Rheology of Cardiovascular Disease
Gordon D. O. Lowe in Clinical Blood Rheology, 2019
Some studies have found significantly increased hematocrit levels in patients with ischemic heart disease,125,127–129,133,134 but others have not126,130–132,135–137 In a study of 12 patients, all had significant plasma volume depletion (mean 82% of predicted) but normal red cell mass (mean 95% of predicted).138 Coronary artery bypass grafting did not alter this contracted plasma volume, despite relief of angina.138 Hence from the limited data available, the increased hematocrit in coronary artery disease appears to result from contracted plasma volume rather than increased red cell mass, as with essential hypertension (see above). This syndrome may merge with relative polycythemia, in which the incidence of cardiovascular events is increased (Chapter 9, Volume II). The cause of plasma volume contraction is obscure. It may reflect an adaptive mechanism to decrease left ventricular volume and systolic wall tension, decreasing myocardial oxygen consumption and relieving angina, since venesection increases the angina threshold and volume expansion decreases it.138 However, reduced plasma volume does not appear to be a result of myocardial ischemia, since it was unaltered by bypass grafting.138 Chronically increased adrenergic activity may be responsible, since catecholamines decrease plasma volume in the short-term.138 This would fit with the hypothesis of increased “stress” in coronary artery disease and hypertension.
Heart failure
Hugh McGavock, Dennis Johnston in Treating Common Diseases, 2017
Reduction of the extracellular fluid volume is a common complication of loop diuretics in heart failure. Volume depletion can lead to impaired renal function and contribute to the metabolic alkalosis which often accompanies diuretic-induced hypokalaemia. In the past, the commonest complication of loop diuretics was hypokalaemia, which increased the risk of digitalis-induced arrhythmias, but with the introduction of ACE inhibitors, angio-tensin-receptor antagonists and spironolactone to the treatment of heart failure, hyperkalaemia is now a more common problem. Hyponatraemia is now the commonest electrolyte abnormality that occurs in heart failure, and further reductions can occur with a high fluid intake. This is in part related to increased anti-diuretic hormone (ADH) release secondary to volume contraction. Acute urinary retention in men with prostatic hypertrophy is relatively common, particularly after intravenous administration.
Cholelithiasis and Nephrolithiasis
John K. DiBaise, Carol Rees Parrish, Jon S. Thompson in Short Bowel Syndrome Practical Approach to Management, 2017
A thorough history often provides the clues necessary for the accurate diagnosis of nephrolithiasis. Volume contraction and oliguria from low fluid intake and excessive stool output need to be recognized. A diet history, including estimated dietary intake of calcium, oxalate, sodium, protein, purine, and potassium-rich citrus fruits, should be determined. Recurrent urinary tract infection with urease-positive organisms (e.g., Proteus, Haemophilus, Corynebacterium, Ureaplasma) should be identified. Attention should be paid to the drugs associated with hypercalcuria (e.g., corticosteroids, vitamin D, calcium supplements, and antacids) or hyperoxaluria (e.g., vitamins C and B6) [49]. Additional evaluation consists of tests to identify both kidney stones and the predisposing factors to stone formation in the individual.
Association between polycythemia and risk of ischemic stroke in males based on the national health insurance service-health screening cohort
Published in Expert Review of Hematology, 2023
Hyo-Sun You, Sang-Jun Shin, Joungyoun Kim, Hee-Taik Kang
Hematologic disorders are common causes of ischemic stroke but are frequently neglected [3]. Polycythemia is a hematological disorder that can cause ischemic stroke. Polycythemia refers to a state in which the hematocrit or hemoglobin concentration in peripheral blood is increased. Polycythemia, or erythrocytosis, is classified into spurious polycythemia and true polycythemia according to its etiology. Spurious polycythemia is induced by volume contraction, severe dehydration, and Gaisbock syndrome. True polycythemia is divided into primary and secondary polycythemia according to serum erythropoietin (EPO) levels. Polycythemia vera and primary familial and congenital polycythemia are the types of primary polycythemia with low serum EPO levels. Secondary polycythemia is caused by various diseases that cause hypoxia in cells, which induces EPO release. High altitude, respiratory diseases such as chronic obstructive pulmonary disease (COPD), cyanotic heart disease, elevated carboxyhemoglobin, hemoglobinopathies, and EPO-secreting tumors can also cause secondary polycythemia [4].
The anti-hypertensive effects of sodium-glucose cotransporter-2 inhibitors
Published in Expert Review of Cardiovascular Therapy, 2023
Luxcia Kugathasan, Lisa Dubrofsky, Andrew Advani, David Z.I. Cherney
It has been postulated that natriuresis, in part, may contribute to the SGLT2 mediated anti-hypertensive effect. Specifically, an acute and transient increase in natriuresis is observed in the early stages of SGLT2 inhibition [71]. Maximal natriuresis is reported within the first 3 days of treatment and eventually returns to baseline over time. Partially by the process of osmoregulation, acute sodium excretion is accompanied by a sustained 7.3% plasma volume contraction, as observed in patients following 8 weeks of dapagliflozin treatment [72,73]. Although the exact mechanisms outlining the transient nature of natriuresis are still unclear, it may be explained by way of a compensatory increase in distal tubule sodium reabsorption to offset the initial increase in sodium excretion at the proximal tubule and may suggest minimal contribution of natriuresis to BP reduction. Despite this, an acute increase in urinary sodium excretion by 10–20% was demonstrated in patients with T2D in response to SGLT2 inhibitor therapy, emphasizing a potential role for natriuresis [74].
The patient with metabolic alkalosis
Published in Acta Clinica Belgica, 2019
Valentine Gillion, Michel Jadoul, Olivier Devuyst, Jean-Michel Pochet
Experimental studies have clearly shown that metabolic alkalosis may persist even if its cause is corrected [27]. Maintenance of metabolic alkalosis generated by chloride depletion was classically attributed to volume contraction (e.g. dehydration) but some studies in rats and humans suggested another mechanism. Indeed, Cl- repletion corrects metabolic alkalosis even when volume contraction is maintained [20]. Given the existence of a distal Cl-HCO3 exchange (Figure 1), the pivotal role of Cl- depletion in the maintenance of metabolic alkalosis is best explained by a shortage of Cl- in the collecting duct. Indeed, reabsorption of Cl- is almost complete upstream in the nephron in case of Cl- depletion leaving no Cl- to be reabsorbed in exchange with bicarbonate. The term chloride depletion alkalosis should then replace the concept of contraction alkalosis.
Related Knowledge Centers
- Bleeding
- Body Fluid
- Dehydration
- Extracellular Fluid
- Hypovolemic Shock
- Osmolyte
- Hypovolemia
- Circulatory System
- Blood Plasma
- Fluid Compartments