Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The existence of treatable postischemic (PI) changes which influence neurological outcome has been documented by this group before. A global brain ischemia model without cardiac arrest was developed in monkeys. It includes high-pressure neck tourniquet inflation plus hypotension for a reproducible ischemic insult; survival with reproducible neurological deficit (ND) under continuous PI life-support for 7 days with control of extracranial variables; and new ND and histopathological damage scoring systems. Hypoxemia, hypercarbia, hypotension, uremia, sepsis, and other extracranial complications PI in 50 unsatisfactory experiments led to immediate worsening in ND and brain death (ND = 100%) in most of these monkeys. In contrast, all monkeys with the same initial insult, with life-support according to protocol, survived with a 7 day ND of 60% or less. In 46 experiments of seven treatment groups, after 16 or 18 min ischemia, life support was according to protocol for 7 days. The control 1 protocol (spontaneous breathing when feasible) resulted in a mean 7-day ND score of 53% (including quadriplegia). Immobilization with pancuronium and controlled ventilation ameliorate deficit to an ND score of 19% (P less than 0.05) (including quadriparesis); this became control 2 protocol. Immobilization resulted in less neuronal damage in the neocortex. Severe repetitive hypertension worsened ND to 46%, versus 19% in controls (P less than 0.05). In separate series, neither heparinization over 72 hours PI, nor hemodilution to hematocrit 25% with dextran 40, changed final ND significantly from that of their control groups. Histopathological damage scores correlated with ND scores.
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PMID:Effect of postcirculatory-arrest life-support on neurological recovery in monkeys. 676 78

Experimental uremia created by obstructing the urethra of 7 cross-bred bulls was associated with significant (P less than 0.05) increases in PCV, blood urea nitrogen concentration, arterial and venous pH and PCO2, arterial bicarbonate, and base excess. Total serum protein concentration decreased nonsignificantly. Arterial PO2 reduced significantly during later stages of uremia. Arterial and venous oxygen saturation, arteriovenous oxygen difference, oxygen extraction ratio, and arteriovenous pH difference were not affected significantly. Uremia was characterized by progressive metabolic alkalosis with, as a compensation, hypercapnia, and arterial hypoxemia. There was no evidence of systemic shunting of blood except in 1 animal.
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PMID:Acid-base status and blood gas alterations following experimental uremia in cattle. 678 24

Delayed awakening from anesthesia remains one of the biggest challenges that involve an anesthesiologist. With the general use of fast-acting anesthetic agents, patients usually awaken quickly in the postoperative period. The time to emerge from anesthesia is affected by patient factors, anesthetic factors, duration of surgery, and painful stimulation. The principal factors responsible for delayed awakening following anesthesia are anesthetic agents and medications used in the perioperative period. Nonpharmacological causes may have a serious sequel, hence recognizing these organic conditions is important. Certain underlying metabolic disorders such as hypoglycemia, severe hyperglycemia, and electrolyte imbalance, especially hypernatremia, hypoxia, hypercapnia, central anticholinergic syndrome, chronic hypertension, liver disease, hypoalbuminemia, uremia, and severe hypothyroidism may also be responsible for delayed recovery following anesthesia. Unexpected delayed emergence after general anesthesia may also be due to intraoperative cerebral hypoxia, hemorrhage, embolism, or thrombosis. Accurate diagnosis of the underlying cause is the key for the institution of appropriate therapy, but primary management is to maintain airway, breathing, and circulation. This comprehensive review discusses the risk factors, causes, evaluation and management of delayed recovery based on our clinical experience, and literature search on the internet, supported by the standard textbooks of anesthesiology.
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PMID:Delayed recovery from anesthesia: A postgraduate educational review. 2721 41