Background Information
Discuss about the Atrial Fibrillation Treatment Rationale And Clinical.
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Mr. X a 60 year old male driver from Australia, married and having six children the youngest being twenty years old, retired driver (was a driver) and cigarette smoker was admitted to the nursing unit from his physician’s office. He was diagnosed with cerebral hemorrhage and hypertension. He complained of a severe headache, nausea and vomiting, weakness on the arm and the leg, trouble with vision and swallowing. Three months ago he was treated with hypertension, with a blood pressure of 170/100 and a reduced urine creatinine removal. He complained of headache and blurred vision. He was recommended three months therapy which included diet restriction such as avoidance of food with high cholesterol did not show a response to the blood pressure elevation. His medical history showed that he had not been complying with reduced sodium, cholesterol diet and medication that were prescribed to him. His social history showed that he has been an alcohol addict and smoked five cigarette per day. An emergent non-contrast head computed tomography showed a left frontal cerebral hemorrhage.
Mr. X was admitted to the hospital complaining of the following sign and symptoms
- Severe headache
- Nausea and vomiting
- Weakness on the arm and leg
- Trouble with vision and swallowing
The client was examined and his vital signs were as follows. Temperature of 36.9, blood pressure of 155/133 mmHg, pulse 69, respiratory rate of 20 and oxygen saturation of 94 %. Both lungs were clear during bilateral auscultation. The client had a normal heart rate with a regular S1 and S2. There was no murmurs and the abdomen was soft with normal bowel sounds. In the peripheral areas there was no sign of edema. Glasgow coma scale was done and the result was a fifteen. He had a best eye response (E4), he was oriented to date and place (V5). He had a fluent speech, his eye were reactive to light bilaterally
Mr. X was diagnosed with hypertension three months ago and he was given the following drugs. Diuretics example hydrochlorothiazide so as to reduce the blood volume and cardiac output. Adrenergic agents’ example clonidine hydrochloride which affects the central nervous system leading to a reduction in blood pressure. Vasodilator example hydralazine hydrochloride which reduces resistance in the periphery.
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Patient
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Control
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White blood cell
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9.7
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4-11
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Hemoglobin
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10.4
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11.5-15.5
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Platelets
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231
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150-450
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Creatinine
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2.34
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0.5-1.2mg/dl
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Blood urea nitrogen
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54
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6-20 mg/dl
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Potassium
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4.4
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3.5-5.5 mmol/l
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Albumin
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3.4/7.2
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Alanine aminotransferase/ Asparate aminotransferase
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19/34
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Up to 33U/L
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Bilirubin
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0.39
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Up to 1.1 mg/dl
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blood glucose
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199
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pH
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7.46
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partial pressure of carbon dioxide
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30-4
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Bicarbonate
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19.5
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- Albumin, IV dose: 100u
- Hydrocortisone, IV dose: 50mg
- Cloxascillin, IV dose: 19m
- Phenytoin, IV dose: 100mg
- Levophed IV dose
Brain hemorrhage is defined as bleeding around the brain, it is either caused by raptured aneurysm also known as hemorrhagic stroke or head trauma. Brain hemorrhage is divided into two types, extra-axial hemorrhage meaning outside the brain tissue and intra-axial hemorrhage which is within the brain tissue. Extra-axial bleeding is also known as intracranial bleeding, this is the bleeding within the skull. Examples of the extra-axial bleeding include the epidural, subdural and subarachnoid. Intra-axial hemorrhage include the intracerebral hemorrhage and intraventricular hemorrhage.
Symptoms and Diagnosis
Extra-axial hemorrhage is bleeding that occurs within the skull but outside the brain tissue. An epidural hemorrhage is a hemorrhage that occurs between the skull and the dura membrane. It’s often as a result of trauma to the head. The bleeding that occurs between the dura and the skull is often from the middle meningeal artery. Clinical manifestation include altered consciousness, headache, vomiting, confusion and aphagia. Subdural hemorrhage is the hemorrhage that occurs below the dura matter. The hemorrhage occurs between the dura matter and the sub-arachnoid membrane. The source of blood is often from the bridging veins. Clinical manifestation of subdural hemorrhage are the same are those occurring in epidural hemorrhage. The final type of extra-axial hemorrhage is the subarachnoid. The bleeding occurs mostly in the subarachnoid space. It is often as a result of the cerebral artery specifically an aneurism within the artery. The most common cause, is a rapture of a saculam type of an aneurism which leads to subarachnoid hemorrhage. The clinical manifestation are the same as those mentioned above except that in subarachnoid hemorrhage there is a sudden severe headache, loss of consciousness and meningismus. Causes of epidural hematoma include head trauma such motor vehicle accident, falls and assault.
