ࡱ> q` }bjbjqPqP .::78\N\X:gh1   d   ֶ z0 q+q(  qf6 DXcsas  School of Nursing Christopher W. Blackwell, Ph.D., ARNP-C Assistant Professor, School of Nursing College of Health & Public Affairs University of Central Florida NGR 5003: Advanced Health Assessment & Diagnostic Reasoning Cardiovascular System: Heart and Blood Vessels: Basic assessment of the cardiovascular system Advanced assessment of the cardiovascular system - Chest X-Ray - 12-lead EKG Assessment findings of abnormal presentations in the cardiovascular system Differential diagnoses of the cardiovascular system Advanced Clinical reasoning: A case study approach advanced assessment of cardiovascular system: heart and blood vessels LEARNING OBJECTIVEs 1. Describe anatomy and physiology of the heart. 2. Identify age and condition variations in the heart. 3. Describe interview questions pertinent to the heart examination. 4. Discuss inspection, palpation, percussion, and auscultation techniques for examination of the heart. 5. Describe age-specific and/or condition-specific variations in examination findings of the heart. 6. Identify examination findings associated with various conditions of the heart. 7. Describe anatomy and physiology of the blood vessels. 8. Identify age and condition variations in the blood vessels. 9. Describe interview questions pertinent to blood vessels examination. 10. Discuss inspection, palpation, percussion, and auscultation techniques for examination of the blood vessels. 11. Describe age-specific and/or condition-specific variations in examination findings of the blood vessels. 12. Identify examination findings associated with various conditions of the blood vessels. Outline for Chapter 14: Heart Anatomy and Physiology The heart lies in the mediastinum, to the left of the midline, just above the diaphragm and is cradled between the medial and lower borders of the lungs. Because of its conelike shape, the hearts upper portion is called the base, and the narrower lower tip is the apex. Structure The pericardium is a double-walled, fibrous sac. Fluid is present between the inner and outer layers of the pericardium. The epicardium, the thin outermost muscle layer, covers the surface of the heart. The myocardium is the thick muscular middle layer responsible for the pumping action of the heart. The endocardium, the innermost layer, lines the chambers of the heart and valves. The heart is divided into four chambers. The right and left atria are the top chambers, and the right and left ventricles are the bottom chambers. The right and left sides of the heart each contain an atrium and a ventricle and are separated by the cardiac septum. The atria act as reservoirs of blood from the veins. The ventricles are large, thick-walled chambers that pump blood to the lungs and throughout the body. The adult heart is 12 cm long, 8 cm wide, and 6 cm thick. The atrioventricular valves include the tricuspid valve, which leads from the right atrium into the right ventricle, and the mitral valve, which leads from the left atrium into the left ventricle. The semilunar valves include the pulmonic valve, which separates the right ventricle from the pulmonary artery, and the aortic valve, which separates the left ventricle from the aorta. The great vessels circulate blood to and from the body and lungs and include the aorta, superior and inferior vena cavae, pulmonary arteries, and veins. The aorta carries oxygenated blood from the left ventricle to the body. The superior and inferior vena cavae carry blood from the body to the right atrium. The pulmonary artery carries blood to the lungs; the pulmonary veins carry oxygenated blood from the lungs to the left atrium. Cardiac Cycle The cardiac cycle includes contraction, or systole, and relaxation, or diastole. As systole begins, ventricular contraction produces S1, the lubb sound, and blood is ejected into the arteries. Aortic and pulmonic valves are then forced open. Valve opening is usually not heard. Closure of the aortic and pulmonic valves causes S2, the dupp sound. Ventricular filling sometimes produces an S3 heart sound; the fourth heart sound, S4, is sometimes produced from atrial contractions. The cardiac cycle is the same on both sides of the heart, but it occurs slightly later on the right side, sometimes causing a split S2 sound. Valve closures are best heard in an area away from the anatomic site. Electric Activity Electric