Overview of the Cardiovascular System PDF

OVERVIEW OF THE CARDIOVASCULAR SYSTEM MEDICAL SURGICAL NURSING II (GNS 213) ALAGBE O. A. SCHOOL OF NURSING, BUTH, OGBOMOSO, OYO STATE.  THE CARDIOVASCULAR SYSTEM 2 Introduction The function of the cardiovascular system is to supply body cells and tissues...

OVERVIEW OF THE CARDIOVASCULAR SYSTEM MEDICAL SURGICAL NURSING II (GNS 213) ALAGBE O. A. SCHOOL OF NURSING, BUTH, OGBOMOSO, OYO STATE.  THE CARDIOVASCULAR SYSTEM 2 Introduction The function of the cardiovascular system is to supply body cells and tissues with oxygen-rich blood and eliminate carbon dioxide (CO2) and cellular wastes. Damage and disease in the cardiovascular system greatly jeopardize a person’s health. In fact, heart disease is the leading cause of death for adults in the United States. Many advanced treatments have been and are being created to treat heart diseases. Human heart transplantation and the temporary use of an artificial heart are realities. Nevertheless, the primary focus remains preserving the natural heart by preventing heart diseases.  THE CARDIOVASCULAR SYSTEM 3 Objectives: By the end of this section, you will be able to: Describe the overview of Cardiovascular system  THE CARDIOVASCULAR SYSTEM: 4 The heart pumps blood, which creates blood pressure, and circulates oxygen, nutrients, and other substances. The heart is located in the mediastinum, the area between the lungs in the thoracic cavity. PERICARDIAL MEMBRANES: These refers to the three layers that enclose the heart.  The outer, fibrous pericardium, made of fibrous connective tissue, is a loose-fitting sac that surrounds the heart and extends over the diaphragm and the bases of the great vessels.  The parietal pericardium is a serous membrane that lines the fibrous pericardium. 5   The visceral pericardium, or epicardium, is a serous membrane on the surface of the myocardium. 6  Serous fluid between the parietal and visceral pericardial membranes prevents friction as the heart beats. CHAMBERS OF THE HEART  Cardiac muscle tissue, the myocardium, forms the walls of the four chambers of the heart.  Endocardium lines the chambers and covers the valves of the heart; is simple squamous epithelium that is very smooth and prevents abnormal clotting.  The right and left atria are the upper chambers, separated by the interatrial septum. The atria receive blood from veins.  The right and left ventricles are the lower chambers, separated by the interventricular septum. The ventricles pump blood into arteries. 7  RIGHT ATRIUM 8 Receives blood from the upper body by way of the superior vena cava and receives blood from the lower body by way of the inferior vena cava. The tricuspid (right AV) valve prevents backflow of blood from the right ventricle to the right atrium when the right ventricle contracts. LEFT ATRIUM Receives blood from the lungs by way of four pulmonary veins. The mitral (left AV or bicuspid) valve prevents backflow of blood from the left ventricle to the left atrium when the left ventricle contracts.  The walls of the atria produce atrial natriuretic peptide when stretched by increased blood volume or BP. ANP 9 increases the loss of Na ions and water in urine, which decreases blood volume and BP to normal. RIGHT VENTRICLE: has relatively thin walls Pumps blood to the lungs through the pulmonary artery. The pulmonary semilunar valve prevents backflow of blood from the pulmonary artery to the right ventricle when the right ventricle relaxes. Papillary muscles and chordae tendineae prevent inversion of the right AV valve when the right ventricle contracts.  LEFT VENTRICLE: 10 has thicker walls than does the right ventricle Pumps blood to the body through the aorta. The aortic semilunar valve prevents backflow of blood from the aorta to the left ventricle when the left ventricle relaxes. Papillary muscles and chordae tendineae prevent inversion of the left AV valve when the left ventricle contracts. The heart is a double pump: The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs; the left side of the heart receives oxygenated blood from the lungs and pumps it to the body. Both sides of the heart work simultaneously.  CORONARY VESSELS 11 Pathway: ascending aorta to right and left coronary arteries, to smaller arteries, to capillaries, to coronary veins, to the coronary sinus, to the right atrium. Coronary circulation supplies oxygenated blood to the myocardium. Obstruction of a coronary artery causes a myocardial infarction: death of an area of myocardium due to lack of oxygen. 12  CARDIAC CYCLE: 13 This is the sequence of events in one heartbeat. The atria continually receive blood from the veins; as pressure within the atria increases, the AV valves are opened. Two-thirds of the atrial blood flows passively into the ventricles; atrial contraction pumps the remaining blood into the ventricles; the atria then relax. The ventricles contract, which closes the AV valves and opens the aortic and pulmonary semilunar valves. Ventricular contraction pumps all blood into the arteries. The ventricles then relax. Meanwhile, blood is filling the atria, and the cycle begins again.   Systole means contraction; diastole means relaxation. In the cardiac cycle, atrial systole is followed by ventricular 14 systole. When the ventricles are in systole, the atria are in diastole.  The mechanical events of the cardiac cycle keep blood moving from the veins through the heart and into the arteries. HEART SOUNDS: This is the two sounds per heartbeat: lub-dup  The first sound is created by closure of the AV valves during ventricular systole.  The second sound is created by closure of the aortic and pulmonary semilunar valves.  Improper closing of a valve results in a heart murmur.  CARDIAC CONDUCTION PATHWAY: 15 This is the pathway of impulses during the cardiac cycle The SA node in the wall of the right atrium initiates each heartbeat; the cells of the SA node are more permeable to Na ions and depolarize more rapidly than any other part of the myocardium. The AV node is in the lower interatrial septum. Depolarization of the SA node spreads to the AV node and to the atrial myocardium and brings about atrial systole. The AV bundle (bundle of His) is in the upper interventricular septum; the first part of the ventricles to depolarize. 16  The right and left bundle branches in the 17 interventricular septum transmit impulses to the Purkinje fibers in the ventricular myocardium, which complete ventricular systole. An electrocardiogram (ECG) depicts the electrical activity of the heart. If part of the conduction pathway does not function properly, the next part will initiate contraction, but at a slower rate. Arrhythmias are irregular heartbeats; their effects range from harmless to life-threatening.  Heart Rate 18 Healthy adult: 60 to 80 beats per minute (heart rate equals pulse); children and infants have faster pulses because of their smaller size and higher metabolic rate. A person in excellent physical condition has a slow resting pulse because the heart is a more efficient pump and pumps more blood per beat.  Cardiac Output 19 Cardiac output is the amount of blood pumped by a ventricle in 1 minute. Stroke volume is the amount of blood pumped by a ventricle in one beat; average is 60 to 80 mL. Cardiac output equals stroke volume pulse; average resting cardiac output is 5 to 6 liters. Starling’s law of the heart—the more cardiac muscle fibers are stretched, the more forcefully they contract. During exercise, stroke volume increases as venous return increases and stretches the myocardium of the ventricles (Starling’s law).  During exercise, the increase in stroke volume and the 20 increase in pulse result in an increase in cardiac output: two to four times the resting level. Cardiac reserve is the difference between resting cardiac output and the maximum cardiac output; may be 15 liters or more. The ejection fraction is the percent of its total blood that a ventricle pumps per beat; average is 60% to 70%.  REGULATION OF HEART RATE 21 The heart generates its own beat, but the nervous system brings about changes to adapt to different situations. The medulla contains the cardiac centers: the accelerator center and the inhibitory center. Sympathetic impulses to the heart increase rate and force of contraction; parasympathetic impulses (vagus nerves) to the heart decrease heart rate. Pressoreceptors in the carotid and aortic sinuses detect changes in blood pressure. Chemoreceptors in the carotid and aortic bodies detect changes in the oxygen content of the blood.  