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Assessment Sequence

Rainey is a 64-year-old woman of Maori descent who has been married for 42 years and has 2 grown up daughters. Both of Rainey’s parents died when they were in the their mid 60s of ‘heart attacks”. Two of her 4 brothers have had heart attacks and have high BP and her remaining uncle had ‘2 heart attacks and a stroke’. Rainey leads a sedentary life style and her diet is mostly high in fat and sugar. Her body mass index is 31 kg/m2 and her waist measurement is 101cm.


Rainey presented to her GP complaining of flu like symptoms. The GP took her BP and found that it was 160/100. He listened to her chest and found it to be clear. He did not prescribe antibiotics but ordered further tests for her elevated BP. Rainey followed up with her GP a few days later, her BP was found to be 165/100. Other tests include serum cholesterol 7.2 mmol/L, LDL 6.2, HDL 0.7 and fasting triglyceride 5.9 mmol/L. The GP suggested she needed to make some lifestyle modifications.


One morning 3 months later, a neighbour found Rainey lying on the lawn complaining of severe, crushing chest pain radiating to the neck and jaw. The neighbour did not know how long she had been there. Rainey was admitted to hospital via ambulance. On the way to the ED, she also vomited. On admission to the ED, an assessment was taken. During the assessment, Rainey admitted that she had been experiencing episodes of chest followed by ear pain over the last three months. She rated the chest pain as 8/10. Using the PQRST method, she confirmed that the pain was provoked by exercise, that is was a crushing feeling radiating to the neck and jaw, that it scored 9/10 at its most severe and lasted for more than 15 minutes.


She was ordered an ECG, blood for serum markers, oxygen via mask, insertion of 2 large IV cannulas, morphine 10mg, aspirin 325 mg, arginine 400 mcg spray, 1-2 sl. The ECG showed ST elevation, the serum cardiac markers showed slightly depressed creatine kinase, and grossly elevated troponin 1 and troponin T. The ischaemia was not immediately reversed and so Rainey developed acute coronary syndrome specifically an ST segment elevation myocardial infarction.
Given the uncertainty of the time of onset of symptoms, Rainey was not offered fibrinolytic therapy. Therefore, the decision was made to undertake a coronary balloon angioplasty with insertion of stent via a right groin puncture.
That evening, Rainey was transferred to the medical ward for further recovery and ongoing assessment and monitoring. 

Lydia Smith is a 23-year-old woman from rural Queensland who was involved in a head on car incident with another car. She did not have any passengers, and the other driver was killed instantly. On arrival at the scene, the ambulance officers noted that Lydia was unconscious, had a strong pulse and even respirations with pupils equal and reacting to
light. Lydia was airlifted to a hospital in Brisbane.


On arrival in the ED 2 hours after the incident, Lydia was classified as ATS 1. Assessments were made, and findings include; temperature 37 C, 98 pulse, 20 respirations, 100% Oxygen saturation. Incomprehensible words, pupils 5 mm and sluggish, bilateral upper and lower spastic flexion, eyes open to pain only.

Cardiovascular Assessment


Lydia was intubated, an IDC inserted and shenwas ventilated in preparation for transport to CT. This showed a right subdural haematoma, cerebral oedema and an intact C spine. She was scheduled for an urgent craniotomy; her GCS had dropped to 6. There was no longer any response from Lydia, her right pupil was sluggish to light. Following drainage of the haematoma and insertion of a EVD, Lydia was transferred to the ICU for ongoing care. In ICU, Lydia continued to be ventilated and was hyperventilated to keep the PaCo2 below 30 mmHg. Ongoing assessment and management of ICP continued.


Lydia stabilised over the next few days and was extubated and her EVD was removed; she was transferred to the ward 72 hours later. Her GCS was 12, she was confused, localised to pain and opened her eyes to speech. Six days later, her GCS was 14, however she was very sleepy and at times continued to be confused. On mobilisation, she was unsteady on her feet. She had a weakness in her left leg. Three weeks later, Lydia was transferred to the rehabilitation unit. While she was no longer confused, her memory was poor, and she lacked concentration, tired easily, tended to be impulsive and easily become distracted. When she became tired her speech slurred and she complained of blurred vision. She also complained of diminished sense of smell.

