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

The effects of fetal hypoxemia on blood coagulation (platelet count, prothrombin time, partial thromboplastin time, fibrinogen, factors II, V, VI, VIII, IX, X, XI, XII, XIII and von Willebrands activities, fibrin degradation products, and fibrin monomer) were evaluated in nine chronically catheterized fetal lambs early in the third trimester of pregnancy (107-110 days gestation). Seven chronically catheterized fetal lambs of similar gestational ages served as controls. The hypoxemic episode (pO2 14 mm Hg) was maintained for 1 hr in the experimental group during which time there were only minimal changes in PCO2, arterial pressure, heart rate, and pH. Epinephrine and norepinephrine levels increased significantly in stressed animals--22 pg/ml pre- to 1025 pg/ml postepinephrine, and 475 pg/ml pre- to 2292 pg/ml postnorepinephrine. There were no significant changes in blood coagulation factor activities related to the hypoxic stress although, one fetus who experienced acidemia did develop a transient increase in fibrin monomer. Slight through significant increases in VIII coagulant activity activity (4.0%), von Willebrand activity (5.9%), and factor XII activity (4.3%) occurred in both the hypoxemic and control fetal lambs. These changes were associated with minimal increases in the white blood cell count (15%) and slight decreases in the mean arterial pressure (3.9 mm Hg) hemoglobin (1.2 g), and hematocrit (2.9%) and may have been related to the blood loss of 25% that occurred as a result of sampling in both groups. There were no differences between the hypoxic and control animals' levels of coagulation factor activities when measured during an 18-day follow-up period except for a slight increase in factor X activity (10%) in the control animals not apparent in the nine hypoxic animals. Thus an episode of severe fetal hypoxemia in the absence of hypotension, acidosis, and hypercarbia does not lead to acute or chronic alterations in blood coagulation factor activities in the fetal lamb.
 ...
PMID:Blood coagulation changes after hypoxemia: a fetal lamb model. 707 Aug 80

Patients undergoing lobectomy are at significantly increased risk of lung injury. One-lung ventilation is the most commonly used technique to maintain ventilation and oxygenation during the operation. It is a challenge to choose an appropriate mechanical ventilation strategy to minimize the lung injury and other adverse clinical outcomes. In order to understand the available evidence, a systematic review was conducted including the following topics: (I) protective ventilation (PV); (II) mode of mechanical ventilation [e.g., volume controlled (VCV) versus pressure controlled (PCV)]; (III) use of therapeutic hypercapnia; (IV) use of alveolar recruitment (open-lung) strategy; (V) pre-and post-operative application of positive end expiratory pressure (PEEP); (VI) Inspired Oxygen concentration; (VII) Non-intubated thoracoscopic lobectomy; and (VIII) adjuvant pharmacologic options. The recommendations of class II are non-intubated thoracoscopic lobectomy may be an alternative to conventional one-lung ventilation in selected patients. The recommendations of class IIa are: (I) Therapeutic hypercapnia to maintain a partial pressure of carbon dioxide at 50-70 mmHg is reasonable for patients undergoing pulmonary lobectomy with one-lung ventilation; (II) PV with a tidal volume of 6 mL/kg and PEEP of 5 cmH2O are reasonable methods, based on current evidence; (III) alveolar recruitment [open lung ventilation (OLV)] may be beneficial in patients undergoing lobectomy with one-lung ventilation; (IV) PCV is recommended over VCV for patients undergoing lung resection; (V) pre- and post-operative CPAP can improve short-term oxygenation in patients undergoing lobectomy with one-lung ventilation; (VI) controlled mechanical ventilation with I:E ratio of 1:1 is reasonable in patients undergoing one-lung ventilation; (VII) use of lowest inspired oxygen concentration to maintain satisfactory arterial oxygen saturation is reasonable based on physiologic principles; (VIII) Adjuvant drugs such as nebulized budesonide, intravenous sivelestat and ulinastatin are reasonable and can be used to attenuate inflammatory response.
 ...
PMID:The Society for Translational Medicine: clinical practice guidelines for mechanical ventilation management for patients undergoing lobectomy. 3096 78

False localizing signs (FLS) and other misleading neurological signs have long been an intractable aspect of neurocritical care. Because they suggest an incorrect location or etiology of the pathological lesion, they have often led to misdiagnosis and mismanagement of the patient. Here, we reviewed the existing literature to provide an updated, comprehensive descriptive review of these difficult to diagnose signs in neurocritical care. For each sign presented, we discuss the non-false localizing presentation of symptoms, the common FLS or misleading presentation, etiology/pathogenesis of the sign, and diagnosis, as well as any other clinically relevant considerations. Within cranial neuropathies, we cover cranial nerves III, IV, V, VI, VII, VIII, as well as multiple cranial nerve involvement of IX, X, and XII. FLS ophthalmologic symptoms indicate diagnostically challenging neurological deficits, and here we discuss downbeat nystagmus, ping-pong-gaze, one-and-a-half syndrome, and wall-eyed bilateral nuclear ophthalmoplegia (WEBINO). Cranial herniation syndromes are integral to any discussion of FLS and here we cover Kernohan's notch phenomenon, pseudo-Dandy Walker malformation, and uncal herniation. FLS in the spinal cord have also been relatively well documented, but in addition to compressive lesions, we also discuss newer findings in radiculopathy and disc herniation. Finally, pulmonary syndromes may sometimes be overlooked in discussions of neurological signs but are critically important to recognize and manage in neurocritical care, and here we discuss Cheyne-Stokes respiration, cluster breathing, central neurogenic hyperventilation, ataxic breathing, Ondine's curse, and hypercapnia. Though some of these signs may be rare, the framework for diagnosing and treating them must continue to evolve with our growing understanding of their etiology and varied presentations.
 ...
PMID:Chameleons, red herrings, and false localizing signs in neurocritical care. 3292 23