Coronary Artery Disease 1 Pathophysiology and Nursing Considerations of Coronary Artery Disease Lyra Sunshine Rider Chico State University, Chico
Coronary Artery Disease 2 Coronary Artery Disease Coronary artery disease also known as atherosclerosis or ischemic heart disease is the mostprevalent cause of cardiovascular disease. (National Heart, Lung, and Blood Institute [NHLBI], 2011b).In America, coronary artery disease (CAD) is the number one cause of death of both men and women(NHLBI, 2011b). Atherosclerosis is believed to begin in childhood and is thought to progress morerapidly as you age (NHLBI, 2011b). Atherosclerosis is the build up of lipids or fatty substances inside thelining of the walls of the arterial blood vessels (Smeltzer, Bare, Hinkle, & Cheever, 2010). This abnormallipid accumulation narrows the vessels and impedes blood flow thus limiting oxygen delivery to the heartand body (Smeltzer et al., 2010). This decrease in blood flow and oxygen delivery can result in anginapectoris, myocardial ischemia or myocardial infarction . Coronary artery disease over time can alsoweaken the heart muscle resulting in heart failure and arrythmias (NHLBI, 2011b). Coronary Atherosclerosis Pathophysiology Atherosclerosis begins when fatty streaks of lipids are deposited in the intima of the arterial wallafter a lesion is created (NHLBI, 2011b). Lesions of the intima of the arterial wall may occur fromdamage caused by smoking, high cholesterol, high blood pressure, and diabetes. These lesions initiate aninflammatory response which stimulates macrophages. Macrophages ingest and transport the lipids intothe arterial walls. These “foam cells” also release biochemicals that irritate and continue to damage thevascular endothelium. This continuous inflammation of the vascular lining attracts platelets and caninitiate clotting inside the arterial lumen (Smeltzer et al., 2010). The inflammation initiates smooth muscle cells to begin proliferating which forms a fibrous capover the initial lipid filled lesion. These fibrous caps are called atherosclerosis or plaques. Plaquesaccumulate and begin to narrow the lumen of the vessel by protruding outward, obstructing flow throughthe vessel which decreases blood and oxygen supply to the heart and body. Plaques are classified as stableor unstable, contingent upon the thickness of the plaque and the degree of inflammation to the vessel.Stable plaques are usually thick and have a fixed lipid pool that can withstand the pressure and stress of
Coronary Artery Disease 3blood flow and vessel contraction and dilation. Unstable plaques are considered vulnerable because theyhave a thin cap and are affected by continued inflammation of the vessel (Smeltzer et al., 2010). If anunstable plaque has an increase to the lipid core, it may rupture and seep into the outer layer of the plaquebecoming a site for platelets to adhere to the injury. Accumulation of platelets form a thrombus whichcan increase the obstruction of blood flow to the heart or completely occlude blood flow (NHLBI,2011b). The obstruction may result in angina pectoris, acute coronary syndrome, myocardial infarction,and even death (Smeltzer et al., 2010). Clinical Manifestations Chest pain is the most common symptom of a plaque or a thrombus decreasing blood flow andoxygen to the heart and is referred to as angina pectoris (Smeltzer et al., 2010). The heart signals the bodyof the unmet myocardial oxygen demand. This often results in a squeezing or pressure felt in the chestfrom the myocardial ischemia. Pain may radiate to the jaw, neck, back or shoulders and may also bemistaken for indigestion (NHLBI, 2011b). If the ischemia lasts for an extended period of time or thedecrease in oxygen is large enough, permanent damage to myocardial cells may result. The damage tomyocardial cells begins scar tissue formation resulting in myocardial dysfunction such as decreasedcardiac output or heart failure. A substantial decrease in blood supply to the heart can also result insudden cardiac death (Smeltzer et al., 2010). Patients may also present asymptomatic of chest pain during a coronary event, although the“epidemiologic study of the people of Framingham, Massachusetts, showed that nearly 15% of men andwomen who had coronary events, which included unstable angina, MIs, or sudden cardiac death events,were totally asymptomatic prior to the coronary event.” (Smeltzer et al., 2010, p.757). Shortness of breathis often reported as a symptom by older patients and patients with a history of diabetes or heart failure.Atypical symptoms are generally experienced by women which may include nausea, weakness, anddyspnea (Smeltzer et al., 2010).
