Heart failure is a medical condition where the heart does not pump blood as normal due to structural and functional impairment of heart filling and ejection of blood (Rich, 2007). This writing is about management of a 72-year-old patient diagnosed with acute heart failure. He is admitted to an emergency department complaining dyspnea and a sensation of suffocating. He has been having difficulty in walking and showering in the last few days. He has swollen feet from the last few weeks a clear evidence of peripheral edema confirmed by pitting edema revealed on examination. He also has widespread course crackles on auscultation indicating a problem with his respiratory system. Giovanni's X-ray results show an enlarged cardiothoracic ratio with white patchy areas with Kerly B lines in the lower lobes. An increase in the endo thoracic ratio indicates that the heart is swollen and this could be an indication of a pulmonary heart failure. In this paper we are going to look at two signs of heart failure and each is having two nursing management options either independent or collaborative.
Difficulty in breathing is usually associated with heart failure. In heart failure, there is increased pressure during the diastolic phase i.e. the relaxation period. The high pressure created backs blood up into the vessels that return blood back into the heart, the pulmonary veins since the heart cannot accommodate the large supply. This results into the fluid leaking into the lungs. The presence of excessive fluid in the lungs cause difficulty in breathing. The accumulated fluid acts as a physical barrier preventing oxygen diffusion. There are several interventions that can be used in the management of dyspnea. Discussed below are two most significant dyspnea management plans. (Yancy et al., 2013)
Drug administration such as captopril
Captopril has been used as an example choice in dyspnea management because it has been effective as a long-term therapy in dyspnea related to heart failure (Remme & Swedberg, 2011).
Mode of action
Converts enzyme inhibitors and block the production of angiotensin II, a potent vasoconstrictor, and thus result in a decrease in arterial resistance. The angiotensin-converting enzyme is a zinc metalloprotease. It works by cutting off a peptide binding in angiotensin I (inactive) that releases angiotensin II. The zinc atom of the active site plays a catalytic role by activating the water molecule which participates in the hydrolysis of the peptide bond. Captopril acts by blocking the vacant coordination of zinc with its thiol function (Rich, 2007).
This class of drug is used primarily in hypertension. Captopril is also used in heart failure and secondary prevention after myocardial infarction. By decreasing blood vessel resistance, the pulmonary blood pressure will be lowered thereby reduce fluid leakage into the lungs.
Captopril is available in scored tablets of 12.5 mg, 25 mg, 50 mg and 100 mg.
An initial dose of 25 milligrams is given orally thrice daily. The maintenance dose is 50 milligrams given orally thrice a day for not less than two weeks to ensure a proper response is realized. Maximum captopril dose is 450 milligrams per day. Many patients experience enough response with 50 or 100 milligrams taken orally three times a day (Remme & Swedberg, 2011).
Adverse drug effects and their prevention
The most common side effects of captopril include: tickly; rashes and other skin disorders such as itching, sores, redness or sensitivity to sunlight. Sometimes there angioneurotic edema, this is fluid accumulation around lips, chin, and mouth. The use of captopril can sometimes bring low blood pressure which makes the patient feel dizzy. Do dose escalation to lower these side effects (Rich, 2007).
Captopril actions can be antagonized by naloxone. As a nurse, one should ensure that these two drugs are not given concurrently. When captopril is administered to a patient also taking naloxone, there is likely to be a little therapeutic response and the patient condition may worsen.
The nurse has a duty of ensuring that the right amounts of doses are given to the patient and consistency in drug administration. These should be efforts aimed at ensuring the treatment plan is successful. After drug administration, a nurse has a responsibility to evaluate the clinical response of the patient. This can be done by carrying out a physical examination of the lung for example through the use of x-ray machines to check the presence of any fluid in the lungs. Other ways involve checking the patient breathing patterns as an improvement in breathing rates will give positive feedback on the effectivity of the drug (Remme & Swedberg, 2011).
