Description of clinical situation and consent
I was on my clinical placement in an emergency department at a metropolitan referral hospital. That day, I was allocated as one of the team members responsible for receiving and admitting patients into the wards. As I sat on the admission desk reviewing the patient’s progress report handed in by the team working on the previous 12-hour night shift, a 40-year-old patient A comes in accompanied by her husband. She complained of retrosternal chest pain which had lasted for the last four weeks. Immediately, I took her to room 6 designated for patient assessment and review. I ensured her privacy and explained the whole medical review procedure. I also sought her consent for the procedure and assured her that the information given by her was deemed confidential.
Assessment framework and analysis
I asked her questions concerning her history and documented it on her medical file. First, I enquired about her biographical data which entails: Name, age, gender, contacts, occupation, marital status, next of kin and occupation. Secondly, I enquired about her chief complaint. She complained of retrosternal chest pain which had lasted for four weeks. She said initially, this pain was not persistent and did not happen so frequently. She said that for the last few days the pain had increased in frequency. She added that the day before it was worse. She described it as an episode of squeezing heavy central pain at the chest. This pain presented at rest and sometimes was accompanied by shortness of breath (Dillon, 2007). That day she had experienced two episodes, one when she was pulling shoes and the other while walking kids to school. She said that before the four weeks she had never experienced chest pain. She added that the pain was increasing in frequency and severity, most of the time self-resolving in five minutes. On the day before admission, she had a pain episode at rest accompanied by sweating and shortness of breath. It lasted for 15 minutes. She confessed that she had never experienced pain like this before.
About her past medical history, she was admitted in 2010 suffering from menorrhagia. She had mirena inserted in the womb and transfused with blood for low haemoglobin level (68 g/l). She has been hospitalized before and undergone surgical operation (cesarean section) and tubal ligation. She suffers from chronic illnesses, which are hypothyroidism, and anaemia. Currently, she is on the following drugs; thyroxin and Fero tablets. She has no history of food, drugs, and environmental allergies.
About her family history, she is married, a mother to four children. She lives with her husband together with three daughters. Her mother lives next door and she receives good support and help from the family. There is a history of ischemic heart disease on a maternal grandfather who died at 60 years of myocardial infarction, her uncle also died of myocardial infarction at age of 55 years. Currently, her mother and brother suffer from thyroid disease (Higgs, Jones, & Christensen, 2008)
Regarding her social history, she works as an early childhood teacher. She has been smoking since she was 12 years of age to early this year (January 2011) an average of six cigars a day. She consumes alcohol but not frequently. She does not engage in exercise or any health practices.
Regarding physical examination, measurements and vital signs indicated that her body metabolic weight was elevated. Her blood pressure was 142/88, high temperature of 38 degrees Celsius, high pulse rate (115 b/m), and elevated respiration rate (26 r/m). She appeared old for her age and portrayed facial grimaces signs of fatigue and discomfort. She was conscious and mobile (Dillon, 2007). Her body physique was obese, able to maintain upright body posture and no obvious physical deformities were noted.
Concerning head examination, her scalp hair was even distributed without any visible injuries or deformities. Her face was sweating, and appeared tired, and exhausted. Her eyes were symmetrical, well vascularised (pinkish cornea), moist and both eyes reflexes and vision were present (Dillon, 2007). Both ears were present, symmetrical, non-tenderness, patent, with conductive and sensorineural hearing ability present. The nose was patent; moist with breathing was present (Bickley, 2007).
On doing mouth and throat examination, the mouth mucous membrane was moist, pink in colour and I did not detect any lesions. She was able to rotate her neck, flex and extend her head (a sign of good muscle tone), no lumps, and carotid artery pulsation was present. Jugular venous pressure was not elevated (Dillon, 2007). On inspecting her neck blood vessels, I was able to differentiate carotid pulsations from venous pulsations. I measured jugular venous pressure at a 45-degree angle to the sternal angle (angle of St Louis). Carotid pulsation was visible without any neck distension. Jugular venous pressure at a 45-degree angle was less than 3cm. On palpating each carotid artery separately noting rate, rhythm amplitude, contour and symmetry, I found lustration and thrills (Dillon, 2007). On auscultating carotid artery by use of both the bell and the diaphragm of the stethoscope with the patient holding their breath, there was no notable carotid bruits. I also auscultated jugular veins. I asked the patient to hold her breath and listen through a stethoscope and I did not hear any venous hums (Dillon, 2007).
