Stressor: Myocardial Ischemia Adaptation: Hypertension and chest pain.

NX DX: Myocardial infarction: High risk related to severe, prolonged myocardial ishemia as manifested by a past hx of MI, hx of hypertension, unstable angina and episodes of severe chest pain.

Goals:

STG: Pt. will experience a resolution of chest pain, upon occurrence within 15 minutes during the length of hospital stay starting 3/6/96

LTG Pt. will show no signs of cardiac arrhythmias as evidenced by AP at 60-100 bpm, systolic BP being less than 140 and EKG showing normal sinus rhythm by end of hopital stay on 3/7/96.

NX INTERVENTIONS:

NI #1: Nurse will assess pt. for chest pain noting the severity, duration, activity that brought pain on and how it was relieved PRN and each shift starting 3/6/96

Scientific Rationale: Any blockage of the coranary arterial circulation can be serious. According to my pt.'s chest x-ray, mild calcification of the aortic arch was present. This is giving rise to an impairment of blood flow to the heart causing him to have angina. Anginina is chest pain caused by fleeting, deficient blood delivery that may result from stress-induced spasms of the coronary arteries or increased physical demands on the heart. The myocardial cells are weakened by a temporary lack of oxygen, but they do not die. Far more serious is a prolonged coronary blockage resulting from an occluding blood clot or severe atherosclerosis. My pt. is putting himself at risk for developing artherosclerosis. His lab data showed a cholesterol level of 217 and a triglyceride level of 463. If this should continue, the ischemic cardiac cells will die, forming an infarct. The resulting myocardial infarction is commonly referred to as a heart attack or a coronary. Because the adult cardiac muscle is amitotic, any areas of cell death are repaired with noncontractile scar tissue. Thus decreasing the amount of oxygen delievered to the heart. So, whether or not a person survives a MI, depends on the extent of cell death and on the location of the damage. Marieb, E.N., (l989) Human Anatomy and Pysiology. The Benjamin/Cumming Publishing Company p.604

NI#2: Nurse will assess respirations noting rate and depth Q4 hours and when/if chest pain occurs starting 3/6/96

Scientific Rationale: Oxygen levels and carbon dioxide levels keep in constand balance with one another. When one goes up, the other goes down, and the same is true of the opposite. My pt. is not getting enough oxygen to his heart which means he is retaining more carbon dioxide. The reason for this lack of oxygen to the heart is because cells sensitive to arterial oxygen levels are found in the peripheral chemo receptors, in the aortic bodies of the aortic arch and in the common carotid arteries. As mentioned, there was a mild calcification present in my pt.'s aortic arch according to his chest x-ray. This is where the carotid bodies, which are the main oxygen censors, are found. Due to this clacification, the carotid bodies are not able to sense the hearts full demand for oxygen. Also the delievery of oxygen by blood to the heart is hampered because of the calcification. It is the effect of the declining oxygen levels on the oxygen -sensitive peripheral chemoreceptors that provide the principle respiratory stimulus. When oxygen is lower, carbon dioxide is higher; now, the respiratory system tries to compensate to maintain equilibrium. Carbon dioxide diffuses easily from the blood into the cerebrospinal fluid, where it is hydrated and forms carbonic acid. As the acid dissociates, hydrogen ions are liberated. Cerebrospinal fluid cantains vertually no proteins that can buffer these free hydrogen ions. Thus, as carbon dioxide levels rise, this is known as hypercapnia and the pH of the cerebrospinal fluid drops, exciting the central chemoreceptors, which make abundant synapses with the respiratory regulatory centers. As a result, the depth and rate of breathing is increased. Hoy, Marianne. RN MSN, Lecture on COPD: Respiratory Mechanism. Given Monday 2/25/96 Marieb, E.N., (l989) Human Anatomy and Pysiology. The Benjamin/Cimmings Publishing Company p. 740

NI #3: Nurse will monitor AP and BP Q4 hours and when/if chest pain occurs starting 3/6/96

Scientific Rationale: Pt. has a history of hypertension which could be made worse due to calcification in his aortic arch and his high cholesterol and high triglycerinde content found in his blood. This could lead to artherosclerosis forcing the heart to pump even harder against more increased resistance. Becuase it must work harder, it will hypertrophy over tyme and then, eventually atrophy when it can no longer keep up with the body's demand. Had this been the case with my pt., the chest x-ray would have shown this. Labe data stated; "top of heart normal in size." So, this has not happened in my pt.'s case as of 3/6/96. Hypertension also ravages blood vessels, causing small tears in the endothelium that accelerate the progress of atherosclerosis and ultimately cause ateriosclerosis. As the blood vessels become increasingly blooked, blood flow to the tissue becomes inadequate and complications begin to occur. This was made evident in my pt.'s stress test: "Study demonstrates a distal anterolateral are of diminished perfusion which appears to reverse itself at rest." Hypertension is defined physiologically as a condition of sustained elevated arterial pressure of 140/90 or higher and the higher the blood pressure, the greater the risk for serious cardiovascular problems. For this pt., one would want to decrease the BP. When BP is decreased, the oxygen demand of the heart is decreased. Since the heart is damaged and the oxygen is having troulbe getting to certian areas, taking steps to decrease oxygen would be beneficial. {please see care plan #2 on MI} When the oxygen demand is decreased, the contractility of the heart is decreased. The muscle relaxes because it does not need to meet the demand for oxygen. This allows for vasodilation of the arteries to the heart. When this occurs, there is an increase in the cornary flow to the heart. This could lead to tachycardia. Therefore, the AP needs to be assessed. Marieb, E.N., (l989) Human Anatomy and Physiology. The Benjamin/Cummings Publishing Company p. 633 Willard, Anne. RN, MSN,CCRN, Lecture on coronary Artery Disease/Myocardial Infarction. Given Monday 2/29/96

