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

1.26 of 340 patients with chronic heart failure (aortic-valve or mitral-valve disease, congestive cardiomyopathy) showed Cheyne-Stokes respiration in supine position. 2. The incidence of Cheyne-Stokes respiration in males is more than twice as high as in females with similar hemodynamic conditions. 3. Lung volumes and airway resistance did not appreciably deviate from the predicted values and are therefore of no etiologic significance. 4. Delay of the feedback between changes in the alveolar gas tensions and respiratory center caused by a prolonged circulation time (decreased cardiac index and increased central blood volume) is the predominant cause of Cheyne-Stokes breathing in patients with chronic heart failure. 5. Metabolic alkalosis (e.g. after diuretics) favors Cheyne-Stokes respiration in patients with congestive heart failure and low cardiac output, by lessening respiratory changes in pH of blood and cerebrospinal fluid.
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PMID:[Cheyne-Stokes respiration in chronic heart insufficiency]. 87 30

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

The cardiorespiratory responses to exercise and forced hyperventilation were measured in 17 unselected patients with syndrome X (angina, positive exercise test, normal coronary arteriogram, no other cardiovascular disease) and compared with those in 15 healthy subjects. Forced hyperventilation produced hypocapnia and metabolic alkalosis but no chest pain or electrocardiographic change. Patients with syndrome X showed reduced maximum oxygen consumption with an increased respiratory exchange ratio at peak exercise, confirming that exercise was limited by skeletal muscle perfusion--and thus that the increase in cardiac output with exercise is limited in syndrome X as in heart failure. Arterial carbon dioxide tension (PCO2) homoeostasis during exercise was normal but the ventilatory cost of carbon dioxide excretion was increased in syndrome X (as in heart failure). End tidal PCO2 measurements correlated only poorly with arterial PCO2 in individual patients with syndrome X, providing a possible explanation for previous reports, based on end tidal PCO2 of inappropriate hyperventilation. Patients with syndrome X did not show inappropriate hyperventilation but they did show hyperventilation that was appropriate to maintain normal arterial PCO2 in the face of reduced cardiac reserve.
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PMID:Syndrome X and hyperventilation. 193 59

A group of 65 patients with advanced heart failure was examined with the aim to disclose changes in serum glucose, creatinine, potassium, chloride, and acid-base balance under the influence of intensive diuretic therapy. 50 patients were treated with ordinary furosemide and amiloride combination (average observation time 25 days), in 15 cases amiloride was replaced by captopril 75-150 mg/day (average observation 15.5 days). The results are as follows: 1. We found no rise of glycaemia in non-diabetics with either ordinary diuretic therapy or captopril. On the contrary: stress hyperglycaemia in the beginning of the therapy normalized in the course of it. 2. There was a significant rise of serum creatinine during the first two weeks of therapy with furosemide and amiloride. Reversal of this trend followed after captopril. 3. There was no fall in the average serum chloride concentration during ordinary diuretic therapy. Adding captopril to the regime brought about a rise in serum chloride. 4. Serum potassium had no tendency to fall either after furosemide and amiloride or furosemide and captopril. 5. The acid-base balance showed no shift towards metabolic alkalosis during an intensive but rational diuretic regime either with or without captopril. On the contrary: mild initial metabolic alkalosis had a tendency to normalize with proceeding cardiac compensation.
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PMID:[Metabolic and acid-base changes in intensive diuretic therapy in heart failure]. 219 96

Side effects and their relationship with the material used were analyzed in 748 plasma exchanges (PE) performed in 75 patients. The total incidence of acute and mild adverse effects (chills and/or fever, paraesthesias, allergic reactions, acute anaemia, vasovagal reactions, abdominal pain and hypotension) was 18.04%. Two patients developed an episode of left cardiac insufficiency. One patient in whom all PE were performed with fresh frozen plasma (FFP) developed metabolic alkalosis. Three patients developed sepsis during treatment with repeated PE and immunosuppressive drugs; in these three patients a permanent vascular inlet was used (shunt or catheter). All patients in whom only FFP was used as replacement solution developed non-A, non-B hepatitis. Neither haemorrhagic nor thrombotic episodes were observed in these patients. It is of the greatest importance to choose the most suitable material for each patient and to develop a careful technique in order to avoid these complications during treatment with PE.
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PMID:Adverse effects secondary to the treatment with plasma exchange. 403 Jan 33

Acid-base equilibrium and electrolyte balance were studied in 80 infants in the immediate postoperative period after surgery for ventricular septal defect under conditions of extracorporeal circulation. Decompensated metabolic alkalosis was the most characteristic disorder of acid-base equillibrium in patients with an uncomplicated postoperative period, whereas decompensated respiratory alkalosis and metabolic acidosis were characteristic of patients with compensated and decompensated forms of cardiac insufficiency. Plasma hypokaliemia and hypochloremia attended by intracellular retention of sodium were typical disorders of the electrolyte balance in all forms of changes in the acid-base equilibrium.
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PMID:[Acid-base state and the electrolyte balance of young infants in the immediate postoperative period after radical correction of an interventricular septal defect under artificial circulation]. 735 5