Coronary Artery Disease 4 Risk Factors and Patient Education Risk factors that increase the probability for coronary artery disease are classified into twocategories, modifiable and non modifiable. Modifiable risk factors are those the patient can change bymaking adjustments to their lifestyle or by using medications. Non modifiable risk factors are those apatient has no control over. Some modifiable risk factors include: hyperlipidemia, cigarette use,hypertension, diabetes mellitus, metabolic syndrome, obesity, diet and physical non activity. Nonmodifiable risk factors include: family history of CAD, increasing age (men over 45, women over 55) andrace (higher incidence in African Americans). Patients with metabolic syndrome are also at high risk forheart disease. Metabolic syndrome has the following risk factors: insulin resistance, central obesity,dyslipidemia, blood pressure higher than 130/85 consistently, pro inflammatory state (high levels c-reactive protein), and pro thrombotic state (Smeltzer et al., 2010). The top four modifiable risk factors for CAD are tobacco use, diabetes mellitus, hypertension, andcholesterol abnormalities. Nursing assessment of these risk factors and patient education on riskmodification are very important for improving health in patients suffering from CAD (Smeltzer et al.,2010). Cigarette cessation is highly encouraged to decrease the risk of developing CAD. Smokingcontributes to CAD by decreasing the amount of oxygen available to the heart and can also lower cardiacoutput. Nicotinic acid in cigarette smoke causes constriction of the coronary vessels and increases heartrate and blood pressure by stimulating the release of catecholamines which are associated with suddencardiac arrest. Cigarette smoking damages the vascular endothelium resulting in an increased number ofplaque and thrombus formations (Smeltzer et al., 2010). Diabetes affects CAD development in various ways and has been known to accelerate heartdisease. Diabetes encourages dyslipidemia, this in turn increases platelet aggregation and thrombusformation. Treatment and control of hyperglycemia can lead to improved endothelial function and patienthealth by reducing the risk of developing plaques (Smeltzer et al., 2010).
Coronary Artery Disease 5 The risk of a cardiovascular event increases in people with a blood pressure over 120/80.Hypertension is a blood pressure that continually exceeds 140/90. Pressures at or above this high levelcontribute to increased stiffness of the walls of the vessels (stenosis). Stenosis leads to increasedinflammation, vessel injury, and occlusion. The workload of the left ventricle is increased byhypertension and this increase causes the heart to hypertrophy and may result in heart failure. Detectionand medical intervention is necessary to decrease this risk (Smeltzer et al., 2010). In an effort to control cholesterol abnormalities all adults over 20 should have a fasting lipid paneland then repeat after every 5 years, more often if there are abnormal results. The normal values for thistest are an LDL count less than 100 mg/dl ( less than 70 mg/dl in high risk patients), total cholesterol lessthan 200 mg/dl, HDL cholesterol grater then 60 mg/dl, and triglyceride levels less than 150 mg/dl. It isrecommended that patients begin the Therapeutic Lifestyle Diet to help control their cholesterol levels.This diet sets fat intake at 25-35% of calories, carbohydrates at 50-60% of intake, dietary fiber at 20-30 Ga day, protein at 15% of caloric intake and cholesterol less than 200 mg a day. Patients are encouraged toincrease their physical activity to 30 minutes of moderate exercise a day which increases LDL levels anddecreases triglyceride levels thus decreasing the risk of a coronary event. Lipid lowering medications canalso be prescribed to help the patient control cholesterol (Smeltzer et al., 2010). Angina Pectoris “Experts believe that nearly 7 million people in the United States suffer from angina. Thecondition occurs equally among men and women.” (NHLBI, 2011a, p.1). Angina pectoris is the mostcommon symptom of coronary artery disease. (NHLBI, 2011a) Atherosclerotic narrowing of vessels isthe main cause of decreased blood flow to the heart resulting in an unmet oxygen demand. This usuallyresults during an increased myocardial demand for oxygen during exertion or emotional stress (Smeltzeret al., 2010). Pathophysiology There are three main types of angina; stable, unstable, and refractory. Stable angina can be