Intracerebral hemorrhage is divided into two, lobam hemorrhage which is the hemorrhage that occurs on specific lobes in the brain, thalamic hemorrhage which is the hemorrhage that occurs in the thalamus pontine hemorrhage which is the hemorrhage that occurs in the pons and lastly cerebellar hemorrhage which occurs in the cerebellar. Intracerebral hemorrhage is the most common cause of stroke.
Cerebral atherosclerosis leads to a condition known as hypertension which is defined as a systolic blood pressure of more than 140mmHg and a diastolic pressure of more than 90mmHg over a long period of time. Cerebral atherosclerosis is caused by several factors. First, high levels of triglycerides and cholesterol in the blood which destroys the endothelium. Second, high blood pressure which is caused by two forces the first is the pressure created by the heart as it pumps blood and the other is resistance in the arteries during blood flow. The harder it is for the blood to flow, the higher the blood pressure. This rapid increase of blood pressure damages the arteries. The third and the last is cigarette smoking. Tobacco particles exacerbate atherosclerosis in the following ways, the tobacco smoke contains toxins which reduce high density lipoprotein while increasing the levels of low density lipoproteins. Carbon monoxide and nicotine found in cigarette smoke destroys the endothelium increasing the risk of plaque formation. Lastly is high blood pressure, smoking by a hypertensive person may increase the risk for malignant hypertension which is a life threatening form of high blood pressure. Atherosclerosis is characterized by fat deposit known as atheroma that infringe on the lumen of the large arteries in the brain. Macrophages which develop from T lymphocytes and monocytes infiltrate the area and eat away the lipids and then die. This causes the proliferation of the smooth muscle cell forming a dead fatty core. This plaque causes an obstruction in the blood flow due to narrowing.
Hypertension and Cerebral Atherosclerosis
Tiny arteries take blood to deep areas in the brain. High blood pressure causes the rapture of the thin walled arteries releasing blood into the tissues. The clotted blood which is enclosed in the rigid skull causes the buildup of fluid which leads to an increase in pressure (Demchuk and Buchan, 2014). The created pressure can compress the brain against the bone or cause a herniation. The distributed blood in the tissue causes a decrease in blood supply in the arteries called a stroke (Alberts, Hademenos and latchaw, 2013). Blood cells contained within the clot die releasing toxins which cause further damage to the brain cells around the hematoma.
A swelling occurs leading to a buildup pressure in the affected area. It’s caused by blood pools in the brain due to blood vessel break. The blood pressure formed cannot be released out through the bone, it pushes and compresses the brain causing damage. The damaged area of the brain affects the body system. Individuals may go through loss of memory, lingering impairments, a delay in reaction time and also death.
Mr. X lived a sedentary lifestyle which included, cigarette smoking and unhealthy diet which included food with high cholesterol intake and sodium intake. This caused abnormal accumulation of fats in the blood vessels leading to cerebral atherosclerosis (Fredman and Rosenman, 2015) hence leading to intracerebral hemorrhage. Fat deposition causes narrowing of the blood vessels which leads to a condition known as hypertension. Hypertension signs and symptoms include severe headache and blurred vision as witnessed in Mr. X. The client never complied with the doctors instructions on high cholesterol restriction and treatment therapy. His main reason for not complying was that he had been busy with work all day. Since the hypertension was left untreated for a long time it resulted to the collapsing of the thin arteries in the brain leading to a release of blood into the brain tissues, leading to a condition known as cerebral hemorrhage which was evidenced by severe headache, nausea and vomiting, weakness on the arm and leg, trouble with vision and swallowing and lastly an emergent non-contrast head computed tomography which showed a left cerebral hemorrhage (Pfohman and Criddle, 2015).
