- Management Strategies for Intracranial Pressure Crises in Subarachnoid Hemorrhage. [Journal Article]
- JIJ Intensive Care Med 2018 Dec 04; :885066618813073
- Standard management strategies for lowering intracranial pressure (ICP) in traumatic brain injury has been well-studied, but the use of lesser known interventions for ICP in subarachnoid hemorrhage (...
Standard management strategies for lowering intracranial pressure (ICP) in traumatic brain injury has been well-studied, but the use of lesser known interventions for ICP in subarachnoid hemorrhage (SAH) remains elusive. Searches were performed in PubMed and EBSCO Host to identify best available evidence for evaluation and management of medically refractory ICP in SAH. The role of standard management strategies such as head elevation, hyperventilation, mannitol and hypertonic saline as well as lesser known management such as sodium bicarbonate, indomethacin, tromethamine, decompressive craniectomy, decompressive laparotomy, hypothermia, and barbiturate coma are reviewed. We also included dose concentrations, dose frequency, infusion volume, and infusion rate for these lesser known strategies. Nonetheless, there is still a gap in the evidence to recommend optimal dosing, timing and its role in the improvement of outcomes but early diagnosis and appropriate management reduce adverse outcomes.
- Respiration and applied tension strategies to reduce vasovagal reactions to blood donation: A randomized controlled trial. [Journal Article]
- TTransfusion 2018 Nov 29
- CONCLUSIONS: While the mechanisms remain somewhat unclear and the interventions did not benefit more fearful, higher-risk donors, respiration control is a promising additional approach to reducing vasovagal symptoms.
- CO2-related vasoconstriction superimposed on ischemic medullary brain autonomic nuclei may contribute to sudden death. [Editorial]
- CPCardiovasc Pathol 2018 Oct 26; 38:42-45
- CONCLUSIONS: Why did not the improved pulmonary ventilation and subsequently improved gas exchange provided during the CPAP and servoventilation clinical trials help to resolve any ischemic lesions that may have been present both in the heart and in the medulla, thereby tending to normalize interactions between the vagal neural structures and the heart? CO2 is a potent dilator of brain vasculature, thereby increasing blood flow to the brain. When ventilation is increased, even if only to improve it back toward normal from a depressed steady-state level, the alveolar partial pressure of carbon dioxide is decreased, likely resulting in a converse relative vasoconstriction in the brain, thereby reducing blood flow in the brain, especially in watershed areas like the solitary tract nucleus. In normal physiology, this is demonstrated impressively by the ability of hyperventilation to induce loss of consciousness.The findings of several clinical trials recently reported, taken together with neuropathology case studies reported elsewhere, suggest that additional research is warranted in regard to the mechanisms by which focal medullary autonomic brain ischemia may be related to sudden death in general medical illnesses - and how it may additionally be influenced by changes in arterial CO2 levels.
- Effect of increased inspiratory muscle work on blood flow to inactive and active limbs during submaximal dynamic exercise. [Journal Article]
- EPExp Physiol 2018 Nov 21
- What is the central question of this study? Increased respiratory muscle activation is associated with neural and cardiovascular consequences via the respiratory muscle metaboreflex. Does increased s...
What is the central question of this study? Increased respiratory muscle activation is associated with neural and cardiovascular consequences via the respiratory muscle metaboreflex. Does increased sympathetic vasoconstriction originating from the respiratory musculature elicit a reduction in blood flow to an inactive limb in order to maintain blood flow to an active limb? What is the main finding and its importance? Arm blood flow was reduced while leg blood flow was preserved during mild leg exercise with inspiratory resistance. Blood flow to the active limb is maintained via sympathetic control of blood flow redistribution when the respiratory muscle-induced metaboreflex is activated.
- Mecp2 Disruption in Rats Causes Reshaping in Firing Activity and Patterns of Brainstem Respiratory Neurons. [Journal Article]
- NNeuroscience 2018 Nov 17
- People with Rett Syndrome (RTT), a neurodevelopmental disorder caused by mutations in the MECP2 gene, have breathing abnormalities manifested as periodical hypoventilation with compensatory hypervent...
People with Rett Syndrome (RTT), a neurodevelopmental disorder caused by mutations in the MECP2 gene, have breathing abnormalities manifested as periodical hypoventilation with compensatory hyperventilation, which are attributable to a high incidence of sudden death. Similar breathing abnormalities have been found in animal models with Mecp2 disruptions. Although RTT-type hypoventilation is believed to be due to depressed central inspiratory activity, whether this is true remains unknown. Here we show evidence for reshaping in firing activity and patterns of medullary respiratory neurons in RTT-type hypoventilation. Experiments were performed in decerebrate rats in vivo. In Mecp2-null rats, abnormalities in breathing patterns were apparent in both decerebrate rats and awake animals, suggesting that RTT-type breathing abnormalities take place in the brainstem without forebrain input. In comparison to their wild-type counterparts, both inspiratory and expiratory neurons in Mecp2-null rats extended their firing duration, and fired more action potentials during each burst. No changes in inspiratory or expiratory neuronal distributions were found. Most inspiratory neurons started firing in the middle of expiration and changed their firing pattern to a phase-spanning type. The proportion of post-inspiratory neurons was reduced in the Mecp2-null rats. With the increased firing activity of both inspiratory and expiratory neurons in null rats, phrenic discharges shifted to a slow and deep breathing pattern. Thus, the RTT-type hypoventilation appears to result from reshaping of firing activity of both inspiratory and expiratory neurons without evident depression in central inspiratory activity.