Coronary Artery Disease 6relieved by rest or nitroglycerin intervention. It normally occurs on exertion and usually follows aconsistent and predictable pattern. Typical stable anginal episodes may be induced by the following:physical exertion, exposure to cold, consuming a heavy meal, and emotional or physical stress. Unstableangina is usually not relieved by rest or nitroglycerine. Symptoms continually increase in severity andfrequency and may occur while at rest. Intractable angina consists of severe incapacitating chest pain thatcan be resistant to treatment (Smeltzer et al., 2010). Physical symptoms of angina can vary from mild indigestion to severe symptoms such as a feelingof impending doom. Common symptoms include pressure on the chest, vice like pain, pain deep in thechest, radiating pain to the jaw or arm, and a strangling sensation. Diabetics may have mild or no paindue to diabetic neuropathy. Women usually experience asymptomatic pain such as weakness or backpain. Angina in the elderly also can present atypically due to diminished neurotransmitter responsesnormal to the aging process. Many elderly people present only with dyspnea. This type of presentation isan example of a “silent” CAD event. Other symptoms of angina include anxiety, weakness or numbnessof the upper extremities, diaphoresis, a pale complexion, dizziness, and nausea and vomiting (Smeltzer etal., 2010). Assessment and Diagnostics Assessment of angina begins with a thorough patient history with an in depth focus on theprecipitating events that occurred before the episode. An ECG can show changes of the heart due toischemia. Lab tests such as a CRP and cardiac biomarkers can be run to rule out acute coronarysyndrome. A patient may also receive an exercise stress test or pharmacological stress test to help withdiagnosis (Smeltzer et al., 2010). Medical and Pharmacologic Management Medical management of angina includes both controlling risk factors and pharmacologicaltherapies. These are usually used in conjunction to decrease the myocardial demand and increase theoxygen supply to the heart. As a last resort reperfusion procedures may be needed to restore blood flow to
Coronary Artery Disease 7the heart. These may include precutaneous transluminal coronary angioplasty (PTCA), Coronary arterybypass graph (CABG), intracoronary stents, and atherectomy (Smeltzer et al., 2010). Medications that may be prescribed to help control angina include: nitroglycerine, calciumchannel blockers, beta adrenergic blockers, antiplatelet medications and anticoagulants. Nitroglycerine isa vasodilator which decreases pain and ischemia by decreasing myocardial oxygen demand. Calciumchannel blockers decrease the workload of the heart by slowing heart rate and decreasing the strength ofmyocardial contractions. Beta blockers block beta adrenergic stimulation of the heart resulting in adecrease in myocardial demand for oxygen. Anti platelet medications such as Aspirin and Plavix inhibitplatelet adhesion and thrombosis generation. Anticoagulants that may be prescribed include Heparin andFragmin which prevent the formation of new blood clots. Oxygen therapy may also be used to decreasepain and increase the amount of oxygen available to the heart with target blood oxygen saturation beingabove 93% (Smeltzer et al., 2010). Nursing Process Nursing assessment of angina includes a full patient history with an emphasis on the patientssymptoms and activities before, during, and after the attack. Questions may include, “Can you rate thepain?”, “When did the pain begin ?”, “What brings on the pain ?”, “What helps the pain go away ?”(Smeltzer et al., 2010, p. 766). The nurse also needs to access the patients risk factors for CAD todetermine an inclusive program of prevention, treatment, and patient education. Nursing diagnosespertaining to angina may include: “ineffective cardiac tissue perfusion secondary to CAD as evidenced bychest pain or other prodromal symptoms.” “Death anxiety related to cardiac symptoms” and “ deficientknowledge about the underlying disease and methods of avoiding complications” (Smeltzer et al., 2010,p. 766). Potential complications that may develop are cardiogenic shock, acute coronary syndrome, MI,dysrhythmias, heart failure, and cardiac death (Smeltzer et al., 2010). Nursing planning goals for anginainclude the prevention of future episodes, reduction of anxiety, education regarding the condition andprescribed treatment, compliance with home care, and absence of complications. Nursing interventions
