Class 14, 15, 16

Hypertension Complications

Target organ diseases occur most frequently in - Heart - Brain - Peripheral vascular disease - Kidney - Eyes The most common complications of hypertension are target organ diseases occurring in the heart (hypertensive heart disease), brain (cerebrovascular disease), peripheral vessels (peripheral vascular disease), kidneys (nephrosclerosis), and eyes (retinal damage).

Echocardiogram

Two commonly used types of echocardiograms are the motion-mode (M-mode) echocardiogram and the two-dimensional (2-D) echocardiogram. In the M-mode, a single US beam is directed toward the heart, recording the motion of the intracardiac structures, as well as detecting wall thickness and chamber size. The 2-D echocardiogram sweeps the US beam through an arc, producing a cross-sectional view. This shows correct spatial relationships among the structures.

Coronary angiography

Uses contrast medium to identify coronary blockages Coronary angiography is done with a left-sided heart catheterization. - The catheter is positioned at the origin of the coronary arteries, and contrast medium is injected into the arteries. Patients often feel a temporary flushed sensation with dye injection. The images identify the location and severity of any coronary blockages. - Complications of cardiac catheterization include bleeding or hematoma at the puncture site, allergic reactions to the contrast media, looping or kinking of the catheter, infection, thrombus formation, aortic dissection, dysrhythmias, MI, stroke, and puncture of the ventricles, cardiac septum, or lung tissue.

Diagnostic Studies for HF

Determine and treat underlying cause - Diagnosing HF is often difficult. Patient signs and symptoms are not highly specific and may mimic those associated with many other medical conditions (e.g., anemia, lung disease). A primary goal in diagnosis is to find the underlying cause of HF. Echocardiogram - Provides information on EF, heart valves and heart chambers - An echocardiogram is a common diagnostic tool used in patients with HF. It provides information on the EF. This helps to differentiate between HFpEF and HFrEF. An echocardiogram also provides information on the structure and function of the heart valves. Heart chamber enlargement or stiffness can also be assessed. ECG, chest x-ray, 6-minute walk test, MUGA scan, cardiopulmonary exercise stress test, heart catheterization, EMB - Other useful tests include electrocardiogram (ECG), chest x-ray, 6-minute walk test, multi-gated acquisition (MUGA) scan, cardiopulmonary exercise stress test, and heart catheterization. Studies for obstructive sleep apnea may be done in select patients. An endomyocardial biopsy (EMB) may be done as part of a heart catheterization in select acutely ill patients who develop unexplained, new onset HF that is unresponsive to usual care. BNP levels - Laboratory studies also aid in the diagnosis of HF. In general, BNP levels correlate positively with the degree of LV failure. Many agencies routinely measure the N-terminal prohormone of BNP (NT-proBNP). This is a more precise test to aid in the diagnosis of HF. Levels are temporarily higher in patients receiving nesiritide (Natrecor) and may be high in patients with chronic, stable HF. Increases in BNP or NT-proBNP levels can be caused by conditions other than HF. - These include pulmonary embolism, renal failure, and acute coronary syndrome.

Nursing and Interprofessional Care: CAD

Health Promotion Identification of people at high risk - Health history, including family history - Presence of cardiovascular symptoms - Environmental patterns: diet, activity - Psychosocial history - Values and beliefs about health and illness The appropriate management of risk factors in CAD may prevent, modify, or slow the progression of the disease. In the United States, there has been a gradual decline in CVD-related deaths over the past 35 years. This relates to the efforts of people to become generally healthier, as well as advances in the treatment of CAD. Prevention and early treatment of heart disease must involve a multifaceted approach and needs to be ongoing throughout the life span. Identification of High-Risk Person - Clinical manifestations of CAD will not be apparent in the early stages of the disease. Therefore, it is extremely important to identify people at risk for CAD. - Risk screening involves obtaining a thorough health history. Question the patient about a family history of heart disease in parents and siblings. - Note the presence of any cardiovascular symptoms. - Assess environmental factors, such as eating habits, type of diet, and level of exercise to elicit lifestyle patterns. - Include a psychosocial history to determine tobacco use, alcohol intake, recent stressful events (e.g., loss of a spouse), and the presence of any negative psychologic states (e.g., anxiety, depression, anger). The place of work and the type of work provides important information on the kind of activity performed, exposure to pollutants or toxins, and the degree of stress associated with work. - Identify the patient's attitudes and beliefs about health and illness. This information can give you insight to how disease and lifestyle changes may affect the patient. It also can reveal possible misconceptions about heart disease. Manage high-risk persons by controlling modifiable risk factors Encourage lifestyle changes - Education - Clarify personal values - Set realistic goals Management of High-Risk Persons - Recommend preventive measures for all persons at risk for CAD. - Risk factors such as age, gender, ethnicity, and genetic inheritance cannot be modified. - However, the person with any of these risk factors can still reduce the risk of CAD by controlling the additive effects of modifiable risk factors. - For example, a young man with a family history of heart disease can decrease the risk of CAD by maintaining an ideal body weight, getting adequate physical exercise, reducing intake of saturated fats, and avoiding tobacco and illicit drug use. - People who have modifiable risk factors should be encouraged to make lifestyle changes to reduce their risk of CAD. You can play a major role in teaching health-promoting behaviors. For highly motivated persons, knowing how to reduce this risk may be the information that they need to get started. - For persons who are less motivated to take charge of their health, the idea of reducing risk factors may be so remote that they are unable to perceive a threat of CAD. Few people desire to make lifestyle changes, especially in the absence of symptoms. First help these patients to clarify their personal values. Then, discuss risk factors and have them identify their individual risks. - This can help patients set realistic goals and choose which risk factor(s) to change first. - Some persons are reluctant to change until they begin to have symptoms or actually suffer an MI. Others, having suffered an MI, may find the idea of changing lifelong habits still unacceptable. You must be able to identify their choices and respect them. Physical fitness - FITT formula: 30 minutes most days plus weight training 2 days a week - Regular physical activity contributes to - Weight reduction - Reduction of >10% in systolic BP - In some men more than women, increase in HDL cholesterol Physical Activity A physical activity program should be designed to improve physical fitness by following the FITT formula: - Frequency (how often) - Intensity (how hard) - Type (isotonic) - Time (how long) Everyone should aim for at least 30 minutes of moderate physical activity on most days of the week. - In addition, adding weight training to an exercise program 2 days a week can help treat metabolic syndrome and improve muscle strength. Examples of moderate physical activity include brisk walking, hiking, biking, and swimming. - Regular physical activity helps with weight reduction, reduces systolic BP, and, in some men more than women, increases in HDL cholesterol. Nutritional therapy ↓ Saturated fats and cholesterol ↑ Complex carbohydrates and fiber ↓ Red meat, egg yolks, whole milk ↑ Omega-3 fatty acids - The National Heart, Lung, and Blood Institute recommends therapeutic lifestyle changes for all people to reduce the risk of CAD by lowering LDL cholesterol. - These recommendations emphasize a decrease in saturated fat and cholesterol and an increase in complex carbohydrates (e.g., whole grains, fruit, vegetables) and fiber. - Red meat, egg yolks, and whole milk products are major sources of saturated fat and cholesterol and should be reduced or eliminated from diets. - If the serum triglyceride level is elevated, alcohol and simple sugars should be reduced or eliminated. - Patients with CAD are encouraged to take EPA and DHA supplements with their diet. The AHA also recommends eating tofu and other forms of soybean, canola, walnut, and flaxseed because these products contain alpha-linolenic acid, which becomes omega-3 fatty acid in the body. - Lifestyle changes, including a low-saturated-fat, high-fiber diet; avoidance of tobacco; and increase in physical activity, can promote the reversal of CAD and reduce coronary events. Drug Therapy Lipid-lowering drug therapy - Drugs that restrict lipoprotein production - Drugs that increase lipoprotein removal - Drugs that decrease cholesterol absorption Anti platelet therapy

Structures of Cardiovascular System

Heart - Four chambers - Composed of three layers 1. Endocardium 2. Myocardium 3. Epicardium Pericardium Left ventricular wall 2-3 times thicker than right. The heart is a four-chambered hollow muscular organ normally the approximate size of a fist. It lies within the thorax in the mediastinal space that separates the right and left pleural cavities. The heart is composed of three layers: a thin inner lining, the endocardium; a layer of muscle, the myocardium; and an outer layer, the epicardium. The heart is covered by a fibroserous sac called the pericardium. This sac consists of two layers: the inside (visceral) layer of the pericardium (the epicardium) and the outer (parietal) layer. A small amount of pericardial fluid (approximately 10 to 15 mL) lubricates the space between the pericardial layers (pericardial space) and prevents friction between the surfaces as the heart contracts. The heart is divided vertically by the septum. The interatrial septum creates a right and a left atrium, and the interventricular septum creates a right and a left ventricle. The thickness of the wall of each chamber is different. The atrial myocardium is thinner than that of the ventricles, and the left ventricular wall is 2 to 3 times thicker than the right ventricular wall.

Hypertension Nursing Implementation

Home BP monitoring Patient teaching is critical for accuracy - Proper equipment - Proper procedure - Frequency - Accurate recording and reporting - Target BP Most patients with known or suspected hypertension should monitor their BP at home. Home BP monitoring reduces the white coat effect of measurement by a HCP. The readings are often lower than those taken in the office setting and are a better predictor of CVD risk. Patient teaching is critical to ensure accuracy. Tell patients to buy an oscillometric BP monitor that uses a cuff for the upper arm or wrist. The patient should bring the BP monitor to the office to verify proper cuff size, accuracy of the device, and the patient's technique. Teach the patient how to obtain a BP. Tell the patient to measure BP in the nondominant arm or arm with the higher BP if there is a known difference between arms. Tell the patient to measure BP first thing in the morning (if possible, before taking medications) and at night before going to bed. Have the patient record all BP measurements and to bring the record to office visits. For clinical decision making (e.g., changes in dosage, start of new drug), tell patients to take BP readings as described for 1 week. Stable, normotensive patients should measure morning and evening BP for at least 1 week every 3 months. Devices that have memory or printouts of the readings are recommended to ensure accurate reporting. Home BP readings may help achieve patient adherence by reinforcing the need to remain on therapy. However, some patients become overly concerned with the BP readings. Discourage too frequent checking of their BP. Generally, home BP monitoring should reassure the patient that the treatment is effective. It is also important for patients to know what their goal or target BP is. Reasons for poor adherence to treatment plan are complex - Inadequate teaching - Low health literacy - Unpleasant side effects of drugs - Return to normal BP while on drugs - High cost of drugs - Lack of insurance A major problem in the long-term management of the patient with hypertension is poor adherence with the treatment plan. The reasons are complex and can include inadequate patient teaching, low health literacy, unpleasant side effects of drugs, return of BP to normal range while on drugs, high cost of drugs, and lack of insurance. It is important to determine the reasons why a patient is not adhering to treatment. Also assess the patient's diet, activity level, and lifestyle as additional indicators of adherence. Measures to enhance compliance - Individualize plan - Active patient participation - Select affordable drugs - Involve caregivers - Combination drugs - Patient teaching Develop a plan with the patient and caregiver to improve compliance. The plan should be compatible with the patient's habits, cultural beliefs, and lifestyle. Active patient participation increases the chance of adherence to the plan. Measures include involving the patient, selecting drugs that are affordable, and involving caregivers to help increase patient adherence. Substituting combination drugs for multiple drugs once the BP is stable may also facilitate compliance. Combination drugs reduce the number of pills that the patient has to take each day and may reduce costs. It is important to help the patient and caregiver understand that hypertension is a chronic illness that cannot be cured. Emphasize that it can be controlled with drug therapy, diet changes, physical activity, periodic follow-up, and other relevant lifestyle modifications

Hypertension Classification

Hypertension is defined as a persistent systolic BP (SBP) of 140 mm Hg or more, diastolic BP (DBP) of 90 mm Hg or more, or current use of antihypertensive medication. Prehypertension is defined as SBP of 120 to 139 mm Hg or DBP of 80-89 mm Hg. Isolated systolic hypertension (ISH) is defined as an average SBP of 140 mm Hg or more, coupled with an average DBP of less than 90 mm Hg. SBP increases with aging. DBP rises until approximately age 55 and then declines. Control of ISH decreases the incidence of stroke, heart failure, and death. BP classification is based on the confirmation of office BP readings with ambulatory BP monitoring.

Diagnostic Studies of Cardiovascular System

Cardiac Biomarkers 1. Creatine kinase (CK) - Three isoenzymes - CK-MB cardiac specific - Rises in 3-6 hours, peaks in 12-24 hours, returns to baseline within 12-48 hours Creatine kinase (CK) enzymes are found in a variety of organs and tissues and occur as three isozymes. These isozymes are specific to skeletal muscle (CK-MM), brain and nervous tissue (CK-BB), and the heart (CK-MB). CK-MB rise is specific for MI or injury. Levels begin to increase 3 to 6 hours after symptom onset, peak in 12 to 24 hours, and return to baseline within 12 to 48 hours after myocardial infarction (MI). The peak level and return to normal can be delayed in a patient with a large MI. Levels drop more rapidly in patients who are quickly and successfully treated for an MI.

Diagnostic Studies of Cardiovascular System

Cardiac Biomarkers 1. Troponin - Troponin T (cTnT) - Troponin I (cTnI) - Rises within 4-6 hours, peaks 10-24 hours, detected for up to 10-14 days When cells are injured, they release their contents, including enzymes and other proteins, into the circulation. These biomarkers are useful in the diagnosis of acute coronary syndrome (ACS). Cardiac-specific troponin is a heart muscle protein released into circulation after injury or infarction. Two subtypes, cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI), are specific to heart muscle. Normally the level in the blood is very low, so a rise in level is diagnostic of myocardial infarction (MI) or injury. cTnT and cTnI are detectable within hours (on average of 4 to 6 hours) of MI or injury, peak at 10 to 24 hours, and can be detected for up to 10 to 14 days. Troponin is the biomarker of choice in the diagnosis ofACS. High-sensitivity troponin (hs-cTnT, hs-cTnI) assays may provide even earlier detection of a cardiac event.

Hypertension Clinical Manifestations

"Silent killer" - Hypertension is often called the "silent killer" because it is frequently asymptomatic until it becomes severe and target organ disease occurs. A patient with severe hypertension may experience a variety of symptoms secondary to the effects on blood vessels in the various organs and tissues or to the increased workload of the heart. Symptoms of severe hypertension - Fatigue - Dizziness - Palpitations - Angina - Dyspnea These secondary symptoms include fatigue, dizziness, palpitations, angina, and dyspnea. In the past, symptoms of hypertension were thought to include headache and nosebleeds. Unless BP is very high, these symptoms are no more frequent in people with hypertension than in the general population. However, patients with hypertensive crisis may experience severe headaches, dyspnea, anxiety, and nosebleeds.

Diagnostic Studies of Cardiovascular System

Additional blood studies - Cardiac natriuretic peptide markers - Three types 1. Atrial natriuretic peptide (ANP) 2. B-type natriuretic peptide (BNP) 3. C-type natriuretic peptide - Increased levels of BNP levels signify heart failure - NT-pro-BNP Cardiac Natriuretic Peptide Markers There are three natriuretic peptides: 1. atrial natriuretic peptide (ANP) from the atrium 2. b-type natriuretic peptide (BNP) from the ventricles 3. c-type natriuretic peptide from endothelial and renal epithelial cells. BNP is the marker of choice for distinguishing a cardiac or respiratory cause of dyspnea. N-terminal pro-brain natriuretic peptide (NT-pro-BNP) is also secreted in the ventricles and is more sensitive but less specific than BNP as a diagnostic marker of heart failure. When DBP increases (e.g., heart failure), BNP and NT-pro-BNP are released and increase natriuresis (excretion of sodium in the urine).

Placement of Coronary Artery Stent

A stent is an expandable meshlike structure designed to keep the vessel open after balloon angioplasty. Because stents are thrombogenic, many different types of drugs are used to prevent platelet aggregation within the stent. Drugs commonly used during PCI are unfractionated heparin (UH) or low-molecular-weight heparin (LMWH), a direct thrombin inhibitor (e.g., bivalirudin [Angiomax]), and/or a glycoprotein IIb/IIIa inhibitor (e.g., eptifibatide [Integrilin]). After PCI, the patient is treated with dual antiplatelet drugs (e.g., aspirin [indefinitely] and clopidogrel) up to 12 months or longer, until the intimal lining grows over the stent and provides a smooth vascular surface. There are two types of stents: bare metal stents (BMS) and drug-eluting stents (DES). DESs are coated with a drug (e.g., paclitaxel, sirolimus) to reduce the risk of overgrowth of the intimal lining (neointimal hyperplasia) within the stent. This is the primary cause of in-stent restenosis (ISR). Following DES placement, dual antiplatelet drugs are taken to prevent thrombus formation within the stent (stent thrombosis) for a minimum of 12 months or longer. The duration of dual antiplatelet drugs for patients with BMS is a minimum of 1 month but ideally one full year after PCI. The most serious complications from stent placement are abrupt closure from coronary artery dissection and vascular injury at the artery access site (femoral or radial), acute MI, stent embolization, coronary spasm, dye allergy, renal compromise, bleeding (e.g., retroperitoneal), infection, stroke and emergent coronary artery bypass graft (CABG) surgery. The possibility of dysrhythmias during and after the procedure is always present.

Pre-PCI and Post-PCI With Stent Placement

A, An occluded coronary artery is shown B, the same artery (now open) after PCI and stent placement.

Vessel Occlusion With Collateral Circulation

A. Open, functioning coronary artery. B. Partial coronary artery closure with collateral circulation being established. C. Total coronary artery occlusion, with collateral circulation bypassing the occlusion to supply blood to the myocardium.

Diagnostic Studies of Cardiovascular System

Additional blood studies 1. C-Reactive protein (CRP) - Marker for inflammation - Linked to atherosclerosis 2. Homocysteine - Elevated levels increased risk for CVAD, peripheral vascular disease (PVD), and stroke C-Reactive Protein - C-reactive protein (CRP) is a protein produced by the liver during periods of acute inflammation. - CRP can be measured using a high-sensitivity test (hsCRP). - An increased level of CRP has been linked with the presence of atherosclerosis and the first occurrence of a cardiac event. In addition, the level of CRP may predict the risk for future cardiac events in patients with MI. However, in general, studies on the usefulness of assessing CRP have produced conflicting results, and measuring CRP routinely in patients with and without CVD is not done. Homocysteine - Homocysteine (Hcy) is an amino acid that is produced during protein catabolism. - Elevated Hcy levels can be either hereditary or acquired from dietary deficiencies of vitamin B6, vitamin B12, or folate. - Elevated levels of Hcy have been linked to a higher risk of CVAD, peripheral vascular disease, and stroke. - It is recommended that Hcy testing be performed in those patients with a familial predisposition for early CVD or a history of CVD in the absence of other common risk factors.

