WRITTEN REPORT IN

MEDICAL-SURGICAL NURSING
Disturbances in Blood Pumping Mechanism

Presented to Prof. Joan Oyangoren Pamantasan ng Lungsod ng Maynila By:

Baraquiel, Patricia Elaine Huilar, Faith Anne Iguia, Shiena Mae Racelis, Glomarie Alyssa Saldo, Jan Robert June 2011

REVIEW OF ANATOMY & PHYSIOLOGY OF THE HEART AND BLOOD VESSELS

The heart is a hollow, muscular organ about a size of a closed fist, located in the center of the thorax, where it occupies the space between the lungs (mediastinum) and rests on the diaphragm. It weighs approximately 300g (10.6 oz); the weight and size of the heart are influenced by age, gender, body weight, extent of physical exercise and conditioning, and heart disease. The Heart spans the area from the 2nd to the 5th intercostal space. The heart pumps blood to the tissues, supplying them with oxygen and other nutrients. The heart is composed of three layers. The inner layer, endocardium, consists of endothelial tissue and lines the outside of the heart and valves. The middle layer, myocardium, is made up of muscle fibers and is responsible for the pumping action. The exterior layer is called the epicardium.

The heart is incased in a thin, fibrous sac called the pericardium, which is composed of 2 layers. Adhering to the epicardium is the visceral pericardium. Enveloping the visceral pericardium is the parietal pericardium, a tough fibrous tissue that attaches to the great vessels, diaphragm, sternum, and vertebral column and supports the heart in the mediastinum. The space between these 2 layers (pericardial space) is normally filled with about 20ml of fluid, which lubricates the surface of the heart and reduces friction during systole. As blood travels through the heart, it enters a total of four chambers and passes through four valves. The two upper chambers, the right and left atria, are separated longitudinally by the interatrial septum. The two lower chambers, the right and left ventricles, are the pumping machines of the heart and are separated longitudinally by the interventricular septum. A valve follows each chamber and prevents the blood from flowing backward into the chamber from which the blood originated. Two prominent grooves are visible on the surface of the heart:

The coronary sulcus (artioventricular groove) marks the junction of the atria and The anterior interventricular sulcus and posterior interventricular sulcus mark the The right atrium, located in the upper right side of the heart, and a small appendage, the

ventricles.

junction of the ventricles on the front and back of the heart, respectively.

right auricle, act as a temporary storage chamber so that blood will be readily available for the right ventricle. Deoxygenated blood from the systemic circulation enters the right atrium through three veins, the superior vena cava, the inferior vena cava, and the coronary sinus. During the interval when the ventricles are not contracting, blood passes down through the right atrioventricular (AV) valve into the next chamber, the right ventricle. The AV valve is also called the tricuspid valve because it consists of three flexible cusps (flaps).

The right ventricle is the pumping chamber for the pulmonary circulation. The ventricle,

with walls thicker and more muscular than those of the atrium, contracts and pumps deoxygenated blood through the three-cusped pulmonary semilunar valve and into a large artery, the pulmonary trunk. The pulmonary trunk immediately divides into two pulmonary arteries, which lead to the left and right lungs, respectively. The following events occur in the right ventricle.

When the right ventricle contract, the right AV valve closes and prevents

blood from moving back into the right atrium. Small tendon like cords, the chordae tendineae, is attached to papillary muscles at the opposite, bottom side of the ventricle. These cords limit the extent to which the AV valve can be forced closed, preventing it from being pushed through and into the atrium.

When the right ventricle relaxes, the initial backflow of blood in the pulmonary

artery closes the pulmonary semilunar valve and prevents the return of blood to the right ventricle.

The left atrium and its auricle appendage receive oxygenated blood from the lungs

though four pulmonary veins (two from each lung). The left atrium, like the right atrium, is a holding chamber for blood in readiness for its flow into the left ventricle. When the ventricles relax, blood leaves the left atrium and passes through the left AV valve into the left ventricle. The left AV valve is also called the mitral or bicuspid valve, the only heart valve with two cusps.

The left ventricle is the pumping chamber for the systemic circulation. Because a greater

blood pressure is required to pump blood through the much more extensive systemic circulation than through the pulmonary circulation, the left ventricle is larger and its walls are thicker than those of the right ventricle. When the left ventricle contracts, it pumps oxygenated blood through the aortic semilunar valve, into a large artery, the aorta, and throughout the body. The following events occur in the left ventricle, simultaneously and analogously with those of the right ventricle.

When the left ventricle contract, the left AV valve closes and prevents blood

from moving back into the right atrium. As in the right AV valve, the chordae tendineae prevent overextension of the left AV valve.

When the left ventricle relaxes, the initial backflow of blood in the aorta
ventricle.

closes the aortic semilunar valve and prevents the return of blood to the left

The pathway of blood through the chambers and valves of the heart.

Two additional passageways are present in the fetal heart:

The foramen ovale is an opening across the interatrial septum. It allows blood to bypass

the right ventricle and the pulmonary circuit, while the nonfunctional fetal lungs are still developing. The opening, which closes at birth, leaves a shallow depression called the fossa ovalis in the adult heart.

The ductus arteriosus is a connection between the pulmonary trunk and the aorta. Blood

that enters the right ventricle is pumped out through the pulmonary trunk. Although some blood enters the pulmonary arteries (to provide oxygen and nutrients to the fetal lungs), most of the blood moves directly into the aorta through the ductus arteriosus. The coronary circulation consists of blood vessels that supply oxygen and nutrients to the tissues of the heart. Blood entering the chambers of the heart cannot provide this service because the endocardium is too thick for effective diffusion (and only the left side of the heart contains oxygenated blood). Instead, the following two arteries that arise from the aorta and encircle the heart in the artioventricular groove provide this function:

The left coronary artery has the following two branches: The anterior interventricular

artery (left anterior descending, or LAD, artery) and the circumflex artery.

The right coronary artery has the following two branches: The posterior

interventricular artery and the marginal artery. Blood from the coronary circulation returns to the right atrium by way of an enlarged blood vessel, the coronary sinus. Three veins, the great cardiac vein, the middle cardiac vein, and the small cardiac vein, feed the coronary sinus. Contractions of the heart occur in a rhythm, the cardiac cycle. And are regulated by impulses that normally begin at the sinoatrial (SA) node, the hearts pacemaker. From there the impulses are conducted throughout the heart. Impulses from the autonomic nervous system affect the SA node and alter its firing rate to meet the bodys needs. The cardiac cycle consists of systole, the period when the heart contracts and sends blood on its outward journey, and diastole, the period when the heart relaxes and fills with blood. During diastole the mitral and tricuspid valves are open, and the aortic and pulmonic valves are closed.

There are various kinds of blood vessels:

Arteries

Aorta (the largest artery, carries blood out of the heart)

Branches of the aorta, such as the carotid artery, the subclavian artery, the celiac

trunk, the mesenteric arteries, the renal artery and the iliac artery.

Arterioles Capillaries (the smallest blood vessels) Venules Veins

Large collecting vessels, such as the subclavian vein, the jugular vein, the renal Venae cavae (the 2 largest veins, carry blood into the heart)

vein and the iliac vein.

They are roughly grouped as arterial and venous, determined by whether the blood in it is flowing away from (arterial) or toward (venous) the heart. The term "arterial blood" is nevertheless used to indicate blood high in oxygen, although the pulmonary artery carries "venous blood" and blood flowing in the pulmonary vein is rich in oxygen. This is because they are carrying the blood to and from the lungs, respectively, to be oxygenated. Structure Arteries Functions The walls (outer structure) of arteries contain smooth muscle fibre that contract and relax under of the the nervous instructions sympathetic Arterioles

Transport

blood

away

from the heart; Transport oxygenated blood only (except in the case of the pulmonary artery). Transport blood from

system. Arterioles are tiny branches of arteries that lead to capillaries. These are also under the control of the sympathetic nervous system, and constrict and dilate, to regulate blood flow.

arteries to capillaries; Arterioles are the main regulators of blood flow and pressure.