The glossopharyngeal nerves are sensory for the 22 carotid receptors. The vagus nerves are sensory for the aortic receptors. If blood pressure to the brain decreases, pressoreceptors in the carotid sinuses detect this decrease and send fewer sensory impulses along the glossopharyngeal nerves to the medulla. The accelerator center dominates and sends motor impulses along sympathetic nerves to increase heart rate and force of contraction to restore blood pressure to normal. A similar reflex is activated by hypoxia. Epinephrine from the adrenal medulla increases heart rate and force of contraction during stressful situations.  AGING AND THE HEART 23 The heart muscle becomes less efficient with age, and there is a decrease in both maximum cardiac output and heart rate, although resting levels may be more than adequate. The health of the myocardium depends on its blood supply, and with age there is greater likelihood that atherosclerosis will narrow the coronary arteries. Atherosclerosis is the deposition of cholesterol on and in the walls of the arteries, which decreases blood flow and forms rough surfaces that may cause intravascular clot formation.  High blood pressure (hypertension) causes the left 24 ventricle to work harder; it may enlarge and outgrow its blood supply, thus becoming weaker. A weak ventricle is not an efficient pump, and such weakness may progress to congestive heart failure; such a progression may be slow, or may be rapid. The heart valves may become thickened by fibrosis, leading to heart murmurs and less efficient pumping. Arrhythmias are also more common with age, as the cells of the conduction pathway become less efficient. 25 ASSESSMENT OF THE CARDIOVASCULAR SYSTEM  MEDICAL SURGICAL NURSING III  (GNS 222) ALAGBE O. A. SCHOOL OF NURSING, BUTH, OGBOMOSO, OYO STATE.  ASSESSMENT OF THE CARDIOVASCULAR SYSTEM 26 The frequency and extent of the nursing assessment of cardiovascular functions are based on several factors, including the severity of the patient’s symptoms, the presence of risk factors, the practice setting, and the purpose of the assessment. An acutely ill patient with CVD who is admitted to the emergency department or coronary intensive care unit requires a very different assessment than a person who is being examined for a chronic stable condition.  A. HISTORY TAKING 27 The initial assessment includes the client’s (or family member’s) description of the symptoms the client experienced before and during admission. The history also includes the client’s past medical history and family medical history. The family medical history is important because many cardiac disorders have a familial or genetic predisposition. The following are the most common signs and symptoms of Cardiovascular diseases, with related medical diagnoses in parentheses:  Chest pain or discomfort (angina pectoris, ACS, dysrhythmias, valvular heart disease).  Shortness of breath or dyspnea (ACS, cardiogenic shock, HF, valvular heart disease).   Peripheral edema, weight gain, abdominal distention due to enlarged spleen and liver or ascites (HF). 28  Palpitations (tachycardia from a variety of causes, including Acute Coronary Syndrome, caffeine or other stimulants, electrolyte imbalances, stress, valvular heart disease, ventricular aneurysms).  Vital fatigue, sometimes referred to as vital exhaustion (an early warning symptom of ACS, HF, or valvular heart disease, characterized by feeling unusually tired or fatigued, irritable, and dejected).  Dizziness, syncope, or changes in level of consciousness (cardiogenic shock, cerebrovascular disorders, dysrhythmias, hypotension, postural hypotension, vasovagal episode).  B. PHYSICAL EXAMINATION 29  General Appearance: An appraisal of the client’s general appearance may suggest problems that require further exploration. The client’s nonverbal behavior and body position may indicate that he or she is anxious, depressed, in pain, or uncomfortable.  Pain: Poor circulation, a common problem in clients with cardiovascular disorders, causes ischemia (reduced blood supply) to body organs. A classic sign of ischemia is pain, which results from a lack of oxygen in the tissue. Chest pain is a manifestation of ischemia to the heart muscle. Leg pain, especially with activity, can indicate inadequate oxygenation to leg muscles.  Vital Signs: Temperature, Pulse, Respiratory Rate, Blood Pressure.   Cardiac Rhythm: The electrical activity that produces the heart rhythm can be observed continuously with bedside 30 cardiac monitoring.  Heart Sounds Normal Heart Sounds: Auscultation of the heart requires familiarization with normal and abnormal heart sounds. The first heart sound (lub), referred to as S1, is the closing of the mitral and tricuspid valves. S1 is heard loudest over the apex of the heart and occurs nearly simultaneously with the palpated pulse. The second heart sound (dub), referred to as S2, is the closing of the aortic and pulmonic valves. S2 is heard loudest with the stethoscope in the aortic area, which is at the second intercostal space to the right of the sternum. Abnormal Heart Sounds: All other heart sounds are abnormal and take considerable practice to recognize. A  sound that follows S1 and S2 is called an S3 heart sound or a ventricular gallop. When the three sounds are heard 31 together, some say the cadence/beat sounds like ‘‘Ken-tuck- y’’ or ‘‘lub-dub-dee.’’ An S3, although normal in children, often is an indication of heart failure in an adult. An extra sound just before S1 is an S4, heart sound, or atrial gallop. Some say this sound resembles the word ‘‘Ten-nes- see’’ or ‘‘lub-lub-dub.’’ An S4 sound often is associated with hypertensive heart disease. In addition to heart sounds, auscultation may reveal other abnormal sounds, such as murmurs and clicks caused by turbulent blood flow through diseased heart valves. A friction rub may cause a rough, grating, or scratchy sound that is indicative of pericarditis (inflammation of the pericardium).  Peripheral Pulses: The nurse palpates the radial arteries and the major arteries of the leg bilaterally during the  physical assessment. He or she records the presence or absence of these pulses and their strength. 32  Skin: Many clients with cardiac disorders exhibit changes in skin color (e.g., cyanosis, pallor). A good light is necessary when assessing skin color. Cyanosis can be detected by carefully noting color changes in the oral mucous membranes as well as on the lips, earlobes, skin, and nail beds. In light-skinned clients, extreme pallor is easy to detect because the skin appears almost bloodless. In dark- skinned clients, a grayish cast to the skin usually indicates pallor.  Peripheral Edema: Edema occurs when blood is not pumped efficiently or plasma protein levels are inadequate to maintain osmotic pressure. When blood has nowhere else to go, the extra fluid enters the tissues. Particular areas for examination are the dependent parts of the body,  such as the feet and ankles. Other areas prone to edema are the fingers, hands, and over the sacrum. To assess for 33 edema, the examiner gently presses his or her fingers into the skin and then quickly releases. If the marks of the fingers remain, the effect is termed pitting edema.  Weight: Weight gain can indicate edema. A rapid gain in weight often means that edema is increasing.  Jugular Veins: If the right side of the heart fails to pump efficiently, blood becomes congested in the neck veins. With the client sitting at a 450 angle, the client turns his or her head to the left or right so the nurse can inspect the external jugular vein. Distention of this vein usually indicates increased fluid volume and pressure in the right side of the heart.  Lung Sounds: If the left side of the heart fails to pump efficiently, blood backs up into the pulmonary veins and  lung tissue. The nurse auscultates the lungs for abnormal and normal breath sounds. With left-sided congestive heart 34 failure, auscultation reveals a crackling sound and possibly wheezes and gurgles. Wet lung sounds are accompanied by dyspnea and an effort to sit up to breathe. If uncorrected, left-sided heart failure is followed by right-sided heart failure because the circulatory system is a continuous loop.  Sputum: Clients with cardiac disease may have a productive or nonproductive cough. The nurse notes the type and frequency of the cough and the amount and appearance of the sputum. These findings can be important in diagnosing heart failure or other pulmonary complications.  Mental Status: Some clients with cardiac disorders may be alert and oriented; others may be confused and disoriented. Confusion or disorientation can result from a  decrease in the oxygen supply to the brain (cerebral ischemia) as a result of poor circulation. 