- Arterial Blood Gas Analysis in Breath-Hold Divers at Depth. [Journal Article]
- FPFront Physiol 2018; 9:1558
- The present study aimed to evaluate the partial pressure of arterial blood gases in breath-hold divers performing a submersion at 40 m. Eight breath-hold divers were enrolled for the trials held at "...
The present study aimed to evaluate the partial pressure of arterial blood gases in breath-hold divers performing a submersion at 40 m. Eight breath-hold divers were enrolled for the trials held at "Y-40 THE DEEP JOY" pool (Montegrotto Terme, Padova, Italy). Prior to submersion, an arterial cannula in the radial artery of the non-dominant limb was positioned. All divers performed a sled-assisted breath-hold dive to 40 m. Three blood samplings occurred: at 10 min prior to submersion, at 40 m depth, and within 2 min after diver's surfacing and after resuming normal ventilation. Blood samples were analyzed immediately on site. Six subjects completed the experiment, without diving-related problems. The theoretically predicted hyperoxia at the bottom was observed in 4 divers out of 6, while the other 2 experienced a reduction in the partial pressure of oxygen (paO2) at the bottom. There were no significant increases in arterial partial pressure of carbon dioxide (paCO2) at the end of descent in 4 of 6 divers, while in 2 divers paCO2 decreased. Arterial mean pH and mean bicarbonate ( HCO 3 - ) levels exhibited minor changes. There was a statistically significant increase in mean arterial lactate level after the exercise. Ours was the first attempt to verify real changes in blood gases at a depth of 40 m during a breath-hold descent in free-divers. We demonstrated that, at depth, relative hypoxemia can occur, presumably caused by lung compression. Also, hypercapnia exists at depth, to a lesser degree than would be expected from calculations, presumably because of pre-dive hyperventilation and carbon dioxide distribution in blood and tissues.
- The effect of isocapnic hyperventilation on early recovery after remifentanil/sevoflurane anesthesia in O2 /air: A randomized trial. [Journal Article]
- AAActa Anaesthesiol Scand 2018 Nov 06
- CONCLUSIONS: Isocapnic hyperventilation only had a small effect on emergence times after anesthesia, suggesting that isocapnic hyperventilation may have limited clinical benefits with modern potent inhaled anesthetics.
- Electroclinical Features of Generalized Paroxysmal Fast Activity in Typical Absence Seizures. [Journal Article]
- JCJ Clin Neurophysiol 2018 Nov 01
- CONCLUSIONS: Generalized paroxysmal fast activity is uncommon in children with typical absence seizures and has medium voltage, posterior predominance, and marked female preponderance. Generalized paroxysmal fast activity is seen during both pharmacoresponsive and drug-resistant epilepsy, and is not affected by antiseizure medications. It may serve as an independent marker of lifelong epilepsy.
- Spontaneous Hyperventilation in Severe Traumatic Brain Injury: Incidence and Association with Poor Neurological Outcome. [Journal Article]
- NCNeurocrit Care 2018 Nov 01
- CONCLUSIONS: SHV is common in patients with a persistent coma after a severe TBI (overall rate: 69%) and was independently associated with unfavorable outcome at 6-month follow-up.
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- Carotid chemoreceptors have a limited role in mediating the hyperthermia-induced hyperventilation in exercising humans. [Journal Article]
- JAJ Appl Physiol (1985) 2018 Nov 01
- Hyperthermia causes hyperventilation at rest and during exercise. We previously reported that carotid chemoreceptors partly contribute to the hyperthermia-induced hyperventilation at rest. However, g...
Hyperthermia causes hyperventilation at rest and during exercise. We previously reported that carotid chemoreceptors partly contribute to the hyperthermia-induced hyperventilation at rest. However, given that a hyperthermia-induced hyperventilation markedly differs between rest and exercise, the results obtained at rest may not be representative of the response in exercise. Therefore, we evaluated whether carotid chemoreceptors contribute to hyperthermia-induced hyperventilation in exercising humans. Eleven healthy young males (23±2 years) cycled in the heat (37°C) at a fixed submaximal workload equal to ~55% of the individual's pre-determined peak oxygen uptake (moderate intensity). In order to suppress carotid chemoreceptor activity, 30-s hyperoxia breathing (100% O2) was performed at rest (before exercise) and during exercise at increasing levels of hyperthermia as defined by an increase in esophageal temperature of 0.5°C (low), 1.0°C (moderate), 1.5°C (high), and 2.0°C (severe) above resting levels. Ventilation during exercise gradually increased as esophageal temperature increased (all P≤0.05), indicating that hyperthermia-induced hyperventilation occurred. Hyperoxia breathing suppressed ventilation in a greater manner during exercise (-9 to -13 L min-1) than at rest (-2±1 L min-1); however, the magnitude of reduction during exercise did not differ at low- (0.5°C) to severe- (2.0°C) increases in esophageal temperature (all P>0.05). Similarly, hyperoxia-induced changes in ventilation during exercise as assessed by %change from pre-hyperoxic levels were not different at all levels of hyperthermia (~15-20%, all P>0.05). We show that in young men, carotid chemoreceptor contribution to hyperthermia-induced hyperventilation is relatively small at low-to-severe increases in body core temperature induced by moderate-intensity exercise in the heat.