Coronary Artery Disease 8would include treating angina, reducing anxiety, and preventing pain. Nursing treatment of anginaincludes assessment of the current episode to see if the condition is worsening. Assessments mayinclude: directing the patient to stop all activity and to sit and rest to see if resting helps alleviate the painor by obtaining an EKG to assess ST segment and T wave changes. Nitroglycerine may also beadministered and the nurse needs to assess the patients response to interventions and monitor vital signscontinually. Oxygen administration of 2 liters by nasal cannula may also be needed by the patient if theiroxygen saturation is low or if their respiratory rate is increased. Expected patient outcomes after anangina attack would include prompt resolution of pain, adherence to therapy program, and patientdemonstration of knowledge on how to prevent and recognize future attacks (Smeltzer et al., 2010). Cultural Considerations Special consideration during nursing assessments need to be give to patients of different culturalbackgrounds. “Native American healing practices vary greatly because there are more than five hundredNative American Nations (commonly called tribes). There are many tribal differences, so it is notsurprising that healing rituals and beliefs vary a great deal” (American Cancer Society, 2008, p.9). InNative American culture it is standard practice to utilize the services of shamanic healers or tribal eldersfor healing (Department of Integrative Medicine [DIM], 2008). They believe health and disease is a directreflection of the patients balance with nature (DIM, 2008). “A common Native American sense of spirituality includes a sense that each and every part of thecosmos is imbued with spirit, not only people but everything including animals, plants, rocks, rivers, andso on (Matheson, 1996).” Trust development with these patients is important for full disclosure of currenthealth practices (American Cancer Society, 2008). “Historically, outside society has sometimesmisinterpreted Native American culture and beliefs, which may increase this reluctance.” (AmericanCancer Society, 2008, p.1). Native American culture is steeped in ceremonial practice. Herbal remedies used in ceremonialhealing need to be identified due to possible interaction with medications (DIM, 2008). It is also
Coronary Artery Disease 9important to ascertain whether the patient has recently gone through a purification or cleansing ritualwhich can alter fluid volume balance and electrolyte levels (American Cancer Society, 2008). The patients spiritual needs must also be addressed (DIM, 2008). “Prayer is also an essential partof all Native American healing techniques.” (American Cancer Society, 2008, p.1). A private room maybe necessary to allow the patient privacy for ceremonies and prayer with members from their tribe (DIM,2008). The burning of herbs and chanting prayers to cleanse and purify the body are common practice(American Cancer Society, 2008). Discharge Planning Before discharge it is the nurses job to educate the patient and family on the disease process, howto identify complications, how to treat the symptoms when they develop, how to prevent recurrentepisodes of angina, and how to prevent further advancement of CAD by decreasing risk factors bytangible lifestyle changes. It is imperative for the patient and their family to understand that any painunresolved after 15 minutes even after nitroglycerine administration needs to be treated and assessed inthe emergency room immediately (Smeltzer et al., 2010). Acute Coronary Syndrome and Myocardial Infarction Coronary artery disease also encompasses Acute coronary syndrome (ACS) (American HeartAssociation [AHA], 2011). ACS includes both unstable angina and myocardial infarction (MI) both non-ST-segment elevation MI and ST segment elevation MI (AHA, 2011). Acute coronary syndrome is anemergent situation in which ischemia to the heart results in permanent damage and even death tomyocardial tissue (Smeltzer et al., 2010). Pathophysiology Unstable angina is usually a consequence from ischemia to the heart due to atheroscleroticplaques, this may result in an MI if not treated promptly. In the occurrence of an MI there is a completeocclusion of the blood flow to the heart. This lack of blood flow results in myocardial injury and death.Additional causes of an MI include situations where an imbalance between myocardial oxygen supply