The aim of the oxygen administration is the metered enrichment of the inhaled air with oxygen, to increase the partial pressure of the oxygen in the arterial blood. Therefore it is sensible to determine the actual values ??in the blood and to adapt the therapy using a blood gas analysis
Oxygenation is considered especially when the patient become hypoxemic. Oxygen therapy is indicated for symptoms that are based on an oxygen deficiency, as well as (acute) shortness of breath at rest or during exercise, weakness, (daily) fatigue; cyanosis. Postoperatively oxygen is used to prevent latent hypoxia or after partial removal of lung tissue (Sullivan et al., 2008).
Oxygen remains the most discussed therapeutic in the event of acute dyspnea and is only an adjunct treatment of other methods.
The use of O2 to treat dyspnea remains controversial because wide variations in PaO2 are needed to stimulate a respiratory response to hypoxia. In hypoxia, tissues are denied of oxygen sources which are necessary for normal body tissue functioning. Carbon dioxide is also accumulated in these tissues. High partial carbon dioxide concentration in the body is very toxic to body tissues (Sullivan et al., 2008).
Oxygen is administered either with a face mask, a probe or nasal glasses. The nasal probe is preferable to the mask that impedes communication and increases the subjective sensation of suffocation. The oxygen can come from a bottle containing the gas in liquid form or from an extractor which, thanks to a pump, extracts the O2 from the ambient air. At home, an extractor is the most convenient system because of its small size, mobility, and non-flammable character. However, it is noisy and can only deliver low flow rates. In the case of higher requirements, bottles must be used (Rich, 2007).
Nurses can initiate oxygen therapy on the patient to enable him to achieve a respiratory oxygen saturation of between 95 and 98 percent. Oxygen therapy is of particular importance when given immediately in emergency situations. Strict aseptic work avoids contamination. For this reason, new tubing systems must be used for each patient. Patients under oxygen therapy require special attention. Care monitoring and documentation cover: breathing, pulse, blood pressure, of consciousness, skin (cyanosis, pressure points), nasal and oral mucosa, oxygen dosage, probe location, and the amount of distilled water. Nurses should take part in monitoring these factors during oxygenation to determine whether the patient is responding well to treatment. Nurses should make sure they are available to the patient when required to administer oxygen therapy (Sullivan et al., 2008).
In many cases, heart failure interferes with the kidney function and its ability to dispose of sodium and water. The decreased blood flow from the heart means fewer amounts of fluid reach the kidney. This results in increased body retention of water. This water further accumulates in the body leaking into the interstitial spaces causing edema. The swelling in the legs experienced by the patient and thus having difficulty in putting on shores is a sign of edema. Pitting edema is also resulted and can be determined when a nurse apply pressure on any part of the leg a pit is formed that takes some time to be resolved (Remme & Swedberg, 2011). Pitting edema is as a result of the reduction of blood flow out of the heart thereby forcing the blood returning to the heart in the veins to back up. Edema can be relieved by the use of diuretic drugs and implementation of special physical activities aimed at reducing water accumulation in the body. An example of a diuretic drug that can be used is furosemide.
Mode of action
Furosemide is a drug from the group of abrasion diuretics. Grinding diuretics lead to the elimination of large amounts of tissue fluid by inhibiting a transport protein (the Na-K-2Cl co-transporter) in the kidney in the ascending part of the Henle loop. For intravenous administration of the drug, excretion rates of up to 50 liters per day are possible. It is a highly diuretic agent (Shiraishi et al., 2016).
Acceptable indications include hypertension, ascites and edema (including cerebral edema) due to cardiac insufficiency or due to the liver, kidney, or burns, and, under certain circumstances, threatened renal failure. Furthermore, furosemide is used in hyperkalemia to purge excess potassium. In sport, furosemide is used as a masking agent, as it helps to remove any traces of doping agents taken from the body; it is therefore on the doping list (Shiraishi et al., 2016).
Furosemide can be administered orally, intravascularly and intramuscularly. It has an oral drug bioavailability of between 43 to 65 percent. The drug undergoes hepatic metabolism and is excreted really in urine and biliary, in feces.
