Angina Pectoris In Patients With Normal Coronary

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Angina Pectoris In Patients With Normal Coronary

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Discuss About The Angina Pectoris In Patients With Normal Coronary.

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Introduction

The case study states the clinical condition of Mr. Ferguson who has been admitted in to the emergency department (ED) with the symptoms of chest heaviness. Mr. Ferguson’s past clinical history tells that he had survived a Non ST Elevated Myocardial infarction (NSTEMI). Some of the complications following an NSTEMI are ischemic angina, re-infarction or infarct extension. The patient in this case is supposedly to be suffering from angina (Grodzinsky et al., 2012). Residual angina after an MI can be common in elderly patients, although residual angina after MI represents poor quality of life and is normally, a major driver of hospitalization. The reasons behind the high burden of angina after a MI is unclear. But it has been well established that stress and anxiety can be related to the standard (Yilmaz & Sechtem, 2012). Whether or not the angina is caused due to the increased pain is still unclear. Angina pectoris is mostly caused due to the myocardial infarction that occurs due to the mismatch between the myocardial blood supply and the oxygen demand. The chest heaviness is mainly caused due to the reduced flow of the blood to the heart (Yilmaz & Sechtem, 2012). As the heart muscles do not get enough oxygen it gives rise to a condition called ischemia. This restriction of the outflow of the myocardial blood is usually caused due to the atherosclerotic narrowing of the epicardial coronary artery (Grodzinsky et al., 2012).
Myocardial ischemia is determined by the increased heart rate which is due to the increased myocardial oxygen demand and the reduced diastolic perfusion. It is revealed from the case study that the patient had medical history of hypertension. Over time uncontrolled high blood pressure can also damage the coronary arteries that can causes blockage, abnormal flow of blood to the heart muscles. Mr. Feguson has been found to be diaphoretic. It has to be remembered that profuse sweating is a specific predictor of the an STEMI, which might have been caused due to the linkage between the sympathetic nervous system innervating the myocardial pain fibers and the sweat gland, originating from the thrombo-occular region (Gokhroo et al., 2012). The patient was probably suffering from unstable angina as detected from the irregular heartbeat.

Pharmacokinetics
It is evident from the case study that the patients has been prescribed with 300 mg of pro Aspirin. The aspirin irreversibly inhibits the action of the cyclooxygenase enzyme in the platelets that prevents the activation and the aggregation of the platelet (Tarkin & Kaski, 2013). This prevents the activation of the clotting cascade. Aspirin may react with some of the anticoagulants like warfarin resulting in excessive bleeding.
Morpine sulphate is a potential analgesic that can be used as it causes peripheral vasodilation and thus lessens the myocardial workload (Tarkin & Kaski, 2013). It is also given as a sedative for enabling relaxation in the patient. It interrupts the flow of the catecholamines and gives relief from the chest discomfort. Some of the side effects involving morphine is vomiting hypotension and respiratory depression (Aronson, 2015). An observational study carried out by Zhang et al., (2016) have indicated the risk of infections in patients receiving morphine. There are authors who have reported that morphine can delay the oral antiplatelet drug adsorption although there is valid reasons behind this. It has to be remembered that rapid inhibition of the platelet is the main treatment in coronary acute syndrome and any delaying in the antiplatelet effect may worsen the outcome (Zhang et al., 2016). Morphine sulphate extended tablets expose he patients to the risks of opoid addiction and misuse. Serious life threatening respiratory depression may be caused due to the use of the morphine sulphate extended tablets (Aronson, 2015). Heparin produces the anticoagulant effect by inactivating the thrombin and the activated factor (Tarkin & Kaski, 2013). It does so by accelerating the rate of the neutralization of certain activated coagulation factors by the help of anti-thrombin. The anti-thrombin effect of the heparin can be correlated to the inhibition factor XA (Husted & Ohman, 2015). It thus prevents the formation of the clots and inhibits further clotting. Long term usage of low dose heparin ,may lead to uncontrolled bleeding. Loss of bone strength and elevated levels of liver enzymes. Heparin induced thrombocytopenia is also common.
Fentanyls are opoids that re used for analgesia or anesthesia. It works by the agonism of the opoid receptors and is more potent than morphine due to its more lipophilicity (Husted & Ohman, 2015). Serious side effect of fentanyl involves vomiting, nausea, dizziness, light headedness, mood changes, abdominal pain, and difficulty in urinating (Aronson, 2015).

Nursing management
The nursing management of the patient with angina initiates with the proper assessment of the patients by using his clinical manifestation. The occurrence of angina or chest discomfort is normally evidenced by pains of varying degree, intensity or duration, narrowed focus, chest tightness or squeezing, diaphoresis and irregular heartbeat (Jorstad et al., 2013). In the first place the patient should be educated to notify the nurse as soon as when chest heaviness or pain occurs because pain and lessened cardiac output helps in the release of more amount of nor-epinephrine that increases the aggregation of the platelets and might result in blood clots. The patient should be observed for the associated symptoms, nausea, dyspnea, vomiting, dizziness, palpitation as decreased cardiac output may stimulate the sympathetic and the parasympathetic nervous system that can cause vague responses that might not be identified as angina ((Jorstad et al., 2013). There should be a continuous monitoring of the vital signs such as the change in the serial ECG. Ischemia at the time of anginal attack can cause ST segment elevation of depression of the T wave inversion. There should be a continuous assessment of the vital signs and the cognitive status and tally with the baseline data. Asympathetic stimulation during angina pectoris may increase the risk of the life threatening dysrhythmias that occurs in response to stress or ischemic changes and hence the heart rate and the heart rhythms should be monitored. In this case the GSW scale is 15 which signifies that the cognitive status of the patient was normal and hence verbalization should be encouraged for reducing the fear and anxiety.
It is revealed from the case study that the patient was having respiratory distress hence it is necessary to administer oxygen and keep the oxygen saturation level to>95% for supplying excess oxygen to the heart muscles (Jorstad et al., 2013). It is necessary to keep the patient in the semi-fowler position as it helps in the gas exchange that decreases the hypoxia and shortness of breath. Proper medications should be administered as per the instruction of the doctors and the medical protocols by maintaining 6 R’s of medicine administration.