Capillaries

Capillaries

are

tiny

Function is to supply tissues with components of, and carried by, the blood, and also to remove waste from the surrounding cells ... as opposed to simply moving the blood around the body (in the case of other blood vessels); Exchange of oxygen, carbon dioxide, water, salts, etc., between the blood and the surrounding body tissues.

(extremely narrow) blood vessels, of approximately 520 (one There micro-metres micro-metre are networks = of diameter.

0.000001metre)

capillaries in most of the organs and tissues of the body. These capillaries are supplied with blood by arterioles and drained by venules. Capillary walls are only one cell thick (see diagram), exchanges capillary Venules which of and permits material the

between the contents of the surrounding tissue. Venules are minute vessels that drain blood from capillaries and into veins. Many venules unite to form Veins a vein. The walls (outer structure) of veins consist of three layers of tissues that are thinner and less elastic than the corresponding layers of arteries. Veins include valves that Transport blood towards the heart; Transport deoxygenated blood only (except in the case of the pulmonary vein).

Drains

blood

from

capillaries into veins, for return to the heart

aid the return of blood to the heart by preventing blood from flowing in the reverse direction. Arteries Transport blood away from the heart; Carry Oxygenated Blood (except in the case of the Pulmonary Artery); Have relatively narrow lumens (see Veins Transport blood towards the heart; Carry De-oxygenated Blood (except in the case of the Pulmonary Vein); Have relatively wide lumens (see

diagram above); Have relatively more muscle/elastic tissue; Transports blood under higher pressure (than veins); Do not have valves (except for the semi-lunar valves of the pulmonary artery and the aorta).

diagram above); Have relatively less muscle/elastic tissue; Transports blood under lower pressure (than arteries); Have valves throughout the main

veins of the body. These are to prevent blood flowing in the wrong direction, as this could (in theory)

return waste materials to the tissues. The central opening of a blood vessel, the lumen, is surrounded by a wall consisting of three layers:

The tunica intima is the inner layer facing the blood. It is composed of an

innermost layer of endothelium (simple squamous epithelium) surrounded by variable amounts of connective tissues.

The tunica media, the middle layer, is composed of smooth muscle with variable The tunica adventitia, the outer layer, is composed of connective tissue.

amounts of elastic fibers.

The cardiovascular system consists of three kinds of blood vessels that form a closed system of passageways:

Arteries carry blood away from the heart. The three kinds of arteries are

categorized by size and function:

Elastic arteries (conducting arteries) are the largest arteries and include the

aorta and other nearby branches. The tunica media of elastic arteries contains a large amount of elastic connective tissue, which enables the artery to expand as blood enters the lumen from the contracting heart. During relaxation of the heart, the elastic wall of the artery recoils to its original position, forcing blood forward and smoothing the jerky discharge of blood from the heart.

Muscular arteries (conducting arteries) branch from elastic arteries and

distribute blood the various body regions. Abundant smooth muscle in the thick tunica media allows these arteries to regulate blood flow by vasoconstriction (narrowing of the lumen) or vasodilation (widening of the lumen). Most named arteries of the body are muscular arteries.

Arterioles are small, nearly microscopic, blood vessels that branch from

muscular arteries. Most arterioles have all three tunics present in their walls, with considerable smooth muscle in the tunica media. The smallest arterioles consist of endothelium surrounded by a single layer of smooth muscle. Arterioles regulate the flow of blood into capillaries by vasoconstriction and vasodilation.

Capillaries are microscopic blood vessels with extremely thin walls. Only the

tunica intima is present in these walls, and some walls consist exclusively of a single layer of endothelium. Capillaries penetrate most body tissues with dense interweaving networks called capillary beds. The thing walls of capillaries allow the diffusion of oxygen and nutrients out of the capillaries, while allowing carbon dioxide and wastes into the capillaries.

Metarterioles (precapillaries) are the blood vessels between arterioles and

venules. Although metarterioles pass through capillary beds with capillaries, they are not true capillaries because metarterioles, like arterioles, have smooth muscle present in the tunica media. The smooth muscle of a metarteriole allows it to acts as a shunt to regulate blood flow into the true capillaries that branch from it. The thoroughfare channel, the tail end of the metarteriole that connects to the venule, lacks smooth muscle.

True capillaries form the bulk of the capillary bed. They branch away

from a metarteriole at its arteriole end and return to merge with the metarteriole at its venule end (thoroughfare channel).

Some true capillaries connect directly from an arteriole to a metarteriole or

venule. Although the walls of true capillaries lack muscle fibers, they possess a ring of smooth muscle called a precapillary sphincter where they emerge from the metarteriole. The precapillary sphincter regulates blood flow through the capillary. There are three types of true capillaries:

Continuous capillaries have continuous, unbroken walls consisting of cells Fenestrated capillaries have continuous walls between endothelial cells,

that are connected by tight junctions. Most capillaries are of this type.

but the cells have numerous pores (fenestrations) that increase their permeability. These capillaries are found in the kidneys, lining the small intestine, and in other areas where a high transfer rate of substances into or out of the capillary is required.

Sinusoidal capillaries (sinusoids) have large gaps between endothelial

cells that permit the passage of blood cells. These capillaries are found in the bone marrow, spleen, and liver.

Veins carry blood toward the heart. The three kinds of veins are listed here in the

order that they merge to form increasingly larger blood vessels: Postcapillary venules, the smallest veins, form when capillaries merge as they exit a capillary bed. Much like capillaries, they are very porous, but with scattered smooth muscle fibers in the tunica media.

Venules form when postcapillary venules join. Although the walls of

larger venules contain all three layers, they are still porous enough to allow white blood cells to pass.

Veins have walls with all three layers, but the tunica intima and tunica

media are much thinner than in similarly sized arteries. Few elastic or muscle fibers are present. The wall consists of primarily of a well-developed tunica adventitia. Many veins, especially those in the limbs, have valves, formed from folds of the tunica intima that prevent the backflow of blood.

Many regions of the body receive blood supplies from two or more arteries. The points where these arteries merge are called arterial anastomoses. Arterial anastomoses allow tissues to receive blood even after one of the arteries supplying blood has been blocked.

ASSESSMENT OF CLIENT WITH DISEASES OF THE CARDIOVASCULAR SYSTEM

I. Assessment Health history Elicit a description of the clients present illness and chief complaints, including onset, course, duration, location, and precipitating and alleviating factors. Cardinal signs and symptoms indicating altered cardiovascular function include: Pain over the lower sterna region and the upper abdomen characterized by heavy vicelike,

belt-squeezing pain that may radiate to the shoulders, neck, and down the arms. (Associated symptoms may include electrocardiogram [ECG] changes and arrhythmias. This pain may indicate myocardial ischemia) Palpitations characterized by rapid irregular or pounding heart beat. (This symptoms may be

associated with arrhythmias or ischemia). Intermittent claudication characterized by extremity pain with exercise (This may indicate

peripheral vascular disease). Dyspnea characterized by difficult breathing or shortness of breath with activity (i.e. dyspnea

on exertion), in the supine position (i.e. orthopnea), or sudden onset at night (i.e paroxysmal nocturnal dyspnea). (This is commonly associated with compromised cardiac function). Fatigue with or without activity (This may be associated with decreased carbon dioxide).