Coronary Artery Disease 10and demand exists such coronary artery vasospasm, decreased oxygen supply (attributed to anemiadecreased blood pressure or blood loss), and increased myocardial oxygen demand (increased hear rate,cocaine use, or thyrotoxicosis) (Smeltzer et al., 2010). The affected area can develop damage very quickly (in minutes) or can develop slowly (overhours or days). Ischemia develops as the calls are deprived of oxygen and then progresses to cellulardamage and infarction of myocardial cells (Smeltzer et al., 2010). “The expression time is muscle reflectsthe urgency of appropriate treatment to improve patient outcomes. Each year in the United States, nearly1 million people have acute MIs, one fourth of these people die as a result (AHA 2007)” (Smeltzer et al.,2010, p. 768). MIs are subcategorized into two categories: non-ST-segment elevation MI (NSTEMI) and ST-segment elevation MI (STEMI). Signs and symptoms of an MI include chest pain that continues despiterest and medication, shortness of breath, chest pain, nausea, indigestion, and anxiety or sense of“impending doom” (Smeltzer et al., 2010). Cool pale diaphoretic skin, dizziness, increased heart rate,increased respiratory rate may also be present (AHA, 2011). An electrocardiogram is used to identify thetype and location of MI. Goals of medical intervention for an MI are to minimize and prevent damage tothe heart and to prevent additional complications (Smeltzer et al., 2010). Assessment and Diagnostics Acute Coronary Syndrome is usually diagnosed with a combination of diagnostic tests and aphysical exam. These tests usually include a 12 lead EKG and a serial cardiac biomarker lab test. An indepth patient cardiac history is also completed which should include a description of the presenting signsand symptoms, previous heart health history for self and immediate family, and the patients risk factorsfor heart disease. This combination of tests and physical examination help differentiate whether thepatient has unstable angina, a NSTEMI, or a STEMI (Smeltzer et al., 2010). Diagnosis of unstable angina include the following assessment results. Clinical manifestations ofcoronary ischemia are present but the EKG and cardiac biomarker lab tests show no evidence of a current
Coronary Artery Disease 11MI. STEMI diagnosis is contingent upon a 12 lead EKG displaying changes of two contiguous leads.Significant damage to the myocardium is evidence of an MI. NSTEMI patients have elevated cardiacbiomarkers but no EKG findings showing MI (Smeltzer et al., 2010). The 12 lead electrocardiogram (EKG) should be obtained within 10 minutes of the patients arrivalto the hospital. Serial EKGs show changes in the recording of the heart rhythm such as T-wave inversiondue to myocardial ischemia that alters repolarization of cardiac cells. ST segment elevation (1 mm aboveisometric line) which is a consequence of myocardial injury. The injured myocardial cells re-polarizefaster than normal cells causing the ST elevation. This elevation in two leads is a main diagnostic findingof a MI. The development of abnormal Q waves resulting from the absence of depolarization currentfrom the infarcted myocardial tissue is also a main diagnostic finding of a MI. R wave height may alsodecrease after a MI. An echocardiogram may be used for MI diagnosis in conjunction with the EKG. Theechocardiogram evaluates ventricular function and the hearts ejection fraction (Smeltzer et al., 2010). Lab tests to help diagnose an acute MI include myoglobin and troponin cardiac biomarker panels.Cardiac enzymes such as Creatinine kinase, myoglobin, and troponin are released into the blood uponcellular cardiac injury and death. An elevated Creatinine Kinase MB is specific to damage to cardiaccells and only increases when they are damaged thus being an indicator of acute MI (Smeltzer et al.,2010). The level increases within a few hours of cardiac cellular damage and peaks within 24 hours of aMI. Myoglobin which is found in both skeletal and heart muscle begins to increase within 1-3 hours ofinjury and peaks at approximately 12 hours. Myoglobin level increase is not cardiac specific but theabsence of a level increase helps to rule out a MI. Troponin isomers I and T are specific for cardiacmuscle and are used to diagnose myocardial injury and MI. A Troponin level increase can be detected afew hours after injury and can remain elevated for as long as 3 weeks (Smeltzer et al., 2010). Medical and Pharmacologic Management Medical management goals of acute coronary syndrome are to minimize myocardial damage,preserve function, and prevent further complications. “These goals are facilitated by the use of guidelines
