patients with the Prader-Willi syndrome (PWS). We measured rebreathing hypercapnic and hypoxic ventilatory responses (HCVR and HPVR, respectively) during wakefulness in 8 nonobese PWS (NOB-PWS) and 9 obese PWS (OB-PWS) patients and compared their results with those from 24 healthy nonobese control (NOB-CON) and 10 obese control (OB-CON) subjects. The slope of HCVR was similar in NOB-PWS patients and NOB-CON subjects (NS). However, HCVR was significantly lower in OB-PWS patients than in OB-CON subjects (P < 0.02). In PWS patients, the mean point of origin of the positive slope of HCVR occurred at a significantly higher end-tidal PCO2 than in either control group. During isocapnic hypoxic challenges, six PWS patients had no significant HPVR. In the remainder, mean slopes of HPVR were -0.80 +/- 0.06 l.min-1.%arterial O2 saturation-1 in five NOB-PWS patients and -0.68 +/- 0.15 l.min-1.%arterial O2 saturation-1 in six OB-PWS patients. These responses were significantly decreased compared with those in the control groups (P < 0.006). We conclude that NOB-PWS patients have normal HCVR, which is blunted in OB-PWS patients. Furthermore, isocapnic HPVR is either absent or markedly reduced in PWS patients. The severity of abnormality of the HPVR is independent of the degree of obesity. We postulate that the primary abnormality of ventilatory control in PWS affects peripheral chemoreceptor pathways.
33
Kobeliatskyi, Yu Yu. "Patients of risk groups in the perioperative period: the review of modern guidelines." Infusion & Chemotherapy, no. 3.2 (December 15, 2020): 129–31. http://dx.doi.org/10.32902/2663-0338-2020-3.2-129-131.
Full textAbstract:
Background. According to the Decree of the Ministry of Health of Ukraine № 275 issued on 11.09.2018, there is a list of measures to ensure surgical safety and patient’s safety. These measures can be divided into those that should be performed 1) before anesthesia; 2) before skin dissection; 3) before the patient leaves the operating room. Perioperative medicine (POM) is a patient-centered and interdisciplinary perioperative care for surgical patients.
Objective. To describe the current recommendations for POM.
Materials and methods. Review of available guidance documents.
Results and discussion. The pathophysiology of postoperative complications (infectious processes, intestinal paralysis, respiratory failure, kidney damage, etc.) includes the following factors: triggers (anxiety, pain, surgical trauma), patient factors (age, comorbid conditions), the consequences of general operative stress (autonomous system imbalance, inflammation, coagulopathy, metabolic imbalance). Clinical evaluation or biomarkers should be used to identify high-risk patients in the perioperative period. Measures to improve postoperative rehabilitation should be carried out in the pre-, intra- and postoperative period. Thus, in the preoperative period it is necessary to examine the patient, to provide the carbohydrate load 2 hours before the intervention, to conduct antibiotic prophylaxis, to correct or stabilize the comorbid diseases (especially cardiovascular and renal diseases, diabetes, anemia). In the intraoperative period it is necessary to maintain normovolemia and normothermia, to use protective mechanical lung ventilation, to limit the use of opioids, to perform extubation immediately after the intervention. In the postoperative period early activation, early enteral nutrition and early removal of drainages and catheters should be used. The key components of POM include the identification of low-risk patients in order to save resources, the identification of high-risk patients with the possible use of alternative management strategies, and the frequent risk reassessment. The main components of the success of anesthesia include preoperative assessment of the patient’s somatic status and risk, use of controlled hypnotics and effective and predictable muscle relaxant, use of analgesics that break down quickly and have no ability to accumulate, control of the hemodynamics stability, blood gases and acid-base balance. To prevent the perioperative myocardial ischemia, it is advisable to use esmolol – a cardioselective β-blocker of ultrashort action. Preoperative anxiety, intubation and extubation, surgical manipulations lead to the excessive adrenergic response, which justifies the use of β-blockers. The pharmacological effects of esmolol (Biblok, “Yuria-Pharm”) include the reduction of myocardial oxygen consumption, increase of the diastole duration, limitation of the free radicals’ production, control of the activity of metalloproteinases, and the reduction of inflammation around atherosclerotic plaques. In addition, esmolol (Biblok) is able to reduce intra- and postoperative use of opioids, and therefore its use as a component of multimodal total intravenous anesthesia has been proposed. Preoperative administration of esmolol may also be an effective and safe method of myocardial protection in patients undergoing cardiac surgery. β-blockers are well tolerated in patients with acute hypovolaemia during anesthesia, however, episodes of hypercapnia should be avoided during their use.