Syncope with or without dizziness (This can result from a sudden decrease in cardiac output) Diaphoresis with associated clamminess and cyanosis (This reflects decreased cardiac output

and decreased peripheral perfusion). Edema or weight gain greater than 3 lbs in 24 hours (This may indicated heart failure)

Explore the clients history for risk factors associated with cardiovascular disease (atherosclerosis): Positive family history for cardiovascular disease Age (the incidence of cardiovascular disease increases after age 40) Gender (mortality from cardiovascular disease is greater than men than in women; however,

this difference decreases after menopause) Race (mortality is greater than nonwhites than whites) Smoking (the risk of cardiovascular diseases is two to four times greater than cigarette

smokers than nonsmokers) Hypertension, particularly elevated systolic pressure Hyperlipidemia (the ratio of high-density lipoproteins [HDL] to low-density lipoproteins

[LDL] is the best predictor) Obesity (contributes to the severity of other risk factors) Sedentary lifestyle

Diabetes (uncontrolled elevated blood glucose level increases risk) Stress (may contribute to developing coronary artery disease) Hormonal contraceptives

Physical Examination Vital signs Assess vital signs, particularly pulse rate, blood pressure, and respirations. Increased blood pressure and pulse may indicate cardiovascular disease. Inspection Observe general appearance for signs of distress, anxiety, and altered level of consciousness. Inspect the lips and buccal mucosa for central cyanosis, which reflects hypoxia. Inspect the peripheral extremities for cyanosis and a capillary refill time of less than 3

seconds. Assess jugular venous pressure and observe for venous distention.

Palpation Palpate all peripheral pulses including carotid, brachial, radial, femoral, popliteal, dorsalis

pedia, and anterior tibial. Grade 0 (no pulse), 1+ (weak), 2+ (normal), 3+ (increased), 4+ (bounding) Palpate the pericardium to locate the point of maximal impulse or the apical impulse.

Auscultation Systematically auscultate the heart for normal and abnormal sounds, murmurs, and friction

rub, covering four main areas: aortic, pulmonary, mitral and tricuspid. Perform a respiratory assessment. Findings pointing to cardiovascular problems may include cough (possibly reflecting

pulmonary congestion); crackles or wheezing (reflecting airway narrowing, atelactasis, or left ventricular failure); hemoptysis (possibly pointing to acute pulmonary edema), Cheyne-stokes respiration (possibly associated with severe left ventricular failure) Perform abdominal assessment
Noting liver enlargement and ascites (indicating decreased venous return secondary to right

ventricular failure); bladder distention (pointing to decrease cardiac output); and bruits just above the umbilicus (reflecting abdominal aortic obstruction or aneurysm).

LABORATORY AND DIAGNOSTIC PROCEDURES

A. Erythrocyte Sedimentation Rate (ESR)

It is a measurement of the rate at which RBCs settle out of anticoagulated blood in an hour. It is elevated in infectious heart disorders or myocardial infarction. Normal range is as follows: Males: 15-20 mm/hr. Females: 20-30 mm/hr.

B.

Enzyme Studies Aspartate Aminotransferase (AST) Formerly SGOT. Elevated ievels indicate tissue necrosis. Normal range is 10 40 u/ml Range in MI Initial Elevation: 4-6 hrs Peaks: 24-36 hrs Returns to normal: 4-7 days

Creatinine Phosphokinase (CK-MB) It is the most cardiac specific enzyme It is an accurate indicator of myocardial damage Normal range Males: 50-325 mU/mL Females: 50-250 mU/mL Range with MI Onset: 3-6 hrs Peaks: 12-18 hrs Returns to normal: 3-4 days

Lactic Dehydrogenase (LDH)

Among the five LDH isoenzymes, LDH 1 is the most sensitive indicator of Normal range is 100-225 mU/mL. Range with Myocardial Infarction

myocardial damage.

Onset: 12 hrs Peaks: 48 hrs Returns to normal: 10-14 days

Hydroxybutyrate Dehydrogenase (HBD) Elevation of HBD is always accompanied by elevation of LDH levels. It is valuable in detecting silent MI. Normal range is 140-350 mU/mL. Range with Myocardial Infarction Onset: 10-12 hrs Peaks: 48-72 hrs Returns to normal: 12-13 days

Troponin Best indicator for myocardial infarction (MI). Negative result is normal. Troponin I greater than 1.5 ng/ ml. indicates MI. Troponin T greater than .1 to .2 ng/ ml. indicates MI.

C.

Electrocardigraphy (ECG, EKG) It is the graphical recording of the electrical activities of the heart. It is the first diagnostic test done when cardiovascular disorder is suspected. P wave. Depolarizatin of atria. Duration is .04 to .11 secs.

PR interval. Time of impulse transmission from SA node to the AV node. Duration is .12-.20 secs. ST segment. Represents the plateau phase of the action potencial. T wave. Ventricular repolarization. Should not exceed 5 mm amplitude. Common ECG Changes Hypokalemia U-wave Depressed ST segment Short T wave

Hyperkalemia Prolonged QRS Complex Elevated ST segment Peaked T wave Pathologic Q wave

D.

SONIC STUDIES Echocardiography Uses ultrasound to assess cardiac structure and mobility The client is to remain still, in supine position slightly turned to the left side, with HOB elevated 15-20 degrees Transesophageal Echocardiography (TEE) Allows ultrasonic imaging of the cardiac structures and great vessels via esophagus. Nursing Interventions before TEE Ascertain history of esophageal surgery, malignancy or allergy to anesthetics or sedatives. NPO for 4-6 hours before the procedure. Encourage to void before the procedure.

Administer sedatives as ordered. Keep suction and resuscitation equipment available. Cardiac monitoring is done throughout the procedure. Topical anesthetics to depress gag reflex. Place the patient in chin to chest position to facilitate passage of endoscope.

Nursing interventions After TEE NPO until gag reflex returns. To prevent aspiration. Place patient in lateral or semi-fowlers position. To promote drainage from the mouth and to enhance ventilation. Encourage to cough. Throat lozenges to relieve throat soreness.

Phonocardiography Involves the use of electrically recorded amplified cardiac sounds. It is helpful in assessing the exact timing and characteristics of murmurs and extra heart sounds.

ANGINA PECTORIS
Angina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest. The cause is usually insufficient coronary blood flow. The insufficient flow results in a decreased oxygen supply to meet an increased myocardial demand for oxygen in response to physical exertion or emotional stress. In other words, the need for oxygen exceeds the supply. Etiology and Risk Factors Angina pectoris is associated with atherosclerotic lesions and is a manifestation of CHD. Angina can be caused either by chronic or acute blockage of a coronary artery or by coronary artery spasm. Chronic blockages are associated with fixed calcified (type Vb) or fibrotic (type Vc) atherosclerotic lesions that occlude more than 75% of the vessel lumen. When fixed blockages are present in the coronary arteries, conditions that increase myocardial oxygen demand (e.g., physical exertion, emotion, exposure to cold) may precipitate episodes of angina. Because the severely stenosed arteries cannot dilate to deliver enough oxygen to meet the increased demand, ischemia results. In contrast, acute blockage of a coronary artery results from rupture or disruption of vulnerable atherosclerotic plaques that cause platelet aggregation and thrombus formation. Acute blockages are associated with unstable angina and AMI. Primary prevention is through the lifelong commitment to reducing the risk factors of CHD. Secondary prevention is through recognition and early treatment of angina attacks. Tertiary prevention consists of resolution of angina before myocardial damage occurs.