Concerning chest examination; I inspected the pericardium and noted pulsations at the apex, at the left lower sternal border, bases and xiphoid area. There were positive pulsations notable at the apex. I also noted slight epigastric pulsations. I did not note any thrills, lifts or heaves on palpating pericardium apex, left lateral sternal border, and xiphoid or epigastric areas. I found that point of maximum impact (PMI) at apex 1-2cm, non-sustained and non-palpable. I also found slight epigastric pulsation and without diffusion. On percussion of precordium from the anterior axillary line to the sternum at fifth intercostals space, I did not find any pulsations, lifts, heaves or thrills notable at the base. I discovered dullness at the third, fourth and fifth intercostal space to the left of the sternum at the midclavicular line. While she was sited, I auscultated precordium using the diaphragm of the stethoscope and to note the heart rate and rhythm. I discovered it irregular rhythm of S1 s2 with a soft systolic murmur which was loud on expiration. In the same position, I inspected the anterior/posterior/lateral of her chest. I discovered that the anteroposterior to lateral ratio was 1:2 (Higgs, Jones, & Christensen, 2008). There was no sign of barrel chest or spinal deformities.
I assessed respiratory rate, rhythm, depth, and symmetry of chest movements. Respirations were quiet, symmetrical, regular rhythm and depth. I did not examine any retraction or use of accessory muscles. I palpated the chest from the Interior/posterior/lateral and compared side to side. On the trachea, I placed fingers on either side to assess position (Higgs, Jones, & Christensen, 2008). The trachea was at midline without any deviation. I palpated the chest for tenderness, masses and crepitus. I discovered some tenderness but no masses or crepitus. I also assessed excursions at the bases and found symmetrical excursions anteriorly and posteriorly but without lags. Using the balls of my hands and asking the patient to say “99”, I estimated the level of the diaphragm and I noted increased areas of fremitus (Higgs, Jones, & Christensen, 2008). Tactile fremitus was equal bilaterally, anteriorly and posteriorly. I percussed and noted the general sound of the chest. The anterior chest was resonant to the second intercostal space (ICS) on the left and the fourth intercostal space on the right. Laterally, it was resonant to the eighth intercostal space. Posterior, it was resonant to T10 and T12 on deep inspiration. I percussed the level of the diaphragm on full expiration and full inspiration then measured to assess diaphragmatic excursion. I noted it was resonant, and she experienced shortness of breath (Dillon, 2007).
Using the diaphragm of the stethoscope I auscultated and listened to the air entering and leaving the lungs. I asked her to take slow deep breaths. I compared side to side. I found all lung fields were clear to auscultation. I assessed breath sounds, for abnormal sounds and adventitious sounds. I found that bronchial breath sounds were present over the trachea. Bronchovesicular sounds were present over the manubrium/sternum anteriorly and between scapulae posterior. I noted vesicular sounds at most lung fields (Marieb, 2009).
On inspecting upper and lower extremities they were symmetrical, skin moist, with even hair distribution, with peripheral oedema present, and degree of cyanosis notable. I pressed the base of the nail and great toe to assess capillary refill (Dillon, 2007). Capillary refill was more than 3 seconds. Muscle tone is present evidenced by limbs mobility. Also, sensation and reflexes were present. I located and lightly palpated temporal brachial, radial, femoral, popliteal, posterior tibial, and dorsalis pedis pulses. I noted the rate, rhythm, equality, elasticity, amplitude and thrills. They were irregular rhythm, pulses irregular, amplitude present, soft and pliable and without thrills (Dillon, 2007).
Concerning abdomen examination, I noted size, shape and symmetry, in addition to skin condition, colour, lesions, scars, abdominal movements, respiratory, pulsations, peristalsis, position, colour, contour and umbilicus hernia. Skin colour was consistent, with no lesions, scars, rashes or discolouration. The abdomen was flat or slightly rounded and symmetrical, with no bulges or hernias (Dillon, 2007). There were positive respiratory movements and slight pulsation in the epigastric area. I did not note any peristaltic waves. Umbilicus was at the midline and had no discolouration or discharge. It was smooth, non-tender and without organomegaly (Dillon, 2007).
I auscultated for bowel sounds using the diaphragm and friction rub, and the bell for vascular sounds. I listened in each of the four quadrants for at least 5 minutes and heard bowel sounds. I used the scratch test to locate the inferior edge of the liver. I auscultated for bruits over the aorta, renal, iliac and femoral arteries. I found soft, medium pitched bowel sounds every 5-15 seconds in all four quadrants. There were no borborygmi, rubs. I located the lower edge of the liver at the costal margin (Dillon, 2007).
I did systematic palpation in all 4 abdominal quadrants (bimanual technique) then deep palpation. Her abdomen was soft, tender, with no masses, with positive skin turgor, and without umbilical bulges. I palpated abdominal organs to identify surface characteristics, tenderness, muscular resistance and turgor. I used deep palpation with bimanual technique to palpate liver, spleen, kidneys, bladder and masses. The liver was not palpable but its edge was palpable at the costal margin, firm smooth and not tender (Dillon, 2007).