current stimulates myocardial contraction. The impulse begins in the SA node in the wall of the right atrium, traveling to the AV node located in the atrial septum, then passing down the bundle of His to the Purkinje fibers in the ventricular myocardium. Ventricular contraction is initiated at the apex and proceeds toward the base of the heart. The electrocardiogram (ECG) records electric current caused from ions moving in and out of the myocardial cell membranes. Depolarization is the spread of a stimulus through the heart muscle; repolarization is the return of the stimulated heart muscle to a resting state. The ECG records electric activity as specific waves (Fig. 14-9): P wavethe spread of a stimulus through the atria (atrial depolarization) PR intervalthe time from initial stimulation of the atria to initial stimulation of the ventricles, usually 0.12 to 0.20 second QRS complexthe spread of a stimulus through the ventricles (ventricular depolarization), less than 0.10 second ST segment and T wavethe return of stimulated ventricular muscle to a resting state (ventricular repolarization) U wavea small deflection sometimes seen just after the T wave Q-T intervalthe time elapsed from the onset of ventricular depolarization until the completion of ventricular repolarization, with the interval varying with the cardiac rate Age- and Condition-Related Variations Infants and children. By 1 year of age, the relative sizes of the left and right ventricles are near the adult ratio of 2:1. The heart lies more horizontally in the childs chest than in the adults, and the apex of the heart is higher, sometimes well into the fourth left intercostal space. By age 7, adult heart position is reached. Pregnant women. From 10 to 12 weeks of gestation until 32 to 34 weeks, total blood volume increases 40% to 50%. Plasma volume increases 50% with a single pregnancy, and up to 70% with a twin pregnancy. By 3 to 4 weeks postpartum, blood volume returns to pre-pregnancy levels. The cardiac output increases approximately 30% to 40% over that of the nonpregnant state and reaches its highest level by about 25 to 32 weeks of gestation. This level is maintained until term. The enlarging uterus moves the diaphragm and the position of the heart upward in pregnancy, the position of the heart is shifted toward a horizontal position, and there is slight axis rotation. Older adults. With age, the heart rate slows, stroke volume decreases, cardiac output during exercise declines 30% to 40%, and heart size may decrease. The endocardium thickens, the myocardium becomes less elastic and more rigid, and myocardial contractility and irritability are delayed. Response to stress and increased oxygen demand is less efficient, tachycardia is poorly tolerated, and the return of normal heart rate is prolonged. Fibrosis and sclerosis in the SA node and the heart valves, increased vagal tone, and decreased baroreceptor sensitivity further compromise cardiac function. Electrocardiographic changes occur, including first-degree AV block, bundle branch block, ST-T wave abnormalities, premature systole, left anterior hemiblock, left ventricular hypertrophy, and atrial fibrillation. Review of Related History History of Present Illness Chest pain. Patients with pain should be assessed for onset, duration, characteristics, location, severity, associated symptoms, and treatment of pain. Specific data include factors that influence the pain, the type of discomfort (e.g., any radiation of pain or position-related relief), symptoms (e.g., dizziness or cyanosis), and use of nitroglycerin. Other considerations include cough, difficulty breathing, and loss of consciousness. Fatigue. Relevant data include associated symptoms (e.g., dyspnea or anorexia), as well as any interruption in usual activities or bedtime changes. Cough. Patients with a cough should be assessed for the onset and duration of the cough, as well as the character of the cough (dry, wet, nighttime, aggravated by lying down). Difficult breathing (dyspnea, orthopnea). Relevant data include aggravating factors (e.g., with exertion, lying down, or climbing stairs) and paroxysmal nocturnal dyspnea. Loss of consciousness (transient syncope). Patients should be assessed for associated symptoms. Past Medical History Ask patient about past cardiac surgery or hospitalizations, rheumatic fever or inflammatory problems, rhythm disorders, and chronic