Adverse drug effects, their prevention, and management
Furosemide major side effects include postural hypotension, ringing in the ears, and photosensitivity. The nurse taking care of the patient should ensure he is closely monitored especially his sitting and sleeping habits to prevent postural hypotension from occurring. The patient should also be advised against staying in the sun for long after taking the drug (Remme & Swedberg, 2011).
This medication should not be used in the following cases:
-Allergy to sulfonamides;
-Urinary retention by significant obstruction of the urinary tract;
-Dehydration (especially in the elderly);
Furosemide has a high risk of nephron damage when used with non-steroid anti-inflammatory drugs e.g. aspirin. It can also lead to cardiac toxicity when used concurrently with anti-arrhythmic drugs if hypokalemia results. A nurse also has a duty to ensure that these drugs are not administered concurrently as doing this may complicate the patient treatment plan (Thom & Kannel, 2007).
Use is not recommended in subjects who may develop acidosis. Hepatic and renal assessment is essential, especially in diabetics and elderly patients. Regular monitoring of serum potassium is also essential. Nurses can be actively involved in the regular monitoring of hepatic and renal person the old age of the patient. Renal function monitoring can be done by checking the creatinine levels in the plasma and urine and comparing their rates of elimination (Remme & Swedberg, 2011).
Evaluation of use
Evaluation of the use of furosemide can be done by measuring the amount of urine excreted over a given period. The patient is asked to urinate in a bottle where a nurse can measure the volume of urine produced.
Patient lifestyle management
This is an area where the nurse is independently involved in patient management. A nurse has a huge role to play in advising a heart failure patient in their lifestyle to ensure a good outcome of their management. Patient education about smoking and its effects on his condition should be encouraged. The patient should be advised to stop smoking because this could worsen the disease. Long-term smoking has been closely associated with lung problems, therefore combined with pulmonary edema this could have been the main causative factor for his difficulty in breathing (Yancy et al., 2013)
The nurse can also advise the patient to participate in light exercises as being physically active will reduce the heart workload and enable it to beat more efficiently. The nurse should advise on the types of exercises the patient should take part in because vigorous exercises may strain the heart more quickly and cause pain to the patient. They can do this by offering a suitable program of low-intensity exercises.
Patient advice is also required in the diet. The patient should be advised to take foods with little amounts of salts and fats. Taking foods rich in salts has a danger of increasing body salt concentration that may lead to fluid accumulating thereby causing edema. The patient should not take many fluids, and their fluid intake should be restricted by the nurse. The positive impacts of patient education on their conditions is that it creates an interest in the patient to be the first person in the implementation of their management plans. Weight management should also be considered as the patient should be advised not to engage in activities that can lead them to gain weight, for example, eating junk food with high fatty content (Hosenpud & Greenberg, 2007)
In conclusion, it is imperative to say that clinical management of a cardiac failure patient requires a high-level intervention of the nurse. Nurses form a big part of the healthcare management team to their patient either through their independent efforts such as offering patient advice and collaborative efforts in administering drugs as prescribed by the medical officer. Here they ensure that the drugs prescribed are administered at the right time and the right doses. They also have a responsibility of monitoring the drug actions during therapy. Nurses provide patient support and should be closely associated with their patients. The role of a nurse in patient management should not stop in the hospital when the patient is discharged but should involve following to check whether the patient is complying with the management plan such as engaging in physical activity. It, therefore, means that when nursing roles are well played, positive patient outcomes can be readily achieved (Thom & Kannel, 2007).
Borlaug, B. A., & Paulus, W. J. (2010). Heart failure with preserved ejection fraction: pathophysiology, diagnosis, and treatment. European heart journal, ehq426.
Chawla, L. S., Davison, D. L., Brasha-Mitchell, E., Koyner, J. L., Arthur, J. M., Shaw, A. D., ... & Seneff, M. G. (2013). Development and standardization of a furosemide stress test to predict the severity of acute kidney injury. Critical Care, 17(5), R207.