Risk Factors for Primary Hypertension

Age - SBP rises progressively with increasing age although DBP may decrease with age. - After age 50, SBP >140 mm Hg is a more important cardiovascular risk factor than DBP. Alcohol - Excessive alcohol intake is strongly associated with hypertension. - Moderate intake of alcohol has cardioprotective properties; males with hypertension should limit their daily intake of alcohol to 2 drinks per day, and 1 drink per day for females with hypertension. Tobacco use - Smoking tobacco greatly ↑ risk of cardiovascular disease. - People with hypertension who smoke tobacco are at even greater risk for cardiovascular disease. Diabetes mellitus - Hypertension is more common in diabetics. - When hypertension and diabetes coexist, complications (e.g., target organ disease) are more severe. Elevated serum lipids - ↑ levels of cholesterol and triglycerides are primary risk factors in atherosclerosis. - Hyperlipidemia is more common in people with hypertension. Excess dietary sodium - High sodium intake can contribute to hypertension in salt sensitive patients. - Decrease the effectiveness of certain antihypertensive drugs Gender - Hypertension is more prevalent in men in young adulthood and early middle age. - After age 64, hypertension is more prevalent in women. Family history - History of a close blood relative (e.g., parents, sibling) with hypertension is associated with an ↑ risk for developing hypertension. Obesity - Weight gain is associated with increased frequency of hypertension. - The risk is greatest with central abdominal obesity. Ethnicity - Incidence of hypertension is two times higher in African Americans than in whites. Sedentary lifestyle - Regular physical activity can help control weight and reduce cardiovascular risk. - Physical activity may ↓ BP. Socioeconomic status - Hypertension is more prevalent in lower socioeconomic groups and among the less educated. Stress - People exposed to repeated stress may develop hypertension more frequently than others. - People who develop hypertension may respond differently to stress than those who do not develop hypertension.

Alterations in Cardiac Functioning (Cont.)

Altered cardiac output - Left-sided heart failure - Right-sided heart failure Impaired valvular function Myocardial ischemia - Angina - Myocardial infarction Failure of the myocardium to eject sufficient volume to the systemic and pulmonary circulations occurs in heart failure. Left-sided heart failure is an abnormal condition characterized by decreased functioning of the left ventricle. - If left ventricular failure is significant, the amount of blood ejected from the left ventricle drops greatly, resulting in decreased cardiac output. - Signs and symptoms include fatigue, breathlessness, dizziness, and confusion as a result of tissue hypoxia from the diminished cardiac output. - As the left ventricle continues to fail, blood begins to pool in the pulmonary circulation, causing pulmonary congestion. - Clinical findings include crackles in the bases of the lungs on auscultation, hypoxia, shortness of breath on exertion, cough, and paroxysmal nocturnal dyspnea. Right-sided heart failure results from impaired functioning of the right ventricle. - It more commonly results from pulmonary disease or as a result of long-term left-sided failure. - The primary pathological factor in right-sided failure is elevated pulmonary vascular resistance (PVR). As the PVR continues to rise, the right ventricle works harder, and the oxygen demand of the heart increases. As the failure continues, the amount of blood ejected from the right ventricle declines, and blood begins to "back up" in the systemic circulation. - Clinically the patient has weight gain, distended neck veins, hepatomegaly and splenomegaly, and dependent peripheral edema. Valvular heart disease is an acquired or congenital disorder of a cardiac valve that causes either hardening (stenosis) or impaired closure (regurgitation) of the valves. When stenosis occurs, the flow of blood through the valves is obstructed. When the ventricles contract, blood escapes back into the atria, causing a murmur, or "whooshing" sound. Myocardial ischemia results when the supply of blood to the myocardium from the coronary arteries is insufficient to meet myocardial oxygen demands. Angina pectoris is a transient imbalance between myocardial oxygen supply and demand. The condition results in chest pain that is aching, sharp, tingling, or burning or that feels like pressure. Typically chest pain is left sided or substernal and often radiates to the left or both arms, the jaw, neck, and back. It is usually relieved with rest and coronary vasodilators, the most common being a nitroglycerin preparation. Myocardial infarction (MI) or acute coronary syndrome (ACS) results from sudden decreases in coronary blood flow or an increase in myocardial oxygen demand without adequate coronary perfusion. Infarction occurs because ischemia is not reversed. Cellular death occurs after 20 minutes of myocardial ischemia. - Chest pain associated with MI in men is usually described as crushing, squeezing, or stabbing. The pain is often in the left chest and sternal area; may be felt in the back; and radiates down the left arm to the neck, jaws, teeth, epigastric area, and back. It occurs at rest or exertion and lasts more than 20 minutes. Rest, position change, or sublingual nitroglycerin administration does not relieve the pain. There is a significant difference between men and women in relation to coronary artery disease. Women's symptoms differ from those of men. The most common initial symptom in women is angina, but they also present with atypical symptoms such as fatigue, indigestion, shortness of breath, and back or jaw pain. Women have twice the risk of dying within the first year after a heart attack than men.

Locations and Patterns of Angina and MI

Although most angina pain occurs substernally, it may radiate to other locations, including the jaw, neck, shoulders, and/or arms. Many people with angina complain of indigestion or a burning sensation in the epigastric region. The sensation may also be felt between the shoulder blades. Often people who complain of pain between the shoulder blades or indigestion type pain dismiss it as not being heart related. Some patients, especially women and older adults, report atypical symptoms of angina including dyspnea, nausea, and/or fatigue. This is referred to as angina equivalent.

Etiology of Heart Failure

Anything that interferes with mechanisms that regulate cardiac output (CO) Primary causes - Conditions that directly damage the heart Precipitating causes - Conditions that increase workload of ventricles HF may be caused by any interference with the normal mechanisms regulating cardiac output (CO). - CO depends on (1) preload, (2) afterload, (3) myocardial contractility, and (4) heart rate (HR). - Any changes in these factors can lead to decreased ventricular function and HF. The major causes of HF may be divided into two subgroups: primary and precipitating Primary causes include: - Hypertension, including hypertensive crisis - Coronary artery disease, including myocardial infarction - Rheumatic heart disease - Congenital heart defects (e.g., ventricular septal defect) - Pulmonary hypertension - Cardiomyopathy (e.g., viral, postpartum, substance abuse) - Hyperthyroidism - Valvular disorders (e.g., mitral stenosis) - Myocarditis Precipitating causes often increase the workload of the ventricles, resulting in an acute condition that results in decreased cardiac function. - Anemia (decreased oxygen supply increases workload of heart to meet the demand) - Infection (increased oxygen demand) - Thyrotoxicosis (increased heart rate and workload) - Hypothyroidism (increased risk for atherosclerosis) - Dysrhythmias (decreased CO and increased workload) - Bacterial endocarditis (infection increases workload, can also cause valvular disorders) - Obstructive sleep apnea - Pulmonary embolism (increased workload to pump blood into lungs) - Paget's disease (increased workload secondary to increased vasculature bed) - Nutritional deficiencies (decreased cardiac function increases workload) - Hypervolemia (increased preload increases workload)

Hypertension

As BP increases, so does the risk of - MI - Heart failure - Stroke - Renal disease Affects 1 in 3 adults in United States High priority health concern identified in Healthy People 2020 Hypertension, or high blood pressure (BP), is one of the most important modifiable risk factors that can lead to the development of cardiovascular disease (CVD). As BP increases, so does the risk of myocardial infarction (MI), heart failure, stroke, and renal disease. Heart disease, often directly related to hypertension, accounts for 23.7% of all deaths each year in the United States. Healthy People 2020 lists the number of adults with hypertension whose BP is under control as one of the 26 high-priority, leading health indicators for the coming decade.

Hypertension BP Measurement

Assess for orthostatic hypotension - BP and HR supine, sitting, and standing - Measure within 1 to 2 minutes of position change - Positive if ↓ of 20 mm Hg or more in SBP, ↓10 mm Hg or more in DBP, or ↑ 20 beats/minute or more in heart rate Assess for orthostatic (or postural) changes in BP and pulse in older adults, in people taking antihypertensive drugs, and in patients who report symptoms consistent with reduced BP on standing (e.g., light-headedness, dizziness, syncope). Measure serial BP and HR with the patient in the supine, sitting, and standing positions. First, measure BP and HR with the patient in the supine position after at least 2 to 3 minutes of rest. Reposition the patient in the sitting position with legs dangling and measure BP and HR again within 1 to 2 minutes. Last, reposition the patient to the standing position and measure the BP and HR within 1 to 2 minutes. Usually the SBP decreases slightly (less than 10 mm Hg) on standing, whereas the DBP and pulse increase slightly. Orthostatic hypotension occurs when a patient moves from a supine to standing position and there is a decrease of 20 mm Hg or more in SBP, a decrease of 10 mm Hg or more in DBP, and/or an increase in the heart rate of 20 beats/min. Common causes of orthostatic hypotension include dehydration and inadequate vasoconstrictor mechanisms related to disease or drugs.

Coronary Artery Disease (CAD)

Atherosclerosis - Begins as soft deposits of fat that harden with age - Referred to as "hardening of arteries" - Atheromas (fatty deposits) prefer coronary arteries - Also known as ASHD, CVHD, IHD, CHD Coronary artery disease is a type of blood vessel disorder that is included in the general category of atherosclerosis. The term atherosclerosis comes from two Greek words: athere, meaning "fatty mush," and skleros, meaning "hard." This combination means that atherosclerosis begins as soft deposits of fat that harden with age. Consequently, it is common to refer to atherosclerosis as "hardening of the arteries." Although this disease can occur in any artery in the body, the atheromas (fatty deposits) prefer the coronary arteries. The terms arteriosclerotic heart disease, cardiovascular heart disease, ischemic heart disease, coronary heart disease, and CAD all describe this disease process.

Coronary Artery Disease Etiology and Pathophysiology

Atherosclerosis is major cause of CAD - Characterized by lipid deposits within intima of artery - Endothelial injury and inflammation play a major role in development Atherosclerosis is the major cause of CAD. - It is characterized by deposits of lipids within the intima of the artery. - Endothelial injury and inflammation play a central role in the development of atherosclerosis. C-reactive protein (CRP) - Nonspecific marker of inflammation - Increased in many patients with CAD C-reactive protein (CRP), a protein produced by the liver, is a nonspecific marker of inflammation. It is increased in many patients with CAD. The level of CRP rises when there is systemic inflammation. Collateral circulation - Arterial anastomoses (or connections) within coronary circulation - Increased with chronic ischemia Normally some arterial anastomoses or connections, called collateral circulation, exist within the coronary circulation. Two factors contribute to the growth and extent of collateral circulation: (1) inherited predisposition to develop new blood vessels (angiogenesis) and (2) presence of chronic ischemia. When plaque blocks the normal flow of blood through a coronary artery and the resulting ischemia is chronic, increased collateral circulation develops. When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of collateral circulation developing, and the heart muscle may still receive an adequate amount of blood and oxygen.

Factors Influencing BP

BP = CO x systemic vascular resistance The mechanisms that regulate BP can affect either CO or SVR, or both. Regulation of BP is a complex process involving both short-term (seconds to hours) and long-term (days to weeks) mechanisms. Short-term mechanisms, including the sympathetic nervous system (SNS) and vascular endothelium, are active within a few seconds. Long-term mechanisms include renal and hormonal processes that regulate arteriolar resistance and blood volume. In a healthy person, these regulatory mechanisms function in response to the demands of the body.

Nursing Diagnosis

Based upon your assessment, you develop nursing diagnoses for patients with oxygenation alterations by clustering specific defining characteristics and identifying the related etiology. The defining characteristics for diagnoses related to oxygenation can be similar. A closer review of assessment findings as well as an analysis of the patient's history will help you clarify and select the correct diagnosis. The clustered defining characteristics and related factor must support the nursing diagnosis. Activity intolerance Impaired gas exchange Risk for aspiration Decreased cardiac output Impaired verbal communication Ineffective breathing pattern Fatigue Ineffective airway clearance Ineffective health maintenance

Chronic HF Nursing Intervention

Basic principles of care HF is a progressive disease: establish treatment plans and quality-of-life goals - Many persons with HF will experience one or more episodes of ADHF. When they do, they are usually admitted through the ED, first stabilized, and then cared for in an ICU, an intermediate care unit, or a specialized HF unit with continuous ECG monitoring capability. Use of self-management tools for symptom management - Successful HF care depends on several important principles: (1) HF is a progressive disease, and treatment plans are established along with quality of life goals; (2) symptom management is controlled by the patient with self-management tools (e.g., daily weights, drug regimens, diet, and exercise plans); (3) salt and, at times, water must be restricted; (4) energy must be conserved; and (5) support systems are essential to the success of the entire treatment plan. Restrict salt (and water at times) Conserve energy - Reduction of anxiety is an important nursing function, since anxiety may increase the SNS response and further increase myocardial workload. Reducing anxiety may be facilitated by a variety of nursing interventions and the use of sedatives (e.g., benzodiazepines, morphine sulfate). Maintain support systems - The Joint Commission has selected three core measures in the management of patients with HF to reflect standards of evidence-based care. The AHA has developed a program, Get With The Guidelines-Heart Failure, to improve adherence to standards of evidence-based care of patients hospitalized with HF. Together, these approaches work to ensure high-quality care for patients with HF. Monitor respiratory status - Monitor pulse oxymetry, respiratory rate, rhythm, depth, and effort of respirations to evaluate changes in respiratory status. - Auscultate breath sounds, noting areas of decreased/absent ventilation and presence of adventitious sounds to detect presence of pulmonary edema. - Monitor for increased restlessness, anxiety, and work of breathing to detect increasing hypoxemia. Administer oxygen therapy - Administer supplemental O2 or other noninvasive ventilator support (e.g., bilevel positive airway pressure [BiPAP]) as needed to maintain adequate O2 levels. - Monitor the O2 liter flow rate and position of O2 delivery device to ensure O2 is adequately delivered. - Change O2 delivery device from mask to nasal prongs during meals as tolerated to sustain O2 levels while eating. - Monitor the effectiveness of O2 therapy to identify hypoxemia and establish range of O2 saturation. Semi-Fowler's position - Position to alleviate dyspnea (e.g., semi-Fowler's position), as appropriate, to improve ventilation by decreasing venous return to the heart and increasing thoracic capacity. Monitor hemodynamic status - Perform a comprehensive assessment of peripheral circulation (e.g., check peripheral pulses, edema, capillary refill, color, and temperature of extremity) to determine circulatory status. - Note signs and symptoms of decreased cardiac output (e.g., chest pain, S3, S4, jugular vein distention) to detect changes in status. - Continuously monitor cardiac rhythm to detect dysrhythmias. Daily weights I and O - Monitor fluid balance (e.g., I/O and daily weight) to evaluate renal perfusion. Administer prescribed drugs - Administer prescribed diuretics, as appropriate, to treat hypervolemia. Monitor edema - Monitor for therapeutic effect of diuretic (e.g., increased urine output, decreased CVP/PCWP, and decreased adventitious breath sounds) to assess response to treatment. - Monitor potassium levels after diuresis to detect excessive electrolyte loss. - Monitor changes in peripheral edema to assess response to treatment. Alternate rest with activity - Encourage alternate rest and activity periods to reduce cardiac workload and conserve energy. Provide diversionary activities - Provide calming diversionary activities to promote relaxation to reduce O2 consumption and to relieve dyspnea and fatigue. Monitor response to activity - Monitor patient's O2 response (e.g., pulse rate, cardiac rhythm, and respiratory rate) to self-care or nursing activities to determine the level of activity that can be performed. Collaborate with OT/PT - Collaborate with occupational and/or physical therapists to plan and monitor activity/exercise program. Reduce anxiety - Instruct patient and caregivers on activity restriction and progression to allay fears and anxiety. Evaluate support system - Establish a supportive relationship with the patient and caregiver(s) to promote adherence with the treatment plan. - Evaluate and encourage use of support systems. Patient teaching - Teach patient and caregiver techniques of self-care that will minimize O2 consumption (e.g., self-monitoring and pacing techniques for performance of ADLs). - Inform the patient of the purpose for and benefits of the prescribed activity/exercise.

Factors Influencing BP

Blood Pressure = cardiac output x systemic vascular resistance Blood pressure (BP), the force exerted by the blood against the walls of the blood vessel, is primarily a function of cardiac output (CO) and systemic vascular resistance. CO is the total blood flow through the systemic or pulmonary circulation per minute. It is described as the stroke volume (SV)(amount of blood pumped out of the left ventricle per beat [approximately 70 pum]) multiplied by the heart rate (HR). Systemic vascular resistance is the force opposing the movement of blood within the blood vessels. The radius of the small arteries and arterioles is the principal factor determining SVR. As arteries narrow, resistance to blood flow increases. As arteries dilate, resistance to blood flow decreases. A small change in the radius of the arterioles creates a major change in the SVR. If SVR is increased and CO remains constant or increases, arterial BP will increase. BP must be adequate to maintain tissue perfusion during activity and rest. The maintenance of normal BP and tissue perfusion requires the integration of both systemic factors and local peripheral vascular effects.

Left-Sided Heart Failure

Blood backs up into left atrium and pulmonary veins Increased pulmonary pressure causes fluid leakage →→ pulmonary congestion and edema Left-sided HF results from left ventricular dysfunction. This prevents normal, forward blood flow and causes blood to back up into the left atrium and pulmonary veins. The increased pulmonary pressure causes fluid leakage from the pulmonary capillary bed into the interstitium and then the alveoli. This manifests as pulmonary congestion and edema.

