Discuss about the Critical Care Nursing for Diagnosis and Management.
The systolic blood pressure in a range of 120-129 mmHg and diastolic blood pressure in a range of 80-84 mmHg considered as normal (NHFA, 2016, p.12). The blood pressure ranges for grade – 1 hypertension attribute to 140-159 mmHg (systolic) and 90-99 mmHg (diastolic) (NHFA, 2016). The ranges for grade – 2 hypertension recorded as 160–179mm Hg (systolic) and 100-109mm Hg (diastolic) (NHFA, 2016). Grade – 3 hypertension identified by systolic blood pressure of ≥180 mmHg and diastolic blood pressure of ≥110mm Hg (NHFA, 2016). The systolic blood pressure of >140 mmHg and diastolic pressure of < 90 mmHg is identified as isolated systolic hypertension (NHFA, 2016).
The respiratory rate of the patient requires manual recording by the physician while investing 30 seconds in the process of its observation (Anon., 2010). Respiratory rate warrants its recording with the vital signs during each patient observation. The respiratory rate of the patients needs recording on the general observation chart on a daily basis and the abnormal pattern of respiratory rate requires its counting for one complete minute in the context of retaining the accuracy of the recorded value.
The pattern of high respiratory rate of the patient requires nursing evaluation of his probable clinical manifestations attributing to anxiety, fear, acidosis, hypercapnia, hypoxia and shock (Urden et al., 2014, p.572). The investigation of medication administration and metabolic demand of the patient also required for tracking the causative factor of patient’s elevated respiratory rate. The registered nurse professional requires recording of patient’s ABG and should regularly visit the patient for providing reassurance during the process of clinical intervention. The registered nurse also requires configuring a therapeutic relationship with the patient for reducing the state of distress related to his elevated respiratory rate.
The diabetes educator assists in disseminating the basic information regarding the disease process of diabetes to the affected patients in the context of elevating the level of their awareness regarding the disease (Goldstein & Mueller-Wieland, 2007, p.48). They facilitate the physical activity, nutritional management and medication monitoring of the diabetes patients while coordinating with physicians and nurses. Since, Mr. Hardy exhibits a 30 year history of diabetes type 2, the diabetes educator requires promoting healthy eating habits in the patient while regularly monitoring his blood glucose level. The diabetes educator needs to educate the patient regarding various healthy coping strategies and problem solving skills for reducing his risk of developing the debilitating diabetic manifestations (Goldstein & Mueller-Wieland, 2007).
As per Mr. Hardy’s scenario, the physiotherapist requires customizing appropriate exercise interventions for normalizing his body mass index and blood glucose level (Azurin, 2016). Aerobic exercise approaches along with resistance training interventions require administration by the physiotherapist for stabilizing the HbA1C level of the patient. The physiotherapist needs to monitor the blood glucose level of patient and recommend the exercise interventions in accordance with the allowable limit of blood glucose following its evaluation. The physiotherapist also requires instructing the patient regarding the self-evaluation of skin redness, breaks and swelling for their prophylactic management (Turan et al., 2015). The physiotherapist also needs to facilitate the activities of daily living of the patient while administering therapeutic exercises for increasing his mobility pattern, range of motion, muscular endurance and strength.
Since Mr. Hardy is overweight, the general practitioner requires evaluating the cardiovascular risk of the patient while ordering cholesterol lab interventions (RACGP, 2014, p.xi). The general practitioner requires administering first line pharmacotherapy for controlling the elevated blood pressure of the patient. The physician might utilize thiazide diuretics, beta-blockers, or ACE inhibitors in accordance with the clinical condition and CVA status of the affected patient (Gupta & Guptha, 2010). The general physician should also recommend appropriate life style interventions and weight and diet management approaches for reducing the risk of the patient in terms of developing the cardiovascular manifestations.
The conditions including diabetes, obesity, hypertension and smoking addiction primarily contributed to the development of Mr. Hardy’s cerebrovascular accident (Alkali et al., 2013). The abnormal blood glucose level of the patient over the course of 30 years facilitated the development of clots on the inside walls of the blood vessels that disrupted the brain’s oxygen supply leading to the development of stroke. The state of patient’s obesity could also have resulted in the deposition of plaques on the arterial walls leading to the formation of arterial clots that might have assisted in the development of stroke in the affected patient (NIH, 2012). The hypertensive state resulted in the development of consistent pressure on the blood vessels near the brain of the patient leading to the occurrence of cardiovascular accident. The pattern of patient’s smoking might have assisted in the elevation of triglycerides and damaged the internal lining of the blood vessels (CDC, 2016). It could have increased the viscosity of blood inside the vessels and facilitated the deposition of cholesterol and calcium on the endothelium of the blood vessels. Resultantly the thickened and narrowed blood vessels could have ruptured due to excessive vascular pressure leading to the appearance of stroke.
