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)

Because of the close anatomic and physiologic relationship between the heart and lungs, patients with chronic obstructive lung disease are at special risk of arrhythmias. Effective therapy hinges on identifying the mechanisms of the arrhythmias--hemodynamic, metabolic, or drug-induced. Impulsive use of antiarrhythmic agents may result only in a more complex and dangerous rhythm disorder. Extremes of pH are a major cause of arrhythmias in these patients. Respiratory alkalemia usually originates with inappropriate ventilation, often during mechanical respiration, while metabolic alkalemia generally can be traced to diuretic or bicarbonate therapy. Lidocaine or diphenylhydantoin are of little use, since the alkaline pH inside and outside heart muscle cells hampers drug distribution and activity. At the other extreme, the arrhythmias of acidemia strike patients who have severe respiratory failure with carbon dioxide retention or severe cardiac failure with shock and lactic acidemia. Arrhythmias may develop if vagal restraint is lost, which is especially likely in patients with potassium depletion. Irritant receptors along the bronchopulmonary tree can trigger arrhythmias if stimulated by cough, microembolism, or mechanical irritation, which is a hazard with endotracheal or tracheostomy tubes.
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PMID:Mechanisms of arrhythmias in chronic obstructive lung disease. 1 Feb 30

The authors studied the effect of lidocaine infusion on the ventilatory response to isocapnic hypoxia in nine healthy male subjects. Lidocaine infusion (serum concentration 3.6 +/- 0.1 micrograms/ml) was associated with a decrease in the shape factor, "A," of the hypoxic ventilatory response in eight of our nine subjects (P less than 0.02). Overall, "A" decreased from 419 +/- 102 1 . min-1 . mmHg before lidocaine to 335 +/- 77 1 . min-1 . mmHg during lidocaine infusion (mean +/- SEM, N = 9). The authors conclude that despite significant intersubject variability, clinically useful serum lidocaine concentrations depress hypoxic ventilatory drive. Patients with carbon dioxide retention, whose resting ventilation depends on hypoxic drive, may be at risk of ventilatory failure when lidocaine is administered for arrhythmia control or regional anesthesia.
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PMID:The effect of lidocaine infusion on the ventilatory response to hypoxia. 650 23

Cerebral air embolism can have hemodynamic effects such as increases in blood pressure and cerebral blood flow. It has been suggested that these factors play a role for the induction of the blood-brain barrier (BBB) dysfunction. In the present study, 5 microliters air was injected into the right internal carotid artery from a catheter in the external carotid artery after ligation of the extracerebral branches. No consistent change in blood pressure was observed with this small amount of air. Hypercapnia, which increases protein leakage in the brain under conditions of high intraluminal pressure, significantly reduced the extravasation in air embolism. Lidocaine and SITS (4 acetamido-4-isothiocyano-stilbene-2,2-disulfonic acid disodium), two drugs that effectively reduce the albumin leakage in acute hypertension, had no prophylactic effect in cerebral air embolism. Spontaneously hypertensive rats are less vulnerable than normotensive rats to pressure-induced BBB dysfunction but did not significantly differ from controls regarding albumin leakage in the present study. It is concluded that the increased cerebrovascular permeability in air embolism is not related to hemodynamic factors.
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PMID:Cerebral air embolism and the blood-brain barrier in the rat. 678 18

A 17-month-old boy developed grand mal seizures secondary to lidocaine toxicity during balloon dilatation of a congenital pulmonary valve stenosis. Lidocaine at 38 mg/kg (nine times the recommended maximum dose of 4.5 mg/kg) was administered during a 90-min period in order to optimize local anesthesia. This resulted in toxic serum lidocaine levels (8.7 mg/L; therapeutic range, 1.5-5 mg/L) at the time of seizures. Caution should be exercised with local anesthetics during invasive cardiac catheterizations. Hypercarbia (which lowers the seizure threshold to local anesthetics) should be avoided and the temptation to exceed the maximum recommended dose resisted.
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PMID:Seizures due to lidocaine toxicity in a child during cardiac catheterization. 846 28

The purpose of the first study was to identify the relationship between reflex sympathetic nerve activity and plasma concentration of lidocaine. Lidocaine was infused in 4 different doses: 2 mg.kg-1 bolus + 100 micrograms.kg-1 x min-1, 3 mg.kg-1 bolus + 200 micrograms.kg-1 x min-1, 6 mg.kg-1 bolus + 400 micrograms.kg-1 x min-1 and 12 mg.kg-1 bolus + 800 micrograms.kg-1 x min-1. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 micrograms.kg-1) and phenylephrine (2-4 micrograms.kg-1) were performed before and at 10 min after the start of lidocaine infusion. Plasma lidocaine concentrations determined by HPLC revealed that its steady-state levels were maintained during the baroreflex tests. Baroreflex sensitivity was preserved at clinical concentrations of lidocaine (< 5 micrograms.ml-1). However, baroreflex was significantly attenuated when plasma lidocaine concentrations were above seizure levels (> 10 micrograms.ml-1). This result indicates that hemodynamic derangement observed in the lidocaine-induced CNS toxicity is, at least in part, due to the attenuated arterial baroreflex. In the second study, the author evaluated the effect of respiratory acidosis and alkalosis on the baroreflex with or without lidocaine infusion (2 mg.kg-1 + 100 micrograms.kg-1 x min-1). Respiratory acidosis (PaCO2: 65.6 +/- 3.4) enhanced the baroreflex significantly, but lidocaine infusion abolished this acidosis-induced enhancement. The author concludes that hypercarbia should be avoided in patients receiving intravenous lidocaine infusion.
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PMID:[Effect of intravenous lidocaine infusion on arterial baroreflex]. 851 40

Lidocaine is commonly used for topical anesthesia of the upper airway in patient with anticipated difficult tracheal intubation undergoing awake fiberoptic intubation. Lidocaine toxicity is dose related and proportional to its plasma level. Although neurologic toxicity has been frequently observed with intravenous use, it has also been reported for topical use. We report on a case of a patient with base tongue abscess who developed sudden seizures and coma during application of topical anesthesia with lidocaine for awake fiberoptic intubation. The presence of a deep neck infection that causes hyperemia and edema of the pharyngolaryngeal mucosa may enhance transmucosal systemic absorption of local anesthetic. Moreover, conditions such as hypercarbia, dysphagia, or hepatic diseases are known to facilitate onset of lidocaine neurologic toxicity with serum concentration lower than normal. These findings should be kept in mind before administering topical anesthesia of the upper airway. In the presence of any of these conditions above, either the total dose of local anesthetic or its concentration should be reduced as much as possible.
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PMID:Neurologic toxicity of lidocaine during awake intubation in a patient with tongue base abscess. Case report. 2412 Jun 92