LEFT-SIDED HEART FAILURE Essay Example

  • Category:
    Nursing
  • Document type:
    Case Study
  • Level:
    Undergraduate
  • Page:
    2
  • Words:
    1438

Question 1

Explanation of Pathogenesis leading to Mrs. Brown’s clinical manifestation:

Ischemic heart diseases as a result of atherosclerosis, most commonly a consequence of lipid accumulation leading to formation of atheroma lead to atherosclerosis which then obstructs blood flow to the myocytes and as such lack of adequate oxygen concentration (Carton, 2017). This then reducing the oxidative potential of the myocyte as oxidative phosphorylation depends on oxygen supply. This then leads to reduced contractility of the myocytes leading to reduced contractility of the heart (Carton, 2017). Part of the affected heart is the left atrium which is consequently unable to empty blood into left ventricle from the lungs leading to build up of pressure in the left atrium. This increased pressure is directed towards the pulmonary veins. This causes imbalance in the starling forces as hydrostatic pressure at the arterial ends is reduced compared to the visceral hydrostatic pressure in the pulmonary veins which is increased (Hosenpud & Greenberg, 2007). This then leads to accumulation of fluid in the lungs resulting reduced surface areas for gaseous exchange in the alveoli leading to rapid breathing as seen with Mrs. Brown (24 breaths/min) to meet oxygen demands, and shallow as more force is to be overcome for breathing.

Accumulation of fluid also reduces oxygen exchange rate in the counter current system at the alveoli leading to reduced concentrations of oxygen available to be obtained from the as carbon IV oxide is released. Reduced oxygen concentration was the cause of reduced oxygen saturation with spatial oxygen pressure about 85% for Mrs. Brown.

Increased hydrostatic pressure at the visceral pulmonary veins at the expense of the pressure in the lungs which leads to imbalance in the starling forces leads to accumulation of fluid at the base of the lungs (edema) (Peacock et al., 2016).This then produces the crackles aka rales at the base of the lungs on auscultation with the diaphragm of the stethoscope.

Valvular heart diseases (mitral and aortic) as well as primary diseases o the myocardium such as myocarditis and amyloidosis and to an extent ischemic heart diseases ultimately lead to reduced cardiac output. Compensatory measures such as ventricular dilatation and neurohumoral systems are activated. Activation of neurohumoral system leads to stimulation of juxtaglomerulus cells of the kidney to release renin which then triggers conversion of angiotensinogen to angiotensin I and into angiotensin II by angiotensin converting enzymes leads to production aldosterone and antidiuretic hormone (Jefferies et al., 2017). Aldosterone is a vasoconstrictor and leads to sodium retention after ultrafiltration by the glomerulus. Antidiuretic hormone inserts aquaporin at the renal tubules leading to increased water retention by the kidneys and this further expands the vascular volume. Water will also ordinarily follow sodium through osmosis thus a larger vascular volume will be obtained. This mechanism leads to expansion of the vascular volume leading to hypertension which increases the peripheral resistance (Hosenpud & Greenberg, 2007). This increases the blood pressure to levels witnessed in Mrs. Brown, 170/95mmHg.

Systemic hypertension which leads to increased peripheral pressure exerts a higher force on the heart compelling it to work harder than normal in meeting the oxygen demands of the body (Jefferies et al., 2017). This then results into the rapid pulses Mrs. Brown presented with at the emergency department.

As explained above, ischemic heart conditions led to increased pressure at the left atrium of the heart. This increased pressure was led to dilation of the left atrium which led to atrial fibrillation (Peacock et al., 2016) that Mrs. Brown was diagnosed with from the ECG findings. This usually present as an irregularly irregular heartbeat.

Question 2

Discussion of two high priority nursing strategies to manage Mrs. Brown and their rationale:

The major nurse priorities are alleviation of symptoms of Mrs. Brown to improve functional status and promotion of survival by extending life.

Alleviation of symptoms such as breathlessness should be managed by immediate oxygen supplements. Oxygen supplement is determined by the level of congestion and hypoxia of the patient (LeMone, 2014).

Oxygen is directly delivered into the capillaries and then carried by blood to tissues. This is administered to increase oxygen percentage saturation, partial pressure of oxygen, in blood so as not to deprive other tissues oxygen for oxidative phosphorylation by their cells thus generating ATP for functioning. The nurses would achieve this objective by either continuous positive airway pressure (CPAP) or through pressure-support ventilators (LeMone, 2014). All this is done with facial mask on.