Brain hemorrhage is the leading cause of the severe headache due to the leaking cerebral aneurism. The small arteries around the brain which deliver oxygen around the brain bulge and form an aneurysm. The aneurism causes outflow blood to tissue which causes tissue irritation hence the severe headache. Weakness in the arm and the leg is due to loss of voluntary motor movements. Damage of motor neurons located in the opposite side of the brain is the leading cause of weakness of the arm and the leg. Mr. X visual disturbance is due to damage of the sensory pathways located between the eye and visual cortex. The high blood pressure of 155/133 is due narrowed arteries caused by accumulation of fat lipids in the blood vessel.
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Actual or Potential problem
1. Ineffective cerebral perfusion related to bleeding evidenced by changes in vital signs
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SMART nursing goal(s)
a) The client will show Improvement cerebral perfusion within two months evidenced by strong peripheral pulses and vitals within the normal range.
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Nursing interventions
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Rationale
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Strategies to determine effectiveness of actions
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1. Check for alteration in blood pressure by comparing both readings in both arms
· Make sure the left arm is has rested at the heart level
· The patient should avoid taking caffeine or tobacco at least one hour before taking the measurement (Papakonstaninou, 2016).
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1. A variation in blood pressure may happen when the vasomotor area is injured. Blockage of blood due to clot formation may result to an increase in intracranial pressure. If the results show that there is in readings of both arms this will signify the presence of a blockage in subclavian artery (Qureshi, Tuhrim and Broderick, 2015).
· Placing the clients arm at the arms rest instead of the right atrial level may result to high blood pressure values. This may be important during the diagnosis and later treatment actions for clients with hypertension.
· Caffeine intake results to a striking increase in blood pressure since caffeine blocks a hormone that assists in the widening of the arteries and it also enhances the adrenaline glands to release more adrenaline which cause a sudden increase in blood pressure (Papakonstaninou, 2016).
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1. Attains an optimum cerebral tissue perfusion
· The patients understands the effects caffeine and tobacco in his body
· The client attains a normal blood pressure
· The clients shows no sign of standing hypotension
2. The client attains a normal neurological status
· The client open his eyes on request
· He follows command with appropriate motor response
· The client show no evidence if increased intracranial pressure
· The client speaks eloquently
· The client pupils reacts normally to light
3. The client understands the importance of medication to his health
· The client takes his medication on time
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2. Asses and check the neurological status
· Monitor pupils’ size, reaction to light, and equality.
· Assess and document the changes in vision and give an account for blurred vision and any change in depth perception or visual field.
· Monitor the higher functions which include speech and if the patient is alert
· Check for factors that are associated with the client’s condition for reduces cerebral perfusion and risk for increased intracranial pressure.
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2. It monitors the courses in the degree of consciousness and a possible raise in intracranial pressure. It is useful in finding the position, extension and the progress of damage (Marmarou and Butcher, 2012).
· Any alteration in the client’s pupil’s reaction is an indication of an increased intracranial pressure and the compaction of the optic nerve. The oculomotor cranial nerve controls pupil reaction and it is important in finding out whether the brain stem is damaged. The pupil’s size assessment is important in ascertaining the equilibrium between the sympathetic and parasympathetic innervation. Reaction to light is shows a joined function of the oculomotor and optic cranial nerve. Pupil’s reaction to light should be quick and after the light source is removed the pupil should go back to its original size. Lack of reaction to light maybe induced by a developing mass, which can include a blood clot which causes pressure on the optic nerve the third cranial nerve; the unchanging pupil may be due herniation of the medial temporal lobe.
· Any change in visual alteration shows the areas of the brain involved. Stroke causes blurred vision and headache.
· Any alteration in speech content and cognition is a signal cerebral involvement and the location of damage. It may also indicate and increased intracranial pressure.
· The assessment will influence and establish the alternative of intervention. Failure of the neurological signs may show a reduced intracranial adaptive capacity which may force for intracranial pressure monitoring. If the stroke is developing the client may deteriorate quickly and may demand for continuous assessment and treatment.
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3. Administer medication as prescribed by the doctor.
· Alteplase
· Administer oxygen as indicated
· Administer albumin 100u intravenous
· Hydrocortisone 500mg intravenous
· Cloxascillin 19m IV dose
· Administer phenytoin 100mg IV dose
· Administer levophed IV dose
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3. Medication are important in controlling the chronic condition and an overall long term health.
· Alteplase is a thrombolytic whose function is to dissolve the clot formed in the cerebral vessels (Bubien and Sanchez, 2014). This therapy is based on trying to reduce the size of the infarct and also continuous checking for any signs and symptoms of intracranial hemorrhage (Hirsh, Halperin and Fuster, 2016).