illnesses, such as hypertension or diabetes. Family History Pertinent data include family members with diabetes, heart disease, hyperlipidemia, hypertension, obesity, congenital heart defects, sudden death, and risk factors related to the cardiovascular system. Personal and Social History Relevant data include employment risks, tobacco habits, nutritional status, alcohol consumption, personality assessment, usual exercise activities, relaxation patterns, and drug use. Age- and Condition-Related Variations Infants. Any symptoms of tiring while feeding, breathing changes, cyanosis, unexpected weight changes, knee-chest position, maternal rubella, unexplained fever, or drug use should be noted. Children. Children should be assessed for the following: tiring during play, taking long naps, frequent preference for squatting position, complaints of leg pains during exercise, headaches, nosebleeds, joint pain, fever, and slow weight or height gain. Physical and cognitive development should also be assessed. Pregnant women. History of cardiac disease or surgery; dizziness or faintness on standing; indications of heart disease during pregnancy: progressive or severe dyspnea, progressive orthopnea, paroxysmal nocturnal dyspnea, hemoptysis, syncope with exertion, and chest pain related to effort or emotion. Older adults. Previous cardiovascular disease should be noted. See Box 14-3, Exercise Intensity (p. 426); and Risk Factors: Cardiac Disability (p. 428). Examination and Findings Summary of ExaminationHeart Preparation and Positioning The following techniques are performed with patient sitting and leaning forward, supine, and in the left lateral recumbent positions. All these positions are used to compare findings or enhance the assessment. Inspection Inspect the chest wall for pulsations (carotids, jugular veins), lifts, heaves, and thrusts. Check for symmetry. Inspect for cyanosis of the skin and cyanosis of the nailbeds and capillary refill. Palpation Palpate the precordium, apex, left sternal border, and base. Palpate for an apical impulse. Palpate for thrill or rushing vibration, primarily over the base of the heart. Palpate the carotid pulses, one at a time, avoiding carotid sinuses. Percussion If other facilities are unavailable, you can estimate the size of the heart by percussion. The change from a resonant to a dull note marks the cardiac border. Auscultation Auscultate heart sounds with patient sitting, supine, and on left side. Listen over aortic, pulmonary, mitral, tricuspid, apical, and epigastric areas. Describe rate, rhythm, duration of cycle, timing, intensity, frequency, splitting or murmurs, and quality. Isolate each sound. Auscultate the carotid arteries for bruits or murmurs. A pericardial friction rub can be easily mistaken for cardiac-generated sounds. Summary of Heart Findings Life Cycle VariationsNormal FindingsTypical VariationsFindings Associated with DisordersAdultsResting heart rate is 60 to 90/min and regular. No bruits or murmurs are present.Heart: In a slender person, the heart is more vertical and central. In stocky person, the heart lies horizontally and to the left. Heart sounds: Splitting of S2 is heard with inspiration. S3 is sometimes heard with ventricular filling. S4 is heard with atrial contraction and split S2.Wide apical pulsation may indicate left ventricular hypertrophy. Loss of palpable apical pulsation may indicate fluid, air, or displacement. Thrills are associated with failure of semilunar valve to close, aortic or pulmonary stenosis, or atrial septal defect. Loud S1 suggests increased blood velocity, mitral stenosis, heart block, hypertension, or calcification of mitral valve. Loud S2 suggests hypertension, valve disorder, stenosis, or fluid. Unexpected splitting, extra heart sounds, and heart murmur should be carefully assessed.Infants and ChildrenIn a term infant, apical pulse is best felt at fourth to fifth intercostal space. Murmurs are common 1 to 2 days after birth. Physiologic murmurs are common in children. Venous hum may be associated with childhood murmurs. Sinus arrhythmia often causes heart rate to varyusually faster on inspiration and slower on expiration. Pulse rates decrease as the child grows older.Venous hums seen in children have no pathologic significance.Cyanosis, tiring during play, frequent squatting position, and slow weight or height gain may indicate congenital heart disease. Heart shifts may indicate pneumothorax, dextrocardia, or diaphragmatic hernia. Arrhythmias in children are usually supraventricular and ventricular ectopic beats. Organic murmurs in infants and children are a result of congenital heart disease.Pregnant women Heart rate and position shift during pregnancy. More audible splitting and grade II murmurs are heard.Older adults Older persons exhibit slower heart rate (pulse from the low 40s to 100), ectopic beats, audible S4, and physiologic murmurs. Surface vessels are more tortuous and distended, and the heart is more transverse with age. With age, heart size often decreases, rate slows, stroke volume decreases, and cardiac output declines 30% to 40% (unless heart disease exists).The risk of heart disease and cardiovascular problems increase with age. See Box 14-1: Chest Pain (p. 424); Box 14-5: Procedure for Auscultating the Heart (p.432); Table 14-2: Heart Sounds According to Auscultatory Area (p. 434); Box 14-8: Unexpected Splitting of Heart Sounds (p. 437); and Table 14-3: Extra Heart Sounds (p. 438). See Table 14-1: Hemodynamic Changes During Pregnancy (p. 423). Mosby items and derived items 2006, 2003, 1999, 1995, 1991, 1987 by Mosby, Inc. an affiliate of Elsevier Inc Outline for Chapter 15: Blood Vessels Anatomy and Physiology The great vessels, the arteries leading from the heart and the veins leading to the heart, are located in a cluster at the base of the heart. They include the aorta, superior and inferior venae cavae, pulmonary arteries, and pulmonary veins. The aorta carries oxygenated blood out of the left ventricle to the body. The pulmonary artery, which leaves the right ventricle and divides almost immediately into right and left branches, carries blood to the lungs. The superior and inferior venae cavae carry blood from the upper and lower body, respectively, to the right atrium. The pulmonary veins return oxygenated blood from the lungs to the left atrium. Blood Circulation Blood flows through the pulmonary and systemic circulatory systems. During systole, unoxygenated blood is ejected through the pulmonic valve into the pulmonary artery. Gas exchange occurs in the alveoli. Oxygenated blood returns to the heart through the pulmonary veins into the left atrium. Stroke volume is the volume of blood forced from the left ventricle into the aorta through the arterial system and capillaries. The arteries are tougher, more tensile, less distensible, and subjected to more pressure than are the veins. Veins are less sturdy and more passive. Blood backflow is prevented by venous valves. If volume increases, veins expand to decrease stress on the heart. Arterial Pulse and Pressure The carotid arteries have the most suitable pulse for evaluation of cardiac function. Arterial blood pressure is the force exerted by the blood against the wall of the artery as the ventricles of the heart contract and relax. It has both systolic and diastolic components. Systolic arterial blood pressure is the force exerted against the wall of the artery when the ventricles contract and is largely the result of cardiac output and blood volume. Diastolic pressure is the force exerted against the wall of the artery when the heart is in the filling or relaxed state and is primarily a function of peripheral vascular resistance. During diastole, pressure falls to its lowest point. Pulse characteristics are affected by stroke volume, distensibility of the aorta and large arteries, blood viscosity, rate of cardiac emptying, and peripheral arteriolar resistance. The normal pulse rate is between 60 and 90 beats per minute. Jugular Venous Pulse and Pressure Activity of the right side of the heart is transmitted back through jugular veins as a pulse that has three peaks and two descending slopes (a wave, c wave, v wave, x slope, and y slope). Age- and Condition-Related Variations Infants and children. Fetal circulation compensates for the nonfunctional fetal lung. Changes at birth include closure of the ductus arteriosus within 12 to 24 hours and closure of the interatrial foramen ovale as pressure increases in the left atrium. Pregnant women. Vasodilation of the blood vessels results from hormonal changes. Blood pressure drops during early pregnancy, rises during the third trimester, and varies with position changes. Pregnant women experience increased venous pressure and venous pooling, occasionally resulting in edema of the lower extremities, varicosities