Structures and Functions of Cardiovascular System

Blood pressure - The arterial blood pressure is a measure of the pressure exerted by blood against the walls of the arterial system. Systolic blood pressure (SBP) - < 120 mm Hg - The systolic blood pressure (SBP) is the peak pressure exerted against the arteries when the heart contracts. Diastolic blood pressure (DBP) - < 80 mm Hg - The diastolic blood pressure (DBP) is the residual pressure in the arterial system during ventricular relaxation (or filling). BP is usually expressed as the ratio of systolic to diastolic pressure. BP = CO x SVR - The two main factors influencing BP are CO and systemic vascular resistance (SVR): - SVR is the force opposing the movement of blood. This force is created primarily in small arteries and arterioles. - Normal blood pressure is SBP less than or equal to 120 mm Hg and DBP less than or equal to 80 mm Hg.

Chronic Stable Angina Nursing/ Interprofessional Care

Cardiac catheterization/coronary angiography - For patients with increasing angina a cardiac catheterization is ordered. Cardiac catheterization and coronary angiography use radiation and IV contrast dye to provide images of the coronary circulation and identify the location and severity of any blockage. - If a patient is allergic to IV contrast dye, they must be premedicated with corticosteroids. Patients with chronic kidney disease need hydration pre- and post-procedure. A baseline serum creatinine level is obtained because the IV contrast dye can worsen renal function. Monitor renal function closely after the procedure. This procedure should only be done if the patient is a candidate for percutaneous or surgical coronary revascularization. 1. Visualize blockages (diagnostic) 2. Open blockages (interventional) - Percutaneous coronary intervention (PCI) (If a coronary blockage is amenable to treatment, coronary revascularization with an elective percutaneous coronary intervention (PCI) may be recommended.) - Balloon angioplasty (During PCI, a catheter with a deflated balloon tip is inserted into the appropriate coronary artery. The deflated balloon is positioned in the blockage and inflated. This compresses the plaque against the artery wall, resulting in vessel dilation and a larger vessel diameter. This procedure is called balloon angioplasty.) - Stent (Intracoronary stents are usually placed along with balloon angioplasty.)

Blood Flow Regulation

Cardiac output - Amount of blood ejected from the left ventricle each minute - Cardiac output (CO) = - Normal cardiac output is 4 to 6 L/min in the healthy adult at rest. - The circulating volume of blood changes according to the oxygen and metabolic needs of the body. Stroke volume Amount of blood ejected from the left ventricle with each contraction - Stroke volume (SV) × Heart rate (HR) - Stroke volume is affected by preload, afterload, and myocardial contractility all affect stroke volume. Preload - Preload is the amount of blood in the left ventricle at the end of diastole, often referred to as end-diastolic volume. - The ventricles stretch when filling with blood. The more stretch on the ventricular muscle, the greater the contraction and the greater the stroke volume (Starling's law). - In certain clinical situations, medical treatment alters preload and subsequent stroke volumes by changing the amount of circulating blood volume. - If volume is not replaced, preload, stroke volume and the subsequent cardiac output decreases. After load - Afterload is the resistance to left ventricular ejection. - The heart works harder to overcome the resistance so blood can be fully ejected from the left ventricle. - The diastolic aortic pressure is a good clinical measure of afterload. - In hypertension the afterload increases, making cardiac workload also increase. Contractility - Myocardial contractility also affects stroke volume and cardiac output. Poor ventricular contraction decreases the amount of blood ejected. Injury to the myocardial muscle such as an acute MI causes a decrease in myocardial contractility. The myocardium of the older adult is stiffer with a slower ventricular filling rate and prolonged contraction time. Heart rate affects blood flow because of the relationship between rate and diastolic filling time. With a sustained heart rate greater than 160 beats/min, diastolic filling time decreases, decreasing stroke volume and cardiac output. The heart rate of the older adult is slow to increase under stress, but studies have found that this may be caused more by lack of conditioning than age. Exercise is beneficial in maintaining function at any age.

Cardiovascular Physiology

Cardiopulmonary physiology involves delivery of deoxygenated blood (blood high in carbon dioxide and low in oxygen) to the right side of the heart and then to the lungs, where it is oxygenated. Oxygenated blood (blood high in oxygen and low in carbon dioxide) then travels from the lungs to the left side of the heart and the tissues. The cardiac system delivers oxygen, nutrients, and other substances to the tissues and facilitates the removal of cellular metabolism waste products by way of blood flow through other body systems such as respiratory, digestive, and renal.

Restorative and Continuing Care

Cardiopulmonary rehabilitation - Controlled physical exercise; nutrition counseling; relaxation and stress management; medications; oxygen; compliance; systemic hydration Cardiopulmonary rehabilitation helps patients achieve and maintain an optimal level of health through controlled physical exercise, nutrition counseling, relaxation and stress-management techniques, and prescribed medications and oxygen. - As physical reconditioning occurs, a patient's complaints of dyspnea, chest pain, fatigue, and activity intolerance decrease. In addition, the patient's anxiety, depression, or somatic concerns often decrease. - The patient and the rehabilitation team define the goals of rehabilitation.

Restoration of Cardiopulmonary Functioning

Cardiopulmonary resuscitation (CPR) 1. Circulation 2. Airway 3. Breathing - Defibrillation (automatic external defibrillator [AED]) If a patient's hypoxia is severe and prolonged, cardiac arrest results. A cardiac arrest is a sudden cessation of cardiac output and circulation. When this occurs, oxygen is not delivered to tissues, carbon dioxide is not transported from tissues, tissue metabolism becomes anaerobic, and metabolic and respiratory acidosis occurs. Permanent heart, brain, and other tissue damage occur within 4 to 6 minutes. The previous ABC (establish an Airway, initiate Breathing, and maintain Circulation) of cardiopulmonary resuscitation (CPR) is changed to CAB (Chest compression, Airway, Breathing) for adults and pediatric patients (excluding newborns). - In adults (the majority of cardiac arrests) the critical initial elements found to be essential for survival were chest compressions and early defibrillation. - Ventilation is done after the first cycle of 30 chest compressions. In addition, the American Heart Association (AHA) (2014) has set a goal for hospitals to deliver the first electrical shock to patients in ventricular fibrillation in less than 2 minutes. Defibrillation by automatic external defibrillator (AED) is needed to stop an abnormal heart rhythm, and AEDs are now available in public places such as schools, airports, and workplaces.

Clinical Manifestations of CAD Angina

Chronic and progressive disease O2 demand > O2 supply → myocardial ischemia Angina = clinical manifestation - Occurs when arteries are blocked 70% or more - 50% or more for left main coronary artery CAD is a chronic and progressive disease. Patients may be asymptomatic for many years or they may develop chronic stable chest pain. When the demand for myocardial oxygen exceeds the ability of the coronary arteries to supply the heart with oxygen, myocardial ischemia occurs. Angina, or chest pain, is the clinical manifestation of myocardial ischemia. It is caused by either an increased demand for oxygen or a decreased supply of oxygen. The most common reason for angina to develop is narrowing of one or more coronary arteries by atherosclerosis. This leads to insufficient blood flow to the heart muscle. For ischemia secondary to atherosclerotic plaque to occur, the artery is usually blocked (stenosed) 70% or more (50% or more for the left main coronary artery)

Heart Failure

Complex clinical syndrome resulting in insufficient blood supply/oxygen to tissues and organs - Involves diastolic or systolic dysfunction - Ejection fraction (EF) is amount of blood pumped by LV with each heart beat (The amount of blood pumped by the left ventricle with each heart beat is called the ejection fraction (EF). The American Academy of Cardiology Foundation (ACCF) has adopted the terms heart failure with reduced EF (HFrEF) and heart failure with preserved EF (HFpEF) to describe systolic and diastolic HF.) Heart failure (HF) is a complex clinical syndrome that results in the inability of the heart to provide sufficient blood to meet the oxygen needs of tissues and organs. It is a major health problem in the United States. A defect in either ventricular filling (diastolic dysfunction) or ventricular ejection (systolic dysfunction) are the key manifestations of HF. Associated with CVDs - HF is associated with numerous types of cardiovascular diseases (CVDs), particularly long-standing hypertension, coronary artery disease (CAD), and myocardial infarction (MI). ↑ In incidence and prevalence - Better survival after cardiac events - Aging population (In contrast to other CVDs, HF is increasing in incidence and prevalence. This is due in part to better survival after cardiac events and the aging population.) (HF is primarily a disease of older adults. The incidence is similar in men and women) (HF is the most common reason for hospital admission in adults over the age of 65.) - Costly (This places a significant economic burden on the health care system.) Most common cause for hospital admission in adults over age 65 - The complex, progressive nature of HF often results in poor outcomes, the most costly being hospital readmissions. - Approximately 25% of patients discharged with a primary diagnosis of HF are readmitted within 30 days. The total cost of HF care in the United States exceeds $40 billion annually, with over half of these costs spent on hospitalizations. The American Heart Association (AHA) estimates that over 650,000 new cases are diagnosed each year.

Chronic Heart Failure Clinical Manifestations

Dependent on age, underlying type and extent of heart disease, and which ventricle is affected - Chronic HF is characterized as progressive worsening of ventricular function and chronic neurohormonal activation that result in ventricular remodeling. This process involves changes in the size, shape, and mechanical performance of the ventricle. - The clinical manifestations of chronic HF depend on the patient's age, underlying type and extent of heart disease, and which ventricle is failing to pump effectively. FACES - Fatigue - Limitation of Activities - Chest congestion/cough - Edema - Shortness of breath The Heart Failure Society of America (HFSA) developed the acronym, FACES (fatigue, limitation of activities, chest congestion/cough, edema, and shortness of breath) to help educate patients on identifying HF symptoms. Fatigue - Fatigue is one of the earliest symptoms of chronic HF. The patient notes fatigue after usual activities and eventually limits these activities. The fatigue is caused by decreased CO, impaired perfusion to vital organs, decreased oxygenation of the tissues, and anemia. Anemia can result from poor nutrition, renal disease, or drug therapy (e.g., angiotensin-converting enzyme [ACE] inhibitors). Dyspnea - Dyspnea is a common manifestation of chronic HF. It is caused by increased pulmonary pressures secondary to interstitial and alveolar edema. Dyspnea can occur with mild exertion or at rest. Orthopnea - often accompanies dyspnea. Careful questioning of patients often reveals adaptive behaviors, such as sleeping with two or more pillows or in a chair to aid breathing. Paroxysmal nocturnal dyspnea - (PND) occurs when the patient is asleep. The patient awakes in a panic, has feelings of suffocation, and a strong desire to sit or stand up. PND is caused by the reabsorption of fluid from dependent body areas when the patient is flat. A cough is often associated with HF and may be the first clinical symptom. It begins as a dry, nonproductive cough and may be misdiagnosed as asthma or other lung disease. The cough is not relieved by position change or over-the-counter cough medicine. Tachycardia - Tachycardia is an early clinical sign of HF. One of the body's first responses to compensate for a failing heart is to increase the HR via activation of the SNS. This works to increase CO. Initially this response is favorable, but over time, persistent tachycardia is harmful and may exacerbate HF. Adequate HR control in patients with chronic HF has been associated with better clinical outcomes, including decreased hospitalizations and mortality. Edema - Dependent, liver, abdominal cavity, lungs - Edema may be pitting in nature - Sudden weight gain of >3 lb (1.4 kg) in 2 days may indicate ADHF, an exacerbation of chronic HF - Edema is a common sign of HF. It may occur in dependent body areas (peripheral edema), liver (hepatomegaly), abdominal cavity (ascites), and lungs (pulmonary edema and pleural effusion). If the patient is in bed, sacral and scrotal edema may develop. Pressing the edematous skin with the finger may leave a transient depression (pitting edema). The development of dependent edema or a sudden weight gain of more than 3 lb (1.4 kg) in 2 days is often a sign of ADHF. It is important to note that not all lower extremity edema is a result of HF. Hypoproteinemia, immobility, venous insufficiency, and certain drugs can cause peripheral edema. Nocturia - Nocturia is the tendency to urinate excessively during the night. Chronic HF is frequently associated with poor renal perfusion and function. Patients develop increased peripheral and systemic edema. At night when lying flat, extravascular fluid is reabsorbed from the interstitial spaces back into the circulatory system. This results in increased perfusion to the kidneys. The increased renal blood flow results in diuresis. The patient may complain of having to urinate frequently throughout the night. Skin changes - Because tissue capillary oxygen extraction is increased in a person with chronic HF, the skin may appear dusky. Often the lower extremities are shiny and swollen, with diminished or absent hair growth. Chronic swelling may result in pigment changes. This causes the skin to appear brown or brawny in areas covering the ankles and lower legs. Behavioral changes - Cerebral circulation may be reduced with chronic HF secondary to decreased CO. The patient or caregiver may report unusual behavior, including restlessness, confusion, and decreased attention span or memory. This may also be secondary to poor gas exchange and worsening HF. It is often seen in the late stages of HF. Co-existing psychologic disorders, especially depression and anxiety, contribute a two-fold risk of mortality and higher readmission rates and health care costs in patients with HF. Approximately 1 in 5 patients with HF have clinical depression. In addition, patients with psychologic disorders have poorer adherence to treatment plans. Assess patients with HF for depression and anxiety and, if needed, initiate appropriate consults. Chest pain - HF can precipitate chest pain (angina) due to decreased coronary artery perfusion from decreased CO and increased myocardial work. Chest pain may accompany either ADHF or chronic HF. Weight changes - Many factors contribute to weight changes. First there may be a progressive weight gain from fluid retention. Renal failure may also contribute to fluid retention. Abdominal fullness from ascites and hepatomegaly frequently causes anorexia and nausea. As HF advances, the patient may have cardiac cachexia with muscle wasting and fat loss. This can be masked by the patient's edematous condition and may not be seen until after the edema subsides.

Alterations in Cardiac Functioning

Disturbances in conduction - Electrical impulses that do not originate from the SA node cause conduction disturbances - Dysrhythmias - Atrial fibrillation - Paroxysmal supraventricular tachycardia - Ventricular dysrhythmias - Illnesses and conditions that affect cardiac rate and rhythm, strength of contraction, and blood flow through the chamber and peripheral circulation will cause altered cardiac functioning. - Older adults experience alterations in cardiac function as a result of calcification of the conduction pathways, thicker and stiffer heart valves caused by lipid accumulation and fibrosis, and a decrease in the number of pacemaker cells in the SA node. - Rhythm disturbances are called dysrhythmias, meaning a deviation from the normal sinus heart rhythm. Dysrhythmias occur as a primary conduction disturbance such as in response to ischemia; valvular abnormality; anxiety; drug toxicity; caffeine, alcohol, or tobacco use; or as a complication of acid-base or electrolyte imbalance. - Dysrhythmias are classified by cardiac response and site of impulse origin. 1. Cardiac response is tachycardia (greater than 100 beats/min), bradycardia (less than 60 beats/min), a premature (early) beat, or a blocked (delayed or absent) beat. 2. Tachydysrhythmias and bradydysrhythmias lower cardiac output and blood pressure. Tachydysrhythmias reduce cardiac output by decreasing diastolic filling time. 3. Bradydysrhythmias lower cardiac output because of the decreased heart rate. 4. Atrial fibrillation is a common dysrhythmia in older adults. - Abnormal impulses originating above the ventricles are supraventricular dysrhythmias. The abnormality on the waveform is the configuration and placement of the P wave. Ventricular conduction usually remains normal, and there is a normal QRS complex. - Paroxysmal supraventricular tachycardia is a sudden, rapid onset of tachycardia originating above the AV node. 1. It often begins and ends spontaneously. Sometimes excitement, fatigue, caffeine, smoking, or alcohol use precipitates paroxysmal supraventricular tachycardia. - Ventricular dysrhythmias represent an ectopic site of impulse formation within the ventricles. 1. It is ectopic in that the impulse originates in the ventricle, not the SA node. 2. The configuration of the QRS complex is usually widened and bizarre. P waves are not always present; often they are buried in the QRS complex. 33. Ventricular tachycardia and ventricular fibrillation are life-threatening rhythms that require immediate intervention. Ventricular tachycardia is a life-threatening dysrhythmia because of the decreased cardiac output and the potential to deteriorate into ventricular fibrillation or sudden cardiac death.

