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Query: UMLS:C0018801 (heart failure)
 72,216 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

Left ventricular function was studied at rest and during post-extrasystolic potentiation in 18 patients with chronic obstructive lung disease. The contractility indices used were obtained from pressures recorded in the isovolumetric period (left ventricular end-diastolic pressure, Vmax., VECmax., dP/dtmax.) and from volume variations during ejection (end-diastolic volume, ejection fraction, VCF). Left ventricular diastolic compliance was also evaluated. All patients were hypoxic (PaO2 = 58 +/- 7 torr); six of them had cor pulmonale (group B); the remaining 12 patients constituted group A. Left ventricular function of groups A and B was similar; we conclude that right cardiac failure, in cor pulmonale, is not secondary to left ventricular failure. However, left ventricular dysfunction exists; the left ventricle is hypertrophied (probably resulting from chronic hypoxia). Pump function is altered (abnormal ventricular function points are found), but left ventricular kinetics is normal or exaggerated (ejection fraction and VCF are increased). Isovolumetric phase contractility indices are diminished; however, they may increase normally during post-extrasystolic potentiation. Left ventricular compliance is abnormal due to left and right ventricular hypertrophy and to paradoxical movement of the interventricular septum which impedes diastolic expansion of the left ventricle. These changes are responsible for decreased left ventricular output. There seems to exist an impairment of left ventricular function related to both intrinsic (secondary to hypoxia, hypercapnia, left ventricular hypertrophy) and extrinsic factors (right ventricula hypertrophy deviating interventricular septum, lowering of left ventricular preload).
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PMID:[Left ventricular function in chronic obstructive lung disease (author's transl)]. 15 43

Arterial blood gases were measured during 7 hours of sleep in 15 patients with severe stable chronic obstructive pulmonary discrease (COPD); 6 awake patients with COPD studies in recumbency for an average of 5 hours served as controls. Mean maximal decrease in arterial oxygen partial pressure (PaO2) (plus or minus SD) was 13.5 plus or minus 3.9 mm Hg for sleeping patients (p less than 0.005) and 5.5 plus or minus 1.7 mm Hg for controls (p less than 0.1), respectively. Changes in pH during sleep were of the magnitude expected with acute changes in arterial carbon dioxide partial pressure (PaCO2) in patients with chronic hypercapnia. Consistent changes in heart rate, respiratory frequency or cardiac rhythm were not observed during sleep. Nocturnal worsening of hypoxemia could be explained by alveolar hypoventilation in six sleeping patients and in five controls; in nine sleeping patients, further impariment of ventilation-perfusion mismatch also contributed to worsening of hypoxemia. There was no relationship between the decrease in PaO2 during sleep and the degree of airways obstruction or the PaO2 level when awake. Because of low PaO2, when awake, a fall in PaO2 during sleep brings values into the steep part of the oxyhemoglobin dissociation curve where slight changes in PaO2 result in marked changes in oxygen content. All patients with COPD whose waking PaO2 was below 60 mm Hg had PaO2 below 50 mm Hg during sleep; nocturnal oxygen therapy should be considered in such patients, particularly in the presence of polycythemia or troublesome right-sided heart failure.
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PMID:Arterial blood gases and pH during sleep in chronic obstructive pulmonary disease. 23 52

Changes in pulmonary hemodynamics and acid-base balance were recorded during induction of anesthesia using either intravenous administration of barbiturate (28 patients) or inhalation of N2O-O2-halothane (12 patients). The two types of induction resulted in equal elevations of pressures within the pulmonary circulation. The increase, proportional on the two sides of the heart, was most pronounced immediately before endotracheal intubation. Cardiac index decreased before and during intubation but subsequently increased to levels above control values. Systemic blood pressure increased more during barbiturate than during inhalation induction. Changes in acid-base balance were similar during the two types of induction: arterial blood PCO2 and PO2 increased, pH decreased, and standard bicarbonate remained unchanged. Changes in pulmonary arterial mean pressure and central venous pressure were correlated with changes in PACO2. Pulmonary capillary filtration pressure (i.e., pulmonary capillary wedge pressure minus plasma colloid osmotic pressure) was negative in every patient before anesthesia. During induction of anesthesia, filtration presures became positive in half the patients. Observed changes in circulation may have been caused by hypercapnia alone or by a combination of hypercapnia and vescular reflexes associated with instrumentation during intubation. The increased strain on the heart during induction of anesthesia may lead to cardiac failure in patients with diminished cardiac reserve.
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PMID:Pulmonary hemodynamics during induction of anesthesia. 84 81

Disturbance in acid-base balance is commonly observed in patients with heart failure. The most common disturbance is metabolic alkalosis combined with hypokalemia, as a result of the excessive use of loop diuretics. Occasionary, hypoxia due to pulmonary edema stimulates ventilation, resulting in respiratory alkalosis. When pulmonary edema develops, carbon dioxide retention occurs, resulting in respiratory acidosis. Decreased tissue oxygen delivery may also produce lethal lactic acidosis. Compensatory mechanisms, coexistence of independent acid-base disorders and changes in electrolytes complicate acid-base balance in the individual patients. As acid-base disturbances have harmful effects on the cardiovascular system, precise diagnosis and proper treatment are highly important.
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PMID:[Acid-base disturbances in heart failure]. 143 8