Lucy is a 32-year-old woman, who has had asthma since she was a child. She lives with her mother in Hobart and works as a cleaner at a private aged care facility. Lucy’s father died of complications from asthma when he was 40 years old, her mother is in good health, with mild hypertension.


Lucy’s general health is good, with a past history of an appendectomy when she was 16 years old. Her weight is 63 kg, and her height is 145 cm. She swims 2 km three times per week and walks 5 km three times a week. She eats a balanced diet, does not smoke and drinks alcohol in moderation. Her asthma is well controlled with a daily inhalation of beclomethasone. When she has the occasional common cold she also requires salbutamol to relieve her asthma symptoms, in addition she has a yearly flu injection. While Lucy tries to avoid people with colds and flu, her mother was recently diagnosed with the flu. One week later, Lucy began to feel unwell, she became dyspnoeic within a day, and had a temperature of 39 C. She wheezed and coughed and had chest tightness. She adopted her asthma rescue plan but continued to deteriorate. Her mother took her to the ED.


On assessment, Lucy temp was 38 C, pulse 115, 32 respirations, BP 160/90, SaO2 91%. Lucy was using her accessory muscles to help her breathe and on auscultation, she has decreased breath sounds and both inspiratory ad expiratory wheeze.

ABGs were taken:

Ph. 7.5
Pa CO2 28
Pc O2 74
HCo3 25
Her oxygen saturation dropped to 88%. Lucy was administered salbutamol via a neb and IV. Oxygen was given and a corticosteroid.
Lucy’s chest was again auscultated, and it was found that although she has a loud expiratory wheeze, she had better airflow. However, she was still using her accessory muscles. After the IV medication therapy, her respiratory rate dropped to 28 and her pulse to 110.


Monitoring continued however after four hours in the ED, she again began to deteriorate; further salbutamol was given. Her vitals included, 38.2 C, pulse 145, resp 38, BP 180/90, Sa O2 87%.


She has a slight tremor in both hands and was using her accessory muscles again and was having trouble speaking. She appeared very tired but was also very anxious.


Her medication was reviewed, and she was given IV ipratropium, methyl prednisone and an antibiotic.
A further four hours saw Lucy begin to improve. Her observations had stabilised, and she no longer had difficulty breathing.


A further 20 hours later, she was no longer using her accessory muscles to breathe and was able to speak easily without dyspnoea. Her vital signs included, 37.2 C, 90 pulse, 16 resp, BP 140/85, SaO2 99% on room air.

Assessment Sequence

Health assessment through health history and examination is the cornerstone of nursing diagnosis. Through a focused health assessment, proper diagnosis can be made, augmented by various investigations. Nursing interventions can be formulated following identification of priority issues in the care of the patient. The current paper is a discussion on the focused health assessment and care plan of a patient, Rainey. The sequence of proposed assessment will be discussed with an emphasis on the specific questions that should be asked and how they guide the assessment. The findings of the health history and focused assessment will then be related to the underlying disease pathophysiology. With the outline of the problem identified, evidence-based nursing interventions will be discussed.

The case study refers to Rainey, a 64-year-old man of Maori descent. He had presented to the GP with flu-like symptoms and on further evaluation found to have a hypertension of 160/100 mmHg. On follow-up a few days, he still had a hypertension of 160/100 and deranged labs with a high serum cholesterol of 7.2 mmol/L, a high LDL of 6.2, a low HDL of 0.7 and a high triglyceride level of 5.9 mmol/L. He was discharged on medication only to present three months later with severe, crushing chest pain, radiating to the neck and jaw. Further inquiry at the emergency department revealed that he had been experiencing similar episodes for the past three months and the episodes were provoked by exercise lasting for up to 15 minutes. Relevant family history shows a family history of heart disease with both parents dying in their 60’s due to heart attacks, two of his four brothers had heart attacks and high blood pressure, and his remaining uncle had two heart attacks and a stroke. His lifestyle is sedentary with a diet high in sugars and fats. He is obese with a BMI of 31 Kg/m2 and a waist circumference of 101cm. An ECG done showed ST elevation. Serum markers were done and the results showed a slightly decreased creatine kinase but grossly increased troponin I and T. A diagnosis of ST-elevation myocardial infarction was made and coronary angioplasty with stenting done. He was discharged to the ward for further monitoring and assessment.