Risk Factors of CHD Nonmodifiable Risk Factors Heredity (Including Race) Children whose parents had heart disease are at higher risk for CHD. This increased risk is related to genetic predisposition to hypertension, elevated lipid levels, diabetes, and obesity, all of which increase the risk of CHD. Increasing Age Age influences both the risk and the severity of CHD. Symptomatic CHD appears predominantly in people older than 40 years of age, and 4 of 5 people who die of CHD are age 65 years or older. Angina and MI, however, can occur in a persons 30s and even in ones 20s. At older ages, women who have heart attacks are twice as likely as men to die from the heart attack. Gender Coronary heart disease is the number one killer of both men and women. In 1999 mortality from CHD was almost equal for men and women. Although men are at higher risk for heart attacks at younger ages, the risk for women increases significantly at menopause, so that CHD rates in women after menopause are two to three times that of women the same age before menopause. Women who take oral contraceptives and who smoke or have high blood pressure are at greater risk for CHD. Women with an early menopause are also at higher risk than women with a normal or late menopause. Modifiable Risk Factors Smoking Both active and passive smoking have been strongly implicated as a risk factor in the development of CHD. Currently 23 % of men and 18 % of women are smokers. The prevalence of smoking is higher in people with 11 years of education or less. Smoking triples the risk of heart attack in women and doubles the risk of heart attack in men. It also doubles the risk of dying from a heart attack and may quadruple the risk of sudden death. Nonsmokers who are exposed to second-hand tobacco smoke at home or work may also have a higher death rate from

CHD. The risk of CHD is decreased by 50% 1 year after smokers quit. The risk is further reduced to that of non-smokers within 5 to 10 years after smoking cessation. Tar, nicotine, and carbon monoxide contribute to the damage. Tar contains hydrocarbons and other carcinogenic substances. Nicotine increases the release of epinephrine and norepinephrine, which results in peripheral vasoconstriction, elevated blood pressure and heart rate, greater oxygen consumption, and increased likelihood of dysrhythmias. In addition, nicotine activates platelets and stimulates smooth muscle cell proliferation in the arterial walls. Carbon monoxide reduces the amount of blood available to the intima of the vessel wall and increases the permeability of the endothelium. Hypertension High blood pressure afflicts nearly 1 in 3 adults in the United States. It increases the workload of the heart by increasing the afterload, enlarging and weakening the left ventricle over time. As blood pressure increases, the risk of a serious cardiovascular event also escalates. When clients have hypertension, obesity, tobacco use, high cholesterol levels, and diabetes, the risk of heart attack increases significantly. More men than women have hypertension until the age of 45, when it is more prevalent in women. The prevalence of hypertension in African Africans is among the highest in the world. In addition, African Americans have hypertension at an earlier age and it is more severe at any age. Consequently, the rate of heart disease in African Americans is 1.5 times greater than that of white Americans. Although hypertension cannot always be prevented, it should be treated to lower the risk of CHD and premature death. Elevated Serum Cholesterol Levels The risk of CHD increases as blood cholesterol levels increase. This risk increases further when other risk factors are present. In adults total cholesterol levels of 240 mg/dl are classified as borderline high. At young and middle ages, men have higher cholesterol levels. In women cholesterol levels contimue to increase up to about age 70. A high intake of cholesterol and saturated fats is associated with the development of CHD. Physical Inactivity

In the United States about 25 % of adults report no leisure time physical activity, even though regular aerobic exercise is important in preventing heart and blood vessel disease. There is an inverse relationship between exercise and the risk of CHD. Those who exercise reduce their risk of CHD because they have (1) higher HDL levels; (2) lower LDL cholesterol, triglyceride, and blood glucose levels; (3) greater insulin sensitivity; (4) lower blood pressure; and (5) lower body mass index. The AHA recommends 30 to 60 minutes of physical activity on most days of the week. Obesity Obesity places an extra burden on the heart, requiring the muscle to work harder to pump enough to support added tissue mass. In addition obesity increases the risk for CHD because it is often associated with elevated serum cholesterol and triglyceride levels, high blood pressure, and diabetes. Distribution of body fat is also important. A waist measurement is a way to estimate fat. For men a high-risk waistline measurement is more than 40 inches, and for women a high-risk waist measurement is more than 35 inches. Body mass index (BMI) is another measure to estimate body fat. A BMI from 18.5 to 24.9 is considered healthy. Extreme obesity, or a BMI greater than 40, is estimated to occur in 4.9 % of the population. People can lower their heart disease risk by losing as little as 10 to 20 pounds. An alternating pattern of weight gain and weight loss, however, is associated with an increased risk for CHD. Diabetes A fasting blood glucose level of more than 126 mg/dl or a routine blood glucose level of 180 mg/dl and glucosuria signals the presence of diabetes and represents an increased risk for CHD. Clients with diabetes have a two-to four-fold higher prevalence, incidence, and mortality from all forms of CHD.

Pathophysiology Three coronary arteries normally supply the myocardium with blood to meet its metabolic needs during varying workloads. The right coronary artery supplies arterial blood to the right side of the heart; the left coronary artery divides into the left circumflex artery, which feeds the posterior heart muscle, and the anterior descending artery, which supplies the anterior myocardium, especially the left ventricle. The coronary vessels are usually efficient and perfuse the myocardium during diastole. When the heart needs more blood, the vessels dilate. As the vessels become lined and eventually occluded with atherosclerotic plaques and thrombi, the vessels can no longer dilate properly. If the coronary vessels slowly become occluded, collateral vessels develop to provide the myocardium with needed arterial blood. Collateral vessels are more common in clients with long-term coronary artery disease. Myocardial ischemia develops if the blood supply through the coronary vessels or oxygen content of the blood is not adequate to meet metabolic demands. Disorders of the coronary vessels, the circulation, or the blood may lead to deficits in supply. Myocardial ischemia occurs when either supply or demand is altered. In some people, the coronary arteries can supply adequate blood when the person is at rest; when the person attempts activity or is taxed in some manner, however, angina develops. Myocardial cells become ischemic within 10 seconds of coronary artery occlusion. After several minutes of ischemia, the pumping function of the heart is reduced. The reduction in pumping deprives the ischemic cells of needed oxygen and glucose. The cells convert to anaerobic metabolism, which leaves lactic acid as a waste product. As lactic acid accumulates, pain develops. Angina pectoris is transient, lasting for only 3 to 5 minutes. I f blood flow is restored, no permanent damage myocardial damage occurs. Clinical Manifestations Characteristics of Angina

Angina is a clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back, or arm. Angina pectoris produces transient paroxysmal attacks of substernal or precordial pain with the following characteristics:
o

Onset. Angina can develop quickly or slowly. Some clients ignore the chest pain, thinking that it will go away or that it is indigestion. Ask what the client was doing when the pain began.

Location. Nearly 90 % of clients experience the pain as retrosternal or slightly to the left of the sternum.

Radiation. The pain usually radiates to the left shoulder and upper arm and may then travel down the inner aspect of the left arm to the elbow, wrist, and fourth and fifth fingers. The pain may also radiate to the right shoulder, neck, jaw, or epigastric region. On occasion, the pain may be felt only in the area of radiation and not in the chest. Rarely is the pain localized to any one single small area over the precordium.

Duration. Angina usually lasts less than 5 minutes. However, attacks precipitated by a heavy meal or extreme anger may last 15 to 20 minutes.

Sensation. Clients describe the pain of angina as squeezing, burning, pressing, choking, aching, or bursting pressure. The client often says the pain feels like gas, heartburn, or indigestion. Clients do not describe angina pain as sharp or knife-like.