Within the cardiovascular system, high blood pressure (hypertension) can damage blood vessels by causing the thickening and hardening of the arteries. The pattern of high blood pressure leads to the consistent exertion of additional force against the walls of the arteries. The arteries then eventually narrowed and predisposed towards the development of fibrolipid plaques across their interior walls. The development of stenosis and arteriosclerosis across the arterial region leads to the gradual weakening of the affected arteries and increases their risk of rupture (Carl et al., 2014, p.403).
This damage to the blood vessel walls may cause cerebral ischemia leading to the reduction in the supply of oxygenated blood to the brain vasculature. This vascular insufficiency leads to the development of cerebrovascular accident in the affected patient. It is worth noting that the pattern of narrowing of the lumen of blood vessels, deposition of plaques and platelet adhesion results in the establishment of thrombosis in the blood vessels of the brain that leads to their maximum occlusion (Galvagno, 2003, p.303). The occluded vessels experience high risk of rupture and the eventual establishment of acute ischemic stroke.
Untreated high blood pressure can decrease the vascular resistance and elevates the risk of the development of acute ischemic stroke (Mayo-Clinic, 2016). It also causes arterial narrowing and damage and facilitates the deposition of dietary fats on the arterial lumen. The development of arterial stenosis results in the blockage of vascular supply to the vital organs as well as extremities. High blood pressure, if left untreated, might also cause enlargement and bulging of weakened arteries in the form of aneurysm (Mayo-Clinic, 2016). Untreated high blood pressure also facilitates the development of coronary artery disease, cardiac enlargement and cardiac failure. The other brain conditions that might develop because of untreated blood pressure include transient ischemic attack, dementia and mild cognitive impairment (Mayo-Clinic, 2016).
When a stroke, caused by cerebral hemorrhage within the central nervous system (the brain) occurs, effects depend on the development of hypertension and cerebral amyloid angiopathy (Aguilar & Brott, 2011). Furthermore, conditions arising from factor deficiencies, antiplatelet medication and anticoagulant-induced coagulopathy lead to the establishment of cerebral hemorrhage and subsequent occurrence of stroke in the affected patients. The lymphoproliferative as well as thrombocytopathic conditions also assist in the development of cerebrovascular infarction followed by cerebral hemorrhage (Aguilar & Brott, 2011). Patients affected with white matter ischemic disease and hypertension experience the high risk of developing the pattern of cerebral hemorrhage. The development of cerebral hematoma is also a risk factor for the occurrence of cerebral ischemia, cerebral hemorrhage and associated stroke pattern. Conditions like chronic kidney disease, alcoholism and drug abuse also increase the risk of stroke development among the affected patients. Advancing age of the diabetic patient also influences the occurrence of cerebral hemorrhage and cerebrovascular infarction (Aguilar & Brott, 2011). Age associated degenerative change in the cerebral arterioles facilitates the development of lacunar stroke and associated manifestations. The clinical conditions like hyperlipidemia, smoking addiction, coagulopathy and utilization of recreational drugs also increase the risk of development of cerebral hemorrhage and infarction in predisposed patients (Aguilar & Brott, 2011).
The pattern of hemorrhagic stroke might result in the development of abnormal involuntary movements in the affected patient (Siniscalchi et al., 2012). The patient might also experience headache, nausea, vomiting and alteration in consciousness in relation to the episode of hemorrhagic stroke (Liebeskind & O’Connor, 2016). Hemorrhagic stroke can lead to the development of seizures and increased intracranial pressure. The paralysis of dormant or non-dormant side of the body and weakness of extremities considered as the direct outcomes of hemorrhagic stroke (Liebeskind & O’Connor, 2016). Focal neurological conditions like facial droop, monocolular/binocular blindness, blurred vision, dysarthria, vertigo and aphasia also result from the development of hemorrhagic stroke in the affected patient (Liebeskind & O’Connor, 2016). Stroke that arises from subarachnoid hemorrhage leads to the development of syncope, photophobia, ocular pain and nuchal rigidity (Liebeskind & O’Connor, 2016). Stroke associated with cerebral hemorrhage in many clinical scenarios lead to the development of anemia and fever (Caceres & Goldstein, 2012). The patient might also experience a decline in the blood glucose level after the onset of hemorrhagic cerebral infarction (Caceres & Goldstein, 2012).