The sequence of assessment in this patient should include a cardiovascular assessment, respiratory assessment and pain assessment (LeMone et al., 2015). This is a patient with an established cardiovascular pathology presenting with chest pain. A cardiovascular assessment with measurement of vital signs is therefore warranted (Glynn & Drake, 2017). Presentation of chest pain and the close correlation between the respiratory system and cardiac pathology also make a focused respiratory assessment needed (Glynn & Drake, 2017. Lastly, since the patient presented with chest pain characteristic of angina, pain assessment, and monitoring should be done (Goodlin et al., 2012).

The cardiovascular assessment begins with the measurement of vital signs (Lewis et al., 2016). Blood pressure is an important measurement since the patient was previously hypertensive with a blood pressure of 160/100. The questions in the health history should try to rule out any complications of hypertension (Lewis et al., 2016). The patient should be asked about blurring of vision to rule out hypertensive eye disease, history of loss of consciousness to rule out transient ischemic attacks and palpitations to rule out hypertensive heart disease (Lewis et al., 2016). The pulses should be measured including the radial, femoral, popliteal and dorsalis pedis pulses. Tachycardia is a feature of heart failure and should be monitored in this patient. Worsening vital signs show clinical deterioration and are a subject of inpatient monitoring to guide clinical interventions (Lewis et al., 2016).

Cardiovascular Assessment

The cardiac exam should be conducted by inspection, palpation, and percussion of the precordium (Hinkle & Cheever, 2013). Relevant cardiac history should include questions assessing for difficulty in breathing, dyspnea, palpitations, leg swelling, orthopnea, paroxysmal nocturnal dyspnea, and chest pain. Dyspnea should be based on the level of exercise intolerance experienced. Dyspnea that prevents one from lying supine is termed orthopnea and is a marker of heart failure. Leg swelling is also a marker of heart failure (Hinkle & Cheever, 2013).

On inspection of the precordium, hyperactivity should be noted. A hyperactive precordium denoted cardiomegaly which can occur in hypertension. Palpation for apex deviation should be done. the normal apex beat in an adult is at the fifth intercostal space in the mid-clavicular line. Apex deviation is also a sign of cardiomegaly. Auscultation of the heart sounds should be done next. The first and second heart sounds should be heard and any murmurs noted (Hinkle & Cheever, 2013). Murmurs represent turbulent blood flow and could point to other cardiac pathology. This focused assessment aims at detecting cardiac pathology in this case of myocardial infarction, identify comorbid conditions and complications such as heart failure and cardiogenic shock (Hinkle & Cheever, 2013).

The respiratory assessment begins by assessing the breathing of the patient. This includes signs of breathlessness, increased work of breathing, use of accessory muscles and cyanosis. This is done on inspection (Lewis et al., 2016). The auscultation of the ling fields is done to assess for added sounds such as wheeze, stridor, basal crepitations, rales or crackles. Signs of pulmonary edema in this patient is warranted due to the setting of heart failure. Percussion notes over the lung bases should be done to assess for fluid accumulation which is dull on percussion or a pneumonic process (Lewis et al., 2016).

The respiratory history should incorporate questions on cough, whether productive or nonproduction, the color, and consistency of the sputum, variations of chest pain with respiration and signs of respiratory distress. These questions are important in this assessment as they differentiate respiratory from cardiac pathology and also identify respiratory manifestation of cardiac pathology (Lewis et al., 2016).