Chronic HF Drug Therapy

Diuretics - Reduce edema, pulmonary venous pressure, and preload (Diuretics are used to reduce edema, pulmonary venous pressure, and preload. If excess extracellular fluid is removed, blood volume returning to the heart can be reduced and cardiac function improved.) - Promote sodium and water excretion (Diuretics act on the kidney by promoting excretion of sodium and water. Many varieties of diuretics are available. Loop diuretics (e.g., bumetanide [Bumex]) are potent diuretics. These drugs act on the ascending loop of Henle to promote sodium, chloride, and water excretion. Problems in using loop diuretics include reduction in serum potassium levels, ototoxicity, and possible allergic reaction in patients sensitive to sulfa-type drugs.) - Loop diuretics - Thiazide diuretics (Thiazide diuretics inhibit sodium reabsorption in the distal tubule, thus promoting excretion of sodium and water. They can be added to loop diuretics to obtain results if patients become resistant to loop diuretics. Thiazide diuretics also can cause severe reductions in potassium levels.) - Monitor potassium levels (hypokalemia) (Diuretics are effective in relieving the congestive symptoms of HF. However, their use does activate the SNS and RAAS, which can exacerbate the HF syndrome. In chronic HF, the lowest effective dose of diuretic should be used.) RAAS inhibitors - ACE inhibitors - Angiotensin II receptor blockers - Aldosterone antagonists - Monitor potassium levels (hyperkalemia) Angiotensin-Converting Enzyme Inhibitors - ACE inhibitors are the primary drug of choice for blocking the RAAS system in HF patients with systolic failure. - The conversion of angiotensin I to the potent vasoconstrictor angiotensin II needs ACE. ACE inhibitors block this enzyme, resulting in reduced levels of angiotensin II. - The end result of the neurohormonal blockade is decreased plasma aldosterone levels, decreased SNS activity, vasodilation, and sodium and water excretion. - ACE inhibitors also decrease the development of ventricular remodeling by inhibiting ventricular hypertrophy. - These drugs can cause symptomatic hypotension, intractable cough, hyperkalemia, angioedema (allergic reaction involving edema of the face and airways), and renal insufficiency (high doses of ACE inhibitors). Angiotensin II Receptor Blockers - For patients who are unable to tolerate ACE inhibitors, angiotensin II receptor blockers (ARBs) are recommended. These agents prevent the vasoconstrictor and aldosterone-secreting effects of angiotensin II by binding to the angiotensin II receptor sites. Aldosterone Antagonists - Spironolactone (Aldactone) and eplerenone (Inspra) are aldosterone antagonists. - They block the harmful neurohormonal effects of aldosterone on the heart blood vessels. - Aldosterone antagonists may prolong survival in patients with HFrEF. - They are also potassium-sparing diuretics that promote sodium and water excretion while retaining potassium. - These effects occur because these agents bind to receptors at the aldosterone-dependent sodium-potassium exchange site in the distal renal tubule. β-Blockers - Β-Blockers directly block the negative effects of the SNS (e.g., increased heart rate) on the failing heart. 1. Vasodilators - Nitrates (Nitrates cause vasodilation by acting directly on the smooth muscle of the vessel wall. Nitrates are of particular benefit in the management of myocardial ischemia related to HF because they promote vasodilation of the coronary arteries.) 2. Combination therapy - BiDil (Combination therapy with hydralazine and isosorbide dinitrate (Bidil) may be helpful in African American patients with HF who are getting optimal therapy with ACE inhibitors and β-blockers. The same benefit is not found in white patients. The combination of the two drugs is also associated with a significant improvement in LV EF and exercise tolerance. Although the evidence of benefit is stronger in African American patients, the combination therapy may be used in patients of other races who are already on optimal therapy.) 3. Positive inotropic agents - Digitalis (Digitalis preparations (e.g., digoxin [Lanoxin]) increase the force of cardiac contraction (inotropic action).) Inhibitor of cardiac sinus node 1. Ivabradine (Corlanor) - Ivabradine (Corlanor) is new category of oral drug that inhibits the sinus node and reduces HR. It is used for patients who have symptoms of chronic HF. They must be in sinus rhythm with a resting HR of at least 70 beats per minute and taking β-blockers at the highest dose tolerated. Ivabradine also reduces the risk of hospitalization for worsening HF. - The most common side effects of ivabradine include symptomatic bradycardia, high BP, atrial fibrillation, and vision disturbance (i.e., flashes of light). Tell patients to call their HCP if they experience symptoms of an irregular HR, feel that the heart is pounding or racing, have chest pressure, or worsened dyspnea. Low HR is a common side effect of ivabradine and can be serious. Patients should tell their HCP if they have experience dizziness, weakness, or fatigue. 2. Must be in sinus rhythm with resting HR of > 70 bpm and taking highest dose β-blockers - Inhibits sinus node - Reduces HR - Decreases risk of hospitalization for worsening HF

Diagnostic Studies of Cardiovascular System

Echocardiogram - Ultrasound of heart - With or without contrast - Provides information regarding structures and motion of heart - Measures ejection fraction (EJ) - Stress echocardiography - Transesophageal echo (TEE) The echocardiogram uses ultrasound (US) waves to record the movement of the structures of the heart. In the normal heart, US waves directed at the heart are reflected back in typical patterns. A contrast echocardiography involves the addition of an IV contrast agent (e.g., agitated saline) to assist in defining the images, especially in technically difficult patients (e.g., obese). The echocardiogram provides information about abnormalities of (1) valvular structures and motion, (2) heart chamber size and contents, (3) ventricular and septal motion and thickness, (4) pericardial sac, and (5) ascending aorta. The ejection fraction (EF) or the percentage of end-diastolic blood volume that is ejected during systole can also be measured. The EF provides information about the function of the left ventricle during systole. Stress echocardiography, a combination of treadmill test or pharmacologic test and US images, evaluates wall motion abnormalities. This test combines the information from a stress test with the information from an echocardiogram. For those individuals unable to exercise, an IV drug (e.g., dobutamine [Dobutrex], dipyridamole [Persantine]) is used to produce pharmacologic stress on the heart while the patient is at rest. Transesophageal echocardiography (TEE) provides more precise echocardiography of the heart than surface 2-D echocardiography by removing interference from the chest wall and lungs. The TEE uses a flexible endoscope with an US transducer in the tip for imaging of the heart and great vessels. The scope is passed into the esophagus to the level of the heart, and M-mode, 2-D, Doppler, and color-flow imaging can be obtained. TEE is contraindicated if the patient has a history of esophageal disorders, dysphagia, or radiation therapy to the chest wall. Patients will require sedation during a TEE.

Diagnostic Studies of Cardiovascular System

Electrocardiogram - Resting ECG - Ambulatory ECG monitoring - Event monitor or loop recorder - Exercise or stress testing Electrocardiogram - The basic P, QRS, and T waveforms are used to assess heart activity. Deviations from the normal sinus rhythm can indicate problems in heart function. - There are many types of electrocardiographic monitoring, including a resting 12-lead ECG, ambulatory ECG monitoring, and exercise or stress testing. - Continuous ambulatory ECG (Holter monitoring) can provide diagnostic information over a greater period of time than a resting 12-lead ECG. - An event monitor or loop recorder is used to record less frequent ECG events. An event monitor is a portable unit that uses electrodes to store ECG data once triggered by the patient. A disadvantage of this type of monitoring is that if symptoms occur for only a brief time, they may be over before the patient puts on the device and triggers it to record. Likewise, if patients are extremely symptomatic (e.g., syncopal), they may not be physically able to trigger the ECG recording. - An implantable loop recorder is used for patients who are suspected to have serious yet rare dysrhythmias. This small recorder is implanted though a small incision into the chest wall. It is activated to record either by the patient through a remote device or automatically if the heart rate exceeds or goes below a set rate. - External loop recorders are worn for a month and require electrodes continually placed on the skin. This device only records when activated by the patient when symptoms occur. - Heart symptoms frequently occur only with activity due to the demand on the coronary arteries to provide more oxygen. Exercise testing is used to evaluate the heart's response to physical stress. - This helps to assess CVD and set limits for exercise programs. Exercise testing is used for individuals who are able to walk unassisted or use a bicycle.

Chronic HF Ambulatory Care

Explain to patient and caregiver physiologic changes that have occurred Assist patient to adapt to both physiologic and psychologic changes Include patient and caregiver(s) in overall care plan HF is a chronic illness. When a patient is diagnosed with HF, care should focus on slowing the progression of the disease. Your important nursing responsibilities include (1) teaching the patient about the physiologic changes that have occurred, (2) assisting the patient to adapt to both the physiologic and psychologic changes, and (3) including the patient and the caregiver in the overall care plan.

Resistant Hypertension

Failure to reach goal BP in patients taking full doses of an appropriate 3-drug therapy regimen that includes a diuretic. Reasons include - Improper BP measurement - Drug-induced - Associated conditions - Identifiable causes of secondary hypertension Carefully explore all reasons why a patient may not be at goal BP. Resistant hypertension is the failure to reach goal BP in patients who are taking full doses of an appropriate three-drug therapy regimen that includes a diuretic. Overactive renal nerves can be one cause of resistant hypertension. Percutaneous catheter-based radiofrequency ablation of the renal nerves (known as renal denervation) lowers BP and sympathetic nerve activity in patients with resistant hypertension.

Hypertension Drug Therapy and Patient Teaching

Follow-up care Identify, report, and minimize side effects - Orthostatic hypotension - Sexual dysfunction - Dry mouth - Frequent urination Time of day to take drug Once antihypertensive therapy is started, patients should return for follow-up and adjustment of drugs at monthly intervals until the goal BP is reached. More frequent visits are necessary for patients with stage 2 hypertension or with co-morbidities. After BP is at goal and stable, follow-up visits can usually be at 3- to 6-month intervals. Side effects of antihypertensive drugs are common and may be so severe or undesirable that the patient does not adhere to the therapy. Patient and caregiver teaching related to drug therapy may help the patient comply with therapy. Side effects may be an initial response to a drug and may decrease over time. Telling the patient about side effects that may decrease with time may help the person to continue taking the drug. The number or severity of side effects may relate to the dose. It may be necessary to change the drug or decrease the dosage. A common side effect of several of the antihypertensive drugs is orthostatic hypotension. This condition results from an alteration of the autonomic nervous system's mechanisms for regulating BP, which are needed for position changes. Consequently, the patient may feel dizzy and faint when assuming an upright position after sitting or lying down. Sexual problems may occur with many of the antihypertensive drugs. - This can be a major reason that patients do not comply with the treatment plan. Problems can range from reduced libido to erectile dysfunction. Rather than discussing a sexual problem with a HCP, the patient may decide just to stop taking the drug. Diuretics cause dry mouth and frequent voiding. Sugarless gum or hard candy may help ease dry mouth. Taking diuretics earlier in the day may limit frequent voiding during the night and preserve sleep. Advise the patient to report all side effects to the health care provider who prescribes the drug.

Primary Hypertension Pathophysiology

Genetic links - Different sets of genes regulate BP at different times - Children and siblings of persons with hypertension should be screened and strongly advised to adopt healthy lifestyles to reduce their risk of hypertension Genetic Links - Different sets of genes may regulate BP at different times throughout the life span. - Genetic variations are associated with the development of hypertension. - For example, genetic abnormalities have been associated with a rare form of hypertension characterized by excess levels of potassium. - Several genetic variants of substances on the endothelium affect BP and the development of hypertension by influencing the body's sensitivity to salt. When endothelial surface proteins are activated, proinflammatory properties are stimulated. This impairs the endothelial cells' ability to activate vasodilatory effects, which leads to hypertension. - More research is needed to understand the connection among genetics, endothelial function, and hypertension. In practice, children and siblings of persons with hypertension should be screened and strongly advised to adopt healthy lifestyles to reduce their risk of hypertension. Water and sodium retention Altered renin-angiotensin-aldosterone mechanism Stress and increased SNS activity Insulin resistance and hyperinsulinemia Endothelial dysfunction

Chronic Stable Angina Interprofessional Care

Goal: ↓ O2 demand and/or ↑ O2 supply Short-acting nitrates - Dilate peripheral and coronary blood vessels - Give sublingually or by spray - If no relief in 5 minutes, call EMS; if some relief ,repeat every 5 minutes for maximum 3 doses - Patient teaching - Can use prophylactically The treatment of chronic stable angina aims to decrease oxygen demand and/or increase oxygen supply. Short-acting nitrates are first-line therapy for the treatment of angina. Nitrates produce their principal effects by: 1. Dilating peripheral blood vessels. This results in decreased SVR, venous pooling, and decreased venous blood return to the heart (preload). Therefore myocardial oxygen demand is decreased because of the reduced cardiac workload. 2. Dilating coronary arteries and collateral vessels. This may increase blood flow to the ischemic areas of the heart. However, when the coronary arteries are severely atherosclerotic, coronary dilation is difficult to achieve SL NTG or translingual spray (Nitrolingual) will usually relieve pain in about 5 minutes and has a duration of approximately 30 to 40 minutes. The recommended dose of NTG is one tablet taken sublingually (SL) or one metered spray on the tongue for symptoms of angina. If symptoms are unchanged or worse after 5 minutes, the patient should contact the emergency medical services (EMS) system before taking additional NTG. If symptoms are significantly improved by one dose of NTG, instruct the patient or caregiver to repeat NTG every 5 minutes for a maximum of three doses and contact EMS if symptoms have not resolved completely. Instruct the patient in the proper use of NTG. It should be easily accessible to the patient at all times. The patient should store the tablets away from light and heat sources, including body heat, to protect from degradation. Tablets are packaged in dark, airtight containers to maintain potency. Once opened, the tablets tend to lose potency and should be replaced every 6 months. Tell the patient to sit down and place a NTG tablet under the tongue and allow it to dissolve. If using the spray, it should be directed on or under the tongue, not inhaled. SL NTG should cause a tingling sensation when administered; otherwise it may be outdated. Warn the patient that a headache, dizziness, or flushing may occur. Caution the patient to change positions slowly after NTG use because orthostatic hypotension may occur. Patients can use NTG prophylactically before undertaking an activity that is known to cause an angina. In these cases, the patient can take a tablet 5 to 10 minutes before beginning the activity. Tell the patient to report to the HCP any changes in the usual pattern of pain, especially increasing frequency or nighttime angina, or angina at rest. Long-acting nitrates - To reduce angina incidence - Main side effects: headache, orthostatic hypotension - Methods of administration - Oral - Nitroglycerin (NTG) ointment - Transdermal controlled-release NTG - Long-acting nitrates are used to reduce the frequency of anginal attacks. - The main side effect of all nitrates is headache from the dilation of cerebral blood vessels. Advise patients to take acetaminophen (Tylenol) to relieve the headache. Over time, the headaches may decrease but the antianginal effects are still present. - Orthostatic hypotension is a complication of all nitrates. You should monitor BP after the initial dose as the venous dilation that occurs may cause a drop in BP, especially in volume-depleted patients. Tolerance to long-acting NTG can develop. To limit this, patients are often scheduled a 10-14 hour nitrate-free period every day. Remind patients that taking a long-acting NTG preparation should not keep them from using transligual or SL NTG if angina develops. - Can be given orally, such as isosorbide dinitrate (Isordil) and isosorbide mononitrate (Imdur), - Nitropaste is a 2% NTG topical ointment dosed by the inch. It is placed on the upper body or arm, over a flat muscular area that is free of hair and scars. Once absorbed, it produces anginal prophylaxis for 3 to 6 hours. It is especially useful for nighttime and UA. The ointment should be wiped off to allow for a 10-14 hour nitrate free interval in order to prevent nitrate tolerance. - Currently two systems are available for transdermal NTG drug delivery: silicone gel and polymer matrix. These systems allow timed release of NTG over a 24-hour period. These preparations should also be removed in the evening to allow for a 10-14 hour nitrate free interval. Angiotensin-converting enzyme inhibitors (ACE) and angiotensin receptor blockers (ARBs) - Patients with chronic stable angina who have an ejection fraction [EF] of 40% or less, diabetes, hypertension, or chronic kidney disease should take an ACE inhibitor (e.g., lisinopril [Zestril]) indefinitely, unless contraindicated. Patients with chronic stable angina and a normal EF, diabetes, and one other CAD risk factor should also take an ACE inhibitor to decrease the risk of MI, stroke and death. - These drugs result in vasodilation and reduced blood volume. Most important, they can prevent or reverse ventricular remodeling in patients who have had an MI. For patients who are intolerant of ACE inhibitors (e.g. cough, angioedema), ARBs (e.g., losartan [Cozaar]) are used. β-Blockers - β-Blockers are ordered for relief of angina symptoms in patients with chronic stable angina. Patients who have LV dysfunction, elevated BP, or have had an MI should start and continue β-blockers indefinitely, unless contraindicated. These drugs decrease myocardial contractility, HR, SVR, and BP, all of which reduce the myocardial oxygen demand. β-Blockers that have been shown to reduce the risk of death in patients with LV dysfunction, heart failure (HF) or MI are carvedilol (Coreg), metoprolol (Lopressor, Toprol XL), and bisoprolol (Zebeta). - β-Blockers have many side effects and can be poorly tolerated. Side effects may include bradycardia, hypotension, wheezing from bronchospasm, and GI complaints. Many patients also complain of weight gain, depression, fatigue, and sexual dysfunction. Absolute contraindications to using β-blockers include severe bradycardia and acute HF. Patients with asthma should avoid β-blockers. They are used cautiously in patients with diabetes, since they mask signs of hypoglycemia. β-blockers should not be stopped abruptly without medical supervision as this may result in an increase in the number and intensity of angina attacks. - β-Blockers have many side effects and can be poorly tolerated. Side effects may include bradycardia, hypotension, wheezing from bronchospasm, and GI complaints. Many patients also complain of weight gain, depression, fatigue, and sexual dysfunction. Absolute contraindications to using β-blockers include severe bradycardia and acute HF. Patients with asthma should avoid β-blockers. They are used cautiously in patients with diabetes, since they mask signs of hypoglycemia. β-blockers should not be stopped abruptly without medical supervision as this may result in an increase in the number and intensity of angina attacks. Calcium channel blockers Lipid lowering drugs Diagnostic studies - Chest x-ray (After a detailed health history and physical examination, a chest x-ray is done to look for cardiac enlargement, aortic calcifications, and pulmonary congestion.) - 12-lead ECG (A 12-lead ECG is done and compared with a previous ECG whenever possible to look for any changes.) - Laboratory studies (Laboratory tests (e.g., lipid profile, C-reactive protein) are done to identify specific risk factors for CAD.) - Echocardiogram (An echocardiogram may be done to look for resting LV wall motion abnormalities, which may suggest evidence of CAD.) - Exercise stress test (An exercise stress test with or without echocardiography or nuclear imaging may be ordered. For patients with physical limitations in walking, a pharmacologic (adenosine [Adenocard] or dipyridamole [Persantine]) stress test with nuclear imaging, or a pharmacologic (dobutamine [Dobutrex]) stress echocardiogram may be ordered. Coronary blockages less than 70% are not usually detected with stress testing.) - EBCT (The electron beam computed tomography (EBCT) scan locates and measures coronary calcification. However, additional testing (e.g., stress testing or cardiac catheterization) is needed to further assess the impact of the lesion on coronary blood flow. Further studies are needed to determine the accuracy of the EBCT scan to diagnose high-grade blockages because many atherosclerotic plaques are not calcified) - CCTA (Coronary computed tomography angiography (CCTA) may be considered. Using IV contrast and radiation, CCTA can detect calcified and noncalcified plaques in the artery, as well as other heart conditions. Limitations of using CCTA include patients with rapid HRs (greater than 90 beats per minute), extensive coronary artery calcifications, obesity, and a history of prior coronary artery stent. Patients allergic to IV contrast dye must be premedicated with corticosteroids. Patients with chronic kidney disease need hydration pre- and post-procedure. A baseline serum creatinine level should be obtained as the IV contrast dye can worsen renal function.)