35 C. DIAGNOSTIC TESTS  Laboratory Tests: Various general laboratory tests are used in the diagnosis of heart disease and in monitoring the client’s progress. Laboratory tests may be performed daily or every few days. They may be used to monitor the results of therapy. Blood chemistries, such as fasting blood glucose and serum electrolyte, cholesterol, and triglyceride levels, may be used as parts of the diagnostic process. Analysis of serum enzymes and isoenzymes may also be used. When tissues and cells break down, are damaged, or die, large quantities of certain enzymes are released into the bloodstream. Enzymes can therefore be elevated in response to cardiac or other organ damage.   Radiography and Radionuclide Studies: Chest radiography and fluoroscopy determine the size and 36 position of the heart and condition of the lungs. These studies also are used to guide the insertion and confirm the placement of cardiac catheters and pacemaker wires. CT scanning and magnetic resonance imaging are used to determine heart size and detect lung involvement. Radionuclides are radioactive chemical elements that are injected into and travel through the bloodstream.  Magnetic Resonance Imaging (MRI): MRI is a diagnostic tool used to identify disorders that affect many different structures in the body without performing surgery. The principle underlying MRI is that many elements within the human body, such as hydrogen, are magnetic.  Echocardiography: Echocardiography uses ultrasound waves to determine the functioning of the left ventricle and  to detect cardiac tumors, congenital defects, and changes in the tissue layers of the heart. 37  Electrocardiography: Electrocardiography (ECG) is the graphic recording of the electrical currents generated by the heart muscle. During electrocardiography, color-coded electrodes matched to corresponding lead wires connect the client to the recording machine.  Cardiac Catheterization: Cardiac catheterization is a diagnostic test performed in an operative setting. It can be done for a variety of purposes. In this procedure, a long, flexible catheter is inserted from a peripheral blood vessel in the groin, arm, or neck into one of the great vessels (inferior or superior vena cava which is attached to the heart) and then into the heart. Cardiac catheterization may be carried out on the left side of the heart by way of an artery or on the right side by way of a vein.   Arteriography 38 Coronary Arteriography: The most common use of a left-sided cardiac catheterization is to determine the degree of blockage of the coronary arteries by performing arteriography while the catheter is in place. An arteriography is a diagnostic procedure that involves instilling dye, referred to as contrast medium, into an artery. Angiocardiography: In angiocardiography, a radiopaque dye is injected into a vein, and its course through the heart is recorded by a series of radiographic pictures taken in rapid succession. The pictures reveal the size and shape of the heart chambers and great vessels and the sequence and time of their filling with dye. Angiocardiography is used particularly to diagnose congenital abnormalities of the heart and great vessels.  Aortography: Aortography detects aortic abnormalities such as aneurysms (abnormal dilatation of a blood vessel 39 wall) and arterial occlusions. When aortography is performed, contrast medium is injected and radiographic films are taken of the abdominal aorta and major arteries in the legs. Distribution of the contrast medium also may be observed as it circulates to other vessels, such as the renal arteries. Peripheral Arteriography: Peripheral arteriography is used to diagnose occlusive arterial disease in smaller arteries. Contrast medium is injected into an artery, and radiographic films are taken. After the procedure, the chance for bleeding is greater than after a venipuncture; therefore, a pressure dressing is applied and client activity is restricted for about 12 hours.  DISORDERS OF 40 THE CARDIOVASCULAR SYSTEM  MEDICAL-SURGICAL NURSING III  (GNS 222) ALAGBE O. A. SCHOOL OF NURSING, BUTH, OGBOMOSO, OYO STATE.  CARDIAC HEMODYNAMICS 41 The basic function of the heart is to pump blood. The heart’s ability to pump is measured by cardiac output (CO), the amount of blood pumped per minute. CO is determined by measuring the heart rate (HR) and multiplying it by the stroke volume (SV), the amount of blood pumped out of the ventricle with each contraction. CO usually is calculated using the equation. CO = HR x SV The HR is primarily controlled by the autonomic nervous system. When SV decreases, the nervous system is stimulated to increase HR and thereby maintain adequate CO. SV depends on three factors: preload, afterload, and contractility. Precise measurement of these factors requires hemodynamic monitoring.  HYPERTENSION 42 Blood pressure (BP) is the force produced by the volume of blood in arterial walls. It is represented by the formula: BP = CO (cardiac output) × PR (peripheral resistance) The measured BP reflects: the ability of the arteries to stretch and fill with blood, the efficiency of the heart as a pump, and the volume of circulating blood. Blood pressure is affected by age, body size, diet, activity, emotions, pain, position, gender, time of day, and disease states.  Studies of healthy persons show that BP can fluctuate within a wide range and remain normal. Thus, obtaining several 43 measurements for comparison is important. Hypertension is defined as a blood pressure higher than 140mmg (systolic) or 90mmHg diastolic on three separate readings several weeks apart The autonomic nervous system, the kidneys, and various endocrine glands regulate arterial pressure. BP tends to increase with age, most likely from arteriosclerotic and atherosclerotic changes in blood vessels or other effects of chronic diseases such as diabetes and renal dysfunction.  Systolic Blood Pressure 44 Systolic blood pressure is determined by the force and volume of blood that the left ventricle ejects during systole and the ability of the arterial system to distend at the time of ventricular contraction. Diastolic Blood Pressure Diastolic blood pressure reflects arterial pressure during ventricular relaxation. It depends on the resistance of the arterioles and the diastolic filling times. If arterioles are resistant (constricted), blood is under greater pressure.  Classifications of Hypertension 45 This is done both by its cause and its course thus:  Primary/Essential Hypertension This has no any identifiable cause, although a host of risk factors have been identified.  Secondary Hypertension This results from a known cause mostly as a result of a disease condition such as kidney disease. 46 ACCORDING TO COURSE (PROCESS)  Risk Factors 47  Modifiable Risk factors Mineral Intake e.g. High Sodium Chloride, Low Potassium, Calcium and Magnesium Obesity Insulin Resistance Excess Alcohol Consumption Smoking Physical and/or Emotional Stress  Non-Modifiable Risk factors Family History Age Race  Signs & Symptoms 48 People with hypertension usually have no symptoms other than an increased blood pressure, occasional headaches and dizziness. This is why hypertension is usually regarded as “the silent killer”. Headaches, Epistaxis, Lightheadedness, vertigo, Tinnitus, SOB, dizziness, nervousness, Insomnia, Fatigue, blurred vision, syncope etc. Pathophysiology Blood pressure is the product of cardiac output multiplied by peripheral resistance. Cardiac output is the product of the heart rate multiplied by the stroke volume. In normal circulation, pressure is transferred from the heart muscle to the blood each time the heart contracts, and then pressure is exerted by the blood as it flows through the blood vessels.  Hypertension can result from an increase in cardiac output, an increase in peripheral resistance (constriction of the blood 49 vessels), or both. Although no precise cause can be identified for most cases of hypertension, it is understood that hypertension is a multifactorial condition, because hypertension is a sign, it is most likely to have many causes, just as fever has many causes. Many factors have been implicated as causes of hypertension:  Increased sympathetic nervous system activity related to dysfunction of the autonomic nervous system (ANS)  Increased renal reabsorption of sodium, chloride, and water related to a genetic variation in the pathways by which the kidneys handle sodium  Increased activity of the renin–angiotensin–aldosterone system, resulting in expansion of extracellular fluid volume and increased systemic vascular resistance   Decreased vasodilation of the arterioles related to dysfunction of the vascular endothelium 50  Resistance to insulin action, which may be a common factor linking hypertension, type 2 diabetes mellitus, hypertriglyceridemia, obesity, and glucose intolerance. Structural and functional changes in the heart and blood vessels contribute to increases in blood pressure that occur with aging. These changes include accumulation of atherosclerotic plaque, fragmentation of arterial elastins, increased collagen deposits, and impaired vasodilation. The result of these changes is decreased elasticity of the major blood vessels.  HYPERTENSIVE CRISIS Hypertensive Crisis is defined as a situation when the blood pressure 51 becomes very high, and with possible organ damage (≥ 180/120mmHg). It encompasses the following:  Hypertensive Urgency This is defined as a condition in which there is a very high blood pressure with no evidence of organ damage (≥ 180/120mmHg).  Hypertensive Emergency This is defined as a very high blood pressure with evidence of imminent organ damage e.g. CVA, HF, Unstable Angina, Pulmonary edema, aneurysm, eclampsia, renal failure etc. (≥ 180/120mmHg).  Diagnosis/Investigations  Health history/History taking 52  Physical examination  Laboratory studies e.g. Blood Chemistry (EUCr), Urinalysis, BUN, L/HDL  Electrocardiography  Echocardiography  Radiology (X-Rays)  Etc. Nursing Diagnoses  Deficient knowledge regarding the relation between the treatment regimen and control of the disease process  Noncompliance with therapeutic regimen related to side effects of prescribed therapy  Management Medical Mgt./Chemotherapy 53  Diuretics e.g. Thiazides, Loop, Potassium-sparing, Osmotic  Beta adrenergic blockers e.g. Labetalol, Propranolol etc.  Alpha Blockers e.g. Doxazosin, Terazosin  Angiotensin Receptor Blockers: e.g. Losartan, Valsatan  Calcium-channel blockers e.g. Nifedipine, Amilodipine etc.  ACE Inhibitors e.g. Lisinopril, Elanapril etc.  Vasodilators e.g. Hydralazine, Nitroprusside etc.  Centrally-Acting Sympatholytics e.g. Clonidine, Methyldopa Surgical Mgt.  Coarctation of Aorta, Phaechromocytoma, Renal artery stenosis  Nursing Mgt. 54  Observation  Diet  Rest  Physical Care  Elimination  Prevention & Health Education Complications  CVA  Hypertensive Retinopathy  Hypertensive Encephalopathy  Myocardial Infarction, Heart failure, TIAs etc.  HEART FAILURE 55 Heart failure is the inability of the heart to pump sufficient blood to meet the body’s metabolic needs. Normally, a healthy heart ejects 55% or more of the blood that fills the left ventricle during diastole. As the heart fails, the amount of ejected blood decreases. An estimate of the heart’s efficiency as a pump is its ejection fraction, which is measured using an echocardiogram. The term Congestive heart failure (CHF) describes the accumulation of blood and fluid in organs and tissues from impaired circulation.  SYSTEMATIC ASSESSMENT FOR HEART FAILURE 56 Be alert for the following signs and symptoms: General  Fatigue  Decreased activity tolerance  Dependent edema  Weight gain Cardiovascular  Third heart sound (S3)  Apical impulse enlarged with left lateral displacement  Pallor and cyanosis  Jugular venous distention (JVD)  Respiratory 57  Dyspnea on exertion  Pulmonary crackles that do not clear with cough  Orthopnea  Paroxysmal nocturnal dyspnea (PND)  Cough on exertion or when supine Cerebrovascular  Unexplained confusion or altered mental status  Lightheadedness Renal  Oliguria and decreased frequency during the day  Nocturia  Gastrointestinal 58  Anorexia and nausea  Enlarged liver  Ascites  Hepatojugular reflux  Classifications of Heart Failure 59 A. According to how it develop: Acute Heart Failure e.g. from Myocardial Infarction Chronic Heart Failure e.g. from Hypertension B. According to location Right-sided Heart Failure Left-sided Heart Failure  Etiology 60 Two mechanisms can cause heart failure. The primary reason for failure of either the left or right ventricle is inability of the heart muscle to contract because of direct damage to the muscular wall. Myocardial infarction (MI) usually affects the pumping ability of the left or right ventricle and frequently contributes to acute heart failure. Acute heart failure may immediately follow an MI or develop some time after the initial episode. The second mechanism occurs when the pumping chambers enlarge and weaken, as in cardiomyopathy and hypertension, making it impossible for the ventricles to eject all the blood they receive.  Left-Sided Heart Failure 61 When the left ventricle fails, the heart muscle cannot contract forcefully enough to expel blood into the systemic circulation (cardiac output). Blood subsequently becomes congested in the left ventricle, left atrium, and finally the pulmonary vasculature. The fluid accumulates and creates congestion in the pulmonary vascular bed (the capillary network surrounding the alveoli). Increased pulmonary vascular bed pressure causes fluid to move from the pulmonary capillaries into the alveoli. Gas exchange is impaired, cells become hypoxic (a state of insufficient oxygen), and CO2 accumulates in the blood. Hypertension, tachy-dysrhythmias, valvular disease, cardiomyopathy, and renal failure can contribute to chronic heart failure.  Signs & Symptoms of Left-Sided Failure 62  Fatigue  Paroxysmal nocturnal dyspnea  Orthopnea  Hypoxia  Crackles  Cyanosis  S3 heart sound  Cough with pink, frothy sputum  Elevated pulmonary capillary wedge pressure  Right-Sided Heart Failure 63 When the left ventricle fails, the heart muscle cannot contract forcefully enough to expel blood into the systemic circulation (cardiac output). Blood subsequently becomes congested in the left ventricle, left atrium, and finally the pulmonary vasculature. The fluid accumulates and creates congestion in the pulmonary vascular bed (the capillary network surrounding the alveoli). Increased pulmonary vascular bed pressure causes fluid to move from the pulmonary capillaries into the alveoli. Gas exchange is impaired, cells become hypoxic (a state of insufficient oxygen), and CO2 accumulates in the blood. Hypertension, tachy-dysrhythmias, valvular disease, cardiomyopathy, and renal failure can contribute to chronic heart failure.  When right ventricular failure develops, the right ventricle cannot forcefully contract and push the blood into the 64 pulmonary artery. As a result, congestion of blood and backflow accumulate first in the right ventricle, then in the right atrium, the superior and inferior vena cavae, and subsequently the venous vasculature. MIs that affect the right ventricle also can cause right ventricular failure. Clients with chronic respiratory disorders tend to develop right-sided failure as a consequence of cor pulmonale. Cor pulmonale is a condition in which the heart (cor) is affected secondarily by lung damage (pulmonale). Pulmonary disease impairs exchange of oxygen and CO2 in the alveoli, leading to increased CO2 in the blood. By an unknown mechanism, pulmonary arterial vasoconstriction occurs. Prolonged pulmonary arterial vasoconstriction results in pulmonary hypertension (elevated pressure in the pulmonary arterial system.  With pulmonary hypertension, the right ventricle is forced to pump against a high pressure gradient. Subsequently, the 65 right ventricle enlarges and weakens under the increased workload, leading to failure. When the right ventricle fails to empty completely, blood is trapped in the venous vascular system. Eventually, the fluid is forced to move in retrograde fashion into the interstitial spaces and cells of other organs and tissues of the body. Signs & Symptoms Right-Sided Failure, Weakness, Ascites, Weight gain, Nausea, vomiting, Dysrhythmias, Elevated central venous pressure, Jugular vein distention  COMPENSATORY MECHANISMS 66  The body can compensate for changes in heart function that occur over time. When cardiac output falls, the body uses certain compensatory mechanisms designed to increase stroke volume and maintain blood pressure (BP).  These compensatory mechanisms can temporarily improve the client’s cardiac output but ultimately fail when contractility is further compromised. As cardiac output falls, the client becomes hypotensive. The low BP stimulates the sympathetic nervous system to release catecholamines (e.g., epinephrine, norepinephrine) to raise heart rate and BP. The increased force and contraction of the heart maintain the client’s BP but increase myocardial oxygen demand (the amount of oxygen the heart needs to perform its work).   