Electrolyte and water balance in cardiac insufficiency. Recent clinical and experimental data
| Autor: | G. Riegger, A. Hepp, Karl Hayduk |
|---|---|
| Rok vydání: | 1980 |
| Předmět: |
Male
Cardiac output medicine.medical_specialty Vasopressins Physiology Anemia Hemodynamics Decreased cardiac output Dogs Physiology (medical) Internal medicine Renin Renin–angiotensin system Animals Humans Medicine Cardiac Output Enzyme Inhibitors Aldosterone Heart Failure business.industry Reabsorption Angiotensin II Arteries Water-Electrolyte Balance medicine.disease Vasoconstriction Heart failure Cardiology Vascular Resistance sense organs Cardiology and Cardiovascular Medicine business Antidiuretic |
| Zdroj: | Basic Research in Cardiology. 75:289-293 |
| ISSN: | 1435-1803 0300-8428 |
| DOI: | 10.1007/bf02001426 |
| Popis: | Summazy The reasons for the disturbances of electrolyte and water balance in cardiac failure are not yet clarified. The decrease of cardiac output in cardiac insufficiency causes humoral regulatory mechanisms such as increased activity of the renin angiotensin-aldosterone system and increased secretion of antidiuretic hormone. These mechanisms in turn lead to an enhancement of renal sodium and water reabsorption. The humoral disturbances can be interpreted as ineffective regula tory mechanisms for hemodynamic changes in cardiac insufficiency; in fact, the humoral disturbances increase cardiac failure. In addition, an increased sodium content of the arteries may contribute to the hemodynamic changes in cardiac insufficiency. The mechanisms involved in the disturbances of electrolyte and water balance in cardiac insufficiency are still poorly defined. In congestive heart failure, decreased cardiac output may cause humoral disturbances, such as increased activity of the renin-angiotensin-aldosterone system and enhanced release of antidiuretic hormone. These mechanisms result in an increased renal sodium and water retention. The humoral factors may indicate compensatory mechanisms for hemodynamic changes in congestive heart failure. There are a lot of definitions of congestive heart failure (CHF), but there is no agreement as to which definition meets all kinds of heart failure. There is agreement that in CHF the heart is not able to keep up with the requirements of the periphery. The starting point of CHF is in fact the hemodynamic failure of the heart or at least the disability of the heart to compensate for increased hemodynamic requirements of the periphery (for example, anemia or arterial hypertension). The decreased cardiac output induces changes in the renin-angiotensin-aldosterone system (RAAS) and in. the secretion of antidiuretic hormone (ADH). These mechanisms may be primarily compensatory, but lead in fact by a vicious circle to a worsening of CHF. There are a lot of experimental |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink