Mrs G who has Coronary Artery Disease

In this case study I will present a client from my clinical placement that I will refer to as Mrs G for confidentiality reasons. Mrs G is an 81 year old woman and she was diagnosed with Coronary Artery Disease (CAD).

I will be explaining the signs and symptoms commonly related to CAD and examine how this disease affected her health and how her body tried to compensate. I will also discuss how hypertension relates to CAD. I will examine diagnostic and pharmacological data while discussing nursing interventions in relation to her results. Mrs G has no past history of alcohol intake.

She is an ex-smoker with 20 cigarettes per day, weighs 67kg and is 154cm in height. Mrs G's past medical history includes osteoporosis, (L) THJR, hypertension, Coronary Artery Disease (CAD) with a CABG in 1993. On admission, Mrs G's signs and symptoms consisted of chest pain, tachycardia, tiredness and shortness of breath (SOB). She said she began experiencing these symptoms earlier in the day but they had gotten worse at the time of admission. These are all consistent with CAD. The coronary arteries branch off from the base of the aorta and encircle the heart in the atrioventricular groove.

Oxygen rich blood flows from the left ventricle up through the aorta and into the coronary arteries allowing the heart to receive oxygen and nutrients. Coronary Artery disease (CAD) is a result of chronic and progressive atherosclerosis (fatty and fibrous tissue build up) of the coronary arteries (McCance & Huether, 2002). The atherosclerotic lesions occur primarily within the intimal layer of the arterial wall, therefore if this lesion progresses, it can occlude the arterial lumen and interfere with the myocardial blood supply.This is support by (Kinney & Packa, 1996) that the atherosclerotic tissue protrudes into the blood vessel lumen resulting in a narrower and occluded artery. CAD impairs the pumping ability of the heart, diminishing the myocardial blood supply causing ischaemia, a local condition in which the cells are temporarily deprived of blood supply and consequently oxygen.

There are many risk factors that contribute to the development of CAD. They include non-modifiable risk factors such as advanced age, male gender (until the age of 60) and diabetes mellitus type 1.Modifiable risk factors include dyslipidaemia (high levels of circulating lipoproteins) hypertension, smoking, and obesity and diabetes mellitus type 2. Dyslipidaemia, hypertension and smoking have been identified objectively as most predictive of CAD.

Mrs G's past history of being a heavy ex-smoker is relevant to her diagnosis. According to Kinney ; Packa (1996), nicotine in cigarette smoke stimulates the sympathetic nervous system by releasing epinephrine and norepinephrine.These hormones cause an increased heart rate, peripheral vasoconstrictions and increased blood pressure. These change increased the cardiac workload necessitating greater myocardial oxygen consumption. In the present of CAD, coronary blood flow cannot increase sufficiently to meet the increased demand because of a decreased coronary artery lumen size, which may cause angina pectoris or myocardial dysfunction (Guzzetta ; Dossey, 1992). Mrs G also has hypertension therefore she has a twofold to threefold increased risk of atherosclerotic cardiovascular disease.

Hypertension contributes to endothelial injury, a key step in atherogenesis (the formation of subintimal plaques in the lining of arteries), and causes myocardial hypertrophy, which increases myocardial demand for coronary flow (McCance ; Huether, 2002). Controlling hypertension by a reduction in systolic blood pressure as small as only 12 to 13 mm Hg can reduce the risk of CAD as much as 21%. As Mrs G has already developed CAD, controlling her blood pressure can reduce the risk of myocardial ischaemic occurrences by maintaining a lower myocardial demand for coronary flow.Mrs G's blood pressure had previously been 160 - 170 systolic over 60 - 80 diastolic.