Epinephrine also causes blood vessels to constrict in an effort to raise BP. As the sympathetic nervous system is 67 stimulated, the body shunts more blood to the vital organs of the brain and heart, decreasing blood supply to the kidneys. The kidneys secrete renin in response to decreased blood flow, which initiates the renin- angiotensin-aldosterone mechanism.  Renin activates angiotensin. Angiotensin causes vasoconstriction and increases BP. Angiotensin also stimulates the adrenal gland to secrete aldosterone, a hormone that causes retention of sodium and water to increase BP by increasing the amount of blood returning to the heart. Sensing an increase in fluid pressure within the heart, the ventricles secrete a neurohormone known as b-type natriuretic peptide (BNP). BNP is cardio- protective in nature.   Its function is to decrease blood pressure by increasing 68 the excretion of sodium and water and promoting arterial dilation. It achieves its effects by counteracting renin, angiotensin, and aldosterone. Ultimately, if compensatory mechanisms fail to restore homeostasis, the client’s status is compromised by increased blood volume that the heart must pump and overwhelming the resistance the heart must overcome from arterial constriction.  As cardiac output falls, the body’s cells become deprived of oxygen and switch from aerobic metabolism to the less efficient anaerobic metabolism. Anaerobic metabolism results in an accumulation of lactic acid, which lowers blood pH and can eventually cause metabolic acidosis. 69  Management Medical Mgt./Chemotherapy 70 Management of both left and right-sided heart failure is directed at reducing the heart’s workload and improving cardiac output, primarily through dietary modifications, drug therapy, and lifestyle changes.  Cardiac Glycosides e.g. Digitalis (Digoxin)  Inotropic agents e.g. Dobutamine, Dopamine  Diuretics: Loop, Potassium-sparing, Thiazides etc  Antihypertensives e.g. Vasodilators, ACEs etc. Surgical Mgt.  Cardiomyoplasty  Human Heart transplant  Nursing Mgt. 71  Observation  Diet  Rest  Positioning  Physical Care  Elimination  Prevention & Health Education  CARDIOGENIC PULMONARY EDEMA 72 Pulmonary edema is fluid accumulation in the lungs, which interferes with gas exchange in the alveoli. It represents an acute emergency and is a frequent complication of left-sided heart failure. Cardiac dysrhythmias and cardiac or respiratory arrest are associated complications. Noncardiogenic pulmonary edema, also referred to as acute respiratory distress syndrome, develops when a pulmonary embolism, infection, or blast injury alters the pulmonary capillary membrane.  Pathophysiology and Etiology 73 In cardiogenic pulmonary edema, the left ventricle becomes incapable of maintaining sufficient output of blood with each contraction. The right ventricle continues to pump blood toward the lungs, however, and the left ventricle has difficulty emptying. There is retrograde fluid accumulation in the left atrium and pulmonary veins. The pulmonary capillaries and alveoli become engorged with blood. The lungs rapidly fill with fluid, and acute respiratory distress develops. As CO2 accumulates, respiratory rate and depth increase. Without treatment, hyperventilation becomes insufficient to prevent respiratory acidosis. Metabolic acidosis follows.  Clinical Manifestations 74 Sudden dyspnea, Wheezing, Orthopnea, Restlessness, cough (often productive of pink, frothy sputum), Cyanosis, Tachycardia, and Severe apprehension.  Medical Management 75 Because pulmonary edema can be fatal, lung congestion needs to be relieved as quickly as possible. Supplemental oxygen or mechanical ventilation is used to support breathing. Cardiac Glycosides e.g. Digitalis (Digoxin) Inotropic agents e.g. Dobutamine, Dopamine Diuretics: Loop, Potassium-sparing, Thiazides etc Antihypertensives e.g. Vasodilators, ACEs etc. Oxygenation 76 CORONARY AND PERIPHERAL VASCULAR DISORDERS  MEDICAL-SURGICAL NURSING III  (GNS 222) ALAGBE O. A. SCHOOL OF NURSING, BUTH, OGBOMOSO, OYO STATE.  CORONARY HEART (ARTERY) DISEASES Arteriosclerosis 77 Arteriosclerosis refers to the loss of elasticity or hardening of the arteries that accompanies the aging process. As cells in arterial tissue layers degenerate with age, calcium is deposited in the cytoplasm. The calcium causes the arteries to lose elasticity. As the left ventricle contracts, sending oxygenated blood from the heart, the rigid arterial vessels fail to stretch. The potential result is a reduced volume of oxygenated blood delivered to organs such as the myocardium, brain, kidneys, and extremities. Atherosclerosis Atherosclerosis is a condition in which the lumen of arteries fill with fatty deposits called plaque. The plaque is chiefly composed of cholesterol, a fatty (lipid) substance. Atherosclerosis is a more modifiable contributor than arteriosclerosis to vascular disease. Therefore, it is the focus of attention and research into the mechanisms that contribute to plaque formation and its reduction to decrease vascular disease.  Angina Pectoris Angina pectoris is a clinical syndrome usually characterized by episodes 78 or paroxysms of pain or pressure in the anterior chest. The cause is insufficient coronary blood flow, resulting in a decreased oxygen supply when there is increased myocardial demand for oxygen in response to physical exertion or emotional stress. Types  Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest and/or Nitroglycerin  Unstable angina (also called pre-infarction angina or crescendo angina): symptoms increase in frequency and severity; may not be relieved with rest or nitroglycerin  Intractable or refractory angina: severe incapacitating chest pain  Variant angina (also called Prinzmetal’s angina): pain at rest, caused by coronary artery vasospasm  Silent ischemia: objective evidence of ischemia (e.g. on ECG), but patient reports no pain  Myocardial Infarction 79 An infarct is an area of tissue that dies (necrosis) from inadequate oxygenation. An MI, or heart attack, occurs when there is prolonged total occlusion of coronary arterial blood flow. The larger the necrotic area is, the more serious the damage. An infarct that extends through the full thickness of the myocardial wall is called a transmural infarction. A partial-thickness infarct is called a subendocardial infarction. Each coronary artery supplies oxygenated blood to a different area of the myocardium. The location of the infarction depends on the area where the blood supply to the myocardium is interrupted by the respective occluded coronary artery  Causes of Coronary Artery Disease 80  Artherosclerosis  Coronary Thrombosis Risk Factors Modifiable  Hyperlipidemia  Smoking, tobacco use  Hypertension  Diabetes mellitus  Obesity  Physical inactivity  etc.  Risk Factors cont’d Non-Modifiable 81  Family history of CAD  Aging (more than 45 years for men; more than 55 years for women)  Gender (men develop CAD at an earlier age than women)  Race Signs & Symptoms  Angina Pectoris (Chest pain) (Retrosternal and radiating to the neck, jaws, shoulders, inner aspect of the left arm)  numbness in the arms, wrists, and hands,  shortness of breath, pallor, diaphoresis,  dizziness or lightheadedness,  nausea and vomiting, anxiety  Pathophysiology 82 CAD results from many factors rather than a single cause. Several inherited and behavioral risk factors contribute to the development of CAD. At rest, ample blood flow may be maintained despite considerable CAD. The condition may go unrecognized, particularly among those with a sedentary lifestyle. During situations that increase myocardial oxygen demand (i.e., exercise, emotional stress), however, the compromised coronary arteries cannot adequately oxygenate the myocardium. When the myocardial tissue becomes ischemic (deprived of oxygen), clinical manifestations of CAD, such as angina pectoris (chest pain of cardiac origin) occur. Death of heart muscle does not immediately accompany angina. Subsequently, the other symptoms follow angina pectoris  Diagnosis/Investigations  Health history/History taking 83  Physical examination  Laboratory studies e.g. Serum Lipid Level, RBG,  ECG (Stress Test)  Etc. Nursing Diagnoses  Ineffective cardiac tissue perfusion related to reduced coronary blood flow  Risk for imbalanced fluid volume  Risk for ineffective peripheral tissue perfusion related to decreased cardiac output from left ventricular dysfunction  Death anxiety related to cardiac event  Management Medical Mgt./Chemotherapy 84  Diuretics e.g. Thiazides, Loop, Potassium-sparing, Osmotic  Beta blockers e.g. Atenolol, Labetalol, Propranolol etc.  Thrombolytics e.g. Alteplase (Activase);  Calcium-channel blockers e.g. Nifedipine, Amilodipine etc.  Nitrates (Vasodilators) e.g. Isosorbide dinitrate, Nitroglycerin etc.  Anticoagulants e.g. Heparin Sodium Surgical Mgt.  Percutaneous Transluminal Coronary (balloon) Angioplasty (PTCA), with or without placement of Coronary Stent  Atherectomy  Coronary Artery Bypass Graft (CABG)  Nursing Mgt. 85  Observation  Diet  Rest  Physical Care  Elimination  Prevention & Health Education Complications  Dysrhythmias  Cardiogenic Shock  Ventricular Rupture  Pericarditis, Pulmonary Embolism etc.  PERIPHERAL VASCULAR DISEASES 86 Peripheral vascular disease is a term for disorders that affect blood vessels distant from the large central blood vessels supplying the myocardium or that circulate blood directly in and out of the heart. Common peripheral vascular disorders include Raynaud’s disease, thrombosis, embolism, aneurysms, varicose veins. Raynaud’s Disease Raynaud’s phenomenon is a form of intermittent arteriolar vasoconstriction that results in coldness, pain, and pallor of the fingertips or toes. There are two forms of this disorder.  Primary or idiopathic Raynaud’s (Raynaud’s disease) occurs in the absence of an underlying disease.   Secondary Raynaud’s (Raynaud’s syndrome) occurs in association with an underlying disease, usually a connective 87 tissue disorder, such as systemic lupus erythematosus, rheumatoid arthritis, or scleroderma; trauma; or obstructive arterial lesions. Symptoms may result from a defect in basal heat production that eventually decreases the ability of cutaneous vessels to dilate. Episodes may be triggered by emotional factors or by unusual sensitivity to cold. The disorder is most common in young women (15 - 45years). It is also known as blue-white-red disease Pathophysiology & Manifestations The classic clinical picture reveals pallor brought on by sudden vasoconstriction. The skin then becomes bluish (cyanotic)  because of pooling of deoxygenated blood during vasospasm. As a result of exaggerated reflow (hyperemia) due to 88 vasodilation, a red color (rubor) is produced when oxygenated blood returns to the digits after the vasospasm stops. The characteristic sequence of color change of Raynaud’s phenomenon is described as white, blue, and red. Numbness, tingling, and burning pain occur as the color changes. The manifestations tend to be bilateral and symmetric and may involve toes and fingers. Management Medical Mgt./Chemotherapy  Thrombolytics e.g. Alteplase (Activase);  Calcium-channel blockers e.g. Nifedipine, Amilodipine etc.  Anticoagulants e.g. Heparin Sodium  Nursing Mgt. 89  Observation  Diet  Rest  Physical Care  Elimination  Prevention & Health Education  THROMBOSIS, PHLEBOTHROMBOSIS, AND EMBOLISM 90 A thrombus is a stationary clot. Thrombosis is a state in which a thrombus has formed in a blood vessel. Thrombophlebitis is an inflammation of a vein accompanied by clot or thrombus formation. Phlebothrombosis is the development of a clot within a vein without inflammation. Phlebothrombosis and thrombophlebitis have similar symptoms and treatment. An embolus is a moving mass (clot) of particles, either solid or gas, in the bloodstream.  Risk Factors Signs & Syptoms  Trauma Arterial Embolism (6 Ps) 91  Surgery  Pain,  Central venous catheters  Pallor,  Dialysis access catheters  Pulselessness,  Local vein damage  Paresthesia  Bed rest or immobilization  Poikilothermia/coldness  Obesity  Paralysis.  Oral contraceptive use  Polycythemia  Septicemia  History of varicosities  Spinal cord injury  Age (greater than 65 years) etc.  Etiology and Pathophysiology 92 Thrombosis in the venous system most often occurs in the lower extremities and usually is associated with disorders or circumstances that cause venous stasis (inactivity, immobility, or trauma to a blood vessel). Orthopedic surgical procedures increase the incidence of deep vein thrombosis (DVT) of the lower extremities. Atherosclerosis, endocarditis, pooling of blood in a ventricular aneurysm, and dysrhythmias such as atrial fibrillation can precipitate arterial thrombosis and subsequent embolization. When a thrombus forms or an embolus reaches a blood vessel too small to permit its passage, blood flow is partly or totally occluded. When an arterial clot is present, symptoms arise from ischemia to the tissues that depend on the obstructed vessel for their oxygenated blood supply.  With total occlusion, the extremity suddenly becomes white, cold, and extremely painful. Arterial pulsations are absent below 93 the obstructed area. Numbness, tingling, or cramping also may be present, and surrounding blood vessels spasm. Loss of sensation and ability to move the part follows. Symptoms of shock frequently result if a large vessel is obstructed. When a small vessel is occluded, symptoms of ischemia, such as pallor and coldness, occur but are less severe. Unless blood flow is restored, gangrene develops. Clients with phlebothrombosis may have few, if any, symptoms because inflammation is absent. Signs and symptoms of DVT usually include mild fever and pain, swelling, and tenderness of the affected extremity. A positive Homans’ sign, pain on dorsiflexion of the foot, may be present. A thrombus may become a mobile embolus and lodge in a distal blood vessel, such as the pulmonary capillaries, causing symptoms related to the organ to which circulation has become impaired.  Diagnosis/Investigations  Health history/History taking 94  Physical examination  Laboratory studies e.g. Serum Lipid Level, RBG,  Magnetic Resonance Imaging  Doppler Ultrasound  Etc. Nursing Diagnoses  Ineffective cardiac tissue perfusion related to reduced obstructed blood flow  Acute Pain  Management Medical Mgt./Chemotherapy 95  Analgesics e.g. PCM, Tradyl, Ibuprofen  Vasodilators e.g. Hydralazine etc.  Thrombolytics e.g. Alteplase (Activase)  Anticoagulants e.g. Heparin Sodium etc. Surgical Mgt.  Thrombectomy  Embolectomy  Endarterectomy  VARICOSE VEINS, VENOUS INSUFFICIENCY AND ANEURYSMS 96 VARICOSE VEINS Varicose veins or varicosities are dilated, tortuous veins. Both sexes suffer equally from this disorder. The saphenous leg veins commonly are affected because they lack support from surrounding muscles. Varicose veins also may occur in other body parts, such as the rectum (hemorrhoids) and esophagus (esophageal varices). Pathophysiology and Etiology Varicose veins have a familial tendency. The valves of the veins become incompetent in early adulthood, resulting in varicosities. In others, anything that constricts or interferes with venous return contributes to the formation of varicose veins e.g. Prolonged standing 20 gravity, obesity and pressure on blood vessels from an enlarging fetus, liver, or abdominal tumor contribute to venous  congestion. Thrombophlebitis may lead to varicose veins because the inflammatory process may damage vein valves. Venous 97 congestion and local edema may diminish arterial blood flow, impairing cellular nutrition. Even minor skin or soft tissue injuries easily become infected and ulcerated. The healing of such lesions is slow and uncertain. Signs and Symptoms  The legs feel heavy and tired, particularly after prolonged standing. Activity or elevation of the legs relieves discomfort.  The leg veins look distended and tortuous and can be seen under the skin as dark blue or purple, snakelike elevations.  The feet, ankles, and legs may appear swollen.  The skin may be slightly darker in the areas of impaired circulation. There may be signs of skin ulcerations in various stages of healing.  Diagnosis/Investigations 98  Health history/History taking  Physical examination  Doppler Ultrasound  The Brodie-Trendelenburg: The client lies flat and elevates the affected leg to empty the veins. A tourniquet is then applied to the upper thigh, and the client is asked to stand. If blood flows from the upper part of the leg into the superficial veins when the tourniquet is released, the valves of the superficial veins are considered incompetent.  Venography  Management Medical Mgt./Chemotherapy 99  Exercising (walking, swimming), losing weight (if needed), wearing elastic support stockings, and avoiding prolonged periods of sitting or standing.  The defective vein may be sclerosed or occluded by injecting a chemical that sets up an inflammation in the vein wall. Eventually adhesions form, and blood flow must find an alternate route through collateral veins.  Thrombolytics e.g. Alteplase (Activase)  Anticoagulants e.g. Heparin Sodium etc. Surgical Mgt.  Veinous ligation with or without vein stripping.  VENOUS INSUFFICIENCY Venous insufficiency is a peripheral vascular disorder in which the 100 flow of venous blood is impaired through deep or superficial veins (or both). The condition usually affects the lower extremities, most often the medial aspect of the leg or around the ankle. Pathophysiology and Etiology Venous insufficiency may be a consequence of varicose veins or valvular damage from a previous venous thrombosis. When the forward movement of venous blood is affected, venous congestion develops from the accumulating blood volume. Increased hydrostatic fluid pressure causes fluid to leave the veins and enter interstitial spaces. Localized edema is evident; the skin becomes shiny and hard. Venous congestion and local edema may diminish arterial blood flow, impairing cellular nutrition. Even minor skin or soft tissue injuries easily become infected and ulcerated. The healing of such lesions is slow and uncertain.  Signs and Symptoms 101  The foot or feet appear swollen.  Testing for pitting is difficult because the congested fluid cannot be displaced.  Superficial veins are dilated and obvious during inspection. Skin color is not uniform  Serous fluid may have collected in a pocket beneath the skin.  If an infection is present, the drainage may change from clear to opaque.  Most clients report moderate pain.  Pedal and tibial pulses may be difficult to palpate because of the congestion of venous fluid.  Diagnosis/Investigations 102  Health history/History taking  Physical examination  Doppler Ultrasound  The Brodie-Trendelenburg: The client lies flat and elevates the affected leg to empty the veins. A tourniquet is then applied to the upper thigh, and the client is asked to stand. If blood flows from the upper part of the leg into the superficial veins when the tourniquet is released, the valves of the superficial veins are considered incompetent.  Venography  ANEURYSMS 103 An aneurysm is stretching and bulging (out-pouching) of an arterial wall. Aneurysms of the aorta (aortic arch, thoracic, abdominal) are the most common, but aneurysms can be found in other arteries, such as those in the legs and brain. Pathophysiology and Etiology Arteriosclerosis, hypertension, trauma, or a congenital weakness can affect the elasticity of the tunica media (middle layer of the artery wall), causing part of the vessel to bulge and occasional pain. Once formed, some aneurysms lay down layers of clots, blocking the vessel until blood flow stops. Most aneurysms enlarge until they rupture. Loss of a large volume of arterial blood leads to shock and death if not controlled. Some aneurysms tear and leak blood into surrounding cavities, such as the thorax or abdomen.  Diagnosis/Investigations 104  Health history/History taking  Physical examination  Laboratory studies e.g. Serum Lipid Level, RBG,  Doppler Ultrasound  Radiographs can demonstrate aneurysms when the arterial wall contains calcium deposits.  Aortography identifies the size and exact location of the aneurysm.  Management Medical Mgt./Chemotherapy 105  Analgesics e.g. PCM, Tradyl, Ibuprofen  Antihypertensives e.g. Vasodilators etc.  Thrombolytics e.g. Alteplase (Activase)  Anticoagulants e.g. Heparin Sodium etc. Surgical Mgt.  Arterial Bypass or Graft 106 CARDIAC DYSRHYTHMIAS  MEDICAL-SURGICAL NURSING III  (GNS 222) ALAGBE O. A. SCHOOL OF NURSING, BUTH, OGBOMOSO, OYO STATE.  DYSRHYTHMIAS 107 Dysrhythmias are disorders of the formation or conduction (or both) of the electrical impulse within the heart. These disorders can cause disturbances of the heart rate, the heart rhythm, or both. Dysrhythmias may initially be evidenced by the hemodynamic effect they cause (e.g. a change in conduction may change the pumping action of the heart and cause decreased blood pressure). Dysrhythmias are diagnosed by analyzing the electrocardiographic (ECG) waveform. Their treatment is based on frequency and severity of symptoms produced. Cardiac dysrhythmias may originate in the atria, atrioventricular node, or ventricles.  Dysrhythmias Originating in the Atria 108 Sinus bradycardia: is a dysrhythmia that proceeds normally through the conduction pathway but at a slower than usual rate (60 beats/min). Sinus tachycardia is a dysrhythmia that proceeds normally through the conduction pathway but at a faster than usual rate (100–150 beats/min). Premature Atrial Contractions: Occasionally, neural tissue in the atrial conduction system initiates an early electrical impulse called a premature atrial contraction (PAC), which is identified by an irregularity in the underlying rhythm Supraventricular tachycardia (SVT) is a dysrhythmia in which the heart rate has a consistent  rhythm, but beats at a dangerously high rate (150 109 beats/min). Atrial Fibrillation: In atrial fibrillation, several areas in the right atrium initiate impulses resulting in disorganized, rapid activity. The atria quiver (tremble/shake) rather than contract Atrial flutter: is a disorder in which a single atrial impulse outside the SA node causes the atria to contract at an exceedingly rapid rate (200 - 400 contractions/min).  Dysrhythmia Originating in the Atrioventricular Node: Heart Block 110 Heart block refers to disorders in the conduction pathway that interfere with the transmission of impulses from the SA node through the AV node to the ventricles. Heart block is categorized into:  First degree,  Second degree,  Third degree (also called complete heart block). In first- and second-degree heart block, the impulse is delayed. In complete heart block, the atrial impulse never gets through, and the ventricles develop their own rhythm independent of the atrial rhythm. In complete heart block, the ventricular rate is slow 30–40 beats/min). Pacemaker insertion is the treatment for complete heart block.  Dysrhythmias Originating in the Ventricles Ventricular dysrhythmias include premature ventricular 111 contractions, ventricular tachycardia, and ventricular fibrillation.  Premature ventricular contraction (PVC): is a ventricular contraction that occurs early and independently in the cardiac cycle before the SA node initiates an electrical impulse.  Ventricular tachycardia: is caused by a single, irritable focus in the ventricle. The ventricles beat very fast (150– 250 beats/min), and cardiac output is decreased.  Ventricular fibrillation: is the rhythm of a dying heart. PVCs or ventricular tachycardia can precipitate it. The ventricles do not contract effectively and there is no cardiac output. Ventricular fibrillation is an indication for CPR and immediate defibrillation.  Pathophysiology and Etiology of Cardiac Dysrhythmias Many clinical states predispose clients to dysrhythmias. 112 One of the most common causes of serious dysrhythmias is myocardial ischemia, lack of oxygenated blood to the heart muscle, which can occur secondary to: Coronary Artery Disease (CAD), Congestive heart failure, Inadequate ventilation, and Shock. The conduction system also is susceptible to disturbances from anxiety, pain, endocrine disorders, electrolyte imbalances, valvular heart disease, placement of invasive catheters in the heart, and drug effects. Because of the altered rate and rhythm, all dysrhythmias affect the heart’s pumping action and cardiac output to some degree.  Signs and Symptoms 113 A client whose dysrhythmia causes decreased cardiac output is likely to develop the following signs weak and tired, experience angina pain, or faint. Some clients with tachydysrhythmias (abnormally fast rhythms) describe palpitations or fluttering in their chest. Blood pressure (BP) usually is low. Pulse is irregular or difficult to palpate; the rate is unusually fast or slow. The apical and radial pulse rates may differ. The skin may be pale and cool. The client may be disoriented and confused if the brain is not adequately oxygenated, or there may be loss of consciousness and even clinical death.  Medical & Surgical Management Some dysrhythmias are not life-threatening and may not require 114 treatment. Many are treated with drug therapy and electrical modalities such as elective electrical cardioversion, defibrillation, or temporary or permanent pacing (pacemakers) Chemotherapy  Antidysrhythmic Agents e.g. Amiodarone, Procainamide hydrochloride (Pronestyl), Lidocaine hydrochloride (Xylocaine), Verapamil hydrochloride (Calan)  Inotropic agents e.g. Dobutamine, Dopamine  Diuretics: Loop, Potassium-sparing, Thiazides etc  Antihypertensives e.g. Vasodilators, ACEs etc. Surgical Mgt.  Cardiomyoplasty  Human Heart transplant  Nursing Mgt. 115  Observation  Diet  Rest  Positioning  Physical Care  Elimination  Prevention & Health Education 116 VALVULAR DISORDERS OF THE HEART  MEDICAL-SURGICAL NURSING III  (GNS 222) ALAGBE O. A. SCHOOL OF NURSING, BUTH, OGBOMOSO, OYO STATE.  AORTIC STENOSIS 117 Stenosis means narrowing. Aortic stenosis is a narrowing of the opening in the aortic valve when the valve cusps become stiff and rigid. It is a common valvular disorder in the United States, especially among older adults. CAUSES  Congenital Heart Disease  Aging (Calcium Deposits)  Damages from Infection PATHOPHYSIOLOGY  Narrowing of the aortic valve is an age-related degenerative change from progressive calcium deposits in valve cells. In young adults, aortic stenosis usually is a  later consequence of a congenital defect in which the valve has two instead of three cusps. At birth and throughout 118 childhood, this defect does not produce symptoms. Symptoms appear after several decades, when the same calcification process that affects older adults causes the valves to harden. In others, aortic stenosis results directly from valvular damage related to rheumatic carditis and infective endocarditis.  The stiff, calcified valve cannot open properly and needs more force to push blood through its narrowed opening. The muscular wall of the left ventricle enlarges and thickens (hypertrophies) in response. The blood volume passing through the narrowed valve eventually becomes insufficient to nourish the myocardium and other organs.  Exercise or any circumstance that increases heart rate can cause myocardial ischemia, affecting the heart’s ability to  Signs and Symptoms 119 A client with aortic stenosis may be asymptomatic for several decades. When symptoms develop, they include  dizziness,  fainting, and  angina because of insufficient cardiac output. At first, the client experiences  dyspnea and fatigue during activity.  The carotid pulse feels weak because of a low stroke volume. Signs and Symptoms  Chest X-ray  ECG  AORTIC REGURGITATION 120 Aortic regurgitation occurs when the aortic valve does not close tightly and blood can leak backward. The valve’s inability to close tightly is a condition called valvular incompetence. CAUSES  Congenital Heart Disease  Aging  Infection PATHOPHYSIOLOGY When blood is pumped through the incompetent aortic valve, some leaks backward (valvular regurgitation) into the left ventricle. This backflow reduces cardiac output and  causes fluid overload in the left ventricle, which becomes 121 chronically stretched, hindering its ability to pump effectively. High fluid pressure in the left ventricle causes the mitral valve to shut early, which interferes with left atrial emptying. The blood in the left atrium backs up into the pulmonary circulation. Left ventricular enlargement increases the heart’s need for oxygen. When the coronary arteries cannot supply the heart muscle with enough oxygen because of decreased cardiac output, the myocardium becomes ischemic and the client experiences angina. Dizziness, dyspnea on exertion, confusion, and left ventricular failure may develop.  MITRAL REGURGITATION 122 Mitral regurgitation involves blood flowing back from the left ventricle into the left atrium during systole. Often the edges of the mitral valve leaflets/cusps do not close during systole. The cusps cannot close completely because the leaflets and chordae tendineae have thickened and fibrosed, resulting in their contraction. The most common causes of mitral valve regurgitation in developed countries are degenerative changes of the mitral valve (e.g., mitral valve prolapse) and ischemia of the left ventricle. The most common causes in developing countries are rheumatic heart disease and its sequelae  SEPTAL DEFECTS 123 The atrial or ventricular septum may have an abnormal opening between the right and left sides of the heart (i.e., septal defect). Most septal defects are congenital and are usually identified and repaired during infancy or childhood. Adults may not have undergone early repair or may develop septal defects as a result of myocardial infarction or trauma. In general, pressures in the left atria and ventricle are higher than those on the right, so blood initially flows from the left heart chamber into the right—a left-to- right shunt. With an atrial septal defect (ASD), ultimately the right atrial pressures become greater than  the left atrial pressures, and blood begins to flow from 124 the right atrium into the left atrium—a right-to-left shunt. With a ventricular septal defect (VSD), the extra blood volume causes the right ventricle to dilate, as well as pulmonary vascular congestion and hypertension. Patients with septal defects may not experience any symptoms, gradually develop symptoms, or rapidly develop heart failure. Patients with ASDs who gradually develop symptoms usually describe decreased exercise tolerance, dyspnea on exertion, palpitations, syncope, and symptoms of right ventricular or congestive heart failure. Cyanosis may result, or strokes (cerebrovascular accidents, brain attacks) may occur.  CARDIOMYOPATHY Cardiomyopathy is a heart muscle disease associated with 125 cardiac dysfunction. It is classified according to the structural and functional abnormalities of the heart muscle: Dilated cardiomyopathy (DCM), Hypertrophic cardiomyopathy (HCM), Restrictive or constrictive cardiomyopathy (RCM), Arrhythmogenic right ventricular cardiomyopathy (ARVC), and Unclassified cardiomyopathy A patient may have pathology representing more than one of these classifications, such as a patient with HCM developing dilation and symptoms of DCM. Ischemic cardiomyopathy is a term frequently used to describe an enlarged heart caused by coronary artery disease, which is usually accompanied by heart failure.  Pathophysiology 126 The pathophysiology of all cardiomyopathies is a series of events that culminate in impaired cardiac output. Decreased stroke volume stimulates the sympathetic nervous system and the renin–angiotensin–aldosterone response, resulting in increased systemic vascular resistance and increased sodium and fluid retention, which places an increased workload on the heart. These alterations can lead to heart failure. 127 INFECTIOUS AND INFLAMMATORY HEART DISEASES  MEDICAL-SURGICAL NURSING III  (GNS 222) ALAGBE O. A. SCHOOL OF NURSING, BUTH, OGBOMOSO, OYO STATE.  INFECTIVE ENDOCARDITIS Infective endocarditis (formerly called bacterial endocarditis) 128 is inflammation of the inner layer of heart tissue as a result of an infectious microorganism MYOCARDITIS Myocarditis is an inflammation of the myocardium (the muscle layer of the heart) RHEUMATIC CARDITIS Acute rheumatic fever, which occurs most often in school age children, may develop after an episode of group A betahemolytic streptococcal pharyngitis. Patients with rheumatic fever may develop rheumatic heart disease as evidenced by a new heart murmur, cardiomegaly, pericarditis, and heart failure. Prompt treatment of “strep” throat with antibiotics can prevent the development of rheumatic fever.  PERICARDITIS 129 Pericarditis refers to 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. For example, it may occur after pericardectomy (opening of the pericardium) following cardiac surgery. Most times, it is asymptomatic, however, there is severe chest pain Types: Subacute, Acute, or Chronic. It is also 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 (calcium) deposits, fibrinous (clotting proteins), or sanguinous (blood). Pericarditis also may be described as exudative or non-effusive.  CAUSES OF PERICARDITIS 130  Idiopathic or nonspecific causes  Infection: usually viral (e.g. HIV, influenza); rarely bacterial (e.g. streptococci, staphylococci, meningococci, gonococci, gram-negative rods); and mycotic (fungal)  Disorders of connective tissue: systemic lupus erythematosus, rheumatic fever, rheumatoid arthritis, polyarteritis, scleroderma  Hypersensitivity states: immune reactions, medication reactions, serum sickness  Disorders of adjacent structures: myocardial infarction, dissecting aneurysm, pleural and pulmonary disease (pneumonia)   Neoplastic disease: caused by metastasis from lung cancer or breast cancer, leukemia, and primary 131 (mesothelioma) neoplasms  Radiation therapy of chest and upper torso (peak occurrence 5–9 months after treatment)  Trauma: chest injury, cardiac surgery, cardiac catheterization, implantation of pacemaker or implantable cardioverter defibrillator (ICD)  Renal failure and uremia  Tuberculosis  Medical & Surgical Management 132 Chemotherapy  Anagelsics e.g. Ibuprofen, Aspirin, Diclofenac  Corticosteroids e.g. Prednisolone (If severe, or patient is not responding to NSAIDs)  Diuretics: Loop, Potassium-sparing, Thiazides etc  Antihypertensives e.g. Vasodilators, ACEs etc. Surgical Mgt.  Pericadiocentesis  Pericardial window  Pericardiectomy  Nursing Mgt. 133  Observation  Diet  Rest  Positioning  Physical Care  Elimination  Prevention & Health Education  THANKS 134 FOR LISTENING