Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lidocaine dosage recommendations vary widely. Severe heart failure adds to risk factors when attempting to reach the optimal therapeutic blood level. Fifty-two coronary care unit (CCU) patients, who were treated with lidocaine infusion after an initial bolus injection of 100 mg, were randomly selected for the study. Blood samples were drawn at 2, 6 and 18 h. The material was divided into four groups according to infusion rates: Group A (n = 15) 4 mg/min for 3 h and then 3 mg/min for 15 h, Group B (n = 10) 4 mg/min for 3 h and then 2 mg/min for 15 h, Group C (n = 9) 2 mg/min for 18 h and Group D (n = 18) according to clinical situation by a mean rate of 3.3 mg/min for 2 h, 2.5 mg/min for 4 h and 2.15 mg/min for 12 h. The mean serum lidocaine concentrations were in optimum therapeutic range of 2-4 mg/l in Groups A, B and D at every sampling time point. Percentage of the patients whose lidocaine concentrations at each sampling time were within the optimum range as follows: Group A 72, 67 and 52, Group B 70, 70 and 56%, Group C 0, 38 and 63% and Group D 38, 38 and 30%. Our material indicates that the optimal lidocaine infusion rate for CCU patients should be as in Group B.
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PMID:Optimum dosage of lidocaine. 398 88

Repeated measurements of lidocaine serum levels during antiarrhythmic treatment were performed by enzyme-immunoassay (EMIT) in 16 patients with acute myocardial infarction. In 12 cases the frequently employed standard dose (100 mg i.v. followed by infusion of 2 mg/min) was not sufficient to reach optimum lidocaine (2-5 mg/l) during the first 2 hours. In this period 6 patients had persistent ectopic beats and required additional bolus injections and increased infusion rates. Lidocaine elimination was delayed in patients with heart failure, which led to potentially toxic drug accumulation in 3 instances. This study indicates the need for individual adaptation of lidocaine dosage in patients with myocardial infarction, especially where left ventricular function is impaired. Monitoring of serum lidocaine levels by a rapid and reliable assay such as the EMIT system may greatly facilitate this task.
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PMID:[Serum concentration measurements for the monitoring of anti-arrhythmic therapy with lidocaine]. 615 56

A case of arrhythmogenic right ventricular dysplasia in a 27 year-old woman is presented, the first one published in Mexico. Palpitations and episodes of syncope were the most important symptoms. Ventricular premature beats and bigeminy without evidence of cardiomegaly or heart failure were disclosed on physical examination. Electrocardiograms revealed frequent, multifocal ventricular extrasystoles with complete left bundle branch block morphology suggesting a right ventricular origin. Dilatation, hypokinesia and decreased ejection fraction were found by both, bidimensional, echocardiography and radionuclear grammography. Right heart catheterization revealed normal pressures and confirmed the hypokinesia, dilatation and decreased ejection fraction; furthermore, irregularities in the endocardial contour of the right ventricle produced a "cauliflower-like" image. Lidocaine suppressed the episodes of ventricular tachycardia, but prevention of recurrences was only obtained with the administration of amiodarone. A review of the literature regarding the diagnosis of this disease is discussed; in addition to the clinical, anatomic and functional aspects above mentioned, an electrophysiological study may be indicated to confirm the right ventricular origin of the arrhythmias with re-entry mechanism.
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PMID:[Arrhythmogenic dysplasia of the right ventricle. First case reported in the Republic of Mexico]. 622 23

As lignocaine clearance is influenced by factors such as cardiac failure and liver impairment, clinical pharmacokinetic principles should be used to account for kinetic variability so that target concentrations are achieved consistently throughout the course of intravenous therapy. Two groups of patients with ischaemic heart disease, who received lignocaine, were studied: a control group with no feedback or intervention from therapeutic drug monitoring, and an intervention group in which strict guidelines for lignocaine administration were introduced. Lignocaine plasma concentrations were measured by EMIT (Syva), and rapid feedback of concentration data in the intervention group allowed adjustment of infusion rates using the Chiou equation. The mean concentration in the intervention group remained within the therapeutic range (2-5 micrograms/ml) at all times, whereas it exceeded 5 micrograms/ml after the first 7 h in the control group. The distribution of concentrations in the intervention group was always narrower than that in the control group. The study also included a comparison of the ability of the Chiou equation and a Bayesian optimisation procedure to estimate pharmacokinetic parameters and to forecast lignocaine concentrations over various periods of time. There was no significant difference between prediction errors determined by the two methods at various points throughout a 32-h period; both methods were associated with a negative prediction bias beyond the first 12 h of infusion. It is likely that this reflects assumptions made about lignocaine clearance and indicates the need for more sophisticated kinetic models.
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PMID:Kinetic predictive techniques applied to lignocaine therapeutic drug monitoring. 663 55