NI #4: Nurse will monitor cardiac enzymes (CPK-MB) for elevation each day starting 3/6/96

Scientific Rationale: Since my pt. is at such high risk for having an MI, the CPK levels must be monitored, This is helpful because the CPK-MB levels do not rise after angina but only if a MI has accurred makeing this a very helpful tool in the diagnosis and treatment of ab NI. The enzyme CPK is found predominantly in the heart muscle, skeletal muscle and brain. The serum CPK level rises within 6 hours after damage to the myocardial cells, peaks in 18 hours and returns to normal in 2-3 days. Levels of CPK are generally measured until they peak and deline to ensure no ongoing necrosis and to determine a general idea of the size of the infarction. Fractionation of CPK into isoenzymes to quantitate the cardiac component of the total enzyme provides a more specific index of the cardiac muscle damage. Creatinine phosphokinase can be fractionated into three isoenezymes: CPK-MB, CPK-BB and CPK-MM. The isoenzyme MB provides a unique marker for damaged myocardial cells. The CPK-MB level begins to rise 3-6 hous after the onset of the infarction, peaks in 12-24 hous, and returns to normal in 12-48 hours. Since small infarcts may not eleveate the MB dramatically, it is important to note the time the blood specimen is drawn. Some physicians recommend four specimens, one every 6 hours after the onset of symptoms. Normally, CPK levels consist of 100%. After a myocardial infaction, one may find a 60% elevation of CPK-MB and a 40% elevation of CPK-MM. Pagana, K. D., and Pagana, T. J. (l990) Diagnostic Testing and Nursing Implications: A Case Study Approach. Mosby Co. p. 12

NI #5: Nurse will monitor EKG noting any ST elevations, T or Q wave changes each shift starting 3/6/96

Scientic Rationale: P wave represents arterial depolorization. Duration should not be over 0.11 seconds with no notching or peaking present. Increased amplitude or width-arterial could signify hypertrophy P-R interval represents AV conduction time. Duration is 0.12-0.2 seconds. If the duration was langer than 0.2 seconds, this could signify an AV block, hypoxia or an MI. Beta blockers and Digoxin could also make the duration too long so this one would want to check these factors out. If it was too short, this could signify preexcitation arrythmias. QRS Complex represents ventricular depolorization. Q wave is the first downword deflection. The R wave is the large upward deflection and the S wave is the second downward deflection after the R. Duration is 0.06 to 0.12 seconds wide and at least 5 mm tall. The Q wave is less than 0.04 seconds in duration and less than 1/3 the height of the QRS Complex. If there is a significant downward deflection of the Q wave, the could be a sign of a MI. Otherwise, it is very small and almost nonexistent. The T wave represents ventricular repolorization so the cardiac cells can regain their charge. The ventricles have no physical response to repolarization. It is simply an electrical phenomenon. The artrial repolarization is so small it is lost in the QRS Complex. The peak of the T wave is the most vulnerable period in the cycle. The myocardium is the most unstable point. Inversion of the T wave sgnifies ischemia or subendocardial infarction. The ST segment represents the period of time between ventricular depolarization and the beginning of repolarization. Marked elevation would suggest MI. Depressed at rest would suggest ischemia or subendocardial MI. In a transmural MI, ST elevations appears first followed by T wave inversion and the development of abnormal Q waves. In a nontransmural MI, meaning not all three layers of the heart are involved, there would be ST depression with T wave changes but no changes in the Q wave. In this pt.'s case, one would expect to see a normal or widened Q wave depending on the extent of the ischemia, a ST depression and slight changes in the T wave because he had a MI before but it was a mild one. Stress test did conclude that there was questionable distal anterolateral reversible perfusion so changes in the ST wave, T wave or Q wave would be expected. Willard, Anne. RN, MSN, CCRN, Lecture on CAD/MI: Reading an EKG. Given 2/29/96

EVALUATION:

STG: Met. Pt. came to hospital with c/o severe chest pain. As of 3/6/96 and 3/7/96, no c/o chest pain present.

LTG: Met: Pt. came to ER with an EKG showing sinus bradycardia. Upon discharge on 3/7/96, EKG showed normal sinus rhythm. AP was 64 bpm and BP was 127/70.