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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 12 patients with heart disease, hypercarbia was induced for carotid endarterectomy. Anesthesia was maintained with nitrous oxide in oxygen and methoxyflurane. In addition to intra-arterial measurements of blood pressure, cardiac output, systolic time intervals (STI), and pressure time indices (PTI) were determined in order to assess cardiovascular responses in these patients. Internal carotid stump blood pressure was measured in five patients before and after induction of hypercarbia. Mild elevation of the Paco2 level affected systolic time intervals but not heart rate and blood pressure. When Paco2 levels reached 56 to 65 torr, systolic but not diastolic blood pressure rose significantly, heart rate and cardiac output increased, while the shortening in the preejection period (PEP), left ventricular ejection time (LVET), and the decrease in the PEP/LVET ratio signified increased mechanical cardiac activity. Hypercarbia caused intense sympathetic stimulation as demonstrated by twofold to threefold increases in plasma catecholamine levels. Stump blood pressure was elevated. Cardiac oxygen demand was significantly increased, while coronary filling time was shortened, as indicated by the increase in the tension time index and shortening in the diastolic time. This signified a relative myocardial underperfusion. Thus, while hypercarbia to levels of 66 to 70 torr increased internal carotid artery stump pressure, it also caused increased cardiac mechanical activity and concomitant unfavorable balance between myocardial oxygen consumption and supply. The measurement of STI and the computation of PTI provided early detection of alterations in cardiac function.
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PMID:Cardiac function and hypercarbia. 70 41

Hypoxic vasoconstriction has been the subject of many studies, but little is known about the interaction of hypercapnia and the pulmonary circulation. We performed two haemodynamic studies on each of three patients with pulmonary vascular disease secondary to congenital heart disease. On the first occasion ventilation was inadequate due to technical problems, and the patients were therefore hypercapnic (arterial pCO2 greater than 5.3 kPa). On the second occasion, they were normocapnic. Pulmonary vascular resistance was measured on each occasion while the patients were breathing 100% oxygen (alveolar hyperoxia) and while epoprostenol (prostacyclin) was infused at doses of 5-20 ng/kg/min. Pulmonary vascular resistance was elevated in the presence of hypercapnia and, despite oxygen and epoprostenol, could not be reduced to the levels observed in the normocapnic study. We conclude that hypercapnia causes significant vasoconstriction in infants; and that epoprostenol is a relatively ineffective pulmonary vasodilator in infants who are hypercapnic due to inadequate ventilation. Where possible, respiratory acidosis should be corrected before using oxygen or epoprostenol as a pulmonary vasodilator.
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PMID:Interactions between alveolar hypercapnia and epoprostenol on the pulmonary circulation: clinical and pharmacological implications. 213 21

Respiratory failure accompanied by cardiac failure occurs mostly due to decreased PaO2. However, sometimes we encounter patients with cardiac failure having on increase of PaCO2, who develop CO2 narcosis in the ICU. In this study we evaluated hypoventilation respiratory failure in patients with cardiac failure. Seventy-six patients with both respiratory failure and cardiac failure caused by intrinsic heart disease, who required mechanical ventilation in the ICU were studied. The patients were divided into 2 groups; hypoxic respiratory failure group (n = 53) and hypoventilation respiratory failure group (n = 23). Blood gas analysis and cardiovascular hemodynamics including arterial blood pressure, heart rate and Swan-Ganz catheter findings were performed before, during and after mechanical ventilation in each patient. Mortality rate and its relation to hemodynamic variables were also evaluated in each group. In both groups even when it was possible to maintain oxygenation capacity by conducting mechanical ventilation against severe respiratory failure, what can be said about the prognosis is that it depended totally on the improvement of cardiac function. The mechanism by which hypoxemia is displayed due to cardiogenic pulmonary edema is already well known, but in regard to the mechanism of hypercapnia in cases with hypersensitivity of the airways it is thought that through induction of cardiogenic pulmonary edema bronchial spasms is induced, and this causes hypercapnia. However, it is also possible to consider cardiac asthma as the cause. Among respiratory failure cases due to cardiogenic pulmonary edema that occurs in association with heart failure, there is both hypoxic respiratory failure as well as hypoventilation respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study on the respiratory failure with cardiac failure--focus on hypoventilation respiratory failure]. 221 87