Severity. The pain of angina is usually mild or moderate in severity. It is often called discomfort, not pain. Rarely is the pain described as severe.

Associated characteristics. Women, older adults, and clients with diabetes may have atypical presentations of CHD that are equivalent to angina. In women, CHD may be manifested as epigastric pain, dyspnea, or back pain, whereas older adults frequently experience dyspnea, fatigue, syncope.

Relieving and aggravating factors. Angina is aggravated by continued activity, and most anginal attacks quickly subside with the administration of nitroglycerine and rest.

The typical exertion-pain, rest-relief pattern is the major clue to the diagnosis of angina pectoris.
o

Treatment. Treatments to reduce the demand on the heart, such as rest, or treatments that dilate the coronary arteries will commonly reduce the pain. The client may have used nitroglycetrine and the client should be asked if the angina subsided.

Patterns of Angina Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest Unstable angina (also called preinfarction angina or crescendo angina): symptoms occur more frequently and last longer than stable angina. The threshold for pain is lower, and pain may occur at rest. Intractable or refractory angina: severe incapacitating chest pain Variant angina (also called Prinzmetals angina): pain at rest with reversible ST-segment elevation; thought to be caused by coronary artery vasospasm Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a stress test), but patient reports no symptoms Medical Management Medical management of clients with angina pectoris focuses on three goals: (1) relieve the acute pain, (2) restore coronary blood flow, and (3) prevent further attacks to reduce the risk of AMI. The diagnosis of angina pectoris is confirmed by history and various tests. A complete history of the pain and its pattern is collected to discriminate angina from other causes of chest pain. Clients are encouraged to describe the pain in their own words. Record a complete analysis of manifestations. This description provides a baseline that can be used in ongoing care. Relieve acute pain and restore coronary blood flow The primary goal of pharmacologic treatment of angina is to balance myocardial oxygen supply and demand by altering the various components of the process, thereby increasing oxygen supply to the myocardium or reducing myocardial oxygen demand. The components of myocardial

oxygen consumption that can be pharmacologically treated are (1) blood pressure, (2) heart rate, (3) contractility, and (4) left ventricular volume. The major types of medications used to treat the acute attack in angina pectoris are as follows:
o Opiates analgesics are used to relieve or reduce acute pain. By reducing pain, the heart

rate often lowers and the need for oxygen by the myocardium also is reduced.
o Vasodilators help reduce acute pain and prevent further attacks by widening the diameter

of coronary arteries and increasing the supply of oxygen to the myocardium. Nitroglycerin, a short acting nitrate, has been the treatment of choice against angina attacks since 1867. Administered sublingually, per tablet, or via transligual spray, nitroglycerin helps relieve or reduce angina pain within 1 to 2 minutes. Long-acting nitrates, given orally or transdermally, help maintain coronary artery vasodilation, thereby promoting greater flow of blood and oxygen to the heart muscle.
o Beta-adrenergic blockers help reduce the workload of the heart, decrease myocardial

oxygen demand, and may decrease the number of angina attacks.

o Calcium-channel blockers are used to dilate coronary arteries, thereby increasing

oxygen supply to the myocardium.

o Antiplatelet agents inhibit platelet aggregation and reduce coagulability, thus preventing

clot formation. Prevent further attacks Education and counselling regarding modification of risk factors are necessary to reduce the progression of CHD and to prevent further attacks.

ASSESSMENT

NURSING INFERENCE DIAGNOSIS

PLANNING

INTERVENTION RATIONALE

EVALUATION

Subjective: Sumasakit ang dibdib ko, as verbalized by the patient Objective: (+)Diaphoresis (+)Facial grimace -Pain scale of 8 out of 10 -v/s taken as follows: PR: 112 cpm BP:140/100 mmHg

Acute pain related to myocardial ischemia resulting from coronary artery occlusion

Occlusion of coronary artery Impaired coronary blood flow Ischemia Shift from aerobic to anaerobic metabolism Lactic acidosis Sensitization to pain

After 20 minutes of effective nursing intervention, the client will experience improved comfort in the chest, as evidenced by -decrease in the pain rating -have reduced anxiety -the ability to rest and sleep comfortably

> Establish rapport with patient. >Assess the characteristics of chest pain including location, duration, intensity etc. Have the client rate pain on a scale of 0 to 10.

> To gain cooperation and trust from the client. > To ascertain clients present situation

> Goal met. After 20 minutes of effective nursing intervention, the clients pain was lessen as evidenced by -pain scale of 4 -respiratory rate, cardiac rate, and blood pressure returned to prediscomfort level

> Assess > To determine respirations, any significant blood pressure, changes and heart rate with each episode of chest pain. > Obtain a 12lead ECG on admission and then each time chest pain recurs for evidence of further infarction > Monitor the response to drug therapy. Notify physician if pain does not abate 15-20 minutes > To monitor further cardiac damage and location of myocardial ischemia

> Pain control is a priority because it indicates ischemia

> Provide care in a calm, efficient manner that reassures the client and minimizes anxiety. Stay with the client

> External stimuli may worsen anxiety and increase cardiac workload as well as limit coping abilities

ACUTE MYOCARDIAL INFARCTION

An AMI is also known as a heart attack, coronary occlusion, or simply a coronary, which is a life-threatening condition characterized by the formation of localized necrotic areas within the myocardium. AMI usually follows the sudden occlusion of a coronary artery and the abrupt cessation of blood and oxygen flow to the heart muscle. Because the heart muscle must function continuously, blockage of blood to the muscle and the development of necrotic areas can be lethal. Etiology and Risk Factors The most common cause of AMI is complete or nearly complete occlusion of a coronary artery, usually precipitated by rupture of a vulnerable atherosclerotic plaque and subsequent thrombus formation. Plaque rupture can be precipitated by both internal and external factors. Internal factors include plaque characteristics, such as the size and consistency of the lipid core and the thickness of the fibrous cap, as well as conditions to which it is exposed, such as coagulation status and degree of arterial vasoconstriction. External factors result from actions of the client or from external conditions that affect the client. Strenuous physical activity and severe emotional stress, such as anger, increase sympathetic nervous system responses, that may lead to plaque rupture. At the same time, sympathetic nervous system responses increase myocardial oxygen demand. Scientists have reported that external factors, such as exposure to cold and time of day, also affect plaque rupture. Acute coronary events occur more frequently with exposure to cold and during the morning hours. Researchers hypothesize that the sudden increases in sympathetic nervous system responses associated with these factors may contribute to plaque rupture. The role of inflammation in triggering plaque rupture is currently being studied. Regardless of the cause, rupture of the atherosclerotic plaque results in (1) exposure of the plaques lipid-rich core to flowing blood, (2) seepage of blood into the plaque, causing it to expand, (3) triggering of thrombus formation, and (4) partial or complete occlusion of the coronary artery.

