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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The isolated perfused working rat heart preparation has been used to study the effects of respiratory acidosis on myocardial metabolism and contractilly. Hearts were perfused with 5 mM glucose and 10(-2) U/ml of insulin in order to enhance metabolsim of glucose relative to that of fatty acids. After perfusion with Krebs bicarbonate medium at pH 6.6, hearts rapidly ceased performing external work and peak left ventricular pressure fell by 75% after 5 minutes. Oxygen consumption, rate of ATP generation and overall glycolytic flux also declined rapidly. After about 2 minutes of perfusion, the fall of glycolytic flux showed a partial reversal, which was largely accounted for by increased lactate production, so that glucose oxidation decreased further. The reversal of glycoltic flux could be accounted for by partial release of H+ inhibition of phospho-fructokinase by increased tissue levels of adenosine 5'-diphosphate (ADP), adenosine monophosphate (AMP) and P1 and decreased levels of adenosine triphosphate (ATP) and creatine phosphate. The increased proportion of glucose uptake converted to lactate together with an increase of the tissue lactate/pyruvate ratio could be accounted for by inhibition of the malate-aspartate cycle combined with tissue hypoxia. Lactate accumulated in the tissue as a result of a decreased permeability of the plasma membrane to lactate. Decreased oxygen delivery to the myocardium was caused by secondary constriction of the coronary vessels. In further experiments, the coronary flow was regulated by an external pump which delivered fluid at a controlled rate into the aortic cannula above the coronary arteries, and the degree of tissue hypoxia was monitored by measuring changes of pyridine nucleotide reduction state by surface fluorescence techniques. The effects of acidosis uncomplicated by possible hypoxia were compared directly with those produced by ischemic hypoxia. The effects of acidosis under these conditions were similar to those described above, and to those produced by ischemia. From these and other data it is concluded that the effects of ischemia are caused by a lowering of the intracellular pH, which decreases the rate of energy production relative to the rate of energy demand. However, it is suggested that the primary cause of the decreased peak systolic pressure with either acidosis or ischemia is not a result of a defect of energy metabolism, but is due to alteration of the calcium cycle of the heart. Possible causes of irreversible heart failure after prolonged ischemia are discussed.
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PMID:Contribution of tissue acidosis to ischemic injury in the perfused rat heart. 0 93

The Pickwickian Syndrome stimulated new pathophysiological concepts in regard to control of ventilation. With the advent of sleep laboratories, the peculiar sleep apnea occurring in some of these patients has been explained on the basis of intermittent upper airway obstruction. Two patients with different manifestations of the Pickwickian Syndrome are presented. The suggestion is made that these two subsyndromes should have unique designations. The Auchincloss Syndrome is manifested by right heart failure and respiratory acidosis in obese patients who are alert and have no major abnormality of breathing pattern. The fundamental cause of this abnormality is the increased work of breathing caused by the obesity. The cost of breathing is so high that the ventilatory regulation is compromised and respiratory acidosis results. The Gastaut Syndrome is characterized principally by hypersomnia and sleep apnea. The fundamental defect is upper airway obstruction during sleep, resulting in increased work of breathing, which together with the increased work caused by obesity leads to respiratory acidosis and right ventricular failure. Hypersomnia, rather than heart failure or respiratory acidosis, is the major manifestation of this syndrome, and is the result of sleep loss.
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PMID:Pickwickian syndrome, 20 years later. 117 87

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

Nasal mask ventilation (NMV) has been used successfully in chronic restrictive respiratory failure and more recently in acute exacerbations of chronic obstructive pulmonary disease (COPD). This study aimed to evaluate the possible role of NMV in acute respiratory failure (ARF) episodes when mechanical ventilation with endotracheal intubation is questionable. Thirty patients (age, 76 +/- 8.1 years) were treated by NMV during ARF episodes (COPD, 20; other chronic respiratory failure [CRF], 5; chronic heart failure [CHF], 4). All patients were hypoxemic (PaO2, 5.85 +/- 1.62 kPa) and hypercapnic (PaCO2, 8.63 +/- 1.89 kPa) with respiratory acidosis (pH, 7.29 +/- 0.08). In all cases, clinical or physiologic parameters indicated the need for mechanical ventilation, but endotracheal intubation was either not applied because of the age and the physiologic condition of the patients (17 cases) or was postponed (13 cases). NMV was performed using a volume-cycled ventilator and a customized nasal mask. Ventilation was continuous during the first 12 hours and the following nights and was then intermittent during the day. Twenty-one patients improved clinically, within a few hours. Progressive correction of arterial blood gases was observed: PaO2 increased during the first hour, but PaCO2 decreased more slowly. Eighteen patients were able to be successfully weaned from NMV. Twelve patients failed to improve despite NMV: eight of them died and four required endotracheal intubation. There was no difference in the success rate between patients in whom endotracheal ventilation was contraindicated or postponed. Clinical tolerance was satisfactory in 23 patients and poor in seven patients. A return to the respiratory condition was observed in the surviving patients with subsequent discharge from hospital. NMV therefore successfully treated respiratory distress initially in 60 percent of the 30 patients. These results suggest that NMV could be a possible alternative in the treatment of ARF, even in very ill patients, when endotracheal ventilation is controversial or not immediately required.
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PMID:Nasal mask ventilation in acute respiratory failure. Experience in elderly patients. 840 33