Since starting on Inhibace, a medication used to lower blood pressure, Mrs G's blood pressure has dropped to 130 - 140 systolic over 60 -80 diastolic. Her systolic reading is now within normal limits (100 - 140 mm Hg) (Black, Hawks ; Keene, 2001). Electrocardiography (ECG) is an essential tool in evaluating the heart rhythm. Electrocardiography detects and amplifies the very small electrical potential changes between different points on the surface of the body as the myocardial cells depolarise and repolarise, causing the heart to contract.The same electrical impulses spread outward from the heart to the skin, where they can be detected by electrodes attached to the skin.

The ECG displays the electrical action of the heart. (Black, Hawks ; Keene, 2001). Recording electrodes (leads) are positioned at various sites on the body surface, 12 standard leads are used to record an ECG. Three of these are bipolar leads that measure the voltage difference between the arms, or an arm and a leg, and nine are unipolar leads. Together the 12 leads provide a fairly comprehensive picture of the electrical activity of the heart.

( Marieb, 2001).Mrs G had an EGC performed on her to assess the electrical actions of her heart, and to determine whether any ischaemia occurred. The findings were typical of someone with CAD. When the blood flow to the heart is decreased, ischaemia occurs. This condition is reflected in altered Q wave, ST segment, and T wave on the ECG.

The ST segment indicates completion of ventricular depolarization and that repolarization is about to begin. During myocardial ischaemia the changes occur first in the ST segment, then the T wave. Prolonged the ST segment elevation is a marker of acute Ischemia and injury-infraction (Conover, 1996).The greater the displacement of the St segment, the greater the number of ischemic and injured cells present. The T wave in an ECG reflects the repolarization of the myocardium. In Mrs G's ECG inversion of T wave was showing in leads due to leakage of intracellular potassium from the damaged muscle cells into the extracellular spaces (Goldman, 1993).

According to Black & Matassarin-Jacobs (1993), the Q waves are the classic diagnosis feature of myocardial necrosis. In most instances, a Q wave is not obvious on the ECG of the normal heart. The Q wave change is minor; normally the Q wave is very small or absent.When there is inactive tissue under the electrode, the wave front must travel long distance around the inactive tissue.

Abnormal Q waves reflect this delay. The larger and deeper the lesion, the larger the Q wave. Abnormal Q waves appear as early as 2 hours after the onset of chest pain and are usually fully developed within 9 hours. Although the electrocardiogram can detect evidence of coronary heart disease in asymptomatic persons and identify individuals at increased risk of future coronary events, having regular ECG's can be invasive procedure, especially for female patient.Therefore it is important as a nurse looking Mrs G to maintain as much dignity as possible by ensuring privacy while carry out the ECG. Calcium plays a significant role in the electrical excitation of cardiac cells and in the mechanical contraction of the myocardial and vascular smooth muscle cells.

Calcium (Ca+) is an element within the body and participates in many biochemical reactions. These include the mechanisms for blood coagulation (clotting), nerve impulses, and muscle contractions including the cardiac muscle. Reduced blood levels of ionic calcium depress the hearts function (Marieb, 2001, pg 708).As Mrs G has CAD, a low calcium level would lower the hearts function resulting in further myocardial ischaemia, therefore taking a blood sample to test her calcium levels was required.

Mrs G Ca+ levels were 2. 60 mmol/L. The normal range for serum Calcium is 2. 10 - 2. 65mmol/L (Black, Hawks ; Keene, 2001). As Mrs G is taking Osteo 500, which is a Calcium supplement, her calcium levels were expected to be within normal limits.

We performed a blood test to ensure us that her Ca+ levels are within the normal ranges. I will look at three drugs Mrs G was taking, Cilazapril (Inhibace), Osteo 500 and Lactulose.Cilazapril is an ACE inhibitor and is used to control hypertension. It blocks the action of a chemical in the body called angiotensin converting enzyme.

Normally, this chemical produces another chemical, angiotensin II. Thus cilazapril reduces the amount of angiotensin II in the blood. Angiotensin II has two actions. Firstly it acts on blood vessels to make them narrow and secondly it acts on the kidney to produce less urine.