After carrying out a laboratory diagnostic test, a blood test indicated the presence of troponin I, creatinine phosphokinase and myoglobin features of heart tissue damage. Chest X ray was unremarkable. She underwent an exercise tolerance test (ETT). This was grossly positive with ST depression associated with chest pain. This condition is relieved with glyceryl trinitrate (GTN) admission and rest. ECG returned to baseline with normal sinus rhythm, and T- wave inversion (Dillon, 2007).
Results of assessment (diagnosis)
Diagnosis was crescendo angina. This was evident careful analyzing and putting together suggestive presenting history information like experiencing pain at rest and on minimal exertion. In addition, to the latter, I also used lab diagnostic tests and physical examination information to come up with a diagnosis (Barbara, Rainer & Haddad, 2002). Evidence for crescendo angina was retrosternal chest pain lasting for four weeks. Initially, this pain was not persistent and did not happen so frequently. She said that for the last few days the pain had increased in frequency. She added that the previous day it was worse. She described the pain as an episode of squeezing heavy central pain. This pain presented at rest and sometimes it was accompanied by shortness of breath. She said on the admission day, she had experienced two episodes one when she was pulling shoes and while walking kids to school. She also said that before four weeks she had never experienced chest pain. She added that the pain was increasing in frequency and severity, most self-resolving in 5 minutes.
On the day before admission, she had a pain episode at rest, accompanied by sweating and shortness of breath, which lasted 15 minutes. She said before she had never experienced pain like this. On performing observations, her body mass index (BMI) was elevated and her vital signs were increased. Blood pressure was 142/88 mm/Hg, pulse rate was 115 b/m and respiration rate was 25 b/m. Regarding, the laboratory diagnostic test the results indicated the presence of troponin I, creatinine phosphokinase and myoglobin in the blood; a feature of heart tissue damage. Chest X ray was unremarkable. An exercise tolerance test (ETT) was done and results were grossly positive with ST depression associated with chest pain. This condition is relieved with glyceryl trinitrate (GTN) administration and rest. ECG returned to baseline with normal sinus rhythm, and T- wave inversion. The rhythm of S1 S2 was irregular with a soft systolic murmur loud on expiration (Barbara, Rainer, & Haddad, 2002). Her history had some positive risk factors for crescendo angina. They include; high blood pressure, obesity, smoking, use of alcohol, old age, not being involved in exercise or any other health practice and history of coronary heart disease in the family (Duncan & Brooks,1997).
Probable differential diagnosis
With crescendo angina physical examination it is not always as precise investigation as compared to the history and diagnostic laboratory diagnostic tests. Although patient’s vital signs and cardiac assessment is vital. Some potential differential diagnoses in crescendo angina are; myocardial infarction, chronic stable angina, aortic dissection, pulmonary embolism, pneumothorax, pericarditis with tamponade and leaking or ruptured thoracic aneurysm (Antman, 2007). Crescendo angina varies with stable angina in that the pain and discomfort are easily aggravated, extreme and ST-segment increase or decrease on ECG may occur. Crescendo angina symptoms are almost identical to those of myocardial ischemia like myocardial infarction and chronic stable angina (Antman, 2007).
Crescendo angina occurs in various forms, and investigations are vital to establishing chest pain and discomfort. In addition, establish chest pain location, frequency, and aggravating and relieving factors. Ischemic pain presents as the burning of the chest, heaviness, aching, tightness and burning of the epigastrium or forearm. It may present in the lower jaw, shoulder or neck (Antman, 2007). Closely linked manifestations include fatigue, dyspnea, diaphoresis, nausea, vomiting, abdominal pain and flu like symptoms. Most time atypical signs and symptoms are rampant in female and elderly patients. Manifestation of increased autonomic activity includes; tachycardia, diaphoresis and bradycardia which result from stimulation of the vagal nerve due to inferior wall myocardial ischemia (Stone, Maehara, & Lansky, 2011). Enormous myocardial compromise portrays as transient myocardial dysfunction and it is an indicator for a high-risk situation. These signs include; elevated jugular venous pressure, systolic pressure below 100 mm Hg or overt hypotension, dyskinetic apex, reverse splitting of second heart sound, presence of third or fourth heart sound, new or deteriorating apical systolic murmur because of papillary muscle dysfunction and rales or crackles. Acute coronary syndrome patients manifest symptoms of discomfort or pain in the chest or left arm, which reproduces angina (Stone, Maehara, & Lansky, 2011). Results indicating peripheral arterial occlusive disease or before stroke elevates chances of related coronary artery disease which include; carotid bruit, diminished peripheral pulses or blood pressure and supraclavicular or femoral bruits.