Assessment

In-depth history of a patient's normal and present cardiopulmonary function - Nursing assessment of cardiopulmonary functioning includes an in-depth history of a patient's normal and present cardiopulmonary function, past impairments in circulatory or respiratory functioning, and methods that a patient uses to optimize oxygenation. - The nursing history includes a review of drug, food, and other allergies. Past impairments in circulatory or respiratory functioning Methods that a patient uses to optimize oxygenation - Utilizing assessment values of pulse oximetry and capnography aide in the assessment of patients with spontaneous breathing, intubated patients, and those patients requiring oxygen therapy or mechanical ventilation. - Pulse oximetry provides an instant feedback about the patient's level of oxygenation. - Capnography, also known as end title CO2 monitoring, provides instant information about the patient's ventilation (how effectively CO2 is being eliminated by the pulmonary system), perfusion (how effectively CO2 is being transport through the vascular system), as well as how effectively CO2 is produced by cellular metabolism. Capnography is measured near the end of exhalation. Finally, a review of laboratory and diagnostic test results provides valuable assessment data. Review of drug, food, and other allergies Physical examination - - Physical examination of a patient's cardiopulmonary status reveals the extent of existing signs and symptoms. Laboratory and diagnostic tests

Age-Related Changes

Increased collagen, decreased elastin - With increased age, the amount of collagen in the heart increases, and elastin decreases. These changes affect the heart muscle's ability to stretch and contract. Decreased response to stress -One of the major changes in the cardiovascular system is the response to physical or emotional stress. In times of increased stress, there is a decrease in CO and SV due to reduced contractility and HR response. The resting supine HR is not markedly affected by aging. When the patient changes positions (e.g., sits upright), the sympathetic nerve pathway may be impacted by fibrous tissue and fatty deposits resulting in a blunted (reduced) HR response. Heart valves become thick and stiff - Heart valves become thicker and stiffer from lipid accumulation, degeneration of collagen, and fibrosis. The aortic and mitral valves are most frequently affected. These changes result in either regurgitation of blood when the valve should be closed or narrowing of the orifice of the valve (stenosis) when the valve should be open. The turbulent blood flow across the affected valve results in a murmur. Number of pacemaker cells decrease - The number of pacemaker cells in the SA node decreases with age. By age 75, a person may have only 10% of the normal number of pacemaker cells. This is compatible with adequate SA node function although it may account for the frequency of some sinus dysrhythmias in the older adult. Similar decreases also occur in the number of conduction cells in the internodal tracts, the bundle of His, and the bundle branches. These changes contribute to the development of atrial dysrhythmias and heart blocks. About 50% of older adults will have an abnormal resting ECG that shows increases in the PR, QRS, and/or QT intervals. Decreased number and function of β-adrenergic receptors - The autonomic nervous system control of the cardiovascular system changes with aging. The number and function of β-adrenergic receptors in the heart decrease with age. So, the older adult not only has a decreased response to physical and emotional stress but also is less sensitive to β-adrenergic agonist drugs. The lower maximum HR during exercise results in only a twofold increase in CO compared with the three or four times increase seen in younger adults. Blood vessels thicken and less elastic - Arterial and venous blood vessels thicken and become less elastic with age. - Arteries increase their sensitivity to vasopressin (antidiuretic hormone). Increase in SBP and decrease or no change in DBP - Both of these changes contribute to a progressive increase in SBP and a decrease or no change in DBP with age. Thus, an increase in the pulse pressure is found. Incompetent venous valves -Valves in the large veins in the lower extremities have a reduced ability to return the blood to the heart and may result in the development of dependent edema. Orthostatic hypotension - Orthostatic hypotension is estimated to be present in more than 30% of patients over age 70 with systolic hypertension and may be related to medications and/or decreased baroreceptor function. Postprandial hypotension - Postprandial hypotension (decrease in BP of at least 20 mm Hg that occurs within 75 minutes after eating) may also occur in about a third of otherwise healthy older adults. Both may be a source of falls in the older adult. Despite the changes associated with aging, the heart is able to function adequately under most circumstances.

Gerontologic Considerations CAD

Increased incidence and mortality associated with CAD in older adults - The incidence of heart disease is greatly increased in older adults and is the leading cause of death in older persons. Strategies to reduce risk and treat CAD are effective - Strategies to reduce CAD risk and to treat CAD are effective in this age-group. Treat hypertension, ↑ lipids - Aggressive treatment of hypertension and hyperlipidemia will stabilize plaques in the coronary arteries of older adults, and cessation of tobacco use helps decrease the risk for CAD at any age. Smoking cessation - - In the older adult, CAD is often a result of the complex interaction of nonmodifiable risk factors (e.g., age) and lifelong modifiable risk behaviors (e.g., inactivity, tobacco use). Necessary to modify guidelines for physical activity - Longer warm-up - Longer periods of low-level activity - Longer rest periods - Avoid extremes of temperature - 30 minutes most days minimum Most likely to change when hospitalized or symptomatic Similarly, you should encourage the older patient to consider a planned program of physical activity. Activity performance, endurance, and ability to tolerate stress are improved in the older adult with physical training. Positive psychologic benefits can be derived from physical activity and can include increased self-esteem and emotional well-being and improved body image. For the older adult who is obese, making modest dietary changes and slowly increasing physical activity (e.g., walking) will result in more positive benefits than aiming for a significant weight loss. When planning a physical activity program for the older adult, recommend the following: (1) longer warm-up periods, (2) longer periods of low-level activity, or (3) longer rest periods between sessions. Heat intolerance in the older adult results from a decreased ability to sweat efficiently. Teach the patient to avoid physical activity in extremes of temperature and to maintain a moderate pace. The older adult should exercise a minimum of 30 minutes on most days of the week as able. Encouraging the older patient to adopt a healthy lifestyle may increase the quality of life and reduce the risk of CAD and fatal heart events. The older adult faces many of the same challenges when it comes to making lifestyle changes. There are two points in time when the older adult is more likely to consider change: (1) when hospitalized and (2) when symptoms (e.g., chest pain) are the result of CAD and not normal aging. First, assess the older adult for readiness to change and health literacy. Then help the patient to select the lifestyle changes most likely to produce the greatest reduction in risk for CAD.

Hypertension in Older Persons

Increased incidence with age - The prevalence of hypertension increases with age. The lifetime risk of developing hypertension is approximately 90% for middle-aged (age 55 to 65) and older (age over 65) normotensive men and women. Isolated systolic hypertension (ISH): Most common form of hypertension in individuals age >50 Older adults are more likely to have "white coat" hypertension - Isolated systolic hypertension (ISH) is the most common form of hypertension in people over 50 years of age. Additionally, older adults are more likely to have white coat hypertension. Age-related physical changes contribute to hypertension -The following age-related physical changes play a role in the pathophysiology of hypertension in the older adult: (1) loss of elasticity in large arteries from atherosclerosis; (2) increased collagen content and stiffness of the myocardium; (3) increased peripheral vascular resistance; (4) decreased adrenergic receptor sensitivity; (5) blunting of baroreceptor reflexes; (6) decreased renal function; and (7) decreased renin response to sodium and water depletion. Altered drug absorption, metabolism, and excretion - In the older adult who is taking an antihypertensive drug, absorption of some drugs may be altered as a result of decreased blood flow to the gut. Metabolism and excretion of drugs may also be prolonged. Often a wide gap between first Korotkoff sound and subsequent beats is called auscultatory gap - Careful technique is important in assessing BP in older adults. In some older people, there is a wide gap between the first Korotkoff sound and subsequent beats. This is called the auscultatory gap. Failure to inflate the cuff high enough may result in underestimating SBP. ↑ Risk for orthostatic hypotension - Orthostatic hypotension often occurs in older adults because of varying degrees of impaired baroreceptor reflexes, especially in those with ISH. Orthostatic hypotension in this age-group is often associated with volume depletion or chronic disease states, such as decreased renal and hepatic function or electrolyte imbalance. To reduce the likelihood of orthostatic hypotension, antihypertensive drugs should be started at low doses and increased slowly. Measure BP and heart rate in the supine, sitting, and standing positions at every visit. Also postprandial hypotension - Older adults experience postprandial drops in BP. The greatest decrease occurs approximately 1 hour after eating. BP returns to preprandial levels 3 to 4 hours after eating. Avoid giving vasoactive drugs with meals. BP goal for people > 60 is < 150/90 - The JNC 8 recommends a BP goal less than 150/90 for people older than 60. Preferred antihypertensive drugs - Thiazide diuretic - Calcium channel blockers - ACE inhibitors or ARBs - Preferred first- line antihypertensive drugs are thiazide diuretic, calcium channel blockers, and/or ACE inhibitors or ARBs. - A diuretic should always be the first or second drug ordered for most patients. Caution use of NSAIDS - After CVD, arthritis is the second most prevalent disease in older adults. The most frequently taken drugs by older adults are nonsteroidal antiinflammatory drugs (NSAIDs), both prescription and over-the-counter. Nonselective NSAIDs (e.g., ibuprofen [Advil]) and selective NSAIDs (e.g., celecoxib [Celebrex]) cause loss of BP control and heart failure. Additionally, there is the potential for adverse renal effects and/or hyperkalemia when NSAIDs are used with ACE inhibitors, ARBs, or aldosterone antagonists.

Hypertension Nursing Diagnoses

Ineffective health management - Ineffective health management related to lack of knowledge of pathology, complications, and management of hypertension Anxiety - Anxiety related to complexity of management regimen Sexual dysfunction - Sexual dysfunction related to side effects of antihypertensive medication Risk for decreased cardiac perfusion - Risk for decreased cardiac tissue perfusion Risk for ineffective cerebral and renal perfusion - Risk for ineffective cerebral tissue perfusion - Risk for ineffective renal perfusion Potential complications: stroke, MI - Potential complication: stroke, MI

Compensatory Mechanisms

Neurohormonal response - Renin-angiotensin-aldosterone system - Sympathetic nervous system (SNS) Continued activation of compensatory mechanisms leads to increased workload on heart, ventricular dysfunction, and ventricular remodeling (i.e. hypertrophy and dilation)

Clinical Manifestations of CAD Chronic Stable Angina

Intermittent chest pain that occurs over a long period with same pattern of onset, duration, and intensity of symptoms Few minutes in duration ST segment depression and/or T-wave inversion Control with drugs Chronic stable angina refers to chest pain that occurs intermittently over a long period of time with a similar pattern of onset, duration, and intensity of symptoms. It is often provoked by physical exertion, stress, or emotional upset. When asked, some patients may deny feeling pain but describe a pressure, heaviness, or discomfort in the chest. This discomfort is often described as a squeezing, heavy, tight, or suffocating sensation. It may be associated with other symptoms such as dyspnea or fatigue. Chronic angina pain usually does not change with position or breathing and is rarely described as sharp or stabbing. The pain of chronic stable angina usually lasts for only a few minutes and commonly subsides when the precipitating factor is resolved (resting, calming down, using sublingual NTG). Pain at rest is unusual and is often a symptom of UA. A 12-lead electrocardiogram (ECG) often shows ST segment depression and/or T-wave inversion indicating ischemia. The ECG will return to baseline when the pain is relieved. Chronic stable angina is controlled with drugs on an outpatient basis. Because chronic stable angina is often predictable, drugs are timed to provide peak effects during the time of day when angina is likely to occur. For example, if angina occurs when rising, the patient can take the drug as soon as awakening and wait 30 minutes to 1 hour before engaging in activity.

Classification of Heart Failure

Left-sided HF - Most common form of HF - Results from inability of LV to 1. Empty adequately during systole 2. Fill adequately during diastole - Further classified as 1. Systolic (inability of heart to pump blood effectively, decreased EF) 2. Diastolic (inability of ventricles to relax and fill during diastole; HTN most important cause) 3. Mixed systolic and diastolic The most common form of HF is left-sided HF. Left-sided HF results either from (1) the inability of the left ventricle (LV) to empty adequately during systole or (2) fill adequately during diastole. Left-sided HF can be further classified as systolic, diastolic, or mixed systolic and diastolic failure.

Risk Factors for CAD

Nonmodifiable risk factors: - Risk factors are characteristics or conditions that are linked with a high incidence of a disease. Many risk factors have been associated with CAD. They are grouped as nonmodifiable and modifiable Age - Nonmodifiable risk factors are age, gender, ethnicity, family history, and genetic inheritance. Gender - The incidence of CAD is highest among middle-aged men. After age 75, the incidence of serious heart events in men and women equalizes, although CVD causes more deaths in women than men. - On average, women with CAD are older than men who have CAD, and are more likely to have co-morbidities (e.g., hypertension, diabetes). Most women have atypical symptoms of angina rather than symptoms of MI when presenting with their initial heart event. Ethnicity - African Americans have an earlier onset and more severe CAD than there CAD counterparts. - Additionally, CAD incidence and mortality rates are greater in African American women than their white counterparts. Family history - Family history is a risk factor for CAD and MI. Often, patients with angina or MI can name a parent or sibling who has died of CAD. Genetic predisposition - The genetic basis of CAD/MI is complex and poorly understood. It is estimated that the genetic contribution to CAD/MI is as high as 40% to 60%. This proportion relates mainly to genes that control known risk factors (e.g., lipid metabolism). Major modifiable risk factors: Elevated serum lipids - Cholesterol >200 mg/dL (5.2 mmol/L) - Triglycerides >150 mg/dL (3.7 mmol/L) - High-density lipoproteins (HDL) - Low-density lipoproteins (LDL) - Treatment according to guidelines based on 10-year and life time risk score Elevated Serum Lipids - An elevated serum lipid level is one of the four most firmly established risk factors for CAD. The risk of CAD is associated with a serum cholesterol level of more than 200 mg/dL (5.2 mmol/L) or a fasting triglyceride level of more than 150 mg/dL (3.7 mmol/L). - For lipids to be used and transported by the body, they must become soluble in blood by combining with proteins. Lipids combine with proteins to form lipoproteins. Lipoproteins are vehicles for fat mobilization and transport, and vary in composition. Three major lipoproteins are high-density lipoproteins (HDLs), LDLs, and very-low-density lipoproteins (VLDLs). - HDLs carry lipids away from arteries and to the liver for metabolism. Therefore, high serum HDL levels are desirable and lower the risk of CAD. - In general, HDL levels are higher in women, decrease with age, and are low in persons with CAD. Physical activity and moderate alcohol intake increase HDL levels. - LDLs contain more cholesterol than any of the lipoproteins and have an attraction for arterial walls. Elevated LDL levels correlate most closely with an increased incidence of atherosclerosis and CAD. Therefore, low serum LDL levels are desirable. - Guidelines for treating elevated LDL cholesterol are based on a person's 10-year and life time risk for having heart disease or stroke. The following data generate a risk score: (1) age, (2) gender, (3) race, (4) use of tobacco, (5) diabetes, (6) systolic BP (7) diastolic BP, (8) use of BP drugs, (9) total cholesterol level, and (10) HDL cholesterol level. A 10-year risk calculator is available. - In general, persons with no or only one risk factor are considered at low risk for the development of CAD, and their LDL goal is <160 mg/dL (4.14 mmol/L). Those at very high risk for developing CAD have multiple risk factors. They have an LDL goal of <70 mg/dL (1.8 mmol/L). Major modifiable risk factors Hypertension - >140/90 mm Hg - Goal for > age 60 is <150/90 mm Hg - Begin lifestyle changes for prehypertension - Treat stage 1 or 2 hypertension with drugs Hypertension - The second major risk factor in CAD is hypertension, which is defined as a BP >140/90 mm Hg. For people older than 60 years, a goal BP of less than 150/90 mmHg is recommended (JNC8 recommendations) to prevent stroke, CVD, and heart failure. Hypertension increases the risk of death from CAD 10-fold in all persons. - The stress of an elevated BP increases the rate of atherosclerosis. This relates to the shearing stress that causes endothelial injury. - Therapeutic lifestyle changes should begin in people with prehypertension (BP of 120 to 139 mm Hg/80 to 89 mm Hg). Normal BP is <120/80 mm Hg. Stage 1 hypertension is 140 to 159/90 to 99 mm Hg. Stage 2 hypertension is BP > 160/100 mm Hg. - Those with stage 1 or 2 hypertension often require more than one drug to reach therapeutic goals Major modifiable risk factors - Tobacco use - Increased catecholamine release - ↑ LDL, ↓ HDL, ↑oxygen radicals - ↑ Carbon monoxide Second-hand smoke Tobacco Use - A third major risk factor in CAD is tobacco use. The risk of developing CAD is two to six times higher in those who smoke tobacco or use smokeless tobacco than in those who do not. Further, tobacco smoking decreases estrogen levels, placing premenopausal women at greater risk for CAD. Risk is proportional to the number of cigarettes smoked. - Nicotine in tobacco smoke causes catecholamine (i.e., epinephrine, norepinephrine) release. These neurohormones cause an increased heart rate (HR), peripheral vasoconstriction, and increased BP. These changes increase the heart's workload. - Tobacco smoke is also related to an increase in LDL level, a decrease in HDL level, and release of toxic oxygen radicals. All of these add to vessel inflammation and thrombosis. - Carbon monoxide, found in tobacco smoke, affects the oxygen-carrying capacity of hemoglobin by reducing the sites available for oxygen transport. Thus the effects of an increased cardiac workload, combined with the oxygen-depleting effect of carbon monoxide, significantly decrease the oxygen available to the heart muscle. There is also some indication that carbon monoxide is a chemical irritant, and causes injury to the endothelium. - The benefits of smoking cessation are dramatic and almost immediate. CAD mortality rates drop to those of nonsmokers within 12 months. However, nicotine is highly addictive and often calls for intensive intervention to assist people to quit. - Chronic exposure to environmental tobacco (secondhand) smoke also increases the risk of CAD. People who live in the same house as the patient should be encouraged to stop smoking. This reinforces the person's effort and decreases the risk of ongoing exposure to environmental smoke. Pipe and cigar smokers, who often do not inhale, have an increased risk of CAD similar to those exposed to secondhand smoke. Major modifiable risk factors - Physical inactivity - Obesity Physical Inactivity - Physical inactivity is the fourth major modifiable risk factor. Physical inactivity implies a lack of adequate physical exercise on a regular basis. An example of health-promoting regular physical activity is brisk walking (3 to 4 miles per hour) for at least 30 minutes 5 or more times a week. - Physically active people have increased HDL levels. Exercise improves thrombolytic activity, thus reducing the risk of clot formation. Exercise may also encourage the development of collateral circulation in the heart. Obesity - The death rate from CAD is higher in obese persons. Obesity is defined as a body mass index (BMI) of >30 kg/m2 and a waist circumference ≥40 inches for men and ≥35 inches for women. - The increased risk for CAD is proportional to the degree of obesity. - People who tend to store fat in the abdomen (an "apple" figure) rather than in the hips and buttocks (a "pear" figure) have a higher incidence of CAD. - Obesity is often linked with hypertension and insulin resistance. Contributing modifiable risk factors - Diabetes - Metabolic syndrome Diabetes Mellitus - The incidence of CAD is 2 to 4 times greater among persons who have diabetes, even those with well-controlled blood glucose levels, than the general population. The patient with diabetes manifests CAD not only more often but also at an earlier age. - The person with diabetes has an increased tendency toward endothelial dysfunction. This may account for the development of fatty streaks seen in these patients. Patients with diabetes also have changes in lipid metabolism and tend to have high cholesterol and triglyceride levels. Management of diabetes should include lifestyle changes and drug therapy to achieve a hemoglobin A1c (Hb A1c) level <7%. Metabolic Syndrome - Metabolic syndrome refers to a cluster of risk factors for CAD whose underlying pathophysiology may be related to insulin resistance. - These risk factors include central obesity, hypertension, abnormal serum lipids, and an elevated fasting blood glucose Contributing modifiable risk factors - Psychologic states - Homocysteine level - Substance abuse Psychologic States - Certain behaviors and lifestyles may contribute to the development of CAD. - One type of behavior, referred to as type A, includes perfectionism and a hardworking, driving personality. The type A person often suppresses anger and hostility, has a sense of time urgency, is impatient, and often creates stress and tension. This person may be more prone to MIs than a type B person, who is more easygoing, takes upsets in stride, knows personal limitations, takes time to relax, and is not an overachiever. However, the relationship between behaviors and the risk for CAD/MI remains controversial and complex. - Psychologic risk factors thought to increase the risk of CAD include depression, acute and chronic stress (e.g., poverty, serving as a caregiver), anxiety, hostility and anger, and lack of social support. In particular, depression is a risk factor for both the development and worsening of CAD. Depressed patients have elevated levels of circulating catecholamines. This may contribute to endothelial injury and inflammation and platelet activation. - Higher levels of depression are also associated with an increased number of adverse heart events. - Stressful states can contribute to the development of CAD. Sympathetic nervous system (SNS) stimulation and its effect on the heart are the physiologic mechanisms by which stress predisposes a person to the development of CAD. SNS stimulation causes an increased release of catecholamines (i.e., epinephrine, norepinephrine). This stimulation increases HR and the force of myocardial contraction. Both results increase myocardial oxygen demand. Also, stress-induced mechanisms can cause elevated lipid and glucose levels and changes in blood coagulation, which can lead to increased atherosclerosis. Homocysteine - High blood levels of homocysteine have been linked to an increased risk for CAD and other CVDs. - Homocysteine is produced by the breakdown of the essential amino acid methionine, which is found in dietary protein. High homocysteine levels may contribute to atherosclerosis by (1) damaging the inner lining of blood vessels, (2) promoting plaque buildup, and (3) altering the clotting mechanism to make clots more likely to occur. - B-complex vitamins (B6, B12, folic acid) have been shown to lower blood levels of homocysteine. - Generally, a screening test for homocysteine is limited to those suspected of having elevated levels. Theses include older patients with pernicious anemia or people who develop CAD at an early age. Substance Abuse - The use of illicit drugs, such as cocaine and methamphetamine, can produce coronary spasm resulting in myocardial ischemia and chest pain. - Most people who are seen in the emergency department (ED) with drug-induced chest pain are initially indistinguishable from those with CAD. - Although MI can occur, these patients often have sinus tachycardia, high BP, angina, and anxiety.

