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

Local anaesthetic systemic toxicity is a rare but often dramatic complication of regional anaesthesia. Convulsions often follow warning signs, easily recognized when looked for; but they may occur from the first. They are rapidly followed by hypoxia and hypercapnia which greatly enhance the risk of severe cardiac depression, mainly with bupivacaine or etidocaine. Thiopentone is able to stop convulsions quickly, but may further depress the cardiovascular system. Diazepam has been shown to be effective in the treatment of local anaesthetic-induced convulsions. It gives less myocardial depression, but is much slower in effect. Midazolam, a new short-acting benzodiazepine, should be the best choice. Should tracheal intubation become necessary, suxamethonium can be used. Indeed, the principal use of these drugs is to make ventilation easier, so as to restore rapidly correct oxygenation. Severe cardiac depression, often leading to cardiac arrest, may occur from the first or after the appearance of convulsions. It generally follows a regional block carried out with bupivacaine. A few antiarrhythmic drugs have been used to treat ventricular arrhythmias, either in experimental studies (lidocaine, bretylium) or after clinical accidents (lidocaine). Their efficacy and innocuity have to be proved before they can be proposed to treat these accidents. Bradycardia only needs treatment with atropine when it causes severe haemodynamic disturbances. When cardiac arrest occurs, cardiopulmonary resuscitation must be carried out; its mainstays are: oxygen, sodium bicarbonate, adrenaline, calcium and perhaps glucagon. This must be continued for a long time, as late successes have been published.
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PMID:[How should a toxic accident be treated?]. 290 Jun 15

The effects of respiratory acidosis on renal inorganic phosphate (Pi) handling are controversial. Clearance experiments, therefore, were performed in fasted, chronically parathyroidectomized (PTX), dietary Pi-deprived rats. The objectives were twofold: to study the effects of compensated and uncompensated hypercapnia per se on renal Pi excretion and to examine the interaction between acute hypercapnia, dietary Pi, and parathyroid hormone (PTH) on the renal handling of Pi. Acute hypercapnia increased the plasma Pi (delta 2.82 +/- 0.65 mg/dl, P less than 0.05) without altering the glomerular filtration rate (GFR). The FEPi increased (delta 7.26 +/- 0.48%, P less than 0.001) but the TRPi/GFR also increased. PTH (3 U X kg-1 X h-1) superimposed on hypercapnia resulted in a plasma Pi comparable to hypercapnia alone. The FEPi (7.56 +/- 0.78 vs. 24.43 +/- 2.20%; P less than 0.001) was higher and the TRPi/GFR (117 +/- 4 vs. 80 +/- 2 micrograms/min, P less than 0.01) lower, in the former group. PTH infusion during normocapnia resulted in a lower FEPi (0.20 +/- 0.10 vs. 24.43 +/- 2.20%, P less than 0.001) and a higher TRPi/GFR (106 +/- 2 vs. 80 +/- 2 micrograms/min, P less than 0.01) compared with PTH infusion during hypercapnia. Urinary adenosine 3',5'-cyclic monophosphate (cAMP) excretion was similar between the groups. During hypercapnia, when the extracellular acidemia was neutralized, the phosphaturic action of PTH persisted. These studies offer direct evidence that in chronically PTX, dietary Pi-deprived rats, the phosphaturic action of PTH is restored by hypercapnia per se. This effect appears to be independent of extracellular acidemia, changes in the plasma Pi and calcium, urinary pH and Na and cAMP excretion.
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PMID:Effect of acute hypercapnia on PTH-stimulated phosphaturia in dietary Pi-deprived rat. 303 23