In 21 patients with acute coronary artery disease the influence of cardiac failure on the elimination of lidocaine (L) was evaluated by repeated serum level measurements during and after a therapeutic L-infusion. Lidocaine clearance (Cl) was less than 8 ml/min/kg in 9 of 13 cases with congestive heart failure (CHF), while in 7 out of 8 patients without CHF Cl-values were 8-12 ml/min/kg. Due to wide interindividual variability in the CHF group, however, mean values were not significantly different: 7.3 +/- 2.9 vs. 9.52 +/- 1.54 ml/min/kg (p greater than 0.05). In 3 patients receiving a simultaneous nitroglycerine infusion Cl was greater than 10 ml/min/kg despite clinical signs of CHF. The t 1/2 of L was significantly prolonged in patients with CHF: 4.29 +/- 2.14 vs. 2.43 +/- 0.58 h (p less than 0.05). It was not possible to determine individual L-dose requirements by bedside clinical examination alone. Serum level monitoring is therefore recommended in order to optimize L-therapy in patients with life-threatening arrhythmias, severe congestive heart failure and hypotension.
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PMID:[Slower lidocaine elimination and dose adjustment in patients with heart failure]. 680 62

Lidocaine plasma levels and indocyanine green clearance were measured in five normal volunteers and eight patients admitted to the coronary care unit. All individuals received lidocaine as a 1 mg/kg bolus and a 35 microgram/kg/min constant infusion for 180 minutes. Eight of the 13 (62 per cent) individuals studied (all normal volunteers and three patients) developed early, potentially subtherapeutic plasma lidocaine levels (less than or equal to 2.4 microgram/ml) within 15 minutes after starting therapy. Those individuals with subtherapeutic levels had either minimal (American Heart Association Class) or no clinical evidence of congestive heart failure. The use of indocyanine green (ICG) clearance as an estimate of hepatic plasma flow showed that individuals with early, subtherapeutic lidocaine levels had higher ICG clearance (9.33 +/- 0.32 ml/min . kg versus 2.90 +/- 1.74 ml/min . kg) and shorter ICG t 1/2 (2.02 +/- 0.99 minutes versus 3.6 +/- 0.69 minutes) and larger volume of distribution (36.1 +/- 16.3 ml/kg versus 19.5 +/- 12.8 ml/kg) than patients without subtherapeutic levels. This study suggests that early lidocaine kinetics may be significantly altered by clinical conditions that alter hepatic blood flow. The reappearance of arrhythmias shortly after initiating lidocaine therapy in patients without heart failure may be due to rapid hepatic clearance and subtherapeutic blood levels rather than lidocaine-resistant arrhythmias.
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PMID:Lidocaine kinetics: relationships between early lidocaine kinetics and indocyanine green clearance. 722 15

Recent studies suggest that lidocaine hydrochloride continues to accumulate during prolonged infusions. Plasma levels of lidocaine and monoethylglycinexylidide (MEGX) were measured in 26 patients with cardiac arrhythmias during lidocaine infusions of 15 to 69 hours' duration. Clearance varied, ranging from 3.2 to 14.7 mL/min/kg, and was significantly less in the ten patients with heart failure (5.8 +/- 1.7 mL/min/kg) as compared with the remaining 16 (8.4 +/- 2.6 mL/min/kg; P < .05). The MEGX levels were < 1 microgram/mL. In four patients, steady states were achieved at two different infusion rates, and changes in lidocaine plasma levels were generally proportional to changes in infusion rates. Lidocaine elimination half-lives ranged from 3.2 to 8.7 hours, and no accumulation continued beyond four half-lives. Clearance values, elimination half-lives, apparent volumes of distribution, and, consequently, steady-state levels were widely variable, which can be partly explained by the inclusion of patients with congestive heart failure. Monitoring of serum lidocaine levels may aid in individualization of therapy.
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PMID:Continuous infusion of lidocaine in patients with cardiac arrhythmias. Unpredictability of plasma concentrations. 744 83