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

Two cases of malignant hyperthermia (MH) are presented. The first patient presented initially with tachyarrhythmia intraoperatively and rapid onset of MH crisis. Nasopharyngeal temperature of 43 degrees C was attained after 15-20 minutes of anaesthesia. The patient eventually died of myocardial failure despite external cardiac massage, inotropic support and ventricular pacing. The second patient presented with increasing endogenous hypercarbia following the administration of suxamethonium and isoflurane. The use of the end tidal carbon dioxide monitor led to an early diagnosis of MH. The early use of dantrolene may have contributed to the favourable outcome.
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PMID:Malignant hyperthermia. 239 48

The long-term clinical course of six patients with congenital central hypoventilation syndrome is described. During the neonatal period, the patients had prolonged apneas and hypoventilation, in the absence of cardiac, pulmonary, or neuromuscular disease. After an initial period of respirator dependency, they became able to sustain normal gas exchange while awake. During sleep, however, profound hypoventilation developed, and tracheostomy and mechanical ventilation were required. Ventilatory responses to hypercapnia and hypoxia were depressed or absent and did not improve with time. One patient was able, at 2 years of age, to breathe spontaneously during sleep with only moderate hypoventilation. The others, now 4 to 14 years of age, still need ventilatory support during sleep. Complications, such as cardiac failure and hypoxic seizures, mostly occurred early in the course and resolved with correction of insufficient mechanical ventilation. Speech acquisition was possible with the use of a special stoma plug. All patients were managed at home, and with appropriate support, the parents were able to provide safe ventilatory care with low morbidity and no mortality.
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PMID:Long-term follow-up of children with congenital central hypoventilation syndrome. 244 98

To assess arteriovenous differences in acid-base status, we measured the pH and partial pressure of carbon dioxide (PCO2) in blood drawn simultaneously from the arterial and central venous circulations in 26 patients with normal cardiac output, 36 patients with moderate and 5 patients with severe circulatory failure, and 38 patients with cardiac or cardiorespiratory arrest. The patients with normal cardiac output had the expected arteriovenous differences: venous pH was lower by 0.03 unit, and venous PCO2 was higher by 0.8 kPa (5.7 mm Hg). These differences widened only slightly in those with moderate cardiac failure. Additional simultaneous determinations in mixed venous blood from pulmonary arterial catheters were nearly identical to those in central venous blood. In the five hypotensive patients with severe circulatory failure there were substantial differences between the mean arterial and central venous pH (7.31 vs. 7.21) and PCO2 (5.8 vs. 9.0 kPa [44 vs. 68 mm Hg]). Large arteriovenous differences were present during cardiac arrest in patients whose ventilation was mechanically sustained, whether sodium bicarbonate had been administered (pH, 7.27 vs. 7.07; PCO2, 5.8 vs. 8.6 kPa [44 vs. 65 mm Hg]) or not (pH, 7.36 vs. 7.01; PCO2, 3.7 vs. 10.2 kPa [28 vs. 76 mm Hg]). By contrast, in patients with cardiorespiratory arrest, large arteriovenous differences were noted only when sodium bicarbonate had been given (pH, 7.24 vs. 7.01; PCO2, 9.5 vs. 16.9 kPa [71 vs. 127 mm Hg]). We conclude that both arterial and central venous blood samples are needed to assess acid-base status in patients with critical hemodynamic compromise. Although information about arterial blood gases is needed to assess pulmonary gas exchange, in the presence of severe hypoperfusion, the hypercapnia and acidemia at the level of the tissues are detected better in central venous blood.
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PMID:Assessing acid-base status in circulatory failure. Differences between arterial and central venous blood. 258 59

During the last years, medical interest has focused on sleep related diseases, especially the sleep apnea syndrome (SAS) and the nocturnal breathing abnormalities associated with broncho-pulmonary diseases. It now appears that SAS is far more prevalent than previously believed. In this review article we present the clinical features, the investigations and the current therapeutic methods. We also discuss the recent developments in our understanding of the SAS pathophysiology and their implications in the disease's management. Clinical importance of sleep related disorders of breathing is appreciated when one looks at some of the secondary effects including hypertension, angina pectoris, cardiac insufficiency and worsening of a broncho-pulmonary disease (hypoxemia, hypercapnia); these are associated with a high degree of morbidity. The recent advent of ambulatory screening systems allows an easier evaluation of patients at risk, such as obese or hypertensive snorers and patients with hypersomnolence; then the diagnostic polysomnographic studies can be reserved for subjects in whom home recording is abnormal. A precise and early diagnosis is important to allow the initiation of treatment such as Continuous Positive Airway Pressure (CPAP) or naso-pharyngeal surgery.
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PMID:[The sleep apnea syndrome. A general review]. 265 45


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