Cardiac and Vascular Care Plans

Chapter 5


Cardiac and Vascular Care Plans



Acute Coronary Syndromes/Myocardial Infarction


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Unstable Angina; ST-Segment Elevation Myocardial Infarction; Non–ST-Segment Elevation Myocardial Infarction; Non–Q-Wave Myocardial Infarction; Q-Wave Myocardial Infarction


Acute coronary syndromes (ACSs) represent a spectrum of clinical conditions associated with acute myocardial ischemia. Most patients who experience ACS have atherosclerotic changes in the coronary arteries. Chronic inflammatory processes play a key role in the pathogenesis of atherosclerosis. The presence of atherosclerotic plaques narrows the lumen of the arteries, and disruption or rupture of those plaques exposes a thrombogenic surface on which platelets aggregate, contributing to thrombus formation that diminishes blood flow to the myocardium. The resulting imbalance between myocardial oxygen demand and supply is the primary cause of the clinical manifestation in ACS. Other causes of ACS include coronary artery spasm and arterial inflammation related to infection. Noncardiac conditions that increase myocardial oxygen demand can precipitate ACS in patients with preexisting coronary artery disease (CAD). These conditions include fever, tachycardia, and hyperthyroidism. Decreased myocardial oxygen supply can occur in noncardiac conditions such as hypotensive states, hypoxemia, and anemia.


Clinical conditions included in ACS are unstable angina, variant angina, non–ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Evaluation of chest pain related to these disorders is a major cause of emergency department visits and hospitalizations in the United States. The term ACS is used prospectively to diagnose patients with chest pain or other clinical manifestations indicating the need to be triaged for treatment of unstable angina or acute MI. Although their pathogenesis and clinical presentation are similar, they differ primarily by whether ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of cardiac biomarkers (e.g., troponin, creatine kinase–myocardial bound [CK-MB], myoglobin) denoting acute MI. Early identification of ACS and intervention to improve myocardial perfusion reduces the risk for sudden cardiac death and acute MI in these patients.


Unstable angina is characterized by: (1) angina that occurs when the patient is at rest, (2) angina that significantly limits the patient’s activity, or (3) previously diagnosed angina that becomes more frequent, lasts longer, and increasingly limits the patient’s activity. Patients typically do not have ST-segment elevation and do not release cardiac biomarkers indicating myocardial necrosis. NSTEMI is distinguished from unstable angina by the presence of cardiac biomarkers, indicating myocardial necrosis. Most patients do not develop new Q waves on the electrocardiogram (ECG) and are diagnosed with non–Q-wave MI. STEMI is characterized by release of cardiac biomarkers and the presence of new Q waves on the ECG.


This care plan focuses on the assessment of and interventions for patients with all of these conditions. The American Heart Association and the American College of Cardiology have developed treatment guidelines for patients with unstable angina and NSTEMI, as well as for STEMI. Each guideline addresses initial and ongoing drug therapy, indications for fibrinolytic and percutaneous coronary interventions, and discharge considerations. For patients with MI, the therapeutic goals are to establish reperfusion, to minimize the infarct size, to prevent and treat complications, and to provide emotional support and education. The Centers for Medicare and Medicaid Services (CMS) and The Joint Commission (TJC) have developed core performance measures/quality indicators for acute MI treatment. This care plan focuses on acute management of ACS. The cardiac rehabilitation care plan presented later in this chapter addresses specific learning needs.




Angina Pectoris, Stable


Chest Pain


Stable angina pectoris is a clinical syndrome characterized by the abrupt or gradual onset of substernal discomfort (often with radiation to the neck, jaw, shoulder, back, or arm) caused by insufficient coronary blood flow and inadequate oxygen supply to the myocardial muscle. The patient with stable angina will have episodes of chest pain that are usually predictable. Chest pain will occur in response to hypoxia, or is aggravated by physical exertion or emotional stressors. Situations that increase myocardial oxygen demand or decrease oxygen supply include both cardiac and noncardiac causes. Stable angina usually persists for only a few minutes and subsides with cessation of the precipitating factor, rest, or use of nitroglycerin (NTG). Patients may present in ambulatory settings or during hospitalization for other medical problems. Stable angina usually can be controlled with medications on an outpatient basis. Stable angina can significantly affect one’s quality of life. A person may limit activities based on fear of precipitating episodes of chest pain.