Pain assessment is an important component of this patient’s assessment. This is because the patient presented with chest pain (Goodlin et al., 2012). The pain was characteristic of angina, which is a cardiac pain due to ischemia (Foreman, Garrett, & Blair, 2015). The patient is an increased risk of recurrent ischemic attacks, monitoring the patient’s pain is important. Assessment of pain involves asking questions that seek to guide one to the site of pain, the onset, duration, aggravating factors, relieving factors, character and associated symptoms such as vomiting (Turk & Melzack, 2011). The character of chest pain differentiates respiratory from cardiovascular pain. respiratory pathology tends to result in pleuritic chest pain while the patient presented with angina which is crushing in nature. The patient is then asked to rate their pain on a scale of 1-10 with 1 being mild and 10 being unbearable. Monitoring for a similar episode could prevent future attacks that might be fatal (Turk & Melzack, 2011).

Respiratory Assessment

Myocardial infarction is among a spectrum of cardiovascular diseases termed acute coronary syndromes (Walker & Colledge, 2013). 90% of these acute coronary syndromes are caused by atherosclerosis. Atherosclerotic plaque rupture and formation of an acute thrombus lead to coronary artery obstruction, ischemia, and infarction (Thygesen et al., 2018). The risk factors associated with atheroma formation and subsequent MI include both modifiable and non-modifiable.

Non-modifiable risk factors include age, sex and family history of heart disease (Huma, Tariq, Amin, & Mahmood, 2012). The patient has these risk factor as she is a 64-year-old female with a family history of heart disease. Her advanced age is an independent risk factor for cardiovascular disease (Dhingra & Vasan, 2012). The family history of heart disease include both parents dying in their 60’s due to heart attacks, two of his four brothers had heart attacks and high blood pressure, and his remaining uncle had two heart attacks and a stroke. The family history of myocardial infarction is an independent risk factor with up to a double risk of MI if a first-degree relative had MI (Ranthe et al., 2015).

Modifiable risk factors are those that can be altered to change the course of the disease (Oliveira, Avezum, & Roever, 2015). They include smoking, diabetes mellitus, hypertension, hypercholesterolemia, dyslipidemia, truncal obesity, stress, sedentary lifestyle and poor fatty diet (Canto et al., 2011). The patient clearly has several modifiable risk factors as evidenced by the health history. The patient leads a sedentary lifestyle with a diet high in sugars and fats. The patient is hypertensive with a blood pressure of 160/100 and lab investigations relieved dyslipidemia with high LDL, triglycerides, cholesterol and low HDL (Voight et al., 2012). The patient is also obese with a BMI of 31 kg/m2 and a truncal obesity evidenced by a waist circumference of 101 cm. All these risk factors increased the probability of developing acute coronary syndrome and other cardiovascular pathology (Canto et al., 2011).

The pathology in acute coronary syndromes involves obstruction of coronary blood flow leading to ischemia and infarction (Frangogiannis, 2011). Ischemia is due to hypoperfusion of the myocardium and occurs in angina. The patient had symptoms of stable angina for three months prior to the presentation. Myocardial infarction can be preceded by periods of stable or unstable angina. It occurs when the obstruction becomes irreversible causing distal loss of perfusion and eventual death of myocardium (Frangogiannis, 2011).

Acute myocardial infarction presents with chest a crushing chest pain, radiating to the jaw or neck. The pathophysiology of angina is due to microvascular obstruction leading to an imbalance between oxygen supply and demands (Heusch & Gersh,2016). Other presentations of MI include autonomic symptoms due to activation of the sympathetic nervous system causing nausea, vomiting, and pallor. The patient had an episode of vomiting on her way to the emergency department.

Acute coronary syndromes include unstable angina which is angina even at rest, ST-elevation myocardial infarction (STEMI) and non- ST-elevation myocardial infarction (NON-STEMI) (Lewis et al., 2016). The patient had a STEMI evidenced by the ECG findings. An ECG recording is therefore important in characterizing the type of MI and also diagnosing acute coronary syndromes. Another needed requirement is an elevation in serum cardiac markers (Lewis et al., 2016). This includes creatine kinase (CK-MB), and troponin I and T. These enzymes are released from myocardium during infarction and are used to monitor the progress of infarction, detect reinfarction and monitor treatment. The patient had elevated troponins with a reduced creatine kinase.