Coronary Artery Disease 12developed by the American College of Cardiology (ACC) and the AHA.” (Smeltzer et al., 2010, p.770).Myocardial damage is reduced by re perfusing the area by PCI or thrombolytic therapy Reducingmyocardial demand and increasing the available oxygen supply via medications, as well as oxygentherapy and bed rest can also lessen further damage to the myocardial cells (Smeltzer et al., 2010). Pharmacologic therapy for a MI includes Aspirin, nitroglycerine, morphine, IV beta blockers, antiplatelet medication, angiotensin-converting enzyme inhibitors and non steroidal anti inflammatory drugs(NSAIDS). Suspected MI patients are given an initial loading dose of a minimum of 162-325 mg dose ofAspirin as an anti thrombolytic (Hennekens, C.H., Dyken, M.L., & Fuster, V., 2009). Morphine decreasesthe workload of the heart by decreasing both preload and after load of the heart while reducing pain andanxiety, thus making it the first choice in treatment of a MI. ACE inhibitors prevent the conversion ofangiotensin I to angiotensin II, resulting in a decrease in blood pressure and the excretion of sodium andfluid from the kidneys thereby decreasing the workload and demand on the heart (Smeltzer et al., 2010). Beta blockers such as Metoprolol and Atenolol are used to reduce the myocardial oxygen demandby blocking the beta adrenergic stimulation of the heart which reduces heart rate by slowing theconduction of electrical impulses through the heart. Blood pressure reduces as well as myocardialcontractility, helping balance the myocardial supply and demand of oxygen. Beta blockers help preventthe recurrence of angina and MI by delaying the onset of ischemia (Smeltzer et al., 2010). Newrecommendations for the safety of acute usage of beta blockers during an MI have been released.(Kontos, M.C., Diercks, D.B., Ho, P.M., Wang, T.Y., Chen, A. Y., & Roe, M.T., 2011). In a recent studyfrom the American College of Cardiology it was found that the emergent use of Beta blockers in MIpatients showed an increase of in hospital complications versus a later use of beta blockers after 24 hoursafter MI . The complications included an increase of cardiogenic shock in both STEMI and NSTEMIpatients (Kontos, M.C., Diercks, D.B., Ho, P.M., et al., 2011). “Risk factors for shock are common inSTEMI and NSTEMI patients treated with early BBs. Increasing numbers of risk factors were associatedwith increased risk for shock or death in patients treated with BBs. These results are consistent with
Coronary Artery Disease 13current recommendations for avoiding early BB treatment for patients with acute MI.” (Kontos, M.C.,Diercks, D.B., Ho, P.M., Wang, T.Y., Chen, A. Y., Roe, & M.T., 2011 p. 1). The most used thrombolytic agent by hospitals is Alteplase (t-pa). Thrombolytics dissolve clotblockages in coronary arteries therefore increasing perfusion and minimizing the area of infarcted tissue.Thrombolytics have specific protocols that need to be followed for administration. Thrombolytic patientsshould be assessed by a nurse for contraindications to thrombolytic therapy. Some contraindicationsinclude active bleeding, recent surgery, head trauma, and pregnancy. Thrombolytic therapy needs to beadministered 3-6 hours after arrival at the hospital. Nursing considerations for patients on thrombolytictherapy include minimizing the number of times a patients skin is punctured, avoid intramuscularinjection, monitor for dysrhythmias and hypotension, check for signs and symptoms of bleeding(Smeltzer et al., 2010). Emergent treatment of a STEMI patient may be accomplished by Percutaneous coronaryintervention (PCI). PCI re-perfuses the ischemic myocardial tissue by opening the occluded artery. Thetypes of PCI vary and include percutaneous transluminal coronary angioplasty (PTCA), intracoronarystent implantation, atherectomy, and brachytherapy. Patients should arrive to the cardiac catheter labwithin 60 minutes or less of arriving at the hospital for treatment (Smeltzer et al., 2010). In PTCA a balloon tipped catheter is inserted into coronary vessels to re perfuse the heart byreducing the blockage by either compressing the plaque or by breaking it apart. The body initiates aninflammatory response (restenosis) after a PTCA procedure which causes vasoconstriction of the vesselsand may result in scaring and clot formation. A coronary artery stent may be placed after PTCA to keepthe artery open and provide structural support. Atherectomy is an invasive procedure that removes thecoronary plaque by grinding, cutting, or shaving and may be used in conjunction with PTCA.Brachytherapy prevents vessel restenosis by gamma or beta radiation which inhibits smooth muscle cellproliferation (Smeltzer et al., 2010). ACS patients may undergo coronary artery revascularization procedures such as a coronary artery