Variations of arterial PCO2 and pH are known to influence myocardial blood flow (MBF) in that hypercapnia results in a coronary vasodilatation, while hypocapnia possibly decreases MBF. The present study was performed to examine if hypocapnia and hypercapnia might influence the sensitivity to exogenous administration of adenosine. Aminophylline, an adenosine receptor blocking agent, was administered to rule out the effect of endogenously liberated adenosine during variations of PCO2 and pH. In the last part of the study, it was examined whether verapamil, a calcium-channel blocker, might influence the MBF response to variations in PCO2 and pH. Closed-chest dogs were anaesthetized with pentobarbital, and hypocapnia induced by hyperventilation. Carbon dioxide was added to the inspiratory gas to create normocapnia and hypercapnia. In the control group hypocapnia did not significantly reduce MBF although a decrease in coronary sinus (CS) SO2 indicated a coronary vasoconstriction. During continuous adenosine infusion (7.5 +/- 0.3 mg/kg/h) which increased MBF 116% during normocapnia, creating hypocapnia caused a 40% decrease in MBF. Hypercapnia seemed to potentiate the vasodilating effect of adenosine. During administration of aminophylline hypocapnia did not cause any decrease in MBF, while hypercapnia increased MBF by 39%, and these results are in harmony with the results obtained in the control group without aminophylline. Verapamil did not result in any altered MBF response to hypocapnia and hypercapnia when compared to the unblocked control group. These observations do not support the idea of any major influence of the Ca2+ fluxes blocked by verapamil as the cause of MBF changes during variations in PCO2 and pH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adenosine modifies canine myocardial blood flow response to hypocapnia and hypercapnia, while aminophylline and verapamil do not. 312 Mar 3

In 60%-90% of cases head injury is a part of multisystem trauma and of very decisive importance for the post-traumatic prognosis. Hypoxia, hypercarbia, and hypotension increase the primary lesion and cause secondary brain damage. Therefore, emergency measures must be directed to the essentials of sustaining vital functions, i.e. intubation/ventilation/oxygenation and stabilization of the circulatory system. All trauma-specific measures should avoid additional increases in intracranial pressure or should decrease it if already elevated. Moderate hyperventilation not only causes cerebral vasoconstriction with a concomitant decrease in intracranial blood volume and intracranial pressure, but also partly restores the disturbed cerebral autoregulation, and is therefore an important part of the emergency care and anesthetic procedure in patients with severe head injuries. It is supplemented by analgesia and sedation to prevent intracranial pressure increases due to painful external stimuli. Elevation of the head and upper part of the body by 30 degrees causes a decrease in intracranial pressure by decreasing intracranial blood volume due to improved venous return from the brain; however, this measure is to be applied only in stable circulatory conditions. The head should be put in mid-position avoiding sideways rotation, flexion, and hyperextension. Osmotically active agents are only indicated in emergency situations when there are signs of clinical deterioration. High-dose barbiturate therapy is reserved as a "last resort", under intensive care conditions, for controlling an otherwise intractable intracranial pressure rise. Calcium antagonists have no indication in this context. Anesthesia in patients with severe head injury must involve only those techniques that do not further increase an already elevated intracranial pressure. As inhalational anesthetics, including nitrous oxide, elevate the intracranial pressure to varying extents due to cerebral vasodilation with a concomitant rise in intracranial blood volume, these substances have to be avoided whenever raised intracranial pressure cannot be excluded. Narcotics, benzodiazepines, small dosages of barbiturates, and long-lasting muscle relaxants can be regarded as useful.
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PMID:[Pathophysiologic principles, emergency medical aspects and anesthesiologic measures in severe brain trauma]. 331 Jul 24