· Tissue hypoxia is a serious condition that requires medical attention. Oxygenation reduces hypoxemia. This condition causes cerebral vessel to dilate this may cause edema to form or increase intracranial pressure.
· Serum albumin is a protein which functions by maintain and controlling the blood colloidal osmotic pressure. It also raises the volume of the circulating plasma hence reducing blood viscosity and hemoconcentration. It functions as a protein drug carrier by transporting fatty acids, steroids and lastly hem (Sugio et al., 2012).
· Hydrocortisone acts by regulating homeostatic, metabolic and cardiovascular functions (Knight, Kornfeld and Glaser, 2012). They bind to cortisol receptor and suppress call mediated immunity by preventing cytokines IL-1 to IL-8. (De Werth, Zijl and Buitelaar, 2012) They also suppress humoral immunity leading to lower amounts of IL-2, reduced amount of IL-2 causes T lymphocytes reduction.
· Cloxacillin is semisynthetic. It is used in the treatment of beta lactamase producing staphylococci. This is because of its large R chain which does not allow binding of the beta-lactamase (Greenwood, 2012).
· Phenytoin acts on the sodium channels found on the neural cell membrane, this causes a reduction in the spread of seizure activity. Promotion of sodium efflux from neurons, phenytoin helps by stabilizing hyper excitability caused by excessive stimulation (De Marco and Felipe, 2018).
· Levophed is a powerful peripheral vasoconstrictor. In the coronary arteries, it causes dilation thereby increasing the coronary blood flow (Campschroer, Zhu and Grobbee, 2014).
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Actual or Potential problem
2. Ineffective coping related to situational crises evidenced by inability to meet basic needs
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SMART nursing goal(s)
a. The client will employs effective coping methods within one month evidenced by the patient verbalizing feelings.
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Nursing interventions
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Rationale
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Strategies to determine effectiveness of actions
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1. Monitor the degree of altered perception and record the functional independence score.
· Explain the meaning of dysfunction and change to the client. Observe if the client is able to understand and allow for appraisal of the situation.
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1. Checking for the individual factors assist in developing a good care plan.
· Independency is highly evaluated in the American culture but it is not important in some culture. Some clients accept and handle with small adjustments, on the other hand, it may look difficult for others to adjust to deficits (Robinson-Smoth, Johnston and Allen, 2012).
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1. The client understands the meaning of dysfunction and dependency
2. The client recognizes the outside stressors
· The client gives a description on the feelings concerning the lifestyle
· The client uses accessible resources and coping methods
· The client uses community resources that are needed
· The clients take part in the development of a care plan.
3. Client remains mentally alert and satisfy psychological needs evidenced by appropriate feelings of expression.
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2. Check for the outside stressors
· Advice the client to show concerns
· Encourage the use of coping methods
· Inform social services if it is mandatory
· Encourage the client to take part in healthcare planning
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2. The information helps identifying the special needs, it also provides information that will assist in solving the problem. Social factors will help in providing discharge destination (Philips, Anna and Douglas, 2018).
· Verbalization assists the client to deal with his problems and feelings
· Coping methods reduces the effects of stress, sharing problems relieves the burden that on has (Eckhard and James, 2015).
· Anxiety may be caused by social or financial problems, it helps in solving management problems which are linked to continuing care (Plant, Ashby and Patricia, 2014).
· Participation in health care planning allow for some control in self
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3. Check for sleep disturbance, concentration problems, weakness, withdrawal, and lastly arguments of inability to cope
· Recommend for neuropsychological assessment and cancelling if needed
· Assess for orientation status
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3 It may signify the beginning of depression which is common after the effect of stroke (Jing Wang, 2013).
· Neuropsychological evaluation assists in adjustment to role changes that are important self-esteem and the sense of being a productive person. Depression may result to brain damage.
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Causes of Brain Hemorrhage
Conclusion
Assessment tools
Tools used to check for vital sign include stethoscope, it’s an instrument used listen to sounds produced by the heart and lungs. It is used by placing the circular piece on the chest. The other tool used was sphygmomanometer was used for checking blood pressure, it made of inflatable rubber cuff, a bulb whose function is to inflate the cuff. The cuff pressure is released slowly by opening the valve. Blood begins flowing when arterial systolic pressure is equal the cuffs pressure.