Unstable angina is associated with short-term partial occlusion of a coronary artery, whereas AMI results from significant or complete occlusion of a coronary artery that lasts more than 1 hour. When blood flow ceases abruptly, the myocardial tissue supplied by the artery dies. Coronary artery spasm can also cause acute occlusion. The risk factors that predispose a client to a heart attack are the same as for all forms of CHD. Pathophysiology AMI can be considered the end-point of CHD. Unlike the temporary ischemia that occurs with angina, prolonged unrelieved ischemia causes irreversible damage to the myocardium. Cardiac cells can withstand ischemia for about 15 minutes before they die. Because the myocardium is metabolically active, manifestations of ischemia can be seen within 8 to 10 seconds of decreased blood flow. When the heart does not receive blood and oxygen, it converts to anaerobic metabolism, creating less adenosine triphosphate (ATP) and more lactic acid as a by-product. Myocardial cells are very sensitive to changes in pH and become less functional. Acidosis causes the myocardium to become more vulnerable to the effects of the lysosomal enzymes within the cell. Acidosis leads to conduction system disorders, and dysrhythmias develop. Contractility is also reduced, decreasing the hearts ability to pump. As the myocardial cells necrose, intracellular enzymes are introduced into the bloodstream, where they can be detected by laboratory tests. Cellular necrosis occurs in one layer of myocardial tissue in subendocardial, intramural, and subepicardial infarctions. In a transmural infarction, cellular necrosis is present in all three layers of myocardial tissue. The infarct site is called the zone of infarction and necrosis. Around it is a zone of hypoxic injury, also called a penumbra. This zone can return to normal but may also become necrotic if blood flow is not restored. The outermost zone is called the zone of ischemia; damage to this area is irreversible.

Clinical Manifestations The clinical manifestations associated with AMI result from ischemia of the heart muscle and the decrease in function and acidosis associated with it. The major clinical manifestation of AMI is chest pain which is similar to angina pectoris but more severe and unrelieved by nitroglycerine.

The pain may radiate to the neck, jaw, shoulder, back, or left arm. The pain also may present near the epigastrium, simulating indigestion. AMI may also be associated with less common clinical manifestations, including the following: o Atypical chest, stomach, back, or abdominal pain o Nausea, or dizziness o Shortness of breath o Unexplained anxiety, weakness, or fatigue o Palpitations, cold sweat, or paleness Women experiencing AMI frequently present with one or more of the less common clinical manifestations. Medical Management Major goals of care for clients with AMI include the following: o Initiating prompt care o Determining the type of AMI (STEMI vs NSTEMI) o Reducing pain o Delivering successful treatment for the acute pain and reperfusion of the myocardium o Preventing complications o Preventing remodelling and heart failure o Rehabilitating and educating the client and significant others Treat the acute attack immediately Clients with manifestations of AMI must receive immediate treatment. Delays may increase damage to the heart and reduce the chance of survival. The goal for treatment of AMI is door to

needle in less than 30 minutes, or specifically from onset of pain till thrombolytic therapy within 30 minutes or percutaneous angioplasty within 1 hour. Until EMS personnel arrive, keep the client quiet and calm. It is recommended that, if conscious, a client chew an aspirin at the onset of manifestations, because mortality is reduced 23 % with this action alone. While waiting for EMS to arrive, elevate the clients head and loosen any tight clothing around the neck. Once EMS workers arrive, the client is assessed and transported quickly to an emergency department.

ASSESSMENT

NURSING INFERENCE DIAGNOSIS

PLANNING

INTERVENTION RATIONALE

EVALUATION

S/O: -(+) Dyspnea -(+) Crackles -(+) Cyanosis - Impaired capillary refill -PaO2:60 mmHg

Impaired gas exchange related to decreased cardiac output as evidenced by cyanosis

Occlusion of coronary artery Impaired coronary circulation Decreased cardiac output Ischemia Decreased exchange of O2 and CO2 Anaerobic metabolism Decreased oxygenation Cyanosis

After 1 hour of effective nursing intervention, the client will demonstrate improved gas exchange, as evidenced by -absence of dyspnea, crackles -absence of cyanosis -brisk capillary refill - ABG levels within normal limits

> Establish rapport with patient. >Administer oxygen as ordered; maintain continuous oximetry

> To gain cooperation and trust from the client. > To increase amount of oxygen available for myocardial uptake ; measures peripheral oxygen saturation > To monitor data on adequacy of tissue perfusion and oxygenation > Capillary refill greater than 3 seconds indicates poor perfusion and hypoxia

> Goal met. After 1 hour of effective nursing intervention, the clients breath sounds were clear and the ABG values are within normal limits

> Monitor ABGs as ordered

> Continue to assess clients skin, capillary refill, and the level of consciousness every 2-4 hours as needed > Assess respiratory status for dyspnea and crackles

> Dyspnea may indicate inadequate oxygenation

> Provide care in a calm, efficient manner that reassures the client and minimizes anxiety. Stay with the client

> External stimuli may worsen anxiety and increase cardiac workload as well as limit coping abilities

ENDOCARDITIS
- A microbial infection of the endothelial surface of the heart. - It is most common in older people, who are more likely to have degenerative or calcific valve lesions, reduced immunologic response to infection, and the metabolic alterations associated with aging. Pathophysiology

Clinical Manifestations - The primary presenting symptoms of infective endocarditis are fever and heart murmur. - Fever may be intermittent or absent, especially in patients who are receiving antibiotics or corticosteroids, in those who are elderly, or those who have heart failure or renal failure. - Heart murmur may be absent initially but develops in almost all patients. Murmurs that worsen over time indicate progressive damage from vegetations or perforation of the valve or the chordae tendineae. - Clusters of petechiae may be found on the body. - Small, painful nodules (Osler nodes) may be present in the pads of finger or toes. - Irregular, red pr purple, painless, flat macules (Janeway lesions) may be present on the palms, fingers, hands, soles, and toes. - Hemorrhages with pale centers (Roth spots) caused by emboli may be observed in the fundi of the eyes. - Splinter hemorrhages (ie, reddish-brown lines and streaks) may be seen under the fingernails and toenails, and petechiae may appear in the conjunctiva membranes. - Cardiomegaly, heart failure , tachycardia, or splenomegaly may occur. - CNS manifestations of infective endocarditis include headache; temporary or transient cerebral ischemia; and strokes, which may be caused by emboli to the cerebral arteries. - Valvular stenosis or regurgitation, myocardial damage, and mycotic (fungal) aneurysm are potential cardiac complications. - First-degree, second-degree, and third degree atrioventricular blocks may occur and are often a sign of a valve ring abscess. and mucous

Assessment and Diagnostic Findings

- Vague complaints of malaise, anorexia, weight loss, cough, and back and joint complain may be mistaken for influenza. - A definitive diagnosis is made when a microorganism is found in two separate blood cultures, in a vegetation, or in an abscess. - Three sets of blood cultures (with each set including oneaerobic and one anaerobic culture) drawn over a 24-hour period (or every 30 minutes if the patients condition is unstable) should be obtained before administration of any antimicrobial agents. - Negative blood cultures do not definitely rule out infective endocarditis. - Patients may have elevated WBC counts. - In addition, patients may be anemic and have a positive rheumatoid and an elevated erythrocyte sedimentation rate (ESR) or C-reactive protein. - Micrscopic hematuria may be present on urinalysis. - Doppler echocardiography may assist in the diagnosis by demonstrating a mass on the valve, prosthetic valve, or supporting structures and by identifying vegetations, abscesses, new prosthetic valve dehiscence, or new regurgitation. Medical Management - The objective of treatment is to eradicate the invading organism through adequate doses of an appropriate antimicrobial agent. - Antibiotic therapy is usually administered parenterally in a continuous IV infusion for 2 to 6 weeks. - Parenteral therapy is adminstered in doses that produce a high serum concentration for a significant period to ensure eradication of the dormant bacteria within the dense vegetations. - If there is insufficient bactericidal activity, increased dosages of the antibiotic are prescribed or a different antibiotic is used.

- Penicillin is usully the medication of choice. - Blood cultures are taken periodically to monitor the effect pf therapy. - In addition, the patients temperature is usually monitored at regular intervals because the course of the fever is one indication of the effectiveness of treatment.

