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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute postoperative hypertension (APH) has been documented in the PACU. Over half of the patients who exhibit APH have pre-existing primary hypertension. Sustained blood pressure (BP) elevation increases the risk of myocardial ischemia, infarction, surgical site bleeding, or cerebral hemorrhage in these patients. Following surgery and anesthesia, increased sympathetic stimulation caused by a high level of circulating catecholamines can lead to APH. Some direct perioperative stimulants include pain, anxiety, hypoxia, hypercapnia, hypothermia, shivering, volume overload, and bladder distension. Nursing interventions are directed toward identifying and relieving the cause of APH. Antihypertensive drug therapy with vasodilators or adrenergic inhibitors is used if initial nursing interventions are not effective. Vasodilators frequently used are hydralazine, sodium nitroprusside, and nitroglycerin. Nicardipine has recently been introduced as an intravenous calcium channel blocker. Vasodilators are effective in BP reduction but may cause reflex tachycardia when used alone. Adrenergic inhibitors, such as esmolol and labetalol, block alpha and/or beta receptors to decrease heart rate and BP. Labetalol's effectiveness, relative freedom from side effects, and ease of administration have made it a useful drug in the treatment of APH.
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PMID:Acute postoperative hypertension in the hypertensive patient. 173 70

Exposure of rainbow trout to environmental hyperoxia (PIO2 approximately 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (PIO2 approximately 145 Torr) at this time induced a metabolic alkalosis which was corrected by 24 h. Intracellular pHi ([14C]DMO method), fluid volumes [3H]PEG-4000 method), and electrolytes were monitored. Environmental hypercapnia (PICO2 approximately 6.5 Torr) was employed to confirm that intracellular responses were specific to respiratory acidosis. Gill pHi did not change during respiratory acidosis despite a very low non-HCO3- buffer capacity, but gill ICFV decreased markedly. A large loss of gill intracellular [Cl-]i in excess of [Na+]i, combined with a substantial gain in [K+]i, contributed to gill pHi regulation by raising branchial [SID]i. In weakly buffered brain tissue, active adjustment of pHi started within 3 h, but two well buffered tissues, RBC and white muscle, exhibited compounding metabolic acidoses during the first 12-24 h. The muscle response was associated with small increases in ICFV and [Cl-]i, and a large decrease in [K+]i which reduced muscle [SID]i. We hypothesize that this initial export of K+ and basic equivalents served to regulate pH in more critical compartments (e.g. gills, brain) at the expense of muscle acidosis. By 48 h, pHi restoration in all tissues was complete, in advance of pHe regulation (72 h). Return to normoxia at 72 h elevated muscle, brain, and gill pHi, but there was no evidence of a comparable 'altruistic' role of muscle during this metabolic alkalosis. Regulation of pHi was complete by 24 h recovery, accompanied by partial or complete restoration of intracellular ions and fluid volumes.
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PMID:Intracellular acid-base responses to environmental hyperoxia and normoxic recovery in rainbow trout. 175 56

We investigated the effects of arterial carbon dioxide tension on the myocardial tissue oxygen tensions of subepicardium and subendocardium in the anesthetized dogs. The study was done in fourteen open-chest mongrel dogs, weighing 13 +/- 1 kg, anesthetized with sodium pentobarbital (30 mg.kg-1 iv), and mechanically ventilated with 100% oxygen to maintain normocapnia. End tidal CO2 fraction (FECO2) was monitored continuously by capnograph. Regional myocardial tissue PO2 was measured using a monopolar polarographic needle electrode. Two pairs of combined needle sensors were carefully inserted, one in the epicardial and the other in the endocardial layer of the beating heart. Electromagnetic blood flow probe was applied on the left anterior descending artery (LAD). After a stable normocapnic ventilation, hypocapnia was induced by increasing the respiratory rate, and this mechanical hyperventilation was kept fixed throughout the experiments. To induce hypercapnia, exogenous carbon dioxide was added to the inspired gas step-wise until FECO2 reached 10%. Hypocapnic hyperventilation (PaCO2: 22 mmHg) invariably resulted in a significant reduction of coronary blood flow (LADBF) and left ventricular myocardial tissue PO2 in both epicardial and endocardial layers, while addition of carbon dioxide to the inspired gas (hypercapnic hyperventilation) reversed the change by increased LADBF and arterial PaCO2 in a dose-dependent manner. These results indicate that injudicious and severe hypocapnic hyperventilation may induce impaired myocardial tissue perfusion and oxygenation although normal cardiac output and arterial blood oxygenation are maintained.
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PMID:[Effect of arterial carbon dioxide tension on regional myocardial tissue oxygen tension in the dog]. 176 12