As Cilazapril stops the production of angiotensin II, these actions are reversed. Therefore the kidneys produce more urine, which results in less fluid in the blood vessels. The blood vessels also widen.The overall effect of this is a drop in blood pressure and a decrease in the workload of the heart. Hypertension adds to the workload of the heart and arteries.

If it continues for a long time, the heart and arteries may not function properly. This can damage the blood vessels of the brain, heart, and kidneys, resulting in a stroke, heart failure, or kidney failure. Hypertension may also increase the risk of heart attacks. These problems may be less likely to occur if blood pressure is controlled (Woods, Froelicher ; Motzer, 2000).

Hypertension causes myocardial hypertrophy thus increasing the myocardial demand for coronary flow.Giving Cilazapril will prevent hypertension therefore helping to prevent further ischaemic attacks due to her Coronary Artery Disease. Principle adverse effects are persistent cough, first dose hypotension and hyperkalemia (Lehne, 2001). Persistent, dry, irritating, non-productive cough can develop with ACE inhibitors.

Cough is caused by accumulation of bradykinin. Cough is more trouble-some when the patient is supine. A precipitous drop in blood pressure may occur following the ACE inhibitors. This reaction is caused by widespread vasodilation secondary to abrupt lowering of angiotensin II levels (Kinney ; Packa, 1996).

Before initiation of therapy, a baseline serum creatine level should be drawn and blood pressure obtained. It is of utmost important that patients receiving ACE inhibitor therapy be monitored closely for hypotension. It is important for nurses to make sure Mrs G's BP is monitored constantly, to ensure her BP does not drop down to dangerous level. Kinney & Packa (1996), states that inhibitor of aldosterone release can cause potassium retention by the kidney. Because of the fact that ACE inhibitors decrease the formation of Angiotensin II, which results in decreased production of aldosterone this can cause an increase in K+ serum levels.Therefore patients should be instructed to avoid potassium supplements or potassium-sparing diuretic.

Another caution should be used when administering Cilazapril as renal impairment, liver cirrhosis or aortic stenosis can occur with toxicity. According to Souhami & Moxham (1999) in patient with renal insufficiency, the elimination half-life of Cilazapril increase as creatinine increases, there is a linear correlation between plasma Cilizaprilat clearances. In studies done on patients with renal impairment, the elimination and half-life all increased as the renal impairment became greater.Therefore with a normal dose of Cilazapril can be toxicity for a patient with renal insufficiency. Not surprisingly, ACE inhibitors are contraindicated for patients with renal artery stenosis. Mrs G was also on Osteo 500.

As she has osteoporosis, she needs to take a calcium supplement to slow the degenerative process of osteoporosis, as well as include more dairy and calcium rich products in her diet. Osteo 500 is a calcium supplement; it consists of 1250mg of calcium carbonate. High dose of Osteo 500 can be resulting in hypercalcemia. This can cause confusion, abdominal pain, muscle pain and weakness.Extremely high levels of blood calcium may result in shock, kidney failure and death. It is important to ensure that Mrs G has regular blood test to monitor her calcium levels.

A high level of calcium in the blood can also cause constipation. Surprisingly in light of the common belief that calcium carbonate may have constipation as a side effect, the belief is not substantiated by scientific evidence (Thompson, 2000). Another drug Mrs G is taking is Lactulose. She normally has regular bowel movements, once a day, but she does say that taking the Osteo 500 does cause her to get constipation.

Therefore taking Lactulose helps her with this. Lactulose is an osmotic laxative and is made up of sugar molecules, which are broken down by the bacteria that live in the lower part of the gut. This leads to the contents of the gut becoming more acidic. The acidification of the contents of the gut causes a reduction in the absorption of chemical called ammonia. The presence of ammonia in the gut causes water to be drawn into the lower bowel, which causes an increase in the water content and volume of the stools, therefore relieving constipation, though sometimes they may cause diarrhoea (New Ethicals Compendium, 2000).