Pain Assessment

The priorities of care in this patient include acute pain, the risk of decreased cardiac output, the risk of ineffective tissue perfusion, anxiety, the risk for excess fluid volume and activity intolerance (Lewis et al., 2016). Nursing interventions should be centered around these priority issues to ensure the optimal patient outcome.


Nursing problem: acute pain

Related to the decreased myocardial blood flow and tissue ischemia

Possibly evidenced by reports of patient’s pain, behavior such as moaning, clutching, restlessness and autonomic responses such as excessive sweating, blood pressure, and pulse rate changes.

Goals of care

Nursing intervention

Rationale

Expected outcome

Pain relief with reduced anginal episodes.

Instruct the patient to verbalize any episodes of chest pain when it occurs.

Pain and the reduced perfusion in this condition lead to a sympathetic nervous system activation with increased platelet aggregation and thromboxane A2 release. These are potent vasoconstrictors that may precipitate an angina attack by causing coronary artery spasm (Shilo & Pascoe, 2013).

The patient verbalizes relief of pain evidenced by rested demeanor, normalization of vital signs and relaxed posture.

Assess the site, frequency, intensity, character, and duration of pain.

This helps in differentiating chest pain and linking it to its etiology. Angina pain is characteristic with unstable angina lasting up to 15minutes while stable angina lasting from 3 to 15 minutes. Stable angina s relieved by rest (Goodlin et al., 2012).

Monitor pain in the jaw, neck, hand, arm or shoulder.

This represents cardiac pain and the pattern is due to referral of pain to areas sharing a dermatome (Goodlin et al., 2012).

During periods of pain, ensure the patient is at rest.

This reduces the myocardial oxygen demands hence reducing tissue ischemia and necrosis.

Put the patient in a relaxed position with the head elevated.

This ensures maximum gaseous exchange and reduces hypoxia (LeMone et al., 2015).

Monitor the patient’s vital signs including the blood pressure, and heart rate.

Blood pressure may rise due to sympathetic stimulation or fall when cardiac output is reduced. Sympathetic stimulation will also increase the heart rate (Lord & Woollard, 2011).

Maintain the patient in a comfortable, quiet and conducive environment.

Anxiety and stress lead to the release of catecholamines that increase the heart's workload and may worsen angina pain (LeMone et al., 2015).

Administer supplemental oxygen as indicated

Helps in reversing ischemia by increasing the available oxygen.

Administer anti-angina medication as prescribed including

· Nitrates such as nitroglycerine

· Beta blockers such as atenolol

· Calcium channel blockers

· Analgesics such as morphine and acetaminophen

Nitrates are potent vasodilators and cause coronary vessel dilatation relieving angina and reversing it in the acute setting (Katzung, Masters, & Trevor, 2012).

Help in reducing myocardial workload by reducing contractility (Katzung et al., 2012).

Cause coronary smooth muscle relaxation thus reducing coronary artery obstruction and resultant ischemia (Katzung et al., 2012)  

Beneficial in causing sedation, vasodilation and reduced myocardial workload. May also improve headaches caused by nitrates (Katzung et al., 2012).

Nursing problem: risk for decreased cardiac output

Related to myocardial ischemia, medications, and changes in rhythm, rate, and electrical conduction

Goals of care

Nursing intervention

Rationale

Expected outcome

The patient will demonstrate activity tolerance and decreased episodes of dyspnea, angina or dysrhythmias

Patient to maintain bedrest with adequate sleep.

This reduces the oxygen demands of the body reduces the metabolic demands of the myocardium.

The patient will show normalized vital signs including normal blood pressure, heart rate and absence of signs of heart failure.

Monitor the patient’s vital signs and heart rhythm

Hypotension, hypertension or tachycardia represent changes in patient condition and may be due to a reduction in cardiac output, pain, anxiety or hypoxemia.

Advice the patient to avoid excessive bearing down and straining.

This causes bradycardia which is usually followed by rebound tachycardia which will impair cardiac output.