Chronic HF Nutritional Therapy

Low sodium diet - Individualize recommendations and consider cultural background - Recommend Dietary Approaches to Stop Hypertension (DASH) diet - Sodium is usually restricted to 2 g/day Poor adherence to a low-sodium diet and failure to take prescribed drugs as directed are the two most common reasons for readmissions of HF patients to the hospital. Therefore, it is critical that you accurately assess a patient's diet and teach both the patient and caregiver about the importance of diet. Obtain a detailed diet history. Determine not only what foods the patient eats but also when, where, and how often the patient dines out. In addition, assess the cultural value of food. Use this information to assist the patient in making appropriate dietary choices when developing a diet plan. The National Heart, Lung, Blood Institute (NHLBI) provides helpful dietary guidelines for heart-healthy food preparation for people of various cultures The edema associated with chronic HF is often treated by dietary restriction of sodium. The Dietary Approaches to Stop Hypertension (DASH) diet is effective as a first-line therapy for many individuals with hypertension (discussed in Chapter 32). This diet is now also widely used for the patient with HF, with or without hypertension. The average American adult's daily intake of sodium ranges from 7 to 15 g. A commonly prescribed diet for a patient with HF is a 2-g sodium diet. All foods high in sodium (over 400 mg per serving) should be avoided. Fluid restriction not generally required - Fluid restrictions are not commonly ordered for the patient with mild to moderate HF. However, in moderate to severe HF and renal insufficiency, fluids are limited to less than 2 L/day. If required, < 2L/day - Ice chips, gum, hard candy, ice pops to help thirst - Helping patients deal with thirst as a side effect of the drugs is important. To deal with the thirst, suggest ice chips, gum, hard candy, or ice pops. Daily weights important - Same time, same clothing each day - Tell patients to weigh themselves daily as this is important for monitoring fluid status. Tell patients to weigh themselves at the same time each day. Ideally this should be before breakfast, using the same scale, wearing the same type of clothing. This helps ensure valid comparisons from day to day and helps identify early signs of fluid retention. Weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3 kg) gain over a week should be reported to HCP - For patients with visual limitations, suggest scales with larger numbers and/or an audible response. Tell patients to call the HCP if they see a weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3-kg) gain over a week.

Chronic HF Interprofessional Care

Main treatment goals 1. Treat the underlying cause and contributing factors 2. Maximize CO 3. Reduce symptoms 4. Improve ventricular function 5. Improve quality of life 6. Preserve target organ function 7. improve mortality and morbidity With the addition of new drugs and devices, the management of HF has dramatically changed in the past few years. Because of the large number of patients and the high cost of care related to hospital readmissions, strategies to improve outcomes have been developed. One example is the use of guideline-directed medical therapy as defined by the AACF/AHA. Another example is specialized HF inpatient units with transitional programs to the outpatient setting to help manage these patients. These units are staffed with multidisciplinary HF teams, including nurses who are educated in the care of these patients. The main goals in the treatment of chronic HF are to treat the underlying cause and contributing factors, maximize CO, reduce symptoms, improve ventricular function, improve quality of life, preserve target organ function, and improve mortality and morbidity risks. Oxygen therapy - Relieves dyspnea and fatigue - In a person with HF, oxygen saturation of the blood can be reduced because the blood is not adequately oxygenated in the lungs. The use of supplemental oxygen improves saturation and assists in meeting tissue oxygen needs. This helps to relieve dyspnea and fatigue. Optimally, either pulse oximetry or arterial blood gases (ABGs) are used to monitor the need for and effectiveness of oxygen therapy. Physical and emotional rest - Conserve energy and decrease oxygen needs - Dependent on severity of HF - Physical and emotional rest allows the patient to conserve energy and decreases the need for additional oxygen. The degree of rest recommended depends on the severity of HF. A patient with severe HF may be on bed rest with limited activity. A patient with mild to moderate HF can be ambulatory with restriction of strenuous activity. Structured exercise program - CR associated with better outcomes - The patient should be told to participate in prescribed activities with adequate recovery periods. A structured exercise program, such as cardiac rehabilitation (CR), should be considered for all patients with chronic HF. - CR has been associated with decreased hospitalizations and reduced mortality. Patients enrolled in CR programs have also reported improved quality of life and less depression.

Hypertension Diagnostic Studies

Measurement of BP - Measurement of BP is essential in assessing and monitoring hypertension. There is some controversy as to what the diagnostic workup should be in the initial assessment of a person with hypertension. Most hypertension is classified as primary hypertension, and testing for secondary causes is not routinely done. Urinalysis - Routine urinalysis, BUN, and serum creatinine levels are used to screen for renal involvement and to provide baseline information about kidney function. BUN and serum creatinine Creatinine clearance - Creatinine clearance reflects the glomerular filtration rate. Decreases in creatinine clearance indicate renal insufficiency. Serum electrolytes, glucose - Measurement of serum electrolytes, especially potassium, is important to detect hyperaldosteronism, a cause of secondary hypertension. Blood glucose levels assist in the diagnosis of diabetes mellitus. Serum lipid profile - A lipid profile provides information about additional risk factors that lead to atherosclerosis and CVD. Uric acid levels - Uric acid levels establish a baseline, because the levels often rise with diuretic therapy. ECG - An ECG provides baseline information about cardiac status. It can identify the presence of LVH, cardiac ischemia, or previous MI. Echocardiogram - If LVH is suspected, echocardiography is often performed. Basic laboratory studies are performed to (1) identify or rule out causes of secondary hypertension, (2) evaluate target organ disease, (3) determine overall cardiovascular risk, or (4) establish baseline levels before initiating therapy. If the patient's age, history, physical examination, or severity of hypertension points to a secondary cause, further diagnostic testing is indicated.

Chronic HF Evaluation

Monitoring to assess outcomes and prevent/ limit future hospitalizations - Vital signs - Weight - Pulse oximetry - Dyspnea Home health nurses can be essential Can use electronic monitoring Managing HF patients out of the hospital is a priority. Effective home health care can prevent or limit future hospitalizations by providing ongoing assessments (e.g., monitoring vital signs and weight, evaluating response to therapies). Many agencies offer specialized programs dedicated to managing HF patients at home. For example, these programs may include the use of telehealth monitoring technology (e.g., electronic scale, BP cuff, pulse oximeter) to collect physiologic data. The technology may also be able to audibly ask the patient questions such as, "Are you short of breath today?" Results are transmitted telephonically or by computer to the home care agency. Once received, the data are reviewed. Based on the findings, the patient may be called to further assess the situation or a visit may be scheduled. Home health nurses frequently work with protocols set up with the patient's health care team. The protocols enable you and the patient to identify problems, such as an increase in weight or dyspnea as evidence of worsening HF. Interventions can be started to prevent hospitalization. These may include changing drugs and restricting fluids. Home health nursing care of HF patients is vital in reducing the number of hospitalizations, increasing functional capacity, and increasing the quality of life.

Hypertension Nursing Management

Nursing Evaluation Patient will: - Achieve and maintain goal BP - Understand, accept, and implement treatment plan - Report minimal side effects of therapy The overall expected outcomes are that the patient with hypertension will: 1. Achieve and maintain goal BP as defined for the individual 2. Understand, accept, and implement the treatment plan 3. Report minimal side effects of therapy

Hypertension Interprofessional Care

Overall Goals - Control blood pressure - Reduce CVD risk factors and target organ disease Goals include achieving and maintaining goal BP, and reducing cardiovascular risk and target organ disease. Lifestyle modifications, directed toward reducing the patient's BP and overall cardiovascular risk, are indicated for all patients with prehypertension and hypertension.

Assessment: Nursing History

Pain - The nursing history for cardiac function includes pain and characteristics of pain, fatigue, peripheral circulation, cardiac risk factors, and the presence of past or concurrent cardiac conditions. Ask specific questions related to cardiopulmonary disease. - The presence of chest pain requires an immediate thorough evaluation, including assessment of location, duration, radiation, and frequency. Note any other symptoms associated with chest pain, such as nausea, diaphoresis, extreme fatigue or weakness. - Pleuritic chest pain results from inflammation of the pleural space of the lungs, the pain is peripheral and radiates to the scapular regions. - Musculoskeletal pain is often present following exercise, rib trauma, and prolonged coughing episodes. Dyspnea - The nursing history focuses on the patient's ability to meet oxygen demands. - Dyspnea is a clinical sign of hypoxia. It is the subjective sensation of difficult or uncomfortable breathing. - Dyspnea is associated with exaggerated respiratory effort, use of the accessory muscles of respiration, nasal flaring, and marked increases in the rate and depth of respirations. The use of a visual analogue scale (VAS) helps patients objectively assess their dyspnea. - Orthopnea is an abnormal condition in which a patient uses multiple pillows when reclining to breathe easier or sits leaning forward with arms elevated. Wheezing - The nursing history for respiratory function includes the presence of a cough, shortness of breath, dyspnea, wheezing, pain, environmental exposures, frequency of respiratory tract infections, pulmonary risk factors, past respiratory problems, current medication use, and smoking history or secondhand smoke exposure. - Wheezing is a high-pitched musical sound caused by high-velocity movement of air through a narrowed airway. It is associated with asthma, acute bronchitis, and pneumonia. Respiratory infection - - Environmental exposure to inhaled substances is closely linked with respiratory disease. - With CO poisoning, the patient will have vague complaints of general malaise, flulike symptoms, and excessive sleepiness. - Radon gas is a radioactive substance from the breakdown of uranium in soil, rock, and water that enters homes through the ground or well water. - Obtain information about the patient's frequency and duration of respiratory tract infections. Ask about any known exposure to tuberculosis (TB) and the date and results of the last tuberculin skin test. - Determine the patient's risk for human immunodeficiency virus (HIV) infection. Patients with a history of intravenous (IV) drug use and multiple unprotected sexual partners are at risk of developing HIV infection. Health risks - Determine familial risk factors such as a family history of lung cancer or cardiovascular disease. Documentation includes blood relatives who had cardiopulmonary disease and their present level of health or age at time of death. Other family risk factors include the presence of infectious diseases, particularly TB. Fatigue - Fatigue in the patient with cardiopulmonary alterations is often an early sign of worsening of the chronic underlying process. Cough - Patients with a chronic cough tend to deny, underestimate, or minimize their coughing. Often, because they are so accustomed to it, they are unaware of how frequently it occurs. - Patients with chronic sinusitis usually cough only in the early morning or immediately after rising from sleep. - If hemoptysis (bloody sputum) is present, determine whether it is associated with coughing and bleeding from the upper respiratory tract, sinus drainage, or the gastrointestinal tract (hematemesis). Smoking - It is important to determine patients' direct and secondary exposure to tobacco. Ask about any history of smoking; include the number of years smoked and the number of packs smoked per day. This is recorded as pack-year history. Allergies - When obtaining information about allergies, ask specific questions about the types of allergens, responses to these allergens, and successful and unsuccessful relief measures. Medications - Medications include prescribed medications, over-the-counter medications, folk medicines, herbal medicines, alternative therapies, and illicit drugs (such as opioids, marijuana, cocaine) and substances. - It is important to determine if a patient uses illicit drugs. - Assess the patient's knowledge and ability to self-administer medications correctly.

Stages of Atherosclerosis

Pathogenesis of atherosclerosis. A, Damaged endothelium. B, Fatty streak and lipid core formation. C, Fibrous plaque. Raised plaques are visible: some are yellow; others are white. D, Complicated lesion: thrombus is red; collagen is blue. Plaque is complicated by red thrombus deposition. A. The endothelium (the inner lining the vessel wall) is normally nonreactive to platelets and leukocytes, as well as coagulation, fibrinolytic, and complement factors. However, the endothelial lining can be injured as a result of tobacco use, hyperlipidemia, hypertension, toxins, diabetes, hyperhomocysteinemia, and infection causing a local inflammatory response. - CAD is a progressive disease that develops over many years. When it becomes symptomatic, the disease process is usually well advanced. - The stages of development in atherosclerosis are (1) fatty streak, (2) fibrous plaque, and (3) complicated lesion. B. Fatty Streak - Fatty streaks, the earliest lesions of atherosclerosis, are characterized by lipid-filled smooth muscle cells. As streaks of fat develop within the smooth muscle cells, a yellow tinge appears. Fatty streaks can be seen in the coronary arteries by age 15 and involve an increasing amount of surface area as one ages. C. Fibrous Plaque - The fibrous plaque stage is the beginning of progressive changes in the endothelium of the arterial wall. These changes can appear in the coronary arteries by age 30 and increase with age. Once endothelial injury has taken place, lipoproteins (carrier proteins within the bloodstream) transport cholesterol and other lipids into the arterial intima. Collagen covers the fatty streak and forms a fibrous plaque with a grayish or whitish appearance. These plaques can form on one portion of the artery or in a circular fashion involving the entire lumen. The result is a narrowing of the vessel lumen and a reduction in blood flow to the distal tissues. D. Complicated Lesion - The final stage in the development of the atherosclerotic lesion is the most dangerous. As the fibrous plaque grows, continued inflammation can result in plaque instability, ulceration, and rupture. Once the integrity of the artery's inner wall is compromised, platelets accumulate in large numbers, leading to a thrombus. The thrombus may adhere to the wall of the artery, leading to further narrowing or total occlusion of the artery. At this stage, the plaque is referred to as a complicated lesion.

Hypertension Nursing Planning

Patient will - Achieve and maintain goal BP - Follow the therapeutic plan Including HCP appointments - Experience minimal side effects of therapy - Manage and cope with this condition The overall goals for the patient with hypertension are that the patient will 1. achieve and maintain the goal BP 2. follow the therapeutic plan, including appointments with the HCP 3. experience minimal side effects of therapy 4. manage and cope with this condition. In acute care settings, BP measurement is usually done to evaluate vital signs, volume status, and effects of drugs, rather than to diagnose hypertension. Trends in BP are more important than a single value. Inform the HCP of any patient with a persistent elevated BP. These patients should be evaluated for hypertension before discharge, if appropriate, or after discharge.

Pitting Edema

Pitting edema. Note the finger-shaped depressions that do not rapidly refill after an examiner has exerted pressure.

Heart Failure Complications

Pleural effusion - Pleural effusion is a common complication in HF. There are two pleural layers or membranes: the visceral pleura lines the lungs, whereas the parietal pleura lines the chest cavity. Normally a small amount of fluid is between the two layers for lubrication and to aid breathing. A pleural effusion occurs when excess fluid builds up in the pleural cavity of the lungs secondary to increasing pressure in the pleural capillaries. Fluid then moves from these capillaries into the pleural space. Pleural effusions may result in symptoms of dyspnea, cough, and chest pain. (Pleural effusion is discussed in Chapter 27.) Dysrhythmias - atrial and ventricular - Chronic HF causes enlargement of the chambers of the heart. This enlargement can cause changes in the normal electrical pathways. When numerous sites in the atria fire spontaneously and rapidly (atrial fibrillation), the organized atrial depolarization (contraction) no longer occurs. Atrial fibrillation also promotes thrombus formation within the atria. Thrombi may break loose and form emboli. This places patients with atrial fibrillation at risk for stroke. They require treatment with anticoagulants, cardioversion, ablation and antidysrhythmic drugs. - Patients with HF are also at risk for ventricular dysrhythmias (e.g., ventricular tachycardia [VT], ventricular fibrillation [VF]). Patients with decreased LV function are at the greatest risk for SCD. Guidelines recommend implantation of a prophylactic implantable cardioverter-defibrillator (ICD). Left ventricular thrombus - With ADHF or chronic HF, the enlarged LV and decreased CO combine to increase the risk of thrombus formation in the LV. Once a thrombus has formed, it may also decrease left ventricular contractility, decrease CO, and worsen the patient's perfusion. The development of emboli from the thrombus also places the patient at risk for stroke. Hepatomegaly - HF can lead to severe hepatomegaly, especially with RV failure. The liver becomes congested with venous blood. The hepatic congestion leads to impaired liver function. Eventually liver cells die, fibrosis occurs, and cirrhosis can develop (see Chapter 43). Renal failure - The decreased CO that accompanies chronic HF results in decreased perfusion to the kidneys and can lead to renal insufficiency or failure.

