Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Records of all patients with a clinical diagnosis of septic shock were reviewed retrospectively; cases occurred from August 1968-July 1971 in a general teaching hospital with 667 beds. In the 3-year period, 80 patients (38 males and 42 females) presented with 82 episodes of septic shock; this represented 14% of total hospital admissions to Intensive Care. The age range was from 15-78 years, with a mean of 52+ or -16 years. The incidence of the syndrome increased with age, reaching a maximum in the 7th decade. 66 (0f 71) of the surgical/gynecological referrals followed operative procedures, of which 1/2 were undertaken electively. By the time of referal to the Intensive Care Unit, pyrexia, hyperventilation, cyanosis, vasoconstriction, pallor, and sweating were commonly present, although 16 patients presented with warm hypotension; moderate hypotension was present in 48 patients, and severe hypotension was present in 18. Dehydration, oliguria, and azotemia were frequently present on admission. Abnormalties in serum electrolytes were common. Blood gas analysis on admission revealed that marked hypoxemia was commonly present in association with hypocapnia and metabolic acidosis. Blood cultures were performed in 62 patients and positive results were obtained in 38 on at least 1 occasion. Of a total of 47 positive blood cultures, 33 were gram-negative organisms and 5 were gram-negative anaerobic bacilli. The former were sensitive to gentamisin and the latter were resistant to both the cephalosporins and ampicillin. Gram-positive organisms were sensitive to cloxacillin and cephalosporins. Initial mortality was 64%, which increased to 70% including late deaths after return to wards. Nonsurvivors were significantly older than survivors (P .005); they were more frequently dehydrated (P .005); and they were more subject to the development of tachycardia and cardiac arrhythmias. Nonsurvivors were also considerably more hypoxemic than survivors. There was a marked difference between nonsurvivors and survivors in mode of presentation and infection source; nonsurvivors were characterized by either mediastinitis as a consequence of leakage of an esophageal anasotmosis or fecal peritonitis.
 ...
PMID:A three year retrospective analysis of septic shock in a general hospital. 23 90

Infants born to opiate-dependent women frequently have low birth weights and low 1- and 5-min Apgar scores. Significant postnatal problems, excluding neonatal withdrawal, can include jaundice, infection, aspiration pneumonia, transient tachypnea, and hyaline membrane disease. Neonatal abstinence may be severe and persist for as long as 3 months. Abstinence symptoms can include central nervous system hyperirritability, gastrointestinal dysfunction, respiratory distress, tremors, fever, high-pitched cry, increased muscle tone, uncoordinated sucking and swallowing reflexes, dehydration, and possible electrolyte imbalance. During the first week of life, increased respirations associated with hypocapnia and alkalosis may occur. The Brazelton Neonatal Behavioral Assessment Scale has been used to quantify the neurobehavioral effects on neonates of narcotics administered prenatally. A marked decline in mortality rates of infants born to opiate-dependent mothers is evident. In Philadelphia, infant morbidity has been related not only to the type of maternal narcotic dependence, but also to the amount of prenatal care. Infants whose mothers received prenatal care have been found to have higher birth weights similar to infants of control mothers. Although the newborn with intrauterine exposure to narcotic agents may appear normal at birth, the effects of the pharmacologic agent may not become apparent until later in development. To obtain a more favorable outcome for the high-risk mother and child involved in the problems of perinatal addiction, several recommendations are proposed.
 ...
PMID:Effects of maternal opiate abuse on the newborn. 388 86

1. Birds lose water in evaporation from the respiratory tract and, in many species, through the skin. Anatomical arrangements in the nasal passages to conservation of water and hear from the expired air in the absence of heat loads. However, most species still expend more water in evaporation than they produce in metabolism when either quiescent or vigorously active. Certain small birds, several of them associated with arid environments, represent exceptions to this and their more favorable situation appears in part to reflect as an ability to curtail cutaneous water loss. 2. Birds typically resort to panting in dealing with substantial heat loads developing in hot environments or accumulated over bouts of activity. In a number of species this form of evaporative cooling is supplemented by gular fluttering. 3. The ubiquitousness of active heat defense appears to reflect more the importance for birds of dealing with heat loads existing following flight or sustained running than any universal affinity for hot climates. Panting can be sustained for hours, despite progressive dehydration and, in some instances, hypocapnia and respiratory alkalosis. The prominent involvement of thermoreceptors in the spinal cord in its initiation is of considerable interest.
 ...
PMID:Evaporative losses of water by birds. 612 38