Conclusions. 1. For the optimal POM, the individual risk of perioperative complications should be determined. 2. POM includes a number of pre-, intra- and postoperative measures. 3. The use of ultrashort-acting β-blocker esmolol prevents intraoperative myocardial ischemia, has antioxidant and anti-inflammatory effects, reduces the need for opioids.
34
Garcia, Bryan, and Patrick A. Flume. "Pulmonary Complications of Cystic Fibrosis." Seminars in Respiratory and Critical Care Medicine 40, no. 06 (October 28, 2019): 804–9. http://dx.doi.org/10.1055/s-0039-1697639.
Full textAbstract:
AbstractCystic fibrosis (CF) lung disease is characterized by the development of progressive bronchiectasis and impaired lung function with severe airflow obstruction. CF patients suffer from shortened life expectancy, primarily driven by respiratory failure. The mechanism by which CF lung disease develops is the result of an interplay of multiple intrinsic and extrinsic factors including genotype, abnormalities in mucus composition and movement, chronic inflammation, and chronic airway infection. Although all CF patients are at increased risk for pulmonary complications including hemoptysis, pneumothorax, pulmonary hypertension, and chronic hypoxic and hypercapnic respiratory failure, the risk of developing these complications increases with progression of lung disease. The focus of this article is to summarize the pathophysiology, epidemiology, and management of these key pulmonary complications.
35
Cahill, Lindsay S., Lisa M. Gazdzinski, Albert KY Tsui, Yu-Qing Zhou, Sharon Portnoy, Elaine Liu, C. David Mazer, Gregory MT Hare, Andrea Kassner, and John G. Sled. "Functional and anatomical evidence of cerebral tissue hypoxia in young sickle cell anemia mice." Journal of Cerebral Blood Flow & Metabolism 37, no. 3 (July 20, 2016): 994–1005. http://dx.doi.org/10.1177/0271678x16649194.
Full textAbstract:
Cerebral ischemia is a significant source of morbidity in children with sickle cell anemia; however, the mechanism of injury is poorly understood. Increased cerebral blood flow and low hemoglobin levels in children with sickle cell anemia are associated with increased stroke risk, suggesting that anemia-induced tissue hypoxia may be an important factor contributing to subsequent morbidity. To better understand the pathophysiology of brain injury, brain physiology and morphology were characterized in a transgenic mouse model, the Townes sickle cell model. Relative to age-matched controls, sickle cell anemia mice demonstrated: (1) decreased brain tissue pO2 and increased expression of hypoxia signaling protein in the perivascular regions of the cerebral cortex; (2) elevated basal cerebral blood flow , consistent with adaptation to anemia-induced tissue hypoxia; (3) significant reduction in cerebrovascular blood flow reactivity to a hypercapnic challenge; (4) increased diameter of the carotid artery; and (5) significant volume changes in white and gray matter regions in the brain, as assessed by ex vivo magnetic resonance imaging. Collectively, these findings support the hypothesis that brain tissue hypoxia contributes to adaptive physiological and anatomic changes in Townes sickle cell mice. These findings may help define the pathophysiology for stroke in children with sickle cell anemia.
36
Fabricius, Martin, Nuran Akgören, Ulrich Dirnagl, and Martin Lauritzen. "Laminar Analysis of Cerebral Blood Flow in Cortex of Rats by Laser-Doppler Flowmetry: A Pilot Study." Journal of Cerebral Blood Flow & Metabolism 17, no. 12 (December 1997): 1326–36. http://dx.doi.org/10.1097/00004647-199712000-00008.