During the winter of 1986-1987, 64 children with respiratory syncytial virus (RSV) infection were admitted to our hospital. The diagnosis was made by direct immunofluorescent antibody technique. Twenty-three children (36%) needed intensive care treatment. Nearly 11 (52%) had a preexisting disease state, identified as a risk factor i.e., prematurity (n = 8), bronchopulmonary dysplasia (n = 2), congenital heart disease (n = 1). Twelve patients (50%) were intubated and ventilated. Conditions for intubation and ventilation were repetitive apnea with or without bradycardia (n = 4), clinical deterioration (n = 3) or hypercarbia (n = 5). Seventy-five percent of the patients who needed intensive care management were under three months of age compared to 34% of the children who were admitted to the clinical ward. The mean age for ventilated patients was 7.9 weeks. The mean duration of ventilation was 5.5 days. Volume controlled ventilation was initially applied to all patients. Pulmonary complications (atelectasis, pneumonia, pneumothorax or adult respiratory distress syndrome) were present in 15 (65%) IC patients. Nine (39%) of them also had symptoms of inappropriate antidiuretic hormone secretion (IADHS). Only two patients had symptoms of IADHS and two others had convulsions. Three children (5%) died as a result of respiratory insufficiency. Two of these infants belonged to the risk group.
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PMID:Respiratory syncytial virus infections in children admitted to the intensive care unit. 281 76

Snoring usually is trivial and unimportant, but it can turn into a social or medical problem. Obesity, hypertension and heart disease are more frequent among snorers than among nonsnorers, and especially snorers with hypersomnia during the day are at risk. Hypersomnia in association with snoring usually signifies obstructive sleep apnea. Increased resistance in the upper airways, together with negative inspiratory pharyngeal pressure and muscular hypotonia during deep non-REM and REM sleep, lead to collapse of the pharynx, hypoxia and hypercapnia. Only after arousal from sleep does muscle tone return, pharyngeal obstruction reopen and airflow resume. Since this process can occur 300 or 400 times a night, repetitive alveolar hypoventilation leads to pulmonary-arterial hypertension and cor pulmonale, and the repetitive sympathetic activations can cause systemic hypertension or serious cardiac arrhythmias. The countless arousals deprive the sufferer of deep non-REM and REM sleep and their consequence is sleep fragmentation. The symptoms are excessive daytime sleepiness, intellectual deterioration and personality and behavioral changes. Oronasomaxillofacial, endocrine and neuromuscular anomalies and diseases predispose to sleep apnea, and alcohol or CNS-depressant drugs can favour its occurrence. Diagnosis is made by nighttime oxymetry, and if this is abnormal, by polysomnography. After polysomnography it is possible to distinguish between obstructive and nonobstructive sleep apnea, and the decisions for an adequate treatment can be made.
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PMID:[Dangerous snoring. Sleep-apnea syndrome]. 331 92