Monitor the patient response to medication noting changes in vital signs and heart rhythm

Drugs should decrease the myocardial oxygen demands such as nitrates and beta blockers.

Assess the patient for signs of heart failure including edema, pulmonary edema, dyspnea, orthopnea, paroxysmal nocturnal dyspnea among others.

This condition may present with decompensated heart failure presenting as shown. This is by compromising heart function due to reduced cardiac output.

Measure the peripheral pulses and note the color and temperature of the skin.

The impaired cardiac output will cause a reduction in peripheral circulation causing cold pale skin and reduced strength in the peripheral pulses

Administer medications as indicated.

· Oxygen

· Calcium channel blockers

· Beta-blockers

· Antiplatelets

Oxygen increases supply to the myocardium hence improving contractility and reduces ischemia.

Cause smooth muscle relaxation hence reducing ischemia and improving cardiac function (Katzung et al., 2012)

Reduce cardiac workload by reducing heart rate and blood pressure. Should be used with caution as they can cause decompensation (Katzung et al., 2012).

Aspirin is beneficial in the prevention of coronary artery disease and helps in the relief of angina (Katzung et al., 2012).

Conclusion:

Focused assessment in this patient will include a cardiovascular assessment, respiratory assessment, and pain assessment. The health history should be conducted in a systematic manner to rule out other cardiovascular pathology and complications such as decompensated heart failure. The care planning involved identification of priority nursing problems such as acute pain, the risk of reduced cardiac output and anxiety and creating optimal interventions to counteract them.

References:

Canto, J. G., Kiefe, C. I., Rogers, W. J., Peterson, E. D., Frederick, P. D., French, W. J., ... & Penney, J. (2011). Number of coronary heart disease risk factors and mortality in patients with first myocardial infarction. Jama, 306(19), 2120-2127. doi:10.1001/jama.2011.1654

Dhingra, R., & Vasan, R. S. (2012). Age as a Cardiovascular Risk Factor. The Medical Clinics of North America, 96(1), 87–91. https://doi.org/10.1016/j.mcna.2011.11.003

Foreman, R. D., Garrett, K. M., & Blair, R. W. (2015). Mechanisms of cardiac pain. Compr Physiol, 5(2), 929-960. doi:10.1002/cphy.c140032

Frangogiannis, N. G. (2011). Pathophysiology of myocardial infarction. Comprehensive Physiology, 5(4), 1841-1875. https://doi.org/10.1002/cphy.c150006

Glynn, M., & Drake, W. M. (2017). Hutchison's Clinical Methods E-Book: An Integrated Approach to Clinical Practice. Elsevier Health Sciences.

Goodlin, S. J., Wingate, S., Albert, N. M., Pressler, S. J., Houser, J., Kwon, J., ... & PAIN-HF Investigators. (2012). Investigating pain in heart failure patients: the pain assessment, incidence, and nature in heart failure (PAIN-HF) study. Journal of cardiac failure, 18(10), 776-783. https://doi.org/10.1016/j.cardfail.2012.07.007

Heusch, G., & Gersh, B. J. (2016). The pathophysiology of acute myocardial infarction and strategies of protection beyond reperfusion: a continual challenge. European heart journal, 38(11), 774-784. https://doi.org/10.1093/eurheartj/ehw224

Hinkle, J. L., & Cheever, K. H. (2013). Brunner & Suddarth's textbook of medical-surgical nursing. Lippincott Williams & Wilkins.

Huma, S., Tariq, R., Amin, F., & Mahmood, K. T. (2012). Modifiable and non-modifiable predisposing risk factors of myocardial infarction-A review. Journal of pharmaceutical sciences and research, 4(1), 1649.

Katzung, B. G., Masters, S. B., & Trevor, A. J. (2012). Basic and Clinical Pharmacology (LANGE Basic Science). McGraw-Hill Education.

LeMone, P., Burke, K., Dwyer, T., Levett-Jones, T., Moxham, L., & Reid-Searl, K. (2015). Medical-surgical nursing. Pearson Higher Education AU.