Full textAbstract:
Laser-Doppler flowmetry (LDF) is a reliable method for estimation of relative changes of CBF. The measurement depth depends on wavelength of the laser light and the separation distance of transmitting and recording optical fibers. We designed an LDF probe using two wavelengths of laser light (543 nm and 780 nm), and three separation distances of optical fibers to measure CBF in four layers of the cerebral cortex at the same time. In vitro comparison with electromagnetic flow measurements showed linear relationship between LDF and blood flow velocity at four depths within the range relevant to physiologic measurements. Using artificial brain tissue slices we showed that the signal for each channel decreased in a theoretically predictable fashion as a function of slice thickness. Application of adenosine at various depths in neocortex of halothane-anesthetized rats showed a predominant CBF increase at the level of application. Electrical stimulation at the surface of the cerebellar cortex demonstrated superficial predominance of increased CBF as predicted from the distribution of neuronal activity. In the cerebellum, hypercapnia increased CBF in a heterogeneous fashion, the major increase being at apparent depths of approximately 300 and 600 μm, whereas in the cerebral cortex, hypercapnia induced a uniform increase. In contrast, the CBF response to cortical spreading depression in the cerebral cortex was markedly heterogeneous. Thus, real-time laminar analysis of CBF with spatial resolution of 200 to 300 μm may be achieved by LDF. The real-time in depth resolution may give insight into the functional organization of the cortical microcirculation and adaptive features of CBF regulation in response to physiologic and pathophysiologic stimuli.
37
Liu, Pei-Kang, Tzu-Yu Chiu, Nan-Kai Wang, Sarah R. Levi, and Ming-Ju Tsai. "Ocular Complications of Obstructive Sleep Apnea." Journal of Clinical Medicine 10, no. 15 (July 31, 2021): 3422. http://dx.doi.org/10.3390/jcm10153422.
Full textAbstract:
Obstructive sleep apnea (OSA), the most common form of sleep-disordered breathing, is characterized by repetitive episodes of paused breathing during sleep, which in turn induces transient nocturnal hypoxia and hypercapnia. The high prevalence of OSA and its associated health consequences place a heavy burden on the healthcare system. In particular, the consequent episodic oxygenic desaturation/reoxygenation series and arousals from sleep in patients with OSA have the potential to trigger oxidative stress, elevated systemic inflammatory responses, and autonomic dysfunction with sympathetic activation. Given these adverse side-effects, OSA is highly correlated to many eye diseases that are common in everyday ophthalmic practices. Some of these ocular consequences are reversible, but they may permanently threaten a patient’s vision if not treated appropriately. Here, this article seeks to review the ocular consequences and potential pathophysiologic associations in patients with OSA. Understanding these OSA-related eye diseases may help clinicians provide comprehensive care to their patients.
38
Ahn, Jeeyun, and Michael B. Gorin. "The Associations of Obstructive Sleep Apnea and Eye Disorders: Potential Insights into Pathogenesis and Treatment." Current Sleep Medicine Reports 7, no. 3 (July 23, 2021): 65–79. http://dx.doi.org/10.1007/s40675-021-00215-0.
Full textAbstract:
Abstract Purpose of Review Obstructive sleep apnea (OSA) patients are at significantly increased risks for cardiovascular and cerebrovascular morbidities. Recently, there has been heightened interest in the association of OSA with numerous ocular diseases and possible improvement of these conditions with the initiation of OSA treatment. We reviewed the current evidence with an emphasis on the overlapping pathogeneses of both diseases. Recent Findings Currently available literature points to a substantial association of OSA with ocular diseases, ranging from those involving the eyelid to optic neuropathies and retinal vascular diseases. Since the retina is one of the highest oxygen-consuming tissues in the body, the intermittent hypoxia and hypercapnia ensuing in OSA can have deleterious effects on ocular function and health. Tissue hypoxia, autonomic dysfunction, microvascular dysfunction, and inflammation all play important roles in the pathogenesis of both OSA and ocular diseases. Whether OSA treatment is capable of reversing the course of associated ocular diseases remains to be determined. It is anticipated that future therapeutic approaches will target the common underlying pathophysiologic mechanisms and promote favorable effects on the treatment of known associated ocular diseases. Summary Emerging evidence supports the association of ocular diseases with untreated OSA. Future studies focusing on whether therapeutic approaches targeting the common pathophysiologic mechanisms will be beneficial for the course of both diseases are warranted.
39
Bitterman, Noemi, and Haim Bitterman. "l-Arginine-NO pathway and CNS oxygen toxicity." Journal of Applied Physiology 84, no. 5 (May 1, 1998): 1633–38. http://dx.doi.org/10.1152/jappl.1998.84.5.1633.