In order to minimize heat loss cold stress induces peripheral vasoconstriction via the sympathetic nervous system. This effect is most pronounced in the extremities. Vasoconstriction does not appear in the head-neck region--a fact of great importance in emergency situations. In order to compensate for heat loss shivering is an early event, where involuntary muscle contractions increase metabolic rate 2-6 fold. Early tachycardia and elevated blood-pressure, followed by progressive bradycardia and lowered pressure are common cardiovascular effects of hypothermia. Death due to ventricular fibrillation or asystole occurs between 28 degrees-25 degrees C. Cold stress causes an osmolal diuresis with sodium and chloride as the main constituents. The natriuresis is of tubular origin and could be due to impaired autoregulation in the kidney and/or depend on the natriuretic polypeptide. The augmented urine flow decreases blood volume, lowers physical working capacity and increases blood viscosity--all negative events in a hazardous situation. Sudden immersion initiates hyperventilation for 1-2 minutes with an increasing risk of drowning. Thereafter ventilation decreases to rates consistent with metabolic requirements. In severe hypothermia carbon dioxide retention causes respiratory and metabolic acidosis. Hypothermia induces progressive depression of mental functions starting with apathy and bizarre behaviour and ending in lethargy and coma often between 30 degrees-28 degrees C. The paradoxal feeling of heat with undressing in agony could depend on cerebral receptor disturbances.
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PMID:Human physiology under cold exposure. 181 74

Atrial natriuretic factor (ANF) is a peptide secreted by auricular cardiac cells and acts on the brain; it is a diuretic, a natriuretic and a vasodilator and inhibits the renin angiotensin aldosterone system at several levels. The lungs are rich in specific ANF receptors present both at a vascular cellular level and in the mesothelial cells. These receptors participate in the extraction of ANF during its pulmonary intravascular transit and also in its enzymatic degradation. Endogenous ANF (and exogenous) is a vasodilator of the pulmonary arterial bed, representing a regulatory system for right ventricular afterload and probably modifying pulmonary capillary permeability. Hypoxia and hypercapnia contribute by direct and indirect mechanisms to the stimulation of ANF secretion explaining their elevated levels in pulmonary arterial hypertension and chronic respiratory insufficiency. The lung can under certain conditions synthesise ANF itself as can neuro-endocrine bronchial tumours. ANF may be involved in the understanding of sodium retention during ventilation with PEEP and in the paraneoplastic hyponatraemia of certain bronchial tumours. Finally acute bronchial obstruction leads to hypersecretion of ANF which has some bronchodilator properties.
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PMID:[Atrial natriuretic factor and the lung]. 183 Mar 97