Etiology of Hypertension

Primary hypertension - Also called essential or idiopathic hypertension - Elevated BP without an identified cause - 90% to 95% of all cases - Exact cause unknown but several contributing factors Primary (essential or idiopathic) hypertension is elevated BP without an identified cause, and it accounts for 90% to 95% of all cases of hypertension. Although the exact cause of primary hypertension is unknown, there are several contributing factors. These include changes in endothelial function related to either vasoconstricting or vasodilating agents, increased SNS activity, overproduction of sodium-retaining hormones, increased sodium intake, greater-than-ideal body weight, diabetes, tobacco use, and excessive alcohol intake. Secondary hypertension - Elevated BP with a specific cause - 5% to 10% of adult cases - Clinical findings relate to underlying cause - Treatment aimed at removing or treating cause Secondary hypertension is elevated BP with a specific cause that often can be identified and corrected. This type of hypertension accounts for 5% to 10% of hypertension in adults. Secondary hypertension should be suspected in people who suddenly develop high BP, especially if it is severe. Clinical findings that suggest secondary hypertension will relate to the underlying cause. For example, an abdominal bruit heard over the renal arteries may indicate renal disease. Treatment of secondary hypertension is aimed at removing or treating the underlying cause. Secondary hypertension is a contributing factor to hypertensive crisis.

Risk Factors HF

Primary risk factors 1. Hypertension - Modifiable risk factor - Properly treated and managed, incidence of HF can be reduced by 50% - Hypertension and CAD are the primary risk factors for HF. Hypertension is a modifiable risk factor that should be aggressively treated and managed. Long-term treatment of hypertension reduces the incidence of HF by 50%. 2. CAD Co-morbidities 1. Diabetes, metabolic syndrome, advanced age, tobacco use, vascular disease - Other co-morbidities, such as diabetes, metabolic syndrome, advanced age, tobacco use, and vascular disease also contribute to the development of HF.

Structures and Functions of Cardiovascular System

Pulse pressure - Difference between SBP and DBP - Normally about 1/3 of the SBP - Pulse pressure is the difference between the SBP and DBP. It is normally about one-third of the SBP. If the BP is 120/80, the pulse pressure is 40. An increased pulse pressure may occur during exercise or in individuals with atherosclerosis of the larger arteries as the result of increased SBP. Decreased pulse pressure may be found in heart failure or hypovolemia. Mean arterial pressure - Average pressure within arterial system that is felt by organs in body - MAP = (SBP + 2 DBP) ÷ 3 - Mean arterial pressure (MAP) refers to the average pressure within the arterial system that is felt by organs in the body. It is not the average of the DBP and SBP because the length of diastole exceeds that of systole at normal HRs. MAP is calculated as follows: MAP = (SBP + 2 DBP) ÷ 3. A person with a BP of 120/60 mm Hg has an estimated MAP of 80 mm Hg. A MAP greater than 60 mm Hg is needed to adequately perfuse and sustain the vital organs of an average person under most conditions. When the MAP falls below this number for a period of time, vital organs are underperfused and will become ischemic.

Pathophysiology Right-Sided Heart Failure

RV fails to pump effectively Fluid backs up in venous system Fluid moves into tissues and organs Left-sided HF is most common cause - Other causes include RV infarction, PE, and cor pulmonale (RV dilation and hypertrophy) Right-sided HF occurs when the right ventricle (RV) fails to pump effectively. When the RV fails, fluid backs up into the venous system. This causes movement of fluid into the tissues and organs (e.g., peripheral edema, abdominal ascites, hepatomegaly, jugular venous distention). The most common cause of right-sided HF is left-sided HF. As the LV fails, fluid backs up into the pulmonary system, causing increased pressures in the lungs. The RV has to work harder to push blood to the pulmonary system. Over time, this increased workload weakens the RV and gradually it fails. Other causes of right-sided HF (independent of the function of the LV) include RV infarction, pulmonary embolism, and cor pulmonale (RV dilation and hypertrophy caused by pulmonary disease)

Structures and Functions of Cardiovascular System

Regulation of cardiovascular system - Autonomic nervous system 1. Autonomic Nervous System. The autonomic nervous system consists of the sympathetic nervous system and the parasympathetic nervous system. 2. Stimulation of the sympathetic nervous system increases the HR, speed of impulse conduction through the AV node, and force of atrial and ventricular contractions. Additionally, stimulation of α1-adrenergic receptors in vascular smooth muscle results in vasoconstriction, increasing the blood pressure. 3. In contrast, stimulation of the parasympathetic system (mediated by the vagus nerve) slows HR by decreasing the impulse from the SA node and thus conduction through the AV node. - Baroreceptors 1. Baroreceptors. Baroreceptors in the aortic arch and carotid sinus (at the origin of the internal carotid artery) are sensitive to stretch or pressure within the arterial system. Stimulation of these receptors (e.g., volume overload) sends information to the vasomotor center in the brainstem. This results in temporary inhibition of the sympathetic nervous system and enhancement of the parasympathetic influence, causing a decreased HR and peripheral vasodilation. Decreased arterial pressure causes the opposite effect. -Chemoreceptors 1. Chemoreceptors. Chemoreceptors are located in the aortic and carotid bodies and the medulla. They are capable of causing changes in respiratory rate and BP in response to increased arterial CO2 pressure (hypercapnia) and, to a lesser degree, decreased plasma pH (acidosis) and arterial O2 pressure (hypoxia). When the chemoreceptors in the medulla are triggered, they stimulate the vasomotor center to increase BP.

Counterregulatory Mechanisms

Release of natriuretic peptides (ANP & BNP) Release of nitric oxide and prostaglandin

Cardiac catheterization

Right-sided to measure pressures Left-sided to evaluate coronary arteries Cardiac Catheterization - Cardiac catheterization is a common outpatient procedure. It provides information about CAD, coronary spasm, congenital and valvular heart disease, and ventricular function. - Cardiac catheterization is also used to measure intracardiac pressures and O2 levels, as well as CO and EF. - With injection of contrast media and fluoroscopy, the coronary arteries can be seen, chambers of the heart can be outlined, and wall motion can be observed. - Cardiac catheterization is done by inserting a radiopaque catheter into the right and/or left side of the heart. - For the right side of the heart, a catheter is inserted through an arm vein (basilic or cephalic) or a leg vein (femoral). Pressures are recorded as the catheter is moved into the vena cava, right atrium, right ventricle, and pulmonary artery. The catheter is then moved until it is wedged or lodged in position. This blocks the blood flow and pressure from the right side of the heart and looks ahead through the pulmonary capillary bed to the pressure in the left side of the heart (pulmonary artery occlusive pressure). This pressure assesses the function of the left side of the heart. - The left heart catheterization is done by inserting a catheter into a femoral or brachial artery. The catheter is passed in a retrograde manner up to the aorta, across the aortic valve, and into the left ventricle.

Gerontologic Considerations

Risk for cardiovascular disease (CVD) increases with age - One of the greatest risk factors for cardiovascular disease (CVD) is age. CVD leading cause of death in adults > 65 years of age - CVD remains the leading cause of death in adults older than age 65. Cardiovascular changes result of aging, disease, environmental factors, and lifetime behaviors - The most common cardiovascular problem is coronary artery disease (CAD) due to atherosclerosis. - It is difficult to separate normal aging changes from the pathophysiologic changes of atherosclerosis. Many of the physiologic changes in the cardiovascular system of older adults are a result of the combined effects of the aging process, disease, environmental factors, and lifetime health behaviors rather than just age alone.

Diagnostic Studies of Cardiovascular System

Serum Lipids - Triglycerides - Cholesterol - Phospholipids - Serum lipids consist of triglycerides, cholesterol, and phospholipids. - Triglycerides are the main storage form of lipids and make up about 95% of fatty tissue. - Cholesterol, a structural component of cell membranes and plasma lipoproteins, is a precursor of corticosteroids, sex hormones, and bile salts. In addition to being absorbed from food in the gastrointestinal tract, cholesterol can also be synthesized in the liver. - Phospholipids contain glycerol, fatty acids, phosphates, and a nitrogenous compound. Although formed in most cells, phospholipids usually enter the circulation as lipoproteins synthesized by the liver. Lipoprotein - Lipids must bind to protein to circulate in blood - Serum lipids circulate in the blood bound to protein. Thus they are often referred to as lipoproteins. - Apoproteins are water-soluble proteins that combine with most lipids to form lipoproteins.

Chronic HF Patient Teaching

Signs and symptoms of HF exacerbations - what to do/report - Review the signs and symptoms of HF exacerbations with the patient and caregiver. Give them a clear action plan to follow should symptoms occur. Early detection of worsening HF may help to prevent an acute episode requiring hospitalization. Importance of early detection - Patients with HF are at risk for anxiety and depression. Emphasize to the patient that it is possible to live productively with this chronic illness. Patients with HF usually need to take drugs for the rest of their lives. This often becomes difficult because a patient may be asymptomatic when HF is under control. You must stress that the disease is chronic, and that drugs must be continued to keep the HF under control. Can have positive outlook with chronic health problem if treatment plan is followed Drug therapy - Expected actions - Signs of drug toxicity - How to take HR and what to report - Signs and symptoms of hypokalemia and hyperkalemia - BP monitoring as needed - Teach the patient the expected actions of the ordered drugs and the signs of drug toxicity. - Also teach the patient and caregiver how to take a HR. The HR should always be taken for 1 full minute. A HR less than 50 beats/minute may be a contraindication to taking a digitalis preparation or β-blocker unless specified otherwise by the HCP. However, in the absence of symptoms (e.g., heart block, ventricular ectopy, syncope), a HR less than 50 beats/minute may be acceptable. Include clear information about when a drug, especially digitalis and beta blockers, should be held and a HCP called. - Teach the patient the symptoms of hypokalemia and hyperkalemia if diuretics that deplete or spare potassium are ordered. Weakness, fatigue, constipation, and muscle cramping may occur but often there are no physical signs of hypo- or hyperkalemia. Frequently the patient who takes thiazide or loop diuretics is given supplemental potassium. - It may also be appropriate to teach patients home BP monitoring, especially those with hypertension. Dietary therapy - Written plan - Reading labels for sodium - No added salt - Daily weights - Smaller, more frequent meals 1. Consult the written diet plan and list of permitted and restricted foods. 2. Examine labels to determine sodium content. Also examine the labels of over-the-counter drugs, such as laxatives, cough medicines, and antacids for sodium content. 3. Avoid using salt when preparing foods or adding salt to foods. 4. Weigh yourself at the same time each day, preferably in the morning, using the same scale and wearing the same or similar clothes. 5. Eat smaller, more frequent meals. Activity/rest - Energy-conserving and energy-efficient behaviors - Exercise training (cardiac rehab) - Increase gradually - Avoid heat and cold extremes - Rest after exertion - Avoid emotional upsets - Activity Program 1. Increase walking and other activities gradually, provided they do not cause fatigue or dyspnea. Consider a cardiac rehabilitation program. 2. Avoid extremes of heat and cold. - Rest The physical therapist, occupational therapist, or you can instruct the patient in energy-conserving and energy-efficient behaviors after an evaluation of daily activities has been done. For example, once you understand the patient's daily routine, suggestions can be made to simplify work or modify an activity. Exercise training (e.g., cardiac rehabilitation) improves symptoms of chronic HF but is often underprescribed. Exercise for patients with HF has been found to be safe and to improve the overall sense of well-being. It has also been correlated with mortality reduction. Increase walking and other activities gradually, provided they do not cause fatigue or dyspnea. Avoid extremes of heat and cold. Frequently the patient needs a prescription for rest after an activity. Many hard-driving persons need the "permission" to not feel "lazy." Avoid emotional upsets. Verbalize any concerns, fears, feelings of depression, etc., to HCP. Ongoing monitoring - Know FACES - Reappearance of symptoms - What to report - Regular follow-up - Support group - Ongoing Monitoring 1. Know the signs and symptoms of worsening heart failure. FACES: fatigue, limitation of activities, chest congestion/cough, edema, shortness of breath. 2. Recall the symptoms experienced when illness began. Reappearance of previous symptoms may indicate a recurrence. 3. Report immediately to health care provider any of the following: Weight gain of 3 lb (1.4 kg) in 2 days, or 3 to 5 lb (1.4 to 2.3 kg) in a week Difficulty breathing, especially with exertion or when lying flat Waking up breathless at night Frequent dry, hacking cough, especially when lying down Fatigue, weakness Swelling of ankles, feet, or abdomen; swelling of face or difficulty breathing (if taking ACE inhibitors) Nausea with abdominal swelling, pain, and tenderness Dizziness or fainting 4. Follow up with HCP on regular basis. 5. Consider joining a local support group with your family members and/or caregiver(s). Health promotion - Vaccinations - Reduce risk factors - 1. Obtain annual flu vaccination. 2. Obtain pneumococcal vaccine (e.g., Pneumovax) and revaccination after 5 years (for people at high risk of infection or serious disease). 3. Develop plan to reduce risk factors (e.g., BP control, smoking cessation, weight reduction).

Chronic HF Nursing Assessment

Subjective Data - Past health history (Past health history: CAD (including recent MI), hypertension, cardiomyopathy, valvular or congenital heart disease, diabetes mellitus, hyperlipidemia, renal disease, thyroid or lung disease, rapid or irregular heart rate.) - Any cardiac history or diseases that increase risk for cardiac dysfunction - Fatigue, depression, anxiety - Usual sodium intake - Nausea/vomiting/anorexia - Stomach bloating - Weight gain - Ankle swelling - Nocturia - Decreased daytime urine output - Constipation - Dyspnea, orthopnea, cough - Palpitations - Dizziness, fainting - Number of pillows used for sleeping - Paroxysmal nocturnal dyspnea - Insomnia - Chest pain or heaviness - RUQ pain, abdominal discomfort - Behavioral changes - Visual changes Drugs - Any cardiac drugs, estrogens, corticosteroids, NSAIDs, OTC drugs, herbs - Use of and compliance with any cardiac drugs; use of diuretics, estrogens, corticosteroids, nonsteroidal antiinflammatory drugs (NSAIDs), over-the-counter drugs, herbal supplements. - Carefully review the patient's current prescription and over-the-counter drugs. Assess for use of any NSAIDs as they can contribute to sodium retention. Objective Data - Skin color and temperature (Cool, diaphoretic skin; cyanosis or pallor, peripheral edema (right-sided heart failure) - Edema - Respiratory rate and sounds (Tachypnea, crackles, rhonchi, wheezes; frothy, blood-tinged sputum) - Frothy, blood-tinged sputum - Heart rate and sounds (Tachycardia, S3, S4, murmurs; pulsus alternans, PMI displaced inferiorly and posteriorly, lifts/heaves, jugular vein distention) - Abdominal distention (Abdominal distention, hepatosplenomegaly, ascites) - Changes in LOC (Restlessness, confusion, decreased attention or memory) - Serum electrolytes (Altered serum electrolytes (especially Na+ and K+) - BUN, creatinine (↑ BUN, creatinine, or liver function tests) - Liver function tests - NT-proBNP or BNP (↑ NT-proBNP or BNP) - Chest x-ray (Chest x-ray demonstrating cardiomegaly, pulmonary congestion, and interstitial pulmonary edema) - Echocardiogram (Echocardiogram showing increased chamber size, decreased wall motion, decreased EF or normal EF with evidence of diastolic failure) - ECG (Atrial and ventricular enlargement on ECG) - O2 saturation (↓ O2 saturation)

Hypertension Nursing Assessment

Subjective Data Past health history - Hypertension - Cardiovascular, cerebrovascular, renal, thyroid disease - Diabetes mellitus, pituitary disorders, obesity, dyslipidemia - Menopause or hormone replacement - Known duration and past workup of high BP; cardiovascular, cerebrovascular, renal, or thyroid disease; diabetes mellitus; pituitary disorders; obesity; dyslipidemia; menopause or hormone replacement status Drugs: Use of any prescription or over-the-counter, illicit, or herbal drugs or products; previous use of antihypertensive drug therapy Family history - Health perception-health management: Family history of hypertension or cardiovascular disease; tobacco use, alcohol use; sedentary lifestyle Salt and fat intake Weight gain or loss - Nutritional-metabolic: Usual salt and fat intake; weight gain or loss Nocturia - Elimination: Nocturia Fatigue, dyspnea on exertion, palpitations, pain - Activity-exercise: Fatigue; dyspnea on exertion, palpitations, exertional chest pain; intermittent claudication, muscle cramps; usual pattern and type of exercise Dizziness, blurred vision - Cognitive-perceptual: Dizziness; blurred vision; paresthesia Erectile dysfunction - Sexual-reproductive: Erectile dysfunction, decreased libido Stressful events - Coping-stress tolerance: Stressful life events Objective Data - Blood pressure readings - Heart sounds - Pulses - Edema - Body measurements - Mental status changes Perform a focused physical assessment for the following risk factors and/or clinical manifestations: Cardiovascular - SBP consistently >140 mm Hg or DBP >90 mm Hg for patients <60 yr old or >150 mm Hg or DBP >90 mm Hg for patients >60 years old. Orthostatic changes in BP and HR; bilateral BPs significantly different; abnormal heart sounds; laterally displaced, apical pulse; diminished or absent peripheral pulses; carotid, renal, or femoral bruits; peripheral edema. Gastrointestinal - Obesity (BMI >30 kg/m2); abnormal waist-hip ratio Neurologic - Mental status changes

Mechanical System

Systole: Contraction of heart muscle - Systole, contraction of the myocardium, results in ejection of blood from the ventricles. Diastole: Relaxation of heart muscle - Relaxation of the myocardium, diastole, allows for filling of the ventricles. Stroke volume: Amount of blood ejected with each heart beat - Stroke volume is the amount of blood ejected from the ventricle with each heartbeat. Depolarization triggers mechanical activity.