Mr. X. was admitted for a month where he was carefully monitored for any signs and symptoms of stroke. The nurses on duty ensured that he took his medicine on time and no medication was skipped. He was released after the doctor had confirmed that the condition was well treated. His family members were called to come pick him up, who later on settled the hospital bill. Mr. X was advised on the importance of taking hypertensive drugs. He was also recommended to go to rehabilitation center where he was to be trained on methods of avoiding cigarette smoking since he was a chronic smoker.
Reference
Alberts, M., Hademenos, G. and latchaw, R. (2013). Recommendations for the establishment of primary stroke centers. Journal of the American Medical Association, 283(23), pp.3102-3109.
Bubien, R. and Sanchez, J. (2014). Atrial fibrillation: treatment rationale and clinical utility of nonpharmacologic therapies. AACN clinical issues: advanced practical acute critical care, 12(11), pp.140-155.
Campschroer, T., Zhu, D. and Grobbee, D. (2014). Alpha-blockers as medical expulsive therapy for ureteral stones. Cochrane Database Syst Rev, 23(2), pp.34-36.
De Marco, E. and Felipe, A. (2018). Cerebellar volume and long-term use of phenytoin. European jpournal of Epilepsy, 12(5), pp.312-315.
De Werth, C., Zijl, R. and Buitelaar, J. (2012). Development of cortisol circadian rhthmn in infancy. Early human development, 73(2), pp.39-52.
Demchuk, A. and Buchan, A. (2014). Predictors of stroke outcome. Neurological clinic, 19(2), pp.455-473.
Eckhard, H. and James, M. (2015). Psychophysiology: Human Behavior and Physiological Response. Human Behavior & Physiological Response, 56(3), p.67.
Fredman, M. and Rosenman, R. (2015). Association of specific overt behavior patterns with blood and cardiovascular findings: Blood cholesterol level, blood clotting time, incidence of arcus senilis and clinical coronary artery disease. Journal of the American Medical Association, 169, pp.1286-1297.
Greenwood, D. (2012). Claxacillin sodium analogue-based drug recovery. International drug price indicator, 21(3), pp.5-8.
Hirsh, J., Halperin, S. and Fuster, L. (2016). Guide to anticoagulant therapy: Heparin. A statement for healthcare professionals from the American Heart Association. Circulation, 103(24), pp.1577-1579.
Jing Wang, X. (2013). inhibitory control in the Cortico-basal ganglia thalamocorticol loop: complex regulation and interplay with memory and decision processes. Neuron, 92, pp.1093-1105.
Knight, R., Kornfeld, D. and Glaser, G. (2012). Effects of intravenous hydrocortisone on electrolytes of serum and urine in man. J clinic endocrinal metab, 15(2), pp.176-181.
Marmarou, A. and Butcher, J. (2012). Prognostic value of glasgow coma scale and pupil reactivity in traumatic brain injury accessed, prehospital and on enrollment; an impact analysis. J Neurotrauma, 24(12), pp.270-280.
Papakonstaninou, E. (2016). Acute effects of coffe consumption on self reported gastrointestinal symptoms, blood pressure and stress indices in healthy individual. Nutritional journal, 15, p.26.
Pfohman, M. and Criddle, L. (2015). Epidemiology of intracranial aneurysm and subarachnoid hemorrhage. Journal of Neuroscience Nursing, 33(1), pp.39-41.
Philips, K., Anna, C. and Douglas, D. (2018). Negative life events and symptoms of depression and anxiety: stress caution and or stress generation. Anxeity stress ansd coping, 28(4), pp.357-371.
Plant, E., Ashby, E. and Patricia, G. (2014). The antecedents and Implications of Interracial Anxiety. Personality and Social Psychology Bulletin, 29, pp.790-801.
Qureshi, A., Tuhrim, S. and Broderick, J. (2015). Spontaneous intracerebral hemorrhage. New England Journal of Medicine, 344(19), pp.1450-1460.
Robinson-Smoth, G., Johnston, M. and Allen, J. (2012). Self-care, self-efficacy, quality of life, and depression after stroke. Archives of Physical Medicine and Rehabilitation, 81, pp.460-464.
Sugio, S., Kashima, A., Mochizuki, M. and Kobayashi, K. (2012). Crystal structure of human serum albumin at 2.5 A resolution. Protein Engineering Design and Selection, 12(6), pp.439-446.
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