1. Blood clearances of lignocaine and indocyanine green together with indocyanine green half-lives were measured in 17 post-myocardial infarct patients (one patient was studied twice) between 8 h and 36 h after starting intravenous lignocaine infusions for the treatment of cardiac arrhythmias. 2. Mean +/- s.d. values of lignocaine clearance (ml min-1 kg-1) were higher in patients without heart failure (11.8 +/- 2.6, n = 9) than in those with heart failure (7.2 +/- 1.9, n = 9) (P < 0002). 3. Clearances of lignocaine and indocyanine green were not correlated but lignocaine clearance was directly related to the reciprocal of indocyanine green half-life (rs = 0.67, P < 0.01). 4. In eight patients who received both lignocaine and indocyanine green and in a further five patients received only lignocaine and whose lignocaine infusions lasted 24h or more, a 25% rise in lignocaine concentrations was observed between 8-12h and 24-28h. 5. The mean +/- s.d. post-infusion terminal half-life of lignocaine in four patients whose lignocaine infusions lasted 30h or longer was 7.2 +/- 2.1 h. 6. Heart failure was associated with greater changes in lignocaine kinetics than in indocyanine green kinetics. 72% of the variance between observed and predicted lignocaine clearances could be accounted for by multiple linear regression analysis incorporating indocyanine green half-life and the presence or absence of heart failure. Indocyanine green half-life contributed only 17% of the variance indicating that by itself it is of limited value in predicting lignocaine requirements. 7. Lignocaine kinetics during and after prolonged intravenous infusion were not predicted by data obtained after intravenous bolus injection. 8. A lowering of lignocaine dosage may be clinically desirable in the presence of heart failure and if an infusion lasts longer than 24 h.
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PMID:Lignocaine and indocyanine green kinetics in patients following myocardial infarction. 744 6

1. The effects of veratridine, BDF 9148 and lignocaine on the action potentials and contractile force of the electrically-driven rat right ventricle have been determined. 2. Veratridine at 10(-7)-10(-6) M and BDF 9148 at 10(-7)-10(-5) M had no effect on the threshold potential or amplitude but prolonged the ventricular action potentials. 3. In contractility studies, veratridine at 10(-7)-10(-6) M augmented the cardiac stimulation responses and the augmenting effects with 3 x 10(-7) and 10(-6) M were greater at 2 than 4 Hz. In the presence of veratridine at 3 x 10(-6) M, the ventricle would not pace. 4. BDF 9148 at 10(-7)-10(-5) M augmented the cardiac stimulation responses and the augmenting effects with 10(-7) and 3 x 10(-7) M were greater at 2 than 4 Hz and the effect was maximal at 3 x 10(-7) M and submaximal at 10(-5) M. The effects of BDF 9148 at 10(-5) were not readily reversible. 5. Lignocaine at 10(-4) M had no effect on the ventricular action potential duration but decreased the threshold potential and amplitude and also reduced the cardiac stimulation force responses. In the presence of lignocaine, the augmenting effects of veratridine and BDF 9148 on ventricular force were reduced. 6. In summary this study has shown that BDF 9148 prolongs the action potential and augments the contractile force responses of the rat right ventricle by a lignocaine-sensitive mechanism. BDF 9148 or similar drugs may have potential as positive inotropes in the treatment of heart failure.
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PMID:The effects of veratridine and BDF 9148 on the action potentials and contractility of the rat right ventricle. 778 34

We experienced two cases of circulatory failure after local infiltration of 0.0005% epinephrine solution for the purpose of prophylactic hemostasis during tonsillectomy under sevoflurane anesthesia. Case 1: A 14 year-old girl developed ventricular bigeminy, tachycardia and hypertension following infiltration of the epinephrine solution 6ml around the tonsil. Sinus rhythm returned with intravenous lidocaine 40 mg and propranolol 0.4 mg. However, the patient showed gradually decreasing heart rate, depressed ST segments and inverted T waves and poor peripheral circulation. Her blood pressure decreased abruptly at the same time and finally the pulsation of the radial and femoral arteries was not palpable. She was treated with intravenous ephedrine in vain. Therefore, she received intravenous epinephrine and cardiac massage, and then recovered from the circulatory failure with her ECG showing normal sinus rhythms. Emergence from the anesthesia was smooth. Her cardiac failure may have been caused by the decreasing cardiac contraction and the increasing afterload due to the vasoconstriction after the intravenous beta-blocker. Case 2: An eleven year-old boy showed ventricular tachycardia and hypertension after infiltration of the epinephrine solution 11.5 ml around the tonsil. Lidocaine was given intravenously. This restored sinus rhythm but the ST segments on his ECG were elevated. ST segments became normalized after intravenous nitroglycerin. However, pulmonary edema developed suddenly, and it was cured by intensive treatment. His ventricular tachycardia and hypertension after the local administration of epinephrine were presumably responsible for the acute heart failure causing the pulmonary edema. Our experience suggests that the maintenance of cardiac function and the reduction of afterload are important to overcome the circulatory disaster following the local infiltration of epinephrine.
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PMID:[Two cases of circulatory failure after local infiltration of epinephrine during tonsillectomy]. 975 60


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