Full textAbstract:
The involvement of thel-arginine-nitric oxide (NO) pathway in the pathogenesis of hyperoxia-induced seizures was studied by using agents controlling NO levels. We selected two inhibitors of nitric oxide synthase, the systemic inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) and the novel cerebral-specific inhibitor 7-nitroindazole, and two generators of NO, the NO donor S-nitroso- N-acetylpenicillamine and the physiological precursorl-arginine. Rats with chronic cortical electrodes were injected intraperitoneally with different doses of one of the agents or their vehicles before exposure to 0.5 MPa O2 and O2 with 5% CO2 at an absolute pressure of 0.5 MPa. The duration of the latent period until the onset of electrical discharges in the electroencephalogram was used as an index of central nervous system O2 toxicity. The two nitric oxide synthase inhibitorsl-NAME and 7-nitroindazole significantly prolonged the latent period to the onset of seizures on exposure to both hyperbaric O2 and to the hypercapnic-hyperoxic mixture. Pretreatment with the NO donor S-nitroso- N-acetylpenicillamine significantly shortened the latent period, whereasl-arginine, the physiological precursor of NO, significantly prolonged the latent period to onset of seizures. Our results suggest that thel-arginine-NO pathway is involved in the pathophysiology of hyperoxia-induced seizures via various regulating mechanisms.
40
Cohen, Scott, Ramon M. Esclamado, Louise Aloe, Steven Telian, and Paul Kileny. "Laryngeal Brain Stem Evoked Response in the Porcine Model." Annals of Otology, Rhinology & Laryngology 102, no. 1 (January 1993): 28–34. http://dx.doi.org/10.1177/000348949310200106.
Full textAbstract:
Exaggeration of normally protective laryngeal reflexes is thought to play a role in several disorders, including the sudden infant death syndrome. An analysis of brain stem neural activity following laryngeal stimulation may provide insight into the pathophysiology of pathologic laryngeal reflexes and help to identify individuals at risk for these disorders. The purpose of this study was to define the far-field brain stem activity following laryngeal stimulation in the porcine model. This activity has been termed the laryngeal brain stem evoked response and may represent a potentially useful and objective measure of the neuronal activity in the laryngeal reflex pathway. Electrical stimulation of the superior laryngeal nerve was performed in 14 mixed-breed piglets under a variety of physiologic conditions. A total of six positive and six negative discrete waves were detected, with mean latencies ranging from 1.24 to 7.16 milliseconds. Stimulations performed during hypoxic, hypercapneic, or hypocapneic conditions resulted in no significant differences in waveform latencies. There appears to be a reproducible, but somewhat variable, brain stem response elicited by superior laryngeal nerve stimulation that can be recorded via a far-field technique in the porcine model.
41
Sivakolundu, Dinesh K., Kathryn L. West, Gayathri B. Maruthy, Mark Zuppichini, Monroe P. Turner, Dema Abdelkarim, Yuguang Zhao, et al. "Reduced arterial compliance along the cerebrovascular tree predicts cognitive slowing in multiple sclerosis: Evidence for a neurovascular uncoupling hypothesis." Multiple Sclerosis Journal 26, no. 12 (August 2, 2019): 1486–96. http://dx.doi.org/10.1177/1352458519866605.
Full textAbstract:
Background: Cognitive slowing occurs in ~70% of multiple sclerosis (MS) patients. The pathophysiology of this slowing is unknown. Neurovascular coupling, acute localized blood flow increases following neural activity, is essential for efficient cognition. Loss of vascular compliance along the cerebrovascular tree would result in suboptimal vasodilation, neurovascular uncoupling, and cognitive slowing. Objective: To assess vascular compliance along the cerebrovascular tree and its relationship to MS-related cognition. Methods: We tested vascular compliance along the cerebrovascular tree by dividing cerebral cortex into nested layers. MS patients and healthy controls were scanned using a dual-echo functional magnetic resonance imaging (fMRI) sequence while they periodically inhaled room air and hypercapnic gas mixture. Cerebrovascular reactivity was calculated from both cerebral blood flow (arterial) and blood-oxygen-level-dependent signal (venous) increases per unit increase in end-tidal CO2. Results: Arterial cerebrovascular reactivity changes along the cerebrovascular tree were reduced in cognitively slow MS compared to cognitively normal MS and healthy controls. These changes were fit to exponential functions, the decay constant (arterial compliance index; ACI) of which was associated with individual subjects’ reaction time and predicted reaction time after controlling for disease processes. Conclusion: Such associations suggest prospects for utility of ACI in predicting future cognitive disturbances, monitoring cognitive deficiencies and therapeutic responses, and implicates neurovascular uncoupling as a mechanism of cognitive slowing in MS.