Lewis, S. L., Bucher, L., Heitkemper, M. M., Harding, M. M., Kwong, J., & Roberts, D. (2016). Medical-Surgical Nursing-E-Book: Assessment and Management of Clinical Problems, Single Volume. Elsevier Health Sciences.

Lord, B., & Woollard, M. (2011). The reliability of vital signs in estimating pain severity among adult patients treated by paramedics. Emergency Medicine Journal, 28(2), 147-150.

Oliveira, G. B., Avezum, A., & Roever, L. (2015). Cardiovascular disease burden: evolving knowledge of risk factors in myocardial infarction and stroke through population-based research and perspectives in global prevention. Frontiers in cardiovascular medicine, 2, 32. doi:10.1001/jama.2011.1654

Ranthe, M. F., Petersen, J. A., Bundgaard, H., Wohlfahrt, J., Melbye, M., & Boyd, H. A. (2015). A Detailed Family History of Myocardial Infarction and Risk of Myocardial Infarction – A Nationwide Cohort Study. PLoS ONE, 10(5), e0125896. https://doi.org/10.1371/journal.pone.0125896

 Roest, A. M., Zuidersma, M., & de Jonge, P. (2012). Myocardial infarction and generalized anxiety disorder: a 10-year follow-up. The British Journal of Psychiatry, 200(4), 324-329. https://doi.org/10.1192/bjp.bp.111.103549

Shilo, Y., & Pascoe, P. J. (2013). Anatomy, Physiology, and Pathophysiology of Pain. Pain Management in Veterinary Practice, 9-27. https://doi.org/10.1002/9781118999196.ch2

Thygesen, K., Alpert, J. S., Jaffe, A. S., Chaitman, B. R., Bax, J. J., Morrow, D. A., & White, H. D. (2018). Fourth universal definition of myocardial infarction (2018). Journal of the American College of Cardiology, 25285. DOI: 10.1016/j.jacc.2018.08.1038

Trotter, R., Gallagher, R., & Donoghue, J. (2011). Anxiety in patients undergoing percutaneous coronary interventions. Heart & Lung: The Journal of Acute and Critical Care, 40(3), 185-192. https://doi.org/10.1016/j.hrtlng.2010.05.054

Turk, D. C., & Melzack, R. (Eds.). (2011). Handbook of pain assessment. Guilford Press.

Voight, B. F., Peloso, G. M., Orho-Melander, M., Frikke-Schmidt, R., Barbalic, M., Jensen, M. K., ... & Schunkert, H. (2012). Plasma HDL cholesterol and risk of myocardial infarction: a Mendelian randomization study. The Lancet, 380(9841), 572-580. https://doi.org/10.1016/S0140-6736(12)60312-2 

Walker, B. R., & Colledge, N. R. (2013). Davidson's Principles and Practice of Medicine E-Book. Elsevier Health Sciences.

Nursing problem: anxiety

Related to threat to self, underlying pathologic process and threat to mortality or change in health status

Goals of care

Nursing intervention

Rationale

Expected outcome

Reduce anxiety to manageable levels and demonstrate effective coping mechanisms.

Explain to the patient the purpose of tests and procedures.

This reduces the fear of unknown diagnosis and unknown prognosis (LeMone et al., 2015)

The patient will demonstrate reduced anxiety and effective coping mechanisms when verbalizing feelings.

Promote expressions of feelings in the patient. The patient should be told that they are normal expressions and may include denial, anger, and depression.

Verbalizing concerns reduces tension as unexpressed or internalized emotions lead to internal turmoil. Verbalization of feelings facilitates dealing with the feelings (Roest, Zuidersma, & de Jonge, 2012).

Encourage close family members to treat the patient as they did before.

This reassures the patient that their role has not been greatly altered and may reduce anxiety (LeMone et al., 2015).

Explain the purpose of medical management and the importance of adherence to the program.

This increases confidence in the medical therapy and confidence that it may help reduce future attacks (Trotter, Gallagher, & Donoghue, 2011).

Administer medication as indicated such as sedatives and tranquilizers

This help to relax and calm the patient until beneficial coping means are achieved (LeMone et al., 2015).

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