Surgical Management - Surgical intervention is required if the infection does not respond to medications, the patient has a prothetic heart valve endocarditis, has a vegetation larger that 1 cm, or develops complications such as a septal perforation. - Surgical interventions include valve debridement or excision, debridement of vegetations, debridement and closure of an abscess, and closure of a fistula. - Aortic or mitral valve debridement, excicion, or rreplacement is required in patient who: Develop congestive heart failure despite adequate medical treatment. Have more than one serious systemic embolic episode Develop a periannular (heart valve), myocardial, or aortic abscess Have uncontrolled infection, persistent or recurrent infection, or fungal endocarditis - Most patients who have prosthetic valve endocarditis (ie, infected valve replacement) require valve replacement. Nursing Management - The nurse monitors the patients temperature.

- Heart sounds are assessed. A new or worsening heart murmur may indicate dehiscence of a prosthetic valve, rupture of an abscess, or injury to valve leaflets or chordae tendineae. - The nurse montors for signs and symptoms of systemic embolization, or, for patients with right-sided heart endocarditis, for signs and symptoms of pulmonary infarction and infiltrates. - In addition, the nurse assesses signs and symptoms of organ damage such as stroke (ie, cerebrovascular accident or brain attack), meningitis, heart failure, myocardial infarction, glomerulonephritis, and splenomegaly. - Patient care is directed toward management of infection. - Long-term IV antimicrobial therapy is often necessary; therefore, many patients have peripherally inserted central catheters or other long-term IV access. - All invasive lines and wounds must be assessed daily for redness, tenderness, warmth, swelling, drainage, or other signs of infection. - The patient and family are instructed about activity restrictions, medications, and signs and symptoms of infection. - Patients with infective endocarditis arre at high risk for another episode of infective endo carditis. The nurse emphasizes the antibiotic prophylaxis previously prescribed. - If the patient undergone surgical treatment, the nurse provides postoperative care and instructions. - The nurse provides the patient and family with emotional support and facilitates coping strategies during the prolonged course of the infection and antibiotc treatment.

ASSESSMENT

NURSING INFERENCE DIAGNOSIS

PLANNING

INTERVENTION RATIONALE

EVALUATION

Subjective:

Fever Fever related to Mainit yung increased pakiramdam WBC WBC of ko, as production. 14.4 x 10 9/L, verbalized by suggestive of the patient. infection Objective: Temp: 38.2 C WBC: 15 000 mg/dl Production of heat as a body defense mechanism

After 1 hour Establish of effective rapport nursing intervention, the client will have stable body temperature as Monitor V/S manifested q4 hours by: Increase fluid Temperatur intake, with 1 e within glass of water normal q1 1/2 hours range, 36.5 to 37.5C. Maintain protection against risk factors (e.g. Too cold and too warm environment)

To establish good communicati on, cooperation and gain trust

GOAL MET.

WAS

After 1 hour of effective nursing intervention, the client maintained a For baseline stable body data temperature as To prevent manifested by: dehydration Temperature of 37.5C To prevent from unwanted effect of elevated body temperature

Increased production of heat

Release of prostaglandins

Encourage To facilitate patient to wear body lose clothes temperature Perform TSB To facilitate the heat of the body To facilitate the present condition.

Administer prescribed medication.

PERICARDITIS
- An inflammation of the pericardium, the membranous sac enveloping the heart.

- It may be a primary illness or it may develop during various medical and surgical disorders. - It may be acute, subacute, or chronic. It is classified either as adhesive (constrictive), because the layers of the pericardium become attached to each other and restrict ventricular filling, or by what accumulates in the pericardial sac: serous (serum), purulent (pus), calcific (calciumdeposits), febrinous (clotting protein), or sanguinous (blood). CAUSES: Idiopathic or nonspecific causes Infection: usually viral; rarely bacterial; and mycotic Disorders of connective tissue: systemic lupus erythematosus, rheumatic fever, rheumatoid arthritis, polyarthritis, scleroderma Hypersensitivity state: immune reactions, medication reaction, serum sickness Disorders of adjacent structures: MI, dissecting aneurysm, pleural and pulmonary disease (pneumonia) Neoplastic disease: causes by metastasis from lung cancer or breast cancer, leukemia, and pimary (mesothelioma) neoplams Radiation theraphy of chesst and upper torso (peak occurance: 5-9 mos after treatment) Trauma: chest injury, cardiac surgery, cardiac catheterization, implantation of pacemaker or implantable cardiverter defibrillator (ICD) Renal failure and uremia TB Pathophysiology

Clinical Manifestations - May be asymptomatic - Most characteristic symptom is chest pain, although pain may be located beneath the clavicle, in the neck, or in the left trapezius (scapula) region. - The pain or discomfort usually remains fairly constant, but it may worsen with deep inspiration and when lying down or turning. It may be relieved with a forward-leaning or sitting position. - Most characteristic sign of pericarditis is a creaky or scratch friction rub heard most clearly at the left lower sternal border. - Other signs may include a mild fever, increased WBC count, anemia, and an elevated ESR or C-reactive protein level. - Patients may have a productive or nonproductive cough. - Dyspnea and other signs and symptoms of heart failure may occur as the result of pericardial compression due to constrictive pericarditis or cardiac tamponade. Assessment and Diagnostic Findings - Diagnosis is most often made on the basis of the history, signs, and symptoms. - An echocardiogram may detect inflammation, pericardial effusion or tamponade, and heart failure. It may help confirm the diagnosis and may be used to guide pericardiocentesis (needle or catheter drainage of the pericardium). - Computed tomography (CT) may be the best diagnostic tool for determining the size, shape, and location of the pericardial effusions and may be used to guide pericardiocentesis. - MRI may assist with detection of inflammation and adhesions. Medical Management - The objective are to determine the cause, administer therapy foor treatment and symptom relief, and detect sign and symptom of cardiac tamponade.

- When the cardiac output is impaired, the patient is placed on bed rest until the fever, chest pain, and friction rub have subsided. - Analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin or ibuprofen (Motrin) may be prescribed for pain relief during the acute phase. These agents also hasten the reabsorption of fluid in oatients with rheumatic pericarditis. Indomethacin is contraindicated because it may decrease the coronary blood flow. - Corticosteroids (e.g. Prednisone) may be prescribed if the pericarditis is severe and the patient does not respond to NSAIDs. - Pericardiocentesis, a procedure in which some of the pericardial fluid is removed, is rarely necessary. It may be performed to assist in the identification of the cause or relieve symptoms, especially if there are signs and symptoms of heart failure or tamponade. - Pericardial fluid is cultured if bacterial bacterial, tubercular, of fungal disease is suspected, and a sample is sent for cytology if neoplastic disease is suspected. - A pericardial window, a small opening made in the pericardium, may be oerfoemed to allow continuous drainage inti the chest cavity. - Surgical removal of the tough encasing pericardium (pericardiectomy) may be necessary to release both the ventricles from the constrictive and restrictive inflammation and scarring. Nursing Management - Patients with acute pericarditis require pain management with analgesics, positioning, and psychological support. - Patients with chest pain often benefit from education and reassurance that the pain is not due to a heart attack. - To minimize complication, the nurse helps the patient with activity restrictions until the pain and fever subsude. As the condition of the patient improve, the nurse encourages a gradual increase of activity. However, if pain, fever, or friction rub reappear, activity restrictions must be resumed.

- The educates the patients and the family about a healthy lifestyle to enhance the patients immune system. - Nurse must be alert about cardic tamponade - Nurse monitors the patient for heart failure.

ASSESSMENT

NURSING DIAGNOSIS

INFERENCE

PLANNING

INTERVENTION RATIONALE

EVALUATION

S/O: (+) tachycardia (+)facial grimace (+) guarding behavior Describes pain at the chest From the pain scale 10 is the highest, the patient verbalized 7.