Patient education and details
One of the crucial duty of the nurses are to provide appropriate education to the patient regarding the self-management of the condition such as education regarding the adherence to the drugs and the dosages. The patient should be prescribed with the proper dosages of the medicines. Although Rainsford,(2016) have stated that a long term low doses of aspirin is safe, but many patients taking this can develop ulcers. The risk of bleeding by low doses of aspirin is rare. The patient should be advised to take the morphine sulphate extended release tablet orally as crushing, chewing or dissolving the tablets may result in the uncontrolled delivery of medication and can cause over dosage (McCarthy et al., 2012). A patient is asked to report the doctor as soon as he faces things like hallucinations, confusions, pounding heart beat or the impairments of the adrenal gland (tiredness, loss of appetite and weightless), after the uptake of fentanyl. Since this medicine can trigger constipation the patient should be educated to consume fibrous diets and enough fluids to prevent dehydration. The patient should be given a clear indication regarding the consumption of the long term heparin therapy. The patient should be careful about any bleeding occurring after the consumption of the heparin, or sudden numbness on one side of the body or impairment of speech or balance (Lee & Arepally,2012). The patient should report to the doctor if he gets any allergies after the consumption of the medications.

Clinical considerations to combat the effects of the drug interactions
Reducing the adverse effects of the drugs in elderly patients suffering from the cardiovascular diseases requires close monitoring. The serious manifestations of the adverse drug reactions may include falls, heart failure, hypotension and delirium (Pretorius et al., 2013). Strategies to avoid adverse drug reactions include discontinuation of the medicines, prescribing new set of drugs, reducing the amount and the number of prescribers and reconciling medications. The STOPP (screening tools for the potential inappropriate prescription for the elderly) and START (screening tool for alerting the doctor for the correct treatment) can be helpful to the doctor for identifying the medications causing the adverse drug reaction. It is necessary to involve the patient in the decision making process and individualize the prescribing decisions based in the functional, medical and social conditions.

References
Alomar, M. J. (2014). Factors affecting the development of adverse drug reactions. Saudi Pharmaceutical Journal, 22(2), 83-94.
Aronson, J. K. (Ed.). (2015). Meyler’s side effects of drugs: the international encyclopedia of adverse drug reactions and interactions. Elsevier.
Gokhroo, R. K., Ranwa, B. L., Kishor, K., Priti, K., Ananthraj, A., Gupta, S., & Bisht, D. (2016). Sweating: A Specific Predictor of ST?Segment Elevation Myocardial Infarction Among the Symptoms of Acute Coronary Syndrome: Sweating In Myocardial Infarction (SWIMI) Study Group. Clinical cardiology, 39(2), 90-95.
Grodzinsky, A., Arnold, S. V., Gosch, K., Spertus, J. A., Foody, J. M., Beltrame, J., …&Kosiborod, M. (2015). Angina frequency after acute myocardial infarction in patients without obstructive coronary artery disease. European Heart Journal–Quality of Care and Clinical Outcomes, 1(2), 92-99.
Husted, S. E., & Ohman, E. M. (2015). Pharmacological and emerging therapies in the treatment of chronic angina. The Lancet, 386(9994), 691-701.
Jorstad, H. T., von Birgelen, C., Alings, A. M. W., Liem, A., van Dantzig, J. M., Jaarsma, W., … & Withagen, A. J. (2013). Effect of a nurse-coordinated prevention programme on cardiovascular risk after an acute coronary syndrome: main results of the RESPONSE randomised trial. Heart, 99(19), 1421-1430.
Lee, G., & Arepally, G. M. (2012). Anticoagulation techniques in apheresis: from heparin to citrate and beyond. Journal of clinical apheresis, 27(3), 117-125.
McCarthy, C. P., Mullins, K. V., Sidhu, S. S., Schulman, S. P., & McEvoy, J. W. (2016). The on-and off-target effects of morphine in acute coronary syndrome: A narrative review. American heart journal, 176, 114-121.
Pretorius, R. W., Gataric, G., Swedlund, S. K., & Miller, J. R. (2013). Reducing the risk of adverse drug events in older adults. Am Fam Physician, 87(5), 331-336.
Rainsford, K. D. (Ed.). (2016). Aspirin and related drugs. CRC Press.
Tarkin, J. M., & Kaski, J. C. (2013). Pharmacological treatment of chronic stable angina pectoris. Clinical medicine, 13(1), 63-70.
Yilmaz, A., & Sechtem, U. (2012). Angina pectoris in patients with normal coronary angiograms: current pathophysiological concepts and therapeutic options. Heart, 98(13), 1020-1029.
Zhang, N., Chen, K., Rha, S. W., Li, G., & Liu, T. (2016). Morphine in the setting of acute myocardial infarction: pros and cons. The American journal of emergency medicine, 34(4), 746-748.

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