Pathogenesis of Fluid Volume Excess in an Acute Exacerbation Chronic Heart Failure Patient Essay
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Heart failure is a clinical syndrome of decreased tolerance and fluid retention due to structural heart disease. Despite much advancement in treatment of the treatment of heart failure, there still exists a high annual mortality.
In normal situations, an increase in total blood volume results in an increase in renal levels of sodium and water excretion. These renal excretions are due to reflexes that help maintain normal body volume in increase of atrial pressure. Thus any atrial pressure increase results to a decreased release of antidiuretic hormone, an increased release of atrial natriuretic peptide and a decreased renal sympathetic tone.
In contrast, when a patient has an acute exacerbation of chronic heart failure, the total blood volume does not affect renal excretion of sodium and water. Rather, due to either decreased or increased cardiac output, underfilling of the arterial circulation and systemic arterial vasodilation occurs. To compensate the change, total blood volume is increased by the expansion of blood volume in the venous circulation and the increased after-load (systemic vascular resistance).
This results in an acute increase in left ventricular end-diastolic pressure.
Pulmonary venous pressure and the acute increase in left ventricular end-diastolic leads to increased alveoli pressure which results to pulmonary congestion when the alveoli cells are overwhelmed.
Further, the stimulated normal reflexes, as a result of increased atrial pressure, are affected by reflexes initiated in the high pressure arterial circulation. For example, renin-angiotensin-aldosterone system is activated by increased arterial pressure to release angiotensin II. Angiotensin II acts to help in reabsorption of sodium in the proximal tubules. Glomerular filtration rate and excretion of water and sodium is also increased. This, however, is affected in acute heart failure by renal vasoconstriction and a reduction of sodium delivery to the distal nephron. Resulting in the release of arginine vasopressin, as a result of arterial undefilling, which increases plasma and urine osmolalities and leading to peripheral arterial vasoconstriction and water reabsorption in the cells of the distal tubule and collecting duct in the kidney, promoting hyponatremia.
The Nitroglycerin and Angiotensin II receptor blockers strategies as Nursing strategies used to manage pulmonary oedema.
Pulmonary oedema is the accumulation of excess watery fluids in the air sacs of the lungs and a common result of heart failure.
The main objective in managing pulmonary oedema is to improve oxygenation and reduce pulmonary congestion. Two of the several managing strategies are use of Nitroglycerin (NTG) and Angiotensin II receptor blockers.
Nitroglycerin (NTG) is an effective, predictable and rapidly-acting medication used for preload reduction. According to Sovari 2012, several studies have demonstrated the efficacy, safety and faster action onset of NTG than of furosemide or morphine sulfate.
NTG can be sublingual, topical or intravenous. Sublingual is associated with preload reduction within 5 minutes and with some afterload reduction.
Topical NTG, although as effective as sublingual NTG, should be avoided in patients with severe left ventricular failure because of poor skin perfusion thus poor absorption.
Intravenous NTG is an excellent monotherapy for patients with severe cardiogenic pulmonary oedema. It can be started with 10mcg/min and then rapidly uptitrated to more than100mcg/min. It can be given as 3 mg boluses every 5 minutes (Sovari, 2012).
The short half-life of nitrates justifies the high dosage for cardiogenic pulmonary oedema, especially with patients presenting a hyperadrenergic state and moderately elevated blood pressure. Nitrates, however, should be avoided in hypotensive patients and used with caution in cases of aortic stenosis and pulmonary hypertension.
Angiotensin II Receptor Blockers
Angiotensin II receptor blockers (ARBs) have comparable beneficial effects in heart failure. Studies have proposed a role for ARBs in preventing structural and electrical remodeling of the heart which reduced incidence of arrhuthmias.
The Valsartan Heart Failure Trial showed that valsartan reduces the incidence of atrial fibrillation by 37% (Sovari, 2012).
The Mechanism of Furosemide
Furosemide is a potent diuretic (water pill) that is used to eliminate water and salt from the body.
Implications of administering Furosemide to a patient with an acute exacerbation of chronic heart
Furosemide is often given in conjunction with a potassium supplement or a potassium-sparing diuretic to counteract potassium loss. The medication has a rapid onset of effect of about one hour when taken orally and five minutes by injection. Duration of action is about six hours so it is possible to use a twice daily dose if necessary.
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