The two significant deficits experienced by Mr. Hardy that require nursing care include the pattern of his immobility and lack of personal hygiene. The mobility restriction of Mr. Hardy relates to his left side paralysis in relation to the pattern of cerebrovascular accident. Mr. Hardy’s unwillingness regarding practicing personal hygiene measures relates to the absence of support systems and home care services that has affected his state of mind to a significant extent. Therefore, the administration of appropriate nursing interventions highly warranted for assisting him in terms of activities of daily living and personal care while overcoming the hygiene issues and treatment related challenges.
Nursing interventions warranted for Mr. Hardy include the administration of assistance to facilitate his activities of daily living and mobility level. The reduction in cardiovascular deconditioning of the patient while assisting him in acquiring various sitting postures required for improving his physical condition. The administration of walking intervention required for increasing the confidence of the client in terms of enhancing the level of his mobility. Assisting the patient in accomplishing the requirements of personal hygiene will decrease his risk of acquiring contagious conditions across the hospital environment. The regular evaluation, of patient’s skin condition also required for preventing the onset and establishment of bed sores (in relation to the pattern of his immobility) during the process of clinical intervention. The major barriers to the nursing interventions include the patient’s unwillingness in attaining mobility and hygiene measures with the assistance of nursing professional.
References
Aguilar, M.I. & Brott, T.G., 2011. Update in Intracerebral Hemorrhage. The Neurohospitalist, 1(3), pp.148-59. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3726132/.
Alkali, N.H. et al., 2013. Stroke risk factors, subtypes, and 30-day case fatality in Abuja, Nigeria. Nigerian Medical Journal, 54(2), pp.129-35. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3687865/.
Anon., 2010. Royal Prince Alfred Hospital Patient Observation (Vital Signs) Policy. Policy Directive. Sydney: Sydney South West Area Health Service (NSW Health).
Azurin, C.R., 2016. Physiopedia. [Online] Available at: https://www.physio-pedia.com/Diabetes [Accessed 20 September 2016].
Caceres, J.A. & Goldstein, J.N., 2012. Intracranial Hemorrhage. Emergency Medicine Clinics of North America, 30(3), pp.771–94. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3443867/.
Carl, L., Gallo, J. & Johnson, P., 2014. Practical Pharmacology in Rehabilitation. USA: Human Kinetics.
CDC, 2016. CDC. [Online] Available at: https://www.cdc.gov/tobacco/campaign/tips/diseases/heart-disease-stroke.html [Accessed 20 September 2016].
Galvagno, S.M., 2003. Emergency Pathophysiology: Clinical Applications for Prehospital Care. USA: Teton NewMedia.
Goldstein, B.J. & Mueller-Wieland, D., 2007. Type 2 Diabetes: Principles and Practice. 2nd ed. Florida: CRC.
Gupta, R. & Guptha, S., 2010. Strategies for initial management of hypertension. IJMR, 132(5), pp.531-42. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3028941/.
Liebeskind, D.S. & O’Connor, R.E., 2016. Medscape – Hemorrhagic Stroke Clinical Presentation. [Online] Available at: https://emedicine.medscape.com/article/1916662-clinical [Accessed 20 September 2016].
Mayo-Clinic, 2016. Diseases and Conditions – High blood pressure (hypertension). [Online] Available at: https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/in-depth/high-blood-pressure/art-20045868 [Accessed 20 September 2016].
NHFA, 2016. Guideline for the diagnosis and management of hypertension in adults. Melbourne: National Heart Foundation of Australia.
NIH, 2012. National Heart, Lung, and Blood Institute. [Online] Available at: https://www.nhlbi.nih.gov/health/health-topics/topics/obe/risks [Accessed 20 September 2016].
RACGP, 2014. General practice management of type 2 diabetes. Australia: RACGP.
Siniscalchi, A. et al., 2012. Current Neuropharmacology. Post-stroke Movement Disorders: Clinical Manifestations and Pharmacological Management, 10(3), pp.254-62. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468879/.
Turan, Y., Ertugrul, B.M., Lipsky, B.A. & Bayraktar, K., 2015. Does physical therapy and rehabilitation improve outcomes for diabetic foot ulcers? World Journal of Experimental Medicine, 5(2), pp.130-39. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4436937/.
Urden, L.D., Stacy, K.M. & Lough, M.E., 2014. Critical Care Nursing: Diagnosis and Management. Missouri: Elsevier Mosby.
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