Blood gas and haemodynamic changes caused by chronic respiratory insufficiency affect the right ventricle and produce chronic cor pulmonale. Equally important but less well known modifications affect the left ventricle and the general circulation and are the subject of the present report. Hypoxemia, hypercapnia and acidosis caused by severe hypoxia create functional disturbances in both ventricles that are manifested in a volume overload that added to other major malfunctions provoke congestive heart failure. The coronary circulation is affected by metabolic factors, perfusion alterations, right ventricular hypertrophy and concomitant coronary lesions. Advanced respiratory insufficiency caused by poorly compensated respiratory acidosis and metabolic acidosis reduces cardiac output and frequency so that tissue perfusion is compromised. Furthermore alterations in transmembrane electrolytic concentrations produce repeated multifocal ventricular arrhythmias that expose the patient to the risk of sudden death. Cardiac failure is reflected in other organs like the kidney and the central nervous system and also contributes to tissue and cerebral hypoxia. The later depresses the respiratory centres and develops into often irreversible coma. A better knowledge of these elements may contribute to the development of appropriate treatment.
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PMID:[General cardiocirculatory effects in chronic respiratory insufficiency]. 354 42

The haemodynamic, metabolic and regional blood flow effects of the vasodilator, tolmesoxide (1 mg kg-1 min-1 for 20 min by intravenous infusion) were examined in two groups of greyhound dogs anaesthetized with alpha-chloralose and mechanically ventilated. One group of dogs was thoracotomized and subjected to acute coronary artery occlusion. In these dogs tolmesoxide was infused 2.5 h after occlusion when there was evidence of impaired myocardial function. Tolmesoxide administration resulted in marked systemic hypotension which was associated with myocardial stimulation (increase in heart rate and LVdP/dtmax). These effects were less marked in thoracotomized dogs subjected to coronary artery occlusion. Cardiac stimulation was attenuated by pretreatment with the beta-adrenoceptor antagonist, atenolol. Peripheral resistance and left ventricular end-diastolic pressure (LVEDP) were reduced by tolmesoxide. In spite of the systemic hypotension, the marked reduction in LVEDP resulted in an enhanced subendocardial driving pressure and an increased blood flow to ischaemic regions of the left ventricular wall as measured with Xe133 clearance. Blood flow to normal regions of the left ventricular wall was also increased by tolmesoxide. A metabolic and respiratory acidosis may have contributed to the haemodynamic effects of tolmesoxide. Plasma renin levels were significantly elevated by the drug. Tolmesoxide administration thus resulted in cardiac stimulation, reduced both pre-load and after-load, yet maintained coronary and pulmonary perfusion. This haemodynamic profile of tolmesoxide would explain the beneficial effects obtained with this drug in the treatment of cardiac failure.
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PMID:The haemodynamic and metabolic effects of tolmesoxide with special reference to impaired myocardial function. 377 13