Atrial Fibrillation


Atrial fibrillation is the most common sustained heart rhythm disturbance in the United States, affecting more than 2 million people. It is an abnormal heart rhythm characterized by an irregular or often rapid heart beat causing reduced cardiac output. In this dysrhythmia, the upper chambers of the heart (atria) fibrillate (quiver) rapidly and erratically, resulting in pooling of blood in the atrium and an irregular ventricular HR and pulse. Although atrial fibrillation itself is not life-threatening, if not adequately treated, it can cause significant side effects resulting in a decreased quality of life and can increase the risk for stroke and heart failure. Because the incidence of atrial fibrillation increases with age, this medical condition is projected to be a huge medical problem as the United States and world population ages. Atrial fibrillation is classified by how it terminates: paroxysmal atrial fibrillation, referring to occasional occurrences that start and stop on their own; persistent atrial fibrillation, a condition in which the abnormal rhythm continues for more than a week, does not self-terminate, but can be treated to a return to normal rhythm; and permanent atrial fibrillation, a condition in which the abnormal rhythm is chronic and unresponsive to treatment.


The most common causes and risk factors for atrial fibrillation include age older than 60 years, heart disease including valve disease, hypertension, heart failure, prior open heart surgery, thyroid disease, chronic lung disease, exposure to stimulants or excessive alcohol, viral infections, and sleep apnea. Some people develop atrial fibrillation for no apparent reason (termed “lone afib”).


Symptoms vary with each person depending on age, cause, and how much the atrial fibrillation affects the contractility of the heart. Symptoms can range from pulse rate that is faster than normal or changing between fast and slow with mild fatigue to shortness of breath, heart palpitations or fluttering, decreased BP, chest tightness or discomfort, dizziness, lightheadedness. Atrial fibrillation is diagnosed by an electrocardiogram (ECG) while the abnormal rhythm is occurring, but if the rhythm is intermittent, a portable Holter ECG monitor or an event recorder is used to document the dysrhythmia.


Management of atrial fibrillation can vary depending on the type, how long the person has had it, and factors such as age, underlying heart condition, stroke risk, and the severity of associated symptoms. A variety of treatments are available focused on the goals of resetting the rhythm to normal (for first time and more acute episodes) or controlling the ventricular rate (for more persistent and chronic conditions) and preventing blood clots from forming in the fibrillating atria through anticoagulation. Thus treatments may include antiarrhythmic medications, electrical cardioversion, catheter ablation, and a surgical maze procedure. Because atrial fibrillation increases the risk of development of blood clots in the atria, long-term anticoagulation is required for patients at increased risk for stroke.




Cardiac Rehabilitation


Post–Myocardial Infarction; Post–Cardiac Surgery; Post–Percutaneous Transluminal Coronary Angioplasty; Chronic Heart Failure; Stable Angina; Activity Progression; Cardiac Education


Cardiac rehabilitation is the process of actively assisting patients with known heart disease to achieve and maintain optimal physical and emotional health and wellness. It has undergone significant evolution, redesigning itself from a primarily exercise-focused intervention into a comprehensive disease management program. Core components of these programs include baseline and follow-up patient assessments; aggressive strategies for reducing modifiable risk factors for cardiovascular disease (CVD; e.g., dyslipidemia, hypertension, diabetes, obesity); counseling on heart-healthy nutrition, smoking cessation, and stress management; assistance in adhering to prescribed medications; promotion of lifestyle physical activity; exercise training; and psychosocial and vocational counseling. These integrated services are best provided by a multidisciplinary team composed of physicians, nurses, health educators, exercise physiologists, dietitians, and behavioral medicine specialists. More recently, the nurse has changed from team member to case manager. Cardiac rehabilitation programs typically begin in the hospital setting and progress to supervised (and often electrocardiogram [ECG]-monitored) outpatient programs. However, with shorter hospital stays, little time may be available for adequate instruction regarding lifestyle management and activity progression. Key to providing cost-effective care is an interdisciplinary team and the provision of interventions based on each patient’s unique needs, interests, and skills.