Acute pain Tissue trauma related to inflammation Inflammation of pericardium. Transportatio n of bradykinin and histamine at the site Hyperemia Redness Heat

After 30 Establish To establish minutes of rapport good effective communicati nursing on, intervention, cooperation the patient will and gain experience pain trust alleviation as evidenced by: Monitor V/S For baseline q4 hours data - Verbalization of pain Assess pain To have an alleviation location, intensive - (-) severity/inten assessment tachycardia sity, duration, of pain that - (-) facial and interval the patient grimace feels. - (-) guarding behavior Provide - Pain scale To divert divertional score of 4-5 patients but nonattention energy towards pain exerting and promote activities none such as pharmacolo watching tv, gical pain music, etc. management . Assist client To have less with positioning energy consumption Encourage period of rests To prevent fatigue Administer prescribed medication. To facilitate the present condition.

GOAL MET.

WAS

After 30 minutes of effective nursing intervention, the patient has experienced pain alleviation.

PATHOPHYSIOLOGY OF ACQUIRED VALVULAR DISORDERS

Backward Heart Failure Aoritc stenosis limits forward flow of blood from the left ventricle Aortic regurgitation permits blood flow back into the left ventricle Increased blood volume and pressure in the left ventricle Left ventricular hypertrophy and dilation; blood from the left atrium cannot get Mitral stenosis limits the forward flow of blood into the left ventricle Mitral regurgitation permits blood flow back into the left atrium Forward Heart Failure Not enough blood flows through the aorta for the bodys needs (decreased cardiac Angina pectoris, postural hypotension, fatigue, dizziness

Increased blood volume and pressure in Left atrium hypertrophy and dilation Increased blood volume and pressure in the Pulmonary congestion (shortness of breath and pulmonary edema), increased pulmonary vascular pressure Increased work for the right ventricle, right Right ventricular failure

MITRAL REGURGITATION
Mitral regurgitation involves blood flowing back from the left ventricle into the left atrium during systole. Clinical Manifestations Chronic mitral regurgitation is often asymptomatic, but acute mitral regurgitations (eg, that resulting from a myocardial infarction) usually manifests as severe congestive heart failure. Dysnpea, fatigue, and weakness are the most common symptoms. Palpitations, shortness of breath on exertion, and cough from pulmonary congestion also occur. Assessment and Diagnostic Findings A systolic murmur is heard as a high-pitched, blowing sound at the apex. The pulse may be regular and of good volume, or it may be irregular as a result of extrasystolic beats or atrial fibrillation. Echocardiography is used to diagnose and monitor the progression of mitral regurgitation Medical Management Surgical intervention consists of mitral valve replacement or valvuloplasty (ie, surgical repair of the heart valves).

MITRAL STENOSIS
Mitral stenosis is an obstruction of blood flowing from the left atrium into the left ventricle. It is most often caused by rheumatic endocarditis, which progressively thickens the mitral valve leaflets and chordae tendineae. The leaflets often fuse together. Eventually, the mitral valve orifice narrows and progressively obstructs blood flow into the ventricle.

Clinical Manifestations The first symptom of mitral stenosis is often dyspnea on exertion as a result of pulmonary venous hypertension. Patients with mitral stenosis are likely to show progressive fatigue as a result of low cardiac output. They may expectorate blood (ie, hemoptysis), cough, and experience repeated respiratory infections. Assessment and Diagnostic Findings The pulse is weak and often irregular because of atrial fibrillation (caused by the strain on the atrium). A low-pitched, rumbling diastolic murmur is heard at the apex. As a result of the increased blood volume and pressure, the atrium dilates, hypertrophies, and becomes electrically unstrable, and the patient experience atrial dysrhythmias. Echocardiography is used to diagnose mitral stenosis. Electrocardiography (ECG) and cardiac catheterization with angiography are used to determine the severity of the mitral stenosis. Medical Management Antibiotic prophylaxis therapy is instituted to prevent recurrence of infections. Patients with mitral stenosis may benefit from anticoagulants to decrease the risk for developing atrial thrombus. They may also require treatment for anemia. Surgical intervention consists of valvuloplasty, usually commissurotomy to open or rupture the fused commussures of the mitral valve. Percutaneous transluminal valvuloplasty or mitral valve replacement may be performed.

VALVULAR HEART DISORDERS: NURSING MANAGEMENT Educate the patient regarding the disease: about the diagnosis, the progressive nature, and treatment plan to report any new symptoms or changes in symptoms to the health care provider on emphasis of the need for prophylactic antibiotic therapy before any invasive procedure that may introduce infectious agents to the patients bloodstream infectious agent, usually a bacterium, is able to adhere to the diseased heart valve more readily than to a normal valve. Once attached tot the valve, the infectious agent multiplies, resulting in endocarditis and further damage tot eh valve Assessment: patients vital signs are taken, recorded, and compared with previous data for any changes heart and lung sounds are auscultated and peripheral ppulses palpated. Assess patient for signs and symptoms of heart failure: fatigue, dyspnea with exertion, an increase in coughing, hemoptysis, multiple respiratory infections, orthopnea, or paroxysmal nocturnal dyspnea assess for dysrhythmias by palpating the patients pulse for strength and rhythm (ie, regular or irregular) and asks if the patient has experienced palpitations or felt forceful heartbeats assess for dizziness, syncope, increased weakness, or angina pectoris Collaborative: to develop a medication schedule and teaches about the name, dosage, actions, side effects, and any drug-drug or drug-food interactions of the prescribed medications for heart failure, dysrhythmias, angina pectoris, or other symptoms teach the patient to weigh daily and report the gain of 2 pounds in 1 day or 5 pounds in 1 week to the health care provider

 assist the patient with planning activity and rest periods to achieve a lifestyle acceptable to the patient If the patient is to have surgical valve replacement or valvuloplasty, teaches the patient about the procedure and anticipated recovery.

VALVULOPLASTY AND REPLACEMENT: NURSING MANAGEMENT Patients who have had valvuloplasty or valve replacements area admitted to the intensive care unit; care focuses on recovery from anesthesia and hemodynamic stability. Vital signs are assessed every 5 to 15 minutes and as needed until the patient recovers from anesthesia or sedation and then assessed every 2 to 4 hours and as needed. Intravenous medications to increase or decrease blood pressure and to treat dysrhythmias or altered heart rates are administered and their effects monitored. The intravenous medications are gradually decreased until they are no longer required or the patient takes needed medication by another route (eg, oral, topical). Patient assessments are conducted every 1 to 4 hours and as needed, with particular attention to neurologic, respiratory, and cardiovascular systems. After the patient has recovered from anesthesia and sedation, is hemodynamically stable without intravenous medications, and assessment values are stable, the patient is usually transferred to a telemetry unit, typically within 24 to 72 hours after surgery. Nursing care continues as for most postoperative patients, including wound care and patient teaching regarding diet, activity, medications, and self-care. The nurse educates the patient about long-term anticoagulant therapy, explaining the need for frequent follow-up appointments and blood laboratory studies, and provides teaching about any prescribed medication: the name of the medication, dosage, its actions, prescribed schedule, potential side effects, and any drug-drug or drug-food interactions. Patients with a mechanical valve prosthesis require education to prevent bacterial endocarditis with antibiotic prophylaxis, which is prescribed before all dental and surgical interventions. Patients are discharged from the

hospital in 3 to 7 days. Home care and office or clinic nurses reinforce all new information and self-care instructions with the patient and family for 4 to 8 weeks after the procedure.