42
Choi, Yong Jun, and Jae Hwa Cho. "Current status of treatment of acute respiratory failure in Korea." Journal of the Korean Medical Association 65, no. 3 (March 10, 2022): 124–29. http://dx.doi.org/10.5124/jkma.2022.65.3.124.
Full textAbstract:
Background: Acute respiratory failure (ARF) is one of the most common causes of intensive care unit (ICU) admission and in-hospital mortality. In South Korea, about 25% of patients admitted to the ICU require mechanical ventilation. The in-hospital mortality rate of these patients is 48%. Respiratory failure can be categorized based on pathophysiologic derangements, and the treatment options vary depending on their classification. This study discusses the status and treatment strategies of patients with ARF in Korea.Current Concepts: The most common treatment for ARF was conventional oxygen therapy, being used at least once in 7.0% of all admitted adult patients and 85.1% of patients admitted with respiratory failure. High-flow oxygen therapy was required in 1.4% of all admissions and 17.2% of respiratory failure-related admissions. High-flow oxygen therapy was attempted in 19.1% of patients who needed invasive mechanical ventilation. Non-invasive positive pressure ventilation (NIV) was used in 0.4% of all admissions and 5.1% of respiratory failure-related admissions. Hypercapnic respiratory failure (57.1%) was the most common reason for NIV use. Invasive mechanical ventilation was required in 2.8% of all admissions and 33.8% of respiratory failure-related admissions.Discussion and Conclusion: Despite its clinical significance, no large-scale studies have been performed on the etiology, treatment, and prognosis of patients with ARF in South Korea. A multicenter or a Korean National Health Insurance Service database study is necessary to accurately identify the characteristics, diagnose problems, and develop treatment guidelines for patients with ARF in South Korea.
43
Champagne, Allen Anthony, Nicole Coverdale, Juan Fernandez Ruis, Clarisse Mark, and Douglas J. Cook. "Compromised Resting Cerebral Metabolism After Sport-Related Concussion: A Calibrated MRI Study." Neurology 95, no. 20 Supplement 1 (November 16, 2020): S15.1—S15. http://dx.doi.org/10.1212/01.wnl.0000720012.62957.73.
Full textAbstract:
ObjectiveUse calibrated MRI to model baseline cerebrovascular physiology parameters and investigate whether changes in resting cerebral blood flow (CBF0) following sport-related concussion (SRC) are concordant with changes in resting and dynamic cerebral physiologic markers, within two weeks of the injury.BackgroundAltered CBF0 in the acute phase post-concussion may contribute to neurobehavioral deficiencies, often reported weeks after the injury. However, in addition to changes in CBF0, little is known about other physiologic mechanisms that may be disturbed within the cerebrovasculature. The aim of this study was to assess whether changes in baseline perfusion following SRC were co-localized with changes in cerebral metabolic demand.Design/MethodsForty-two subjects (15 SRC patients 8.0 ± 4.6 days post-injury and 27 age-matched healthy control athletes) were studied cross-sectionally. CBF0, cerebrovascular reactivity (CVR), resting oxygen extraction (OEF0) and cerebral metabolic rate of oxygen consumption (CMRO2|0) were measured using a combination of hypercapnic and hyperoxic breathing protocols, and the biophysical model developed in calibrated MRI. Blood Oxygenation Level Dependent and Arterial Spin Labelling data were acquired simultaneously using a dual-echo arterial spin labelling sequence.ResultsSRC patients showed significant decreases in CBF0 spread across the grey-matter (p < 0.05, corrected), and these differences were also confounded by the effects of baseline end-tidal CO2 (p < 0.0001). Lower perfusion was co-localized with reductions in regional CMRO2|0 (p = 0.006) post-SRC, despite finding no group-differences in OEF0 (p = 0.800). Higher CVR within voxels showing differences in CBF0 was also observed in the SRC group (p = 0.001), compared to controls.ConclusionsReductions in metabolic demand despite no significant changes in OEF0 suggests that hypoperfusion post-SRC may reflect compromised metabolic function after the injury. These results provide novel insight about the possible pathophysiologic mechanisms underlying concussion that may affect the clinical recovery of athletes after sport-related head injuries.