Dantrolene sodium acts primarily by affecting calcium flux across the sarcoplasmic reticulum of skeletal muscle. Recently, dantrolene has been used very successfully in the treatment of several rare hypercatabolic syndromes which have previously been associated with high mortality rates. In malignant hyperthermia, where early diagnosis and treatment usually with intravenous dantrolene in association with other supportive measures (and often subsequent dantrolene therapy) is performed, recovery is seen in virtually 100% of patients. There is a rapid resolution of hyperthermia, dysrhythmias, muscle rigidity, tachycardia, hypercapnia, mottled or cyanotic skin, and metabolic acidosis, and a slower normalisation of myoglobinuria and elevated serum creatine phosphokinase levels. In patients with family history or previous episodes of malignant hyperthermia, prophylactic treatment with dantrolene prior to anaesthesia prevents the syndrome occurring in most cases. Where malignant hyperthermia has developed patients have been successfully treated with further dantrolene therapy. Dantrolene has also been used successfully in the treatment of a few cases of heat stroke and the neuroleptic malignant syndrome--both of which have many similarities to malignant hyperthermia. Dantrolene is well established in the treatment of patients with muscle spasticity where it generally improves at least some of the components of spasticity (i.e. hyper/hypotonia, clonus, muscle cramps and spasms, resistance to stretch and flexor reflexes, articular movement, neurological and motor functions and urinary control). However, in some patients, particularly those with multiple sclerosis, dantrolene may not be effective, and in many cases muscular strength may diminish. Long term dantrolene therapy has been associated with hepatic toxicity and may cause problems in patients treated for disorders of muscle spasticity. Thus, dantrolene offers a unique advance in the therapy available for the treatment of hypercatabolic disorders and is also useful in the treatment of muscle spasticity of various aetiology.
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PMID:Dantrolene. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic use in malignant hyperthermia, the neuroleptic malignant syndrome and an update of its use in muscle spasticity. 352 59

Shifts in the normal balance of neurovegetative and hormonal regulations, modifications in the ionic composition of the plasma and pathological changes such as ischaemia, hypoxia and hypercapnia may lead to changes in permeability of the cardiac cell membranes to different ions, resulting in electrophysiological changes. These are: depressed and non-homogeneous conduction of impulses, lack of homogeneity in excitability and recovery of excitability, increased ectopic automaticity, etc. Interaction of these changes may be responsible for the appearance of arrhythmias. Membrane stabilization in a broader sense means a tendency to restore pathologically altered membrane permeability, permitting normal ionic transport through membranes of the heart muscle cells and protecting the heart from arrhythmia. In this sense not only classical membrane stabilizing agents such as quinidine- or lidocaine-type drugs are antiarrhythmic; so are the very heterogeneous group of agents defined as calcium antagonists or the interventions changing the phospholipid composition of the cardiac cell membrane, such as a linoleic-acid rich diet or adjuvant arthritis. Examples of these actions are given in the heart in situ of the anaesthetized dog and in the conscious rat infarction model.
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PMID:Myocardial cell membrane stabilization and antiarrhythmic action. 353 68

The ionic compensatory response to CO2 breathing for 3 days was studied on intact and cystectomized turtles at 10 and 20 degrees C. Arterial blood gases, pH, ionized calcium, and the plasma concentrations of Na+, K+, Cl-, total Ca2+, and total Mg2+ were measured periodically. At 20 degrees C, ureteral urine was also collected from bladderless turtles and was analyzed for pH, ions, NH3+, total CO2, osmolality, and titratable acid. When CO2 was breathed there was a compensatory change in the strong-ion difference as manifest by an increase in plasma [HCO3-] that was approximately 10 meq/l both in the 10 and 20 degrees C turtles. The only significant associated strong-ion changes observed consistent with the ionic compensatory response were increases in total and ionized Ca2+ and total Mg2+. These results were unaffected at either temperature by surgical removal of the urinary bladder. Urine collected from cystectomized turtles showed no compensatory increase in acid excretion during hypercapnia; in fact, changes occurred in the opposite direction. Urinary excretion of HCO3- and urine pH increased significantly, whereas titratable acidity decreased significantly. No significant change occurred in ammonia excretion over the three days of hypercapnia. These data argue against compensatory roles for the kidneys and urinary bladder in this species and point to internal ionic exchanges involving bone and shell.
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PMID:Ionic compensation with no renal response to chronic hypercapnia in chrysemys picta bellii. 378 4