The object of this review is to provide the definitions and criteria for diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS), and convey current knowledge of the causes of permanent disability or mortality from complications of these conditions, of the risk factors for DKA and HHS, and of early indicators and contemporary treatment of suspected cerebral edema. The frequency of DKA at onset of type 1 diabetes mellitus (DM1) varies from 10-70%, depending on availability of health care and frequency of diabetes. At the onset of type 2 diabetes (DM2), DKA occurs in 5-52%. One study reported HHS in approximately 4% of new patients with DM2. Recurrent DKA rates are equally dependent on variability in medical services and socio-economic circumstances, and are estimated to be eight episodes per 100 patient years, with 20% of patients accounting for 80% of the episodes. Mortality for each episode of DKA internationally varies from 0.15-0.31%, with idiopathic cerebral edema accounting for two-thirds or more of this mortality. Other causes of death or disability include untreated DKA or HHS, hypokalemia, hypophosphatemia, hypoglycemia, other intracerebral complications, peripheral venous thrombosis, mucormycosis, rhabdomyolysis, acute pancreatitis, acute renal failure, sepsis, aspiration pneumonia, and other pulmonary complications. Population-based studies from the UK, Australia, the USA, and Canada report cerebral edema incidence in DKA of 0.5-2.0%. Published information does not support the notion that treatment factors are causal in cerebral edema. Younger age, greater severity of acidosis, degree of hypocapnia, and severity of dehydration have been suggested as risk factors in several studies. Bimodal distribution of the time of onset of cerebral edema and wide variation in brain imaging findings suggest the variability and likely multiple causation of the clinical picture. Functional brain scanning has indicated that DKA is accompanied by increased cerebral blood flow suggesting that the predominant mechanism of edema formation is a vasogenic process. A method of monitoring for diagnostic and major and minor signs of cerebral edema has been proposed and tested which indicates that intervention will be required in five individuals to provide early intervention for a single case of cerebral edema. The preferred intervention of mannitol infusion has typically been accompanied by intubation and hyperventilation, but recent evidence indicates outcome is adversely affected by aggressive hyperventilation. The prevention of DKA and HHS at the onset of diabetes mellitus requires a high degree of awareness and suspicion by primary care providers; prevention of recurrent DKA necessitates a diligent team effort.
 ...
PMID:Hyperglycemic crises and their complications in children. 1731 23

The effects of two transportation periods on physio- metabolic hemodynamic changes and gaseous exchange in commercial swine during transportation to the slaughterhouse was studied in 684 pigs, 357 barrows and 327 gilts, transported in 2 groups for 8 and 16 h. Transportation caused an increase of oxygen consumption and body temperature, a decrease in pH, lactic acid accumulation. Both transportation periods caused higher than normal plasma glucose levels, lactic acidosis and evidence of dehydration. The linear regression analysis for pigs transported for 8h indicates that the PO(2,) lactate and Ca(++) variables correlated negatively with the PCO(2.) Whilst the animals that were transported for 16 h had negative correlations between glucose, and calcium, hematocrit, lactate and potassium levels. It was concluded that regardless of transport time acidosis, hypocapnia, hypoxaemia, hypernatraemia, hypercalcaemia, hyperglycemia, lactacidemia and increased hematocrit levels occurred.
 ...
PMID:Changes in blood constituents of swine transported for 8 or 16 h to an Abattoir. 2073 49

Spinal muscular atrophy type I (SMA-I) is characterized by progressive muscle weakness with onset in early infancy, usually resulting in mortality before two years of age. However, the processes underlying the pathophysiological progression of the disease remain unclear. Prior to the onset of muscle weakness, a regression of local capillaries is observed along with motor neuron loss. Local populations of neurons, astrocytes, and vascular endothelial cells constitute a neurovascular unit (NVU), in which neuronal and synaptic metabolism is tightly coupled to capillary blood flow by astrocyte-mediated vasodilatory control. We hypothesize that survival motor neuron protein deficiency and initial neuronal dysfunction leads to the regression of vascular beds and the disruption of NVU function. As a result, local capillary blood flow becomes insufficient, leading to metabolic stress in neurons, endothelial cells, pericytes, and astrocytes, ultimately disrupting the astrocytic regulation of capillaries. This pathogenic process may accelerate the loss of anterior horn motor neurons, leading to the further regression of capillaries and astroglial dysfunction. Hypocapnia, resulting from dehydration and hyperventilation during therapeutic manual ventilation, might further damage the NVU. Moreover, disruption of the microcirculation may affect sympathetic and sensory neurons in the spinal cord, contributing to sympathetic hyperactivity and sensory nerve degeneration, respectively. These mutually reinforcing processes may underlie the progression of muscle weakness during infancy in SMA-I. Therefore, disruption of the NVU and a stressful neurovascular environment in the anterior horn may play important roles in disease initiation and/or progression in SMA-I. The NVU is therefore a critical therapeutic target for treating SMA-I. Our hypothetical model may provide insight into why most neuroprotective strategies that do not address astroglial and vascular cell dysfunction have limited efficacy.
...
PMID:Early disruption of neurovascular units and microcirculatory dysfunction in the spinal cord in spinal muscular atrophy type I. 2643 86

The most frequent cause of syncope in young athletes is noncardiac etiology. The mechanism of noncardiac syncope (NCS) in young athletes is neurally-mediated (reflex). NCS in athletes usually occurs either as orthostasis-induced, due to a gravity-mediated reduced venous return to the heart, or in the context of exercise. Exercise-related NCS typically occurs after the cessation of an exercise bout, while syncope occurring during exercise is highly indicative of the existence of a cardiac disorder. Postexercise NCS appears to result from hypotension due to impaired postexercise vasoconstriction, as well as from hypocapnia. The mechanisms of postexercise hypotension can be divided into obligatory (which are always present and include sympathoinhibition, histaminergic vasodilation, and downregulation of cardiovagal baroreflex) and situational (which include dehydration, hyperthermia and gravitational stress). Regarding postexercise hypocapnia, both hyperventilation during recovery from exercise and orthostasis-induced hypocapnia when recovery occurs in an upright posture can produce postexercise cerebral vasoconstriction. Athletes have been shown to exhibit differential orthostatic responses compared with nonathletes, involving augmented stroke volume and increased peripheral vasodilation in the former, with possibly lower propensity to orthostatic intolerance.
 ...
PMID:Pathophysiology of Noncardiac Syncope in Athletes. 2960 37