For definitive diagnostic laboratory test evaluation of crescendo, angina includes a blood test to check if there is heart tissue damage or any chance of developing a heart attack. This is indicated by the presence of troponin I, creatine phosphokinase and myoglobin. Other tests include ECG, echocardiography, stress test, chemical or pharmacological stress test, exercise tolerance test, stress echocardiogram, thallium stress test, non-imaging or imaging test and coronary angiography (Stone, Maehara, & Lansky, 2011). An electrocardiogram (ECG) indicates normal waves unless one has cardiac problems. In pain, ST-segment is depressed or elevated. To indicate the change treadmill test should be done. In this case, a patient has to exercise maximum before getting fatigued, breathless, or before pain set (Stone, Maehara, & Lansky, 2011). Changes in ECG waves are recorded. In this case pulse and blood pressure is important for conclusion purpose. The thallium stress test is important for the patient who can not exercise adequately due to arthritis or asthma (Stone, Maehara, & Lansky, 2011).
Crescendo angina pathophysiology
Pathophysiology of crescendo angina includes a change of stable angina to unstable angina. It is caused by the bursting of atherosclerotic plaque causing clot formation and occlusion of the coronary artery (Marieb, 2009). Non-ST elevation myocardial infarction is linked to unstable angina and lead to elevated cardiac marker because of incomplete coronary artery occlusion. ST rise in myocardial infarction is due to sudden occlusion of the involved artery (Porth, 2007). It leads to acute ischemia and necrosis (Bhargav & Guthrie, 2002). This is common in obstruction and coronary artery atherosclerosis (Egger, Spark, & Donovan, 2005).
Treatment and management of crescendo angina
The most specific pharmacological intervention is the use of vasodilator nitroglycerin. It improves oxygen supply to the heart muscle. Calcium channel blockers and beta-blockers reduce heart workload (Stone, Maehara, & Lansky, 2011). The major aim of treatment in crescendo angina is to manage symptoms, their progress and chances of a heart attack. Beta-blockers like atenolol, carvedilol and propranolol help manage this condition (Moliterno, 1999). Also, ACE inhibitors (vasodilators) are widely used. Statin lipid/cholesterol modifiers are used frequently. It has the additional effect of stabilizing existing atheromatous plaque. Aspirin low dose reduces the risk of a heart attack in patients having crescendo angina. Gentle and sustained exercise forms part of good treatment of crescendo angina since it improves blood pressure and promotes collateralization of the coronary artery (Stone, Maehara, & Lansky, 2011). Recognizing and intervening on risk factors is crucial in crescendo angina patients. This includes testing for increased body cholesterol, high body fats, hypertension, and diabetes, urging them to stop smoking and maintain optimal body weight. They should avoid fatty and high cholesterol foods in addition to engaging in frequent body exercise (Australian institute of health and welfare, 2004).
Patient (A) nursing care plan.
References
Antman, E.M. (2007). ST-Elevation Myocardial Infarction: A textbook of Cardiovascular Medicine. (3rd ed.). Saunders: Elsevier.
Australian Institute of health and welfare, (2004). The relationship between overweight, obesity and cardiovascular disease. Pubmed Journal, 23(4), 66-78.
Barbara, M., Rainer. G., & Haddad. L. (2002). Making the Case: Unstable angina. Journal of UN System’s Forum for cardiovascular World Health Organization, 12 (4), 8-15.
Bhargav, A., & Guthrie, J. (2002). Crescendo angina. British Journal of cardiovascular, 10 (6), 719-728.
Bickley, L.S., (2007). Bates’ guide to physical examination and history taking, New York: Lippincott.
Dillon, P.M. (2007). Nursing health assessment: Student applications (2nd ed.). Philadelphia.
Duncan, G. J. & Brooks, J. (1997). Consequences of smoking. New York, NY: Russell Sage Foundation.
Egger. G., Spark. R. & Donovan. R. (2005). Health promotion strategies and methods. Sydney: McGraw-Hill.
Higgs, J., Jones, M.A., & Christensen, N. (2008). Clinical reasoning in the health professions, (3rd.). London: Elsevier
Marieb, E.N., (2009). Pathophysiology: The biologic basis for disease in adults and children, (5th ed.). Missouri: Mosby Elsevier.
Moliterno, D.J. (1999). Management of unstable angina pectoris. Medline journal, 84 (10), 1145-450.
Porth, C. M. (2007). Essentials of pathophysiology: Concepts of altered health states. New York: Lippincott.
Stone, G.W., Maehara, A. & Lansky, A. J. (2011). A prospective natural-history study of coronary atherosclerosis. Journal of medicine, 364(3) 226-35.