An estimate of the total mass of bone in the Channel catfish Ictalurus punctatus Rafinesque, was obtained by dissection. The wet weight of bone constituted 16.3 +/- 1.9% (+/- S.D.) of the total (live) wet weight, and 25.0 +/- 2.1% of the dry weight. Of the dry skeletal material, 66.3 +/- 11.1% was soluble in strong acid. The acid-soluble material was about half mineral salts, consisting of 19.5 +/- 2.21% Ca2+ and 27.6 +/- 3.22% PO4(3-), with minor fractions of Mg2+ (0.33%) and CO3(2-) (1.67%). The pH values of fluid compartments associated with skull and vertebral bone tissues were 7.420 +/- 0.026 and 7.444 +/- 0.017 (+/- S.E.), respectively, at a normocapnic plasma pH of 7.868 +/- 0.020. In response to external hypercapnia (7.5 Torr), the blood response consisted of an immediate decrease in pH, and a subsequent compensatory rise in both pH and [HCO3-]. This compensatory phase was accompanied by a net apparent H+ excretion to the water. The participation of the mineral salts of the bone compartment in compensation appeared to be negligible, since there was no significant change in either blood [Ca2+] or [PO4(3-)], nor any significant increase in calcium efflux to the water. The intracellular pH values of the bone compartments were only slightly higher than other tissues, and the changes in pHi during hypercapnia were similar in bone and white muscle. Thus, the bone compartment in the fish appears to be well regulated, relatively refractory to acute acid-base disturbance, and does not serve as an ion source during acid-base compensation.
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PMID:The bone compartment in a teleost fish, Ictalurus punctatus: size, composition and acid-base response to hypercapnia. 406

Tiapamil was effectively used in 32 surgical patients in the treatment of intra- and postoperative cardiac arrhythmias such as atrial fibrillation, supraventricular paroxysmal tachycardia and extrasystoles and in ventricular ectopic beats. In 28 patients aged between 38 and 82 years, bolus doses of 0.3-1.5 mg/kg were used. Before administration, hypoxaemia, hypercarbia, metabolic acidosis and electrolyte imbalances were excluded. Small doses of 0.3-0.5 mg/kg were only effective in patients with tachycardic atrial fibrillation. In most other arrhythmias the effective dose was between 1 and 1.5 mg/kg. In 4 surgical patients aged between 56 and 82 years, the continuous infusion of 12-25 mg/h (in 2 patients preceded by a bolus injection of 1 mg/kg) was effective in abolishing arrhythmias. In 18 healthy subjects, systolic time intervals were measured continuously and noninvasively before, during and for 9 min after 1 mg/kg tiapamil or 0.13 mg/kg verapamil, given intravenously according to a randomization schedule. Heart rate increased and systolic blood pressure decreased slightly but significantly. A significant improvement in myocardial function, with a decrease in PEP and PEP LVET ratio, was found after both calcium antagonists. The effect of tiapamil on myocardial function lasted significantly longer than that of verapamil.
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PMID:Effect of tiapamil on perioperative cardiac arrhythmias and myocardial function. 618 22

The paper concentrates on measurements of tissue pO2 and local flow, which are both assumed to determine the nervous signal of the carotid body. The measurements were performed with needle electrodes. Inside the specific tissue of the carotid bodies of cat and rabbit, which is assumed to be surrounded by an oxygen barrier, pO2 values between 7 and 25 torr were recorded. From experiments on the fetal carotid body it was concluded that these low values are essential for the chemoreceptive process. Two types of blood flow were observed in the carotid body: high flow running through arteriovenous shunt vessels or flow-through channels (total flow), and low flow running through the capillaries supplying the specific tissue (local flow). Local flow decreases under hypoxia, whereas total flow follows the changes in blood pressure in any case. These pO2-dependent regulatory mechanisms influence the extracellular calcium activity, which determines the calcium uptake of type I cells under hypoxia and, consequently, (by vesicle release) the chemoreceptor discharge. Other mechanisms are assumed to be involved during hypercapnia, since under these conditions local flow does not change.
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PMID:The meaning of tissue pO2 and local blood flow for the chemoreceptive process of the carotid body. 624 45


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