Coronary Artery Disease 14bypass graft (CABG). During a CABG a blood vessel is grafted to an occluded artery so that blood canflow beyond the occlusion and perfuse the heart. “For a patient to be considered for CABG, the coronaryarteries to be bypassed must have 70% occlusion (60% if in the main coronary artery).” (Smeltzer et al.,2010, p.).Complications of a CABG may include MI, dysrhythmias, and hemorrhage (Smeltzer et al.,2010). Nursing Process The nursing process for a patient with Acute coronary syndrome includes an in depth assessmentto determine the patients baseline condition which enables future analysis of any deviations from theinitial assessment. The assessment includes patient cardiac history of chest pain, dyspnea, palpitations,diaphoresis, faintness, and palpitations. All symptoms need to be evaluated relating to onset, duration,and resolution. A physical exam is also essential in determining a baseline of patient health. Two IVs areusually placed for emergent medication administration (Smeltzer et al., 2010). Nursing diagnosis for acute coronary syndrome includes consideration of clinical manifestations,history, and diagnostic findings. Some potential nursing diagnoses may include “Ineffective cardiac tissueperfusion related to reduced coronary blood flow”, “risk for imbalanced fluid volume” and “ deathanxiety related to cardiac event.” (Smeltzer et al., 2010, p.766). Some potential complications mayinclude acute pulmonary edema, cardiogenic shock, heart failure, dysrhythmias, and cardiac death(Smeltzer et al., 2010). Planning and goals for the patient with acute coronary syndrome include the relief of pain,prevention of myocardial damage, and reduced anxiety. Secondary goals include adherence to therapyregimen, early recognition or absence of complications, and a decrease in risk factors contributing toacute coronary syndrome (Smeltzer et al., 2010). Nursing Interventions Nursing interventions for acute coronary syndrome entail the following: relieve pain, improverespiratory function, promote adequate tissue perfusion, reduce anxiety, and manage and identify
Coronary Artery Disease 15potential complications. The top priority for an ACS patient is to balance myocardial oxygen supply anddemand. This can be done through oxygen therapy by titrating the oxygen saturation between 96-100%and administering the prescribed pharmacologic therapy. Vital signs should be assessed frequently alongwith the patients pain rating. Bed rest and elevation of the head of the bed also help to decrease dyspnea.Assessment of fluid volume status improves respiratory function by preventing overloading of the heartand lungs. Frequent position changes should be encouraged to prevent pooling of fluid in the lungs(Smeltzer et al., 2010). Tissue perfusion should be monitored by checking patients skin color, temperature, capillary refill,and peripheral pule strength. Anxiety reduction and alleviation of fear are important nursinginterventions to reduce the sympathetic stress response, development of trust between nurse and patienthelps to facilitate this. Patient education, a restful environment, and relaxation techniques also help thepatient decrease fear and anxiety. Monitoring the patient carefully for changes in heart rate, rhythm, andsound help to monitor for potential complications. The nurse also needs to assess respiratory status, pain,urinary output, blood pressure, and lab values to determine the onset of complications (Smeltzer et al.,2010). Discharge Preparing the ACS patient for discharge and self care at home includes assessing the patientseducation needs. The level of understanding of the patient needs to be determined to ensure a successfuldischarge. The patients understanding and educational needs should be assessed regarding ACS,medication use, risk factors, identifying potential complications and when to seek help. Evaluation of theACS patient and expected patient outcomes include relief of angina, adequate tissue perfusion, decreasedanxiety, no complications, and patient adheres to self care regimen (Smeltzer et al., 2010). A case manager or social worker may need to be involved in helping prepare the patient withCAD for discharge. Arrangements can be made for financial assistance, home health or assisted living,rehabilitation, dietary, transportation and counseling needs (Smeltzer et al., 2010).