Nursing Fundamentals of Lung Auscultation

Question: Discuss about the Nursing for the Fundamentals of Lung Auscultation. Answer: 1. Severe dyspnoeacan be a cause of hypercapnia and hypoxia, consequences mainly from chemically tempted respiratory motor action. The severe breathlessness accompanying with severe hypercapnia is not an image of respiratory muscle action but quite a reflection of respiratory motor action. It has been found that acute breathlessness arises from amplifiedPCo2. Acute dyspnoeamay be associated with a pulmonary or cardiac abnormalities. Cardiac disorders that may precipitate dyspnoeainclude left ventricular systolic or diastolic dysfunction, intra-cardiac or extra-cardiac shunts, arrhythmias, pericardial disease, valvular disease, pulmonary hypertension and myocardial infarction (Janssen et al. 2011). The patient had a previous record of heart failure which suggest the presence of damaged heart muscle. Respiratory rate is an indicator of serious heart condition. 24 breaths/minute was the most important predictor of cardiac arrest in hospitals. Alveolar ventilation (a product of tidal volume and respiratory rate) is generally cautiously controlled by the activities of central and peripheral lung and chemoreceptors receptors. Ventilation is controlled by in cooperation of the arterial fractional pressure of carbon dioxide (PaCo2) and the arterial fractional pressure of oxygen (PaO2) with PaCo2being the most vital factor. The body efforts to treat hypercarbia and hypoxaemia by escalating both respiratory rate and tidal volume (Janssen et al. 2011). Thus these disorders can be spotted by assessing the respiratory rate. The patient showed a drop in oxygen saturation. It can be due to poor pulmonary function. According to Hoeper and Granton (2011), gaseous interchange could be changed even in mild failures. An arterialoxygen saturation rate under 90 percentorigins hypoxemia. This occurs when blood backs up in the pulmonic veins because the heart cannot keep up with the amount, initiating leak of fluid into the lungs and fluid accumulation in the tissues. It is very essential to note that once the oxygen saturation drops to between 80-85 percent it will rapidly fall away without the support of supplementary oxygen. Due to this cause that nurses should effort to keep oxygen saturations of a patient above 90 percent. The patient had a systolic pressure 170 and the diastolic pressure 95 which is a very high blood pressure of stage 2 level. The pathogenesis of high blood pressure can have different causes. Masip et al. (2012) and many other researchers have revealed a direct connection between the level and duration of elevated blood pressure and left ventricular hypertrophy. Diastolic dysfunction accompanied by LVH can lead to high blood pressure during heart failure. Sinus tachycardia was observed in the patient (pulse rate 110/minute). Tachycardia arises when an irregularity in the heart yields rapid electrical motions across the heart tissue. A heart failure that damage the heart tissue can cause it to accelerate (Masip et al., 2012). On auscultation crackles at the base of each lung must be caused by the opening of tiny air passages and alveoli collapsed due to exudate, fluid or lack of aeration during expiration. Pulmonary edema secondary to left-sided heart failurecan originate crackles (Bohadana et al. 2014). 2. First strategy to manage Mrs. Browns condition is to stabilize the declined cardiac output. In a short period (3-4 hours) planning of nursing interventions, the patient shall be contribute in actions that lessens the workload of the heart. After 24 to 48 hours of long term care, the patient should be capable to show hemodynamic strength. These nursing interventions include frequently monitoring of blood pressure and pulse rate because patient with heart problems can experience rennin-angiotensin mechanism; monitoring oxygen saturation and ABGs for checking the hearts capacity to perfuse distal tissues with O2 containing blood and implementing strategies to treat fluid and electrolyte inequities as it can reduce the danger for developing of cardiac output as a result of imbalances (Scherb et al., 2011). Providing oral care Q2 can be beneficial for conditions like Mrs. Brown. Venous congestion can result in increased capillary pressure. Fluid leaks out of the capillaries when hydrostatis pressure surpasses interstitial pressure. It can eventually cause edema in sacrum and legs. Elevation of legs upsurges venous reoccurrence to the heart (Felker et al., 2011). Monitoring distended neck veins and ascites indicates fluid overload. Oral care Q2 with diuretic therapy can be valuable for treating these problems. 3. IV furosemide constrains reabsorption of water in the nephron by checking the sodium-potassium-chloride co-transporter in the thick ascending limb of the Henles loop. This is attained via competitive reticence at the chloride binding sites on the co-transporters, therefore stopping the transportation of sodium from the lumen into the basolateral interstitium. Adverse effects of this drug includes chest pain, fever, weakness, loss of appetite, sore throat, pain in upper stomach and back, breathlessness, wheezing, difficulty in urination, dark colored urine and stool, nausea and vomiting etc. During the treatment with furosemide the renal function should be monitored and renal ultrasonography may be needed. If the patient possess any liver illness, regular checking of the electrolytes is recommended (Fleg et al., 2011). As the body adjusts to the drug during treatment these adverse effects may go away.If any of the problems continue to occur, a change in medication must be done. Glyceryl trinitrate is a vasodilating drug which relaxes vascular smooth muscle and reduces pulmonary vascular resistance by dilating both venous and arterial beds. It produces nitric oxide as an active metabolite which is a potent activator ofguanylyl cyclase. Nitric oxide proliferates the level of cGMPwithin the cell which in turn triggers myosin light chain phosphatase through cGMP-dependent protein kinase. A low blood pressure, headaches, diarrhoea, dizziness, nausea and vomiting are adverse effects of GTN. Caution is essential in vulnerable patients like Mrs. Brown. Reporting suspected adverse reactions after application of the drug is important. It allows sustained nursing of the risk factors of the drug.Lowering of the patient's head or elevation of the legs may be beneficial in case of mild hypotension (Ferreira and Mochly-Rosen, 2012). Estimation of arterial blood gas should be done for examining acidosis. Oxygen therapy can also be given in certain cases. 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