Cutaneous infiltration of dilute solutions of epinephrine for hemostasis during halothane anesthesia can result in ventricular dysrhythmias. Our clinical experience, published reports, and a study comparing piglets with adult swine suggest that children may be less susceptible than adults to dysrhythmias under these conditions. We therefore undertook a prospective survey of heart rate and rhythm in halothane-anesthesized children who received subcutaneous epinephrine for hemostasis. Mass spectrometry was used to quantify end-tidal halothane and to avoid hypercarbia. In 83 children anesthesized with halothane, we continuously recorded ECG, heart rate (HR), end-tidal halothane (ETHalo), and carbon dioxide (ETCO2). The surgeons injected 0.4--15.7 micrograms/kg of epinephrine (in saline or 1% lidocaine) to provide hemostasis at a variety of sites. No child developed a ventricular dysrhythmia. One child had self-limited premature atrial contractions (PAC). Sixty-three children had some increase in heart rate after epinephrine injection, while seven increased their HR 15% or more above pre-injection levels. No relation between any increase in HR and epinephrine dosage, ETHalo, ETCO2, physical status, or age was found by multiple linear regression; however, HR was increased significantly in patients receiving epinephrine in head and neck sites other than the palate. The authors conclude that children tolerate higher doses of subcutaneous epinephrine than adults during halothane anesthesia. The arrhythmogenic dose of epinephrine in children receiving halothane has yet to be determined, but at least 10 micrograms/kg of epinephrine infiltration may be used safely in normocarbic and hypocarbic pediatric patients without congenital heart disease. The presence of PAC and tachycardia emphasize the need for continuous ECG monitoring and caution during halothane anesthesia with epinephrine injection.
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PMID:Epinephrine-halothane interactions in children. 633 28

Cardiac arrhythmias are common in patients with chronic obstructive pulmonary disease. Several factors may contribute to the development of arrhythmias in these patients including hypoxemia, hypercapnia, acid-base disturbances. The aim of the study was to assess QTc dispersion in patients with chronic obstructive pulmonary disease, who are at high risk of arrhythmias. Interlead QT variability as measured on the 12-lead electrocardiogram is not a technical artifact but probably reflects regional differences in ventricular repolarization. Increased dispersion of ventricular recovery time is believed to provide a substrate which supports serious ventricular arrhythmias. We showed that in patients with chronic obstructive pulmonary disease, free of underlying structural heart disease, the QTc dispersion is significant greater (p = 0.036) than in a control group, despite a similar value in mean QTc value. The data of the present study suggest that the determination of dispersion of repolarization times may be affected by metabolic changes occurring in patients with chronic obstructive pulmonary disease.
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PMID:[Assessment of dispersion++ of ventricular recovery in patients with chronic obstructive pulmonary disease]. 755 94

This paper reviews cardiac dysrhythmias occurring in the perioperative period. Electrocardiography was the first application of electronic monitoring to anesthesia care. The detection of dysrhythmias remains the most important use of this technology today. While the description of dysrhythmias dates back to the early 1900's, the first large series was reported in 1936. Early descriptions of the kinds seen and the predisposing factors have changed little in the past 50 years. Several factors tend to emerge when one evaluates perioperative dysrhythmias. These are the anesthetic given, the site of surgery, abnormalities of blood gases or electrolytes, tracheal intubation, reflexes such as vagal slowing and the oculocardiac reflex, stimulation of the central nervous system the presence of pre-existing heart disease, and the use of intracardiac devices. In the evaluation of cardiac dysrhythmias several facts need to be determined. The most important is to determine if there is an underlying complication of anesthesia and surgery which may explain the dysrhythmia. In addition, one needs to evaluate the heart rate, the regularity, the number of P waves per QRS, and the configurations of the QRS. The anesthesiologist needs to determine whether the rhythm is dangerous to the patient and whether it requires treatment. The two major abnormalities of sinus rhythm are sinus bradycardia and the sinus tachycardia. Sinus bradycardia can be due to hypoxia, vagal stimulation, drug effects, a high sympathetic block or an acute myocardial infarction. Sinus tachycardia can be due pain, light anesthesia, hypovolemia, sepsis, hypoxia, hypercapnia and drug effects. The major atrial dysrhythmias are paroxysmal atrial tachycardia, atrial fibrillation and atrial flutter. Each require treatment if perfusion is impaired or if the heart rate is persistently elevated. The new agents esmolol and adenosine are particularly useful in managing atrial dysrhythmias. The major ventricular dysrhythmias are ventricular premature contractions, ventricular tachycardia and ventricular fibrillation. The later two demand emergency management with DC cardioversion when perfusion is impaired. The major abnormality of conduction is complete heart block which usually requires emergency treatment in the perioperative period. Prompt evaluation and management of perioperative dysrhythmias reduce anesthetic morbidity and mortality.
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PMID:Management of perioperative dysrhythmias. 828 46