We tested the hypothesis that cerebral blood flow (CBF) reactivity to CO2 after global ischemia takes longer to recover in 1- to 2-wk-old piglets than in 6- to 10-mo-old pigs. All animals were sedated with ketamine and anesthetized with pentobarbital sodium. Cerebral ischemia was produced by sequentially tightening ligatures around the inferior vena cava and ascending aorta for 10 min. The microsphere-determined CBF response to hypercapnia (arterial PCO2 approximately 65 mmHg) was depressed at 60 min of reperfusion (9 +/- 6% of preischemia; means +/- SE) and remained depressed at 120 min (33 +/- 23% of preischemia, means +/- SE) in young pigs. In older pigs, the response was also depressed at 60 min of reperfusion (21 +/- 9% of preischemia) but was not depressed at 120 min. The pattern for recovery of hypercapnic reactivity was present in most brain regions except cerebellum, where CO2 reactivity returned to control in young animals by 120 min of reperfusion. The response to hypocapnia (arterial PCO2 approximately 25 mmHg) was also better preserved in older pigs. In older pigs recovery of CO2 reactivity during reperfusion paralleled recovery of cerebral O2 consumption over time. We conclude that older pigs have quicker return of CBF CO2 reactivity following transient global ischemia, which may be due to age-related differences in mechanisms of vascular reactivity.
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PMID:Age-related cerebrovascular reactivity to CO2 after cerebral ischemia in swine. 190 1

The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. Metabolic acidosis (pH 7.20) and alkalosis (pH 7.60) were induced with HCl and Carbicarb (isosmolar Na2CO3 and NaHCO3), respectively. Hypercapnia was induced by adding inspiratory CO2, whereas pH was allowed to change (respiratory acidosis, pH 7.20) or maintained constant (isolated hypercapnia). Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.
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PMID:Acid-base status affects gas exchange in canine oleic acid pulmonary edema. 201 14

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 mM) 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 less than 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.
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PMID:The effects of hyponatraemia and subarachnoid haemorrhage on the cerebral vasomotor responses of the rabbit. 205 Jul 54

Neotenic larval Ambystoma tigrinum were subjected to hypercapnia (3% CO2, 22 Torr) for 24 h under different conditions: alpha-adrenergic blockade using phentolamine, beta-adrenergic blockade using propranolol, and sham treatments. The sham animals were able to carry out a partial extracellular pH compensation that consisted of an increase in extracellular [HCO3-]. Animals treated with catecholamine antagonists did not compensate to the same extent. Analysis of plasma samples by high-performance liquid chromatography with electrochemical detection revealed a significant increase in circulating norepinephrine, but not epinephrine, during the high-CO2 exposure. Measurements of cutaneous ion transport showed that beta-antagonists block the increased Na+ influx associated with hypercapnia, whereas alpha-antagonists inhibited the decrease in cutaneous Cl- influx that is also associated with respiratory acidosis. Additionally, both alpha- and beta-blockers inhibited the increase in transcutaneous potential difference that accompanied the respiratory acidosis. The results are consistent with a role for circulating catecholamines in compensatory ion transport responses to respiratory acidosis in this species.
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PMID:Acid-base-electrolyte balance responses to catecholamine antagonists in Ambystoma tigrinum. 211 75

During surgery under pentobarbital sodium anesthesia, 20 rats had heat exchange devices implanted into their abdominal cavity. After recovery, 14 rats underwent two sets of trials, one in which body core temperature (Tbc) was lowered to 34.5-35.5 degrees C and another in which Tbc was raised to 40.5-41.5 degrees C. Rats breathed air and hypoxic (15, 11, and 7% O2 in N2) and hypercapnic (2, 4, and 6% CO2 in air) gas mixtures. Respiratory responses were measured using a barometric method and compared with data from the same rats breathing the gas mixtures at normal Tbc (37.5-38.5 degrees C) before surgery. The six remaining rats served as controls (Tbc unchanged). Lowering Tbc increased respiration in air, whereas heating had no effect. Hypothermia and severe hypoxia combined to inhibit respiration when compared with breathing air at lowered Tbc or low O2 at normal Tbc. The CO2 response slope became steeper when Tbc was raised, suggesting an increased CO2 sensitivity. Possible sites for the hypothermia-hypoxia interaction and the hyperthermia-hypercapnia interaction are discussed.
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PMID:Body temperature effects on hypoxic and hypercapnic responses in awake rats. 211 31


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