Cowie, M. R., Woehrle, H., Wegscheider, K., Angermann, C., d’Ortho, M. P., Erdmann, E., ... & Teschler, H. (2015). Adaptive servo-ventilation for central sleep apnea in systolic heart failure. New England Journal of Medicine, 373(12), 1095-1105.
Heidenreich, P. A., Albert, N. M., Allen, L. A., Bluemke, D. A., Butler, J., Fonarow, G. C., ... & Nichol, G. (2013). Forecasting the impact of heart failure in the United States. Circulation: Heart Failure, 6(3), 606-619.
Hosenpud, J. D., & Greenberg, B. H. (Eds.). (2007). Congestive heart failure. Lippincott Williams & Wilkins.
Keith, J. D. (2010). Congestive heart failure. Adults, 18(3), 491-500.
Kucherenko, Y. V., & Lang, F. (2012). Inhibitory effect of furosemide on non-selective voltage-independent cation channels in human erythrocytes. Cellular Physiology and Biochemistry, 30(4), 863-875.
Mebazaa, A., Yilmaz, M. B., Levy, P., Ponikowski, P., Peacock, W. F., Laribi, S., ... & McDonagh, T. (2015). Recommendations on pre?hospital & early hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency Medicine. European journal of heart failure, 17(6), 544-558.
Medhora, M., Gao, F., Fish, B. L., Jacobs, E. R., Moulder, J. E., & Szabo, A. (2012). Dose-modifying factor for captopril for mitigation of radiation injury to normal lung. Journal of radiation research, 53(4), 633-640.
Münzel, T., Gori, T., Keaney, J. F., Maack, C., & Daiber, A. (2015). Pathophysiological role of oxidative stress in systolic and diastolic heart failure and its therapeutic implications. European heart journal, ehv305.
Paulus, W. J., & Tschöpe, C. (2013). A novel paradigm for heart failure with preserved ejection fraction. Journal of the American College of Cardiology, 62(4), 263-271.
Poppas, A., & Rounds, S. (2012). Congestive heart failure. American journal of respiratory and critical care medicine, 165(1), 4-8.
Remme, _. W., & Swedberg, K. (2011). Guidelines for the diagnosis and treatment of chronic heart failure. European heart journal, 22(17), 1527-1560.
Rich, M. W. (2007). CONGESTIVE HEART FAILURE IN OLDER ADULTS*: Epidemiology, Pathophysiology, and Etiology of Congestive Heart Failure in Older Adults. Journal of the American Geriatrics Society, 45(8), 968-974.
Shiraishi, M., Murakami, T., Nawa, T., Kobayashi, H., Nagamine, H., Shiraga, K.& Nakajima, H. (2016). Hypertonic saline with furosemide for diuretic resistant congestive heart failure in an infant. International journal of cardiology, 215, 127-128.
Sonsalla, P. K., Coleman, C., Wong, L. Y., Harris, S. L., Richardson, J. R., Gadad, B. S., ... & German, D. C. (2013). The angiotensin converting enzyme inhibitor captopril protects nigrostriatal dopamine neurons in animal models of parkinsonism. Experimental neurology, 250, 376-383.
Stock, R. J., Mudge, G. H., & Nurnberg, M. J. (2011). Congestive Heart Failure. Circulation, 4(1), 54-69.
Sullivan, M. J., Higginbotham, M. B., & Cobb, F. R. (2008). Increased exercise ventilation in patients with chronic heart failure: intact ventilatory control despite hemodynamic and pulmonary abnormalities. Circulation, 77(3), 552-559.
Thom, T. J., & Kannel, W. B. (2007). Congestive heart failure. Disease Management & Health Outcomes, 1(2), 75-83.
Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Drazner, M. H., & Johnson, M. R. (2013). 2013 ACCF/AHA guideline for the management of heart failure. Circulation, CIR-0b013e31829e8776.
Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Drazner, M. H., & Johnson, M. R. (2013). 2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation, 128(16), 1810-1852.