Since heart failure may occur in the setting of lung dysfunction and CO2 retention with only modest increases in cardiac work load, we questioned whether myocardial function is impaired by hypercapnic acidosis. To determine the influence of hypercapnic acidosis on right ventricular function, we measured the effects of acute (2 hours) and chronic (2 weeks) hypercapnic acidosis on right ventricular performance during normal and increased right ventricular afterload in five conscious dogs. Systemic hemodynamic and right ventricular functions were unaltered during normal right ventricular afterload by acute hypercapnic acidosis (PaCO2 = 49 +/- 3 mm Hg, pH = 7.27 +/- 0.003). As right ventricular afterload was increased by progressive balloon occlusion of the right ventricular outflow tract during acute hypercapnic acidosis, the rise (slope) in right ventricular end-diastolic pressure was increased 4-fold (P less than 0.01) over that observed in normocapnic control. Maximum isovolumic right ventricular dP/dt rose (P less than 0.05) comparably with increasing right ventricular afterload during normocapnic control and acute hypercapnic acidosis. Chronic hypercapnic acidosis (PaCO2 = 55 +/- 2 mm Hg, pH = 7.28 +/- 0.01) resulted in systemic vasodilation and increased (P less than 0.05) heart rate and cardiac output during normal right ventricular afterload. As right ventricular afterload was increased during chronic hypercapnic acidosis, the rate of rise in right ventricular end-diastolic pressure was 2-fold (P less than 0.01) above normocapnic control but maximum isovolumic right ventricular dP/dt was unchanged in contrast to normocapnic control and acute hypercapnic acidosis. Moreover, cardiac output fell and stroke work was unchanged with increasing afterload during chronic hypercapnic acidosis. beta-Adrenergic blockade resulted in an increased (P less than 0.01) rate of rise in right ventricular end-diastolic pressure with afterload during normocapnic control and chronic hypercapnic acidosis. We conclude that hypercapnic acidosis results in diminished right ventricular performance during increased right ventricular afterload, evidenced by accentuated rise in right ventricular end-diastolic pressure, and may contribute to the congestive heart failure and edema observed in patients with pulmonary hypertension and CO2 retention.
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PMID:Right ventricular performance during increased afterload impaired by hypercapnic acidosis in conscious dogs. 612 76

The mechanism responsible for the depressive myocardial effects of severe respiratory acidosis is unclear; however, sympathetic stimulation and catecholamines are known to be involved. The influence of beta-adrenergic receptor activity on the myocardial response to severe respiratory acidosis was studied in 18 anesthetized, mechanically ventilated dogs. Arterial CO2 tension (PaCO2) was raised by increasing the inspired CO2 fraction in O2. In control animals, as PaCO2 increased, heart rate (HR) decreased (PaCO2 approximately 110 mmHg), then returned to control (PaCO2 approximately 220 mmHg), whereas arterial blood pressure (Pa) and cardiac output (Q) remained unchanged from prehypercapnia levels. At PaCO2 greater than 350 mmHg, Pa, HR, and Q decreased and left ventricular function (LVF) curves were depressed. Death occurred at a PaCO2 of 404 +/- 25 mmHg (pH 6.48 +/- 0.02). In a second group of animals, administration of isoproterenol during the increase in PaCO2 did not result in depression of myocardial function, and death did not occur even at a significantly higher PaCO2 (PaCO2 496 +/- 12 mmHg; pH 6.39 +/- 0.02) than in the control group. Administration of propranolol to a third group of animals as PaCO2 increased did not change Pa, HR, and Q; however, LVF curves indicated a more rapid and severe depression of myocardial performance than in control, and death occurred at a significantly lower PaCO2 (PaCO2 220 +/- 25 mmHg; pH 6.65 +/- 0.02). We conclude that beta-adrenergic receptor stimulation can prevent hypercapnic heart failure and that beta-adrenergic receptor activity is involved in the mechanism responsible for this failure.
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PMID:beta-Adrenergic activity and cardiovascular response to severe respiratory acidosis. 629 89

The authors report two cases of heroin induced pulmonary edema. In both cases the severity of respiratory failure, attested by a deep hypoxemia (paO2 28 and 32 mmHg) and a metabolic and respiratory acidosis (pH 7.07 and 7.14) imposed an artificial ventilation with positive end expiratory pressure (PEEP). Hemodynamic study revealed a noncardiogenic edema. In both cases, a cardiac insufficiency was also present : in the first case it's etiology remained unclear, in the second it was a complication of hyperkalemia.
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PMID:[Pulmonary edema caused by heroin. Hemodynamic study of 2 cases]. 634 28

The mechanisms of oedema in cor pulmonale remain unexplained. On the basis of a small number of studies, cor pulmonale is not caused by cardiac muscle failure, at least in early oedematous phases. Progressive and persistent elevation of pulmonary vascular resistance may exceed the pumping capacity of the right ventricle in later stages. Alternative explanations for the sharp fall in renal blood flow as oedema appears should be sought. The renin-angiotensin-aldosterone system seems causally related to oedema. The curious position of hypercapnia remains an enigma. Surprisingly few studies of hypercapnia, renal blood flow and renal hormones are reported. Redistribution of body water from intracellular to the extracellular space may be in part due to the need to buffer extracellular respiratory acidosis caused by hypercapnia. It provides an explanation for one form of hypercapnic oedema. Cyclical loss and gain of tissue mass seems more evident in cor pulmonale than ischaemic or valvular heart failure.
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PMID:Oedema in cor pulmonale. 703 67


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