Survival would be promoted by administration of drugs that counter heart failure and its pathogenesis. These are drugs that would curtail the progress of imbalances that would lead to heart failure (LeMone, 2014). Among them are vasodilators to expand the pulmonary arteries and the peripheral vasculature to minimize the effect of systemic hypertension. As explained above, drugs that would reduce sodium and water retention are administered. These are basically diuretics including loop diuretics, carbonic anhydrase inhibitors, thiazides, osmotic diuretics and inhibitors of ADH hormone. Another group of drugs are those that target the renin-angiotensin-aldosterone pathways which would include angiotensin receptor blockers (candesartan, telmisartan, losartan) and inhibitors of angiotensin converting enzyme inhibitors (Enalapril, captopril, Lisinopril). In so doing, the nurses should closely monitor the related adverse drug effects of these therapies (Trevor et al., 2016). Most notable adverse drug effects are hyperkalemia, arrhythmias, vasodilator effects such as hypotension, flushing, headache, and GIT effects such as anorexia vomiting, diarrhea and constipation.

Question 3

  1. Mechanism of action of Furosemide and glyceryl trinitrate

Furosemide like other loop diuretics exerts it effects at the thick ascending limb of the loop of henle of the nephron where it decreases reabsorption of sodium chloride and potassium chloride. This decreases the effects of increased vascular volume as a consequence of aldosterone and antidiuretic effects. This would therefore minimize the progress of increased vascular volume to systemic hypertension which would subsequently elevate the peripheral vascular resistance thus exerting more force on the heart (Anatomy, pharmacology, physiology, 2010). The heart workload would therefore be reduced as the peripheral resistance is reduced by decreased NaCl and KCl. It will therefore lead to restoration of salt level and water will follow through osmosis leading to reduced vascular volume.

Glyceryl trinitrate when administered sublingually is carried to the smooth muscles cells of the e vessels where it is dinitrated by either glutathione S-transferase or an isoform of aldehyde dehydrogenase (ALD2 andLD3) releasing nitric oxide. The released nitric oxide combines with guanylyl cyclase activating it leading to increased cGMP which promotes dephosphorylation of the myosin light chains leading to decreased cytosolic calcium channels thus causing relation of the myocytes (Trevor et al., 2016). Its effects are vasodilated blood vessels, reduced myocardial oxygen demand, and decreased cardiac workload. It therefore vasodilates the narrowed blood vessels in atheromatous heart diseases that led to ischemic heart diseases. Blood will therefore adequately reach major organs such as the kidneys reducing the possibility of systemic hypertension by compensatory measures of neurohumoral system. Oxygen saturation of the lungs among other tissues would be improved as well.

  1. Nursing monitoring of adverse effects and evaluation of therapeutic effects:

The adverse effects of furosemide are hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity with aminoglycosides thus care is needed. The nurses should therefore monitor the fluid levels as higher levels would lead to effects of hypovolemia which would subsequently trigger neurohormonal system. Its levels should be maintained on the upper does of 4mglmin and oral dose should be 20-80mg (Champe, 2005). All this while, the levels of fluid intake and output are to be monitored to avoid overload. Blood tests are conducted to evaluate the electrolyte levels in blood and urine.

The adverse effects of glyceryl trinitrate are orthostatic hypotension, orthostatic hypotension, tachycardia and throbbing heart headache (Champe, 2005). The levels should therefore be closely monitored by the nurses to avoid overdoes which could lead to the above complications. First dose should also be monitored as it is bound to have tachycardiac effects.

References

Anatomy, pharmacology, physiology. (2010). Cardiac Anaesthesia. doi:10.1093/med/9780199209101.010.0002

Carton, J. (2017). Cardiac pathology. Oxford Medicine Online. doi:10.1093/med/9780198759584.003.0004

Champe. (2005). Lippincott’s Illustrated Reviews :Pharmacology. Lippincott Williams & Wilkins.

Hosenpud, J. D., & Greenberg, B. H. (2007). Congestive heart failure. Philadelphia: Lippincott Williams & Wilkins.

In Jefferies, J. L., In Blaxall, B. C., In Robbins, J., & In Towbin, J. A. (2017). Cardioskeletal myopathies in children and young adults.

In Peacock, A. J., In Naeije, R., & In Rubin, L. J. (2016). Pulmonary circulation: Diseases and their treatment.

LeMone, P. (Ed.). (2014). Medical-surgical nursing: Critical thinking for person-centred care (2nd Australian ed.). Frenchs Forest, Australia: Pearson Australia.

Trevor, A. J., Katzung, B. G., & Kruidering-Hall, M. (2015). Katzung & Trevor’s Pharmacology: Examination & Board Review.