Classification Systems of Heart Failure

The New York Heart Association (NYHA) developed functional guidelines for classifying people with heart disease based on tolerance to physical activity. Because this system only reflected exercise capacity, the American College of Cardiology Foundation/AHA (ACCF/AHA) developed a staging system that identified disease progression and treatment strategies. This system allows for identification of people at risk for developing HF but who do not currently have heart disease. The ACCF/AHA system encourages clinicians to actively address the patient's risk factors and treat any existing conditions to prevent further disease progression. This may help reduce the growing number of HF patients. Patients may move between levels in the NYHA classification system based on worsening or improving symptoms However, the ACCF/AHA staging system is progressive. Patients can only advance to a higher (worse) stage as the disease progresses.

Conduction System

The conduction system consists of specialized tissue responsible for creating and transporting the electrical impulse, or action potential. This impulse starts depolarization of the cardiac cells and subsequently heart contraction. The electrical impulse normally begins in the sinoatrial (SA) node (pacemaker of the heart). Each impulse coming from the SA node travels through interatrial pathways to depolarize the atria, resulting in a contraction. The electrical impulse travels from the atria to the AV node through internodal pathways. The signal then moves through the bundle of His and the left and right bundle branches. The left bundle branch has two fascicles (divisions): anterior and posterior. The action potential moves through the walls of both ventricles by means of Purkinje fibers. The ventricular conduction system delivers the impulse within 0.12 second. This triggers a synchronized right and left ventricular contraction and ejection of blood into the pulmonary and systemic circulations. Last, repolarization occurs when the contractile fiber cells and the conduction pathway cells regain their resting polarized condition. Heart muscle cells have a compensatory mechanism that makes them unresponsive or refractory to restimulation during the action potential. During ventricular contraction, there is an absolute refractory period during which heart muscle does not respond to any stimuli. After this period, heart muscle gradually recovers its excitability, and a relative refractory period occurs by early diastole. Normal sinus rhythm (NSR) - Originates at the SA node, follows normal sequence through conduction system - P wave 1. The P wave represents the electrical conduction through both atria. Atrial contraction follows the P wave. - PR interval 1. The PR interval represents the impulse travel time from the SA node through the AV node, through the bundle of His, and to the Purkinje fibers. The normal length for the PR interval is 0.12 to 0.2 second. An increase in the time greater than 0.2 second indicates a block in the impulse transmission through the AV node; whereas a decrease, less than 0.12 second, indicates the initiation of the electrical impulse from a source other than the SA node. - QRS complex 1. The QRS complex indicates that the electrical impulse traveled through the ventricles. Normal QRS duration is 0.06 to 0.1 second. An increase in QRS duration indicates a delay in conduction time through the ventricles. Ventricular contraction usually follows the QRS complex. - QT interval 1. The QT interval represents the time needed for ventricular depolarization and repolarization. The normal QT interval is 0.12 to 0.42 second. This interval varies inversely with changes in heart rate. Changes in electrolyte values such as hypocalcemia or therapy with drugs such as disopyramide (Norpace) or amiodarone (Cordarone) increase the QT interval. Shortening of the QT interval occurs with digitalis therapy, hyperkalemia, and hypercalcemia. An electrocardiogram (ECG) reflects the electrical activity of the conduction system. An ECG monitors the regularity and path of the electrical impulse through the conduction system; however, it does not reflect the muscular work of the heart. The normal sequence on the ECG is called the normal sinus rhythm (NSR). NSR implies that the impulse originates at the SA node and follows the normal sequence through the conduction system.

Drug Therapy

The drugs currently available for treating hypertension have two main actions: (1) decrease the volume of circulating blood and (2) reduce SVR. The drugs used in the treatment of hypertension include: - Diuretics promote sodium and water excretion, reduce plasma volume, and reduce the vascular response to catecholamines. - Adrenergic-inhibiting agents act by diminishing the SNS effects that increase BP. Adrenergic inhibitors include drugs that act centrally on the vasomotor center and peripherally to inhibit norepinephrine release or to block the adrenergic receptors on blood vessels. - Direct vasodilators decrease the BP by relaxing vascular smooth muscle and reducing SVR. - Calcium channel blockers increase sodium excretion and cause arteriolar vasodilation by preventing the movement of extracellular calcium into cells. - Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II and reduce angiotensin II (A-II)-mediated vasoconstriction and sodium and water retention. - A-II receptor blockers (ARBs) prevent angiotensin II from binding to its receptors in the walls of the blood vessels.

Goals of Drug Therapy

The following are recommendations for from the JNC 8: - In patients > 60 years, start drug treatment for BP ≥ 150 mm Hg systolic or ≥ 90 mm Hg diastolic and treat to goal BP less than those thresholds - In patients < 60 years, treatment initiation and goals should be 140/90 mm Hg, same threshold used in patients 18 years or older with either chronic kidney disease or diabetes

Cardiac Valves

The four valves of the heart serve to keep blood flowing in a forward direction. The cusps of the mitral and tricuspid valves are attached to thin strands of fibrous tissue termed chordae tendineae. Chordae are anchored in the papillary muscles of the ventricles. This support system prevents eversion of the leaflets into the atria during ventricular contraction. The pulmonic and aortic valves (also known as semilunar valves) prevent blood from regurgitating into the ventricles at the end of each ventricular contraction.

Coronary Arteries and Veins

The myocardium has its own blood supply, the coronary circulation. Blood flow into the two major coronary arteries occurs primarily during diastole (relaxation of the myocardium). The left coronary artery arises from the aorta and divides into two main branches: the left anterior descending artery and the left circumflex artery. These arteries supply the left atrium, the left ventricle, the interventricular septum, and a portion of the right ventricle. The right coronary artery also arises from the aorta, and its branches supply the right atrium, the right ventricle, and a portion of the posterior wall of the left ventricle. In 90% of people, the atrioventricular (AV) node and the bundle of His, part of the cardiac conduction system, receive blood supply from the right coronary artery. For this reason, obstruction of this artery often causes serious defects in cardiac conduction. The divisions of coronary veins parallel those of coronary arteries. Most of the blood from the coronary system drains into the coronary sinus (a large channel), which empties into the right atrium near the entrance to the inferior vena cava.

Physical Examination

The physical examination includes assessment of the cardiopulmonary system. When assessing an older adult patient, give special consideration to changes that occur with the aging process. These changes affect the patient's activity tolerance and level of fatigue or cause transient changes in vital signs and are not always associated with a specific cardiopulmonary disease. Inspection - Skin and mucous membrane color, level of consciousness (LOC), breathing patterns, chest wall movement, general appearance, circulation - Inspection: skin and mucous membranes for color, appearance, level of consciousness, adequacy of systemic circulation, breathing patterns, and chest wall movement. Inspection includes observations of the nails for clubbing. - At rest the normal adult rate is 12 to 20 regular breaths/min. Bradypnea is less than 12 breaths/min, and tachypnea is greater than 20 breaths/min. - In some conditions, such as metabolic acidosis, the acidic pH stimulates an increase in rate, usually greater than 35 breaths/min, and depth of respirations (Kussmaul respiration) to compensate by decreasing carbon dioxide levels. - Apnea is the absence of respirations for lasting for 15 seconds or longer. - Cheyne-Stokes respiration occurs when there is decreased blood flow or injury to the brainstem. - Conditions such as emphysema, advancing age, and COPD cause the chest to assume a rounded "barrel" shape. Palpation - Chest, feet, legs, pulses - Palpation of the chest provides assessment data in several areas. It documents the type and amount of thoracic excursion; elicits any areas of tenderness; and helps to identify tactile fremitus, thrills, heaves, and the cardiac point of maximal impulse (PMI). - Palpation of the extremities provides data about the peripheral circulation (e.g., the presence and quality of peripheral pulses, skin temperature, color, and capillary refill) (see Chapter 31). - Palpation of the feet and legs determines the presence or absence of peripheral edema. Patients with alterations in cardiac function, such as those with heart failure or hypertension, often have pedal or lower-extremity edema. Edema is graded from 1+ to 4+ depending on the depth of visible indentation after firm finger pressure. - Palpate the pulses in the neck and extremities to assess arterial blood flow (see Chapter 31). Use a scale of 0 (absent pulse) to 4 (full, bounding pulse) to describe what you feel. The normal pulse is 2; and a weak, thready pulse is 1. Percussion - Presence of abnormal fluid or air; diaphragmatic excursion - Percussion: detects the presence of abnormal fluid or air in the lungs. It also determines diaphragmatic excursion. Auscultation - Normal and abnormal heart and lung sounds - Auscultation: identification of normal and abnormal heart and lung sounds. - Auscultation of the cardiovascular system includes assessment for normal S1 and S2 sounds and the presence of abnormal S3 and S4 sounds (gallops), murmurs, or rubs. Identify the location, radiation, intensity, pitch, and quality of a murmur. Auscultation also identifies any bruit over the carotid, abdominal aorta, and femoral arteries. - Auscultation of lung sounds involves listening for movement of air throughout all lung fields: anterior, posterior, and lateral. Adventitious, or abnormal, breath sounds occur with collapse of a lung segment, fluid in a lung segment, or narrowing or obstruction of an airway.

Blood Flow Through the Heart

The right atrium receives venous blood from the inferior and superior venae cavae and the coronary sinus. The blood then passes through the tricuspid valve into the right ventricle. With each contraction, the right ventricle pumps blood through the pulmonic valve into the pulmonary artery and to the lungs. Blood flows from the lungs to the left atrium by way of the pulmonary veins. It then passes through the mitral valve and into the left ventricle. As the heart contracts, blood is ejected through the aortic valve into the aorta and thus enters the systemic circulation. Myocardial pump - Two atria and two ventricles As the myocardium stretches, the strength of the subsequent contraction increases (Starling's law). - The pumping action of the heart is essential for oxygen delivery. The ventricles fill with blood during diastole and empty during systole. The volume of blood ejected from the ventricles during systole is the stroke volume. Hemorrhage and dehydration cause a decrease in circulating blood volume and a decrease in stroke volume. - Myocardial fibers have contractile properties that allow them to stretch during filling. - As the myocardium stretches, the strength of the subsequent contraction increases; this is known as the Frank-Starling (Starling's) law of the heart. - In the diseased heart (cardiomyopathy or myocardial infarction [MI]), Starling's law does not apply because the increased stretch of the myocardium is beyond the physiological limits of the heart. The subsequent contractile response results in insufficient stroke volume, and blood begins to "back up" in the pulmonary (left heart failure) or systemic (right heart failure) circulation. Myocardial blood flow - Unidirectional through four valves S1: mitral and tricuspid close S2: aortic and pulmonic close - To maintain adequate blood flow to the pulmonary and systemic circulation, myocardial blood flow must supply sufficient oxygen and nutrients to the myocardium itself. Blood flow through the heart is unidirectional. The four heart valves ensure this forward blood flow. During ventricular diastole, the atrioventricular (mitral and tricuspid) valves open, and blood flows from the higher-pressure atria into the relaxed ventricles. As systole begins, ventricular pressure rises and closes the mitral and tricuspid valves. Valve closure causes the first heart sound (S1). - During the systolic phase, the semilunar (aortic and pulmonic) valves open, and blood flows from the ventricles into the aorta and pulmonary artery. The mitral and tricuspid valves stay closed during systole, so all of the blood is moved forward into the pulmonary artery and aorta. As the ventricles empty, ventricular pressures decrease, allowing closure of the aortic and pulmonic valves; this causes the second heart sound (S2). Some patients with valvular disease have backflow or regurgitation of blood through the incompetent valve, causing a murmur that you can hear on auscultation. Coronary artery circulation - Coronary arteries supply the myocardium with nutrients and remove wastes. - The coronary circulation is the branch of the systemic circulation that supplies the myocardium with oxygen and nutrients and removes waste. - The coronary arteries fill during ventricular diastole. The left coronary artery has the most abundant blood supply and feeds the more muscular left ventricular myocardium, which does most of the work of the heart. Systemic circulation - Arteries and veins deliver nutrients and oxygen and remove waste products. - The arteries of the systemic circulation deliver nutrients and oxygen to tissues, and the veins remove waste from tissues. Oxygenated blood flows from the left ventricle through the aorta and into large systemic arteries. These arteries branch into smaller arteries, then arterioles, and finally the smallest vessels, the capillaries. Exchange of respiratory gases occurs at the capillary level, where the tissues are oxygenated. Waste products exit the capillary network through venules that join to form veins. These veins become larger and form the vena cava, which carries deoxygenated blood to the right side of the heart, from which it then returns to the pulmonary circulation.

Pathophysiology Heart Failure in General

Ventricular failure leads to: - Low blood pressure (BP) - Low CO - Poor renal perfusion Abrupt or subtle onset Compensatory mechanisms mobilized to maintain adequate CO The patient with ventricular failure of any type may have low blood pressure (BP), low CO, and poor renal perfusion. HF can have an abrupt onset as with acute MI or it can be a subtle process resulting from slow, progressive changes. The overloaded heart uses compensatory mechanisms to try to maintain adequate CO. The main compensatory mechanisms include (1) neurohormonal responses: renin-angiotensin-aldosterone-system (RAAS) and the sympathetic nervous system (SNS), (2) ventricular dilation, and (3) ventricular hypertrophy.

Hypertension Lifestyle Modifications

Weight reduction - Weight loss of 22 lb (10 kg ) may decrease SBP by approx. 5 to 20 mm Hg - Calorie restriction and physical activity - Overweight persons have an increased incidence of hypertension and increased risk for CVD. - Weight reduction has a significant effect on lowering BP in many people, and the effect is seen with even moderate weight loss. - A weight loss of 22 lb (10 kg) may decrease SBP by approximately 5 to 20 mm Hg. - When a person decreases caloric intake, sodium and fat intake are usually also reduced. Although reducing the fat content of the diet has not been shown to produce sustained benefits in BP control, it may slow the progress of atherosclerosis and reduce overall CVD risk. - Weight reduction through a combination of calorie restriction and moderate physical activity is recommended for overweight patients with hypertension. DASH eating plan - Fruits, vegetables, fat-free or low-fat milk, whole grains, fish, poultry, beans, seeds, and nuts - The DASH eating plan significantly lowers BP and these decreases compare with those achieved with BP-lowering drug. Additional benefits also include lowering of low-density lipoprotein (LDL) cholesterol. - The DASH eating plan emphasizes fruits, vegetables, fat-free or low-fat milk and milk products, whole grains, fish, poultry, beans, seeds, and nuts. - Compared with the typical American diet, the plan contains less red meat, salt, sweets, added sugars, and sugar-containing beverages. Dietary sodium reduction - < 2300 mg/day for healthy adults - < 1500 mg/day for ---- African Americans ---- Middle-aged and older ---- Those with hypertension, diabetes, or chronic kidney disease - This involves avoiding foods known to be high in sodium (e.g., canned soups, frozen dinners) and not adding salt in the preparation of foods or at meals. - Average sodium intake is about 4200 mg/day. - Patient and caregiver need to learn about sodium-restricted diets. Moderation of alcohol intake - Excessive alcohol intake is strongly associated with hypertension. Drinking three or more alcoholic drinks daily is also a risk factor for CVD and stroke. - Men should limit their intake of alcohol to no more than two drinks per day and women and lighter-weight men to no more than one drink per day. One drink is defined as 12 oz of regular beer, 5 oz of wine (12% alcohol), or 1.5 oz of 80-proof distilled spirits. Excessive alcohol intake that results in cirrhosis is the most frequent cause of secondary hypertension. Physical activity - Moderate-intensity aerobic activity, at least 30 minutes, most days of the week - Vigorous-intensity aerobic activity at least 20 minutes, 3 days a week - Muscle-strengthening activities at least 2 times a week - Flexibility and balance exercises 2 times a week - A physically active lifestyle is essential to promote and maintain good health. - The AHA and American College of Sports Medicine recommend that adults perform moderate-intensity aerobic physical activity for at least 30 minutes most days (i.e., more than 5) per week with a goal of at least 150 minutes per week. - Exercise goals can be accomplished by performing shorter periods of exercise that last at least 10 minutes or more. - Additionally, combinations of moderate and vigorous activity are acceptable (e.g., walking briskly for 30 minutes on 2 days of the week and jogging for 20 minutes on 2 other days). - For adults age 18 to 65, walking briskly at a pace that noticeably increases the pulse defines moderate-intensity aerobic activity. Jogging at a pace that substantially increases the pulse and causes rapid breathing is an example of vigorous activity for this age group. - All adults should perform muscle-strengthening activities using the major muscles of the body at least twice a week. This helps to maintain or increase muscle strength and endurance. - Additionally, flexibility and balance exercises are recommended at least twice a week for older adults, especially for those at risk for falls. - Generally, physical activity is more likely to be done if it is safe and enjoyable, fits easily into one's daily schedule, and is inexpensive. Avoidance of tobacco products - Nicotine causes vasoconstriction and elevated BP - Smoking cessation reduces risk factors within 1 year - Nicotine contained in tobacco causes vasoconstriction and increases BP, especially in people with hypertension. - Smoking tobacco is also a major risk factor for CVD. - The cardiovascular benefits of stopping tobacco use are seen within 1 year in all age groups. Strongly encourage everyone, especially patients with hypertension, to avoid tobacco use. Advise those who continue to use tobacco products to monitor their BP during use. Psychosocial risk factors - Low socioeconomic status, social isolation and lack of support, stress, negative emotions - Activate SNS and stress hormones - Psychosocial risk factors can contribute to the risk of developing CVD and to a poorer prognosis and clinical course in patients with CVD. - These risk factors include low socioeconomic status, social isolation and lack of support, stress at work and in family life, and negative emotions such as depression and hostility. Frequently, these risk factors are clustered together. For example, there tends to be higher rates of depression in individuals who experience job stress. - Psychosocial risk factors have direct effects on the cardiovascular system by activating the SNS and stress hormones. This can cause a wide variety of pathophysiologic responses, including hypertension - Psychosocial risk factors can contribute to CVD indirectly as well, simply by their impact on lifestyle behaviors and choices. Screening for psychosocial risk factors is important. Make appropriate referrals (e.g., counseling), when indicated. Suggest behavioral interventions such as relaxation training, stress management courses, support groups, and exercise training for individuals who are not in acute psychologic distress.