44
Shen, Qiuhua, Qiuhua Shen, John B. Hiebert, and Janet D. Pierce. "Underlying Causes of High Output Heart Failure." Journal of Integrative Cardiology Open Access, December 18, 2020, 1–4. http://dx.doi.org/10.31487/j.jicoa.2020.06.04.
Full textAbstract:
In the U.S., each year, there are more than 500,000 new cases of all types of heart failure. With high output cardiac failure, there is an elevated cardiac output associated with several conditions and diseases, including obesity, chronic anemia, systemic arterio-venous fistula, hypercapnia, mitochondrial dysfunction, and hyperthyroidism. The underlying pathophysiologic mechanisms relate to a reduction in systemic vascular resistance from arterio-venous shunting or peripheral vasodilation. Often there is a decrease in systemic arterial blood pressure and neurohormonal activation leading to heart failure symptoms of dyspnea and fatigue. In a persistent high output state, patients may experience tachycardia, valvular abnormalities, and ventricular dilatation and/or hypertrophy. In this article, there is a review of high output heart failure, including the prevalence, pathophysiology, and common clinical causes of this disease.
45
Wallis, Charles, and Lewis Hendon-John. "Respiratory failure." InnovAiT: Education and inspiration for general practice, November 24, 2022, 175573802211395. http://dx.doi.org/10.1177/17557380221139552.
Full textAbstract:
Respiratory failure is a leading cause of morbidity and mortality in the UK, and a significant burden on the NHS. It occurs when the lungs fail to provide adequate gas exchange leading to hypoxia and/or hypercapnia. Primary care clinicians will often encounter acute and chronic respiratory failure and have a key role in the management of patients. This review aims to provide a broad overview of the pathophysiology, causes, presentation, investigations and management relevant to primary care.
46
Adrogué, Horacio J., and Nicolaos E. Madias. "Respiratory Acidosis and Alkalosis." DeckerMed Medicine, September 25, 2017. http://dx.doi.org/10.2310/im.12004.
Full textAbstract:
Respiratory acid-base disorders are those disturbances in acid-base equilibrium that are expressed by a primary change in CO2 tension (Pco2) and reflect primary changes in the body’s CO2 stores (i.e., carbonic acid). A primary increase in Pco2 (and a primary increase in the body’s CO2 stores) defines respiratory acidosis or primary hypercapnia and is characterized by acidification of the body fluids. By contrast, a primary decrease in Pco2 (and a primary decrease in the body’s CO2 stores) defines respiratory alkalosis or primary hypocapnia and is characterized by alkalinization of the body fluids. Primary changes in Pco2 elicit secondary physiologic changes in plasma [HCO3ˉ] that are directional and proportional to the primary changes and tend to minimize the impact on acidity. This review presents the pathophysiology, secondary physiologic response, causes, clinical manifestations, diagnosis, and therapeutic principles of respiratory acidosis and respiratory alkalosis. This review contains 4 figures, 3 tables, and 59 references. Key words: Respiratory acidosis, respiratory alkalosis, primary hypercapnia, primary hypocapnia, hypoxemia, pseudorespiratory alkalosis
47
Adrogué, Horacio J., and Nicolaos E. Madias. "Respiratory Acidosis and Alkalosis." DeckerMed Nephrology, Dialysis, and Transplantation, September 25, 2017. http://dx.doi.org/10.2310/nephro.12004.