Coronary Bypass/Valve Surgery: Postoperative Care


Coronary Artery Bypass Graft (CABG); Valve Replacement; Minimally Invasive Surgery; Off-Pump CABG (OPCAB)




Coronary Bypass Surgery


The surgical approach to myocardial revascularization for coronary artery disease is bypass grafting. An artery from the chest wall (internal mammary) or a vein from the leg (saphenous) is used to supply blood distal to the area of stenosis. Internal mammary arteries have a higher patency rate. Today’s coronary artery bypass graft (CABG) patients are older (even octogenarians unresponsive to medical therapy or with failed coronary angioplasties or stents), have poorer left ventricular function, and may have undergone prior sternotomies. Older patients are at higher risk for complications and have a higher mortality rate. Women tend to have CABG surgery performed later in life. They have more complicated recovery courses than men because of the smaller diameter of women’s vessels and their associated comorbidity. Women have also been noted to have less favorable outcomes, with more recurrent angina and less return to work. Newer techniques for revascularization are available, such as transmyocardial revascularization with laser and video-assisted thoracoscopy. These techniques use limited incision and reduce the need for cardiopulmonary bypass and related perioperative complications. Surgical procedures for CABG without cardiopulmonary bypass or cardioplegia (off-pump) hold promise for reductions in postoperative morbidity.












Heart Failure, Chronic


Congestive Heart Failure; Cardiomyopathy; Left-Sided Failure; Right-Sided Failure; Pump Failure; Systolic Dysfunction; Diastolic Dysfunction


Heart failure is described as a common clinical syndrome resulting in the inability of the heart to meet the hemodynamic and metabolic demands of the body, producing a variety of biochemical and neurohormonal changes and manifesting in a variety of ways. With more than 5 million people in the United States having heart failure, it is a major health problem associated with high mortality rates, major morbidity, and rehospitalization. There is an increased prevalence with age, especially with women, making this a key geriatric concern. Heart failure remains one of the most disabling conditions, carrying a high economic burden related to the frequency of hospital readmissions.


Heart failure is the final syndrome of a wide spectrum of endothelial and myocardial injuries that produce ventricular systolic dysfunction (poor pumping function) and/or diastolic dysfunction (poor relaxation and filling function). Hypertension and coronary artery disease are the most common contributing factors to heart failure, though the list of causative factors is quite extensive. These causes are often described as resulting from myocardial ischemia and chamber enlargement from a variety of causes, volume-related factors, pressure-loading conditions, and restrictive causes. Because of the health consequences of heart failure, attention is being directed to identifying and treating earlier those at risk for heart failure. A lettered classification system has been developed with characteristics defined for stages A, B, C, and D, with A being high risk but without structural problems or heart failure symptoms to D being refractory heart failure requiring specialized interventions. This somewhat parallels the classic New York Heart Association functional classification system based on severity of symptoms. Class I patients have no symptoms or physical limitations. Class II patients have slight limitations in their physical activity, whereby ordinary physical activities can cause symptoms such as fatigue, palpitations, dyspnea, or angina. Class III patients have marked physical limitations, with less than ordinary level of activities causing symptoms. Class IV patients experience dyspnea even at rest; activity is severely restricted.


The goals of treatment are to prevent progression of heart failure, reduce exacerbations, recognize early signs of decompensation, control symptoms, assist patient in co-managing the disease, and improve quality of life. The basis of medical therapy is neurohormonal inhibition. Angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta-blockers (e.g., carvedilol), and aldosterone antagonists vasodilate, prevent decompensation, and reduce mortality. These drugs are used in combination with diuretics that reduce fluid overload. Digoxin is sometimes used in appropriate patients but does not reduce mortality. As patients deteriorate and experience acute decompensation, additional therapies of IV vasodilators and inotropes are indicated. Additional device therapies are available for patients with more complicated conditions. These include ultrafiltration to remove excess fluids and sodium, cardiac resynchronization therapy pacemakers to optimize cardiac output, implantable defibrillators to reduce risk for sudden cardiac death, and ventricular assist devices to extend life.


Innovative programs such as cardiac case-managed home care, community-based heart failure case management, telemanagement, and heart failure cardiac rehabilitation programs are being developed to reduce the need for acute care or hospital services for this growing population. Because the goal of therapy is to manage patients outside the hospital, this care plan focuses on treatment in an ambulatory setting for patients with heart failure symptoms (Stage C, Functional Class II-III). Note: Several national organizations have performance outcome goals related to heart failure: the American Heart Association’s Get With the Guidelines—Heart Failure initiative and The Joint Commission’s National Patient Safety Goals and National Quality Improvement Goals.



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Dec 3, 2016 | Posted by in NURSING | Comments Off on Cardiac and Vascular Care Plans

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