Severe congestive heart failure (CHF) is often characterised by fluid retention. A (chronic) state of overhydration has a negative influence on both the quality of life and prognosis of these patients. Therefore, the use of diuretics remains a cornerstone in the treatment of heart failure. However, diuretic resistance, a failure to correct the hydration state adequately with the use of conventional dosages of loop diuretics, is a frequently occurring complication in the treatment of advanced stages of CHF. Several intra- and extrarenal mechanisms may be involved in the development of diuretic resistance. An important pathophysiological mechanism leading to diuretic resistance seen after chronic use of loop diuretics is the functional adaptation of the distal tubule. Studies in animals demonstrate that the sodium reabsorption capacity of this nephron segment increases significantly when the sodium delivery to this segment is augmented, as is the case during administration of loop diuretics. The use of combinations of diuretics acting on different segments of the nephron appears to be an effective option in the treatment of diuretic resistance. Several combinations have been used; however, the combination of a loop diuretic and a thiazide drug acting on the distal tubule appears to be the most effective. However, since the use of this combination may lead to serious adverse effects such as hypokalaemia, metabolic alkalosis and dehydration, careful monitoring of the patient of combination diuretic therapy is necessary.
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PMID:Combination diuretic therapy in severe congestive heart failure. 950 39

Patients with advanced heart failure commonly develop simple or mixed acid-base disturbances. The altered acid-base homeostasis can occur as a consequence of the heart failure itself, the therapeutic interventions, or associated conditions. The present study examined acid-base disorders in patients with heart failure who received successful heart transplantation. The information collected should provide light on the determinants of acid-base disorders in this patient population. Seventy status 2 UNOS (United Network Organ Sharing) patients listed for heart transplantation were enrolled in this study. All patients received loop diuretics, spironolactone, ACE inhibitors, carvedilol and digitalis as needed. Patients were studied again at discharge after transplantation, under cyclosporine, azathioprine, steroids, loop diuretics and ACE inhibitors. After heart transplantation, a significant increase of ejection fraction from 19.7 +/- 0.63 to 53.6 +/- 0.9% (p < 0.0001) occurred along with a concomitant reduction of central venous pressure (p < 0.0001) from 12.6 +/- 0.20 to 6.9 +/- 0.21 mm Hg. Before heart transplantation there was high-normal pH (7.43 +/- 0.009), slight loss of hydrogen ions (35.4 +/- 0.4 nmol/l), slightly reduced pCO(2 )(37.6 +/- 1.1 mm Hg). After heart transplantation a stability of blood pH and hydrogen ion concentrations was found but bicarbonate increased significantly (p < 0.02) from 24.2 +/- 0.61 to 26.2 +/- 0.51 mmol/l and pCO(2) from 37.6 +/- 1.1 to 39.3 +/- 0.7 mm Hg (p < 0.05). Plasma renin activity averaged 3.80 +/- 0.6 pg/ml before heart transplantation and 2.82 +/- 0.4 pg/ml after (p < 0.01). Aldosterone concentration averaged 380 +/-15 pg/ml before heart transplantation and 280 +/- 10 pg/ml after (p < 0.01). These data suggest that in patients before heart transplantation there is a mixed acid-base imbalance that includes respiratory alkalosis and metabolic alkalosis. After transplantation the recovery of the abnormal circulatory status erased the initial respiratory alkalosis but metabolic alkalosis persisted and accounted for a further rise in plasma bicarbonate.
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PMID:Acid-base state in patients after cardiac transplantation. 1216 64

We review the diuretics regarding the mechanism of action, way of clinical use and their adverse effects. Recent progress of molecular biology revealed the molecular target of diuretics and thereby, the molecular mechanism of diuretic action became clear to understand. Loop diuretics and thiazides are the most widely used diuretics and the physiologic adaptation to their prolonged use are mentioned. Carbonic anhydrase inhibitors are not used as diuretics but for correction of metabolic alkalosis and treatment of glaucoma. Potassium-sparing diuretics have modest natriuresis but the combination with loop diuretics or thiazides results in strong natriuresis. Adenosine type 1 receptor antagonist has been developed for treatment of edema in chronic heart failure. Vasopressin type 2 receptor antagonists are developed for a new type of diuretics to increase the free water clearance in cases of chronic heart failure and SIADH. The recombinant atrial natriuretic polypeptide is recently used as diuretics in acute heart failure. Knowledge of pharmacological action of diuretics could help the appropriately clinical use of diuretics, in particular the diuretics-resistant edema.
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PMID:[Diuretics; their characteristics and future development]. 1567 32

In end-stage heart failure, various acid-base disorders can be discovered due to the renal loss of hydrogen ions and hydrogen ion movements into cells, the reduction of the effective circulating volume, hypoxemia and renal failure. This justifies the occurrence of metabolic alkalosis, metabolic acidosis, respiratory alkalosis, as well as respiratory acidosis alone or in combination. Several studies have been published on the acid-base state in heart failure. In a 1951 study, Squires et al analyzed the distribution of body fluid in congestive heart failure by taking into consideration the abnormalities in serum electrolyte concentration and in acid-base equilibrium. A recent study by Milionis et al, analyzed 86 patients with congestive heart failure receiving conventional treatment; the majority of these patients exhibited hypokalemia, hyponatremia, hypocalcemia and hypophosphatemia. Disorders in acid-base balance were noted in 37.2% of patients. In a recent study, 70 patients with severe congestive heart failure before heart transplantation showed high-normal pH, slightly reduced pCO 2 and a slight loss of hydrogen ions. After heart transplantation, stability of blood pH and hydrogen ion concentrations was found. In contrast, bicarbonate and pCO 2 increased significantly. The data led us to formulate the diagnosis of a mixed acid-base disorder that includes respiratory alkalosis and metabolic alkalosis before heart transplantation. In heart failure, the presence of acid-base imbalance associated with the activation of mechanisms that lead to salt and water retention reveals evidence concerning the pivotal role of the kidney in determining the outcome of these patients.
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PMID:Acid-base balance in heart failure. 1673 34


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