Full textAbstract:
Respiratory acid-base disorders are those disturbances in acid-base equilibrium that are expressed by a primary change in CO2 tension (Pco2) and reflect primary changes in the body’s CO2 stores (i.e., carbonic acid). A primary increase in Pco2 (and a primary increase in the body’s CO2 stores) defines respiratory acidosis or primary hypercapnia and is characterized by acidification of the body fluids. By contrast, a primary decrease in Pco2 (and a primary decrease in the body’s CO2 stores) defines respiratory alkalosis or primary hypocapnia and is characterized by alkalinization of the body fluids. Primary changes in Pco2 elicit secondary physiologic changes in plasma [HCO3ˉ] that are directional and proportional to the primary changes and tend to minimize the impact on acidity. This review presents the pathophysiology, secondary physiologic response, causes, clinical manifestations, diagnosis, and therapeutic principles of respiratory acidosis and respiratory alkalosis. This review contains 4 figures, 3 tables, and 59 references. Key words: Respiratory acidosis, respiratory alkalosis, primary hypercapnia, primary hypocapnia, hypoxemia, pseudorespiratory alkalosis
48
Taivassalo, Tanja, and Russell T. Hepple. "Integrating Mechanisms of Exacerbated Atrophy and Other Adverse Skeletal Muscle Impact in COPD." Frontiers in Physiology 13 (June 3, 2022). http://dx.doi.org/10.3389/fphys.2022.861617.
Full textAbstract:
The normal decline in skeletal muscle mass that occurs with aging is exacerbated in patients with chronic obstructive pulmonary disease (COPD) and contributes to poor health outcomes, including a greater risk of death. There has been controversy about the causes of this exacerbated muscle atrophy, with considerable debate about the degree to which it reflects the very sedentary nature of COPD patients vs. being precipitated by various aspects of the COPD pathophysiology and its most frequent proximate cause, long-term smoking. Consistent with the latter view, recent evidence suggests that exacerbated aging muscle loss with COPD is likely initiated by decades of smoking-induced stress on the neuromuscular junction that predisposes patients to premature failure of muscle reinnervation capacity, accompanied by various alterations in mitochondrial function. Superimposed upon this are various aspects of COPD pathophysiology, such as hypercapnia, hypoxia, and inflammation, that can also contribute to muscle atrophy. This review will summarize the available knowledge concerning the mechanisms contributing to exacerbated aging muscle affect in COPD, consider the potential role of comorbidities using the specific example of chronic kidney disease, and identify emerging molecular mechanisms of muscle impairment, including mitochondrial permeability transition as a mechanism of muscle atrophy, and chronic activation of the aryl hydrocarbon receptor in driving COPD muscle pathophysiology.
49
Robba, Chiara, Dorota Siwicka-Gieroba, Andras Sikter, Denise Battaglini, Wojciech Dąbrowski, Marcus J. Schultz, Evert de Jonge, Chloe Grim, Patricia RM Rocco, and Paolo Pelosi. "Pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest." Intensive Care Medicine Experimental 8, S1 (December 2020). http://dx.doi.org/10.1186/s40635-020-00307-1.
Full textAbstract:
AbstractPost 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.
50
Ziaka, Mairi, and Aristomenis Exadaktylos. "ARDS associated acute brain injury: from the lung to the brain." European Journal of Medical Research 27, no. 1 (August 13, 2022). http://dx.doi.org/10.1186/s40001-022-00780-2.
Full textAbstract:
AbstractA complex interrelation between lung and brain in patients with acute lung injury (ALI) has been established by experimental and clinical studies during the last decades. Although, acute brain injury represents one of the most common insufficiencies in patients with ALI and acute respiratory distress syndrome (ARDS), the underlying pathophysiology of the observed crosstalk remains poorly understood due to its complexity. Specifically, it involves numerous pathophysiological parameters such as hypoxemia, neurological adverse events of lung protective ventilation, hypotension, disruption of the BBB, and neuroinflammation in such a manner that the brain of ARDS patients—especially hippocampus—becomes very vulnerable to develop secondary lung-mediated acute brain injury. A protective ventilator strategy could reduce or even minimize further systemic release of inflammatory mediators and thus maintain brain homeostasis. On the other hand, mechanical ventilation with low tidal volumes may lead to self-inflicted lung injury, hypercapnia and subsequent cerebral vasodilatation, increased cerebral blood flow, and intracranial hypertension. Therefore, by describing the pathophysiology of ARDS-associated acute brain injury we aim to highlight and discuss the possible influence of mechanical ventilation on ALI-associated acute brain injury.