It is well known that the incidence of cardiac arrhythmia is particularly high in patients with chronic respiratory insufficiency (CRI). This study examines the prevalence, incidence and prognostic clinical importance of arrhythmia occurring during the course of CRI on the basis of data taken from the literature and the authors' personal experience using dynamic electrocardiographic diagnosis (24-hour Holter monitoring). The majority of arrhythmias observed in these patients appeared to take the form of premature ventricular and/or supraventricular beats and less frequently of atrial fibrillation and/or attacks of supraventricular paroxysmal tachycardia. Cardiac rhythm alterations were observed using Holter monitoring in 70-90% of patients. No cardiac rhythm disorder is specific to this pathological condition. The aim of this study was to formulate, as far as was possible, a rational therapeutic approach which took account of the electrogenesis of arrhythmic phenomena, variations in the type of arrhythmia and the hemodynamic conditions under which they occur. The etiopathogenesis of arrhythmias within the framework of CRI is relatively complex and probably multifactorial since there are a number of concomitant pathological conditions able to trigger off arrhythmogenic processes both inducing the onset of reflux circuits and enhancing cardiac automatism centres. Many studies correlate the presence of arrhythmia with hypoxemia, hypercapnia and both respiratory and metabolic alkalosis. Even the combined effect of hypoxia with respiratory acidosis and the integrity or otherwise of cardiac function (chronic pulmonary heart, right ventricular hypertrophy, ischemic cardiopathy) have a notable pro-arrhythmic effect. Hypokalemia induced by both respiratory alkalosis and by drugs used during the course of CRI (eg diuretics and/or steroids) may induce a marked dispersion of refractory periods of the various fibrocells thus encouraging the onset of arrhythmia. With regard to drugs, it has been observed that both digitalis and theophylline and beta-2 stimulants if frequently used during the course of CRI may possibly induce arrhythmia. It is therefore important to underline that they should be used with particular caution. As far as concerns the use of beta-2 adrenergic compounds, it is advised that they be administered using an aerosol rather than systemic route. Digitalis has limited indications; the molecules of the methylxanthine classes require careful pharmacological dose monitoring. Arrhythmic therapy should also be seen in terms of prophylaxis and the correction of predisposing and decisive factors such as hypoxemia, hypercapnia, hemoglobin and electrolyte levels, and alterations in blood pH following the obstruction of small airways.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Respiratory insufficiency and cardiac arrhythmia: the rationale of treatment]. 833 38

Patients with chronic obstructive pulmonary disease (COPD), especially during acute exacerbations of their disease, show a greater incidence of cardiac arrhythmias than healthy subjects of the same age. The type of arrhythmias found may be supraventricular (premature atrial beats, paroxysmal supraventricular tachycardia, multifocal atrial tachycardia, atrial flutter, atrial fibrillation) or ventricular (premature ventricular beats, sustained ventricular tachycardia, torsades de pointes, ventricular fibrillation) that may lead to sudden cardiac death. The pathogenesis of arrhythmias is complex and many factors may be involved such as hypoxemia, hypercapnia, respiratory acidosis, metabolic and respiratory alchalosis, hypokalemia, concomitant ischemic heart disease, chronic cor pulmonale, left ventricular diastolic dysfunction. Remarkable attention has been drawn to the possible arrhythmogenic effect of drugs such as theophylline, beta-adrenergic stimulants and digitalis which are commonly used in the therapy of COPD. Both of the main classes of bronchodilators (methylxanthynes and beta-adrenergic agonists), even when used together, apparently do not increase the incidence of dangerous cardiac arrhythmias. However, these drugs should be used with caution in the elderly, in patients with preexisting cardiac arrhythmias, with heart disease or with reduced hepatic function. In these cases Holter monitoring, repeated measurements of plasma drugs concentration and prompt hospitalization of high risk patients in Intensive Care Unit may be needed.
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PMID:[Evaluation of hyperkinetic cardiac arrhythmia in chronic obstructive bronchopneumopathy]. 944 64


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