of the legs and vulva, and hemorrhoids. Older adults. Calcification of the artery walls causes dilation and tortuosity of the aorta, aortic branches, and the carotid arteries. The superficial vessels of the forehead, neck, and extremities become tortuous and more prominent. The arterial walls lose elasticity and vasomotor tone. Increased vasopressor lability tends to increase both systolic and diastolic blood pressures progressively. Review of Related History History of Present Illness Leg pain or cramps. Patients having leg discomfort should be assessed for onset and duration of pain and whether leg elevation or immobilization changes pain. The character of discomfort should be described, and questions should be directed toward any burning in toes, changes in skin color or temperature, dizziness, limping, or discomfort during the night. Severe headaches. Patients having severe headaches should be assessed for onset and duration, location, character, and known history of hypertension. Swollen ankles. Patients having swollen ankles should be assessed for onset and duration, related circumstances, and associated symptoms. Treatment includes rest, massage, heat, elevation, and medication. Past Medical History Ask patient about past cardiac surgery or hospitalizations, rheumatic fever or inflammatory problems, and chronic illnesses such as hypertension or diabetes. Family History Pertinent data include family members with diabetes, heart disease, hyperlipidemia, hypertension, congenital heart defects, sudden death, risk factors related to the cardiovascular system, and peripheral vascular disease. Personal and Social History Relevant data include employment risks, tobacco habits, nutritional status, alcohol consumption, personality assessment, usual exercise activities, relaxation patterns, and drug use. Age- and Condition-Related Variations Infants. Any symptoms of tiring while feeding; breathing changes; cyanosis; unexpected weight changes; knee-chest position; maternal rubella, unexplained fever, or drug use should be noted. Children. Children should be assessed for the following: tiring during play, taking long naps, frequent preference for squatting position, complaints of leg pains during exercise, headaches, nosebleeds, joint pain, fever, and slow weight or height gain. Physical and cognitive development should also be assessed. Pregnant women. Areas of concern are blood pressures before, during, and after pregnancy; associated symptoms of edema (facial, abdominal, or peripheral); varicosities; epigastric pain; right upper quadrant pain; oliguria; hyperreflexia; and proteinuria. Older adults. Related symptoms such as respiratory or peripheral problems, should be analyzed. Previous cardiovascular disease should be noted. See Risk Factors: Varicose Veins (p. 467). Examination and Findings Summary of ExaminationBlood Vessels Preparation and Positioning The following techniques are performed with patient sitting and leaning forward, supine, and in the left lateral recumbent positions. All these positions are used to compare findings or enhance the assessment. Peripheral Arteries Inspection Inspect the chest wall for pulsations (carotids, jugular veins), lifts, heaves, and thrusts. Check for symmetry. Inspect for the color of the extremities, hair distribution, and venous distention. Inspect for the apical and carotid pulses. Inspect for cyanosis of the skin and cyanosis of the nailbeds and capillary refill. Palpation Palpate the precordium, apex, left sternal border, and base. Palpate for thrill or rushing vibration, primarily over the base of the heart. Palpate the carotid pulses, one at a time, avoiding carotid sinuses. Palpate for temporal, brachial, radial, femoral, popliteal, posterior tibial, and dorsalis pedis pulses. Palpate the extremities for temperature and venous distention. Auscultation Isolate each sound. Auscultate the carotid arteries for bruits or murmurs. Listen to the jugular veins for venous hums. Blood Pressure Measure blood pressure in the upper extremities bilaterally in the sitting, standing, and supine positions. Summary of Blood Vessels Findings Life Cycle VariationsNormal FindingsTypical VariationsFindings Associated with DisordersAdultsPatient exhibits no visible pulsations or heaving chest. Pulses are symmetric. Bilaterally, pulse amplitude is 2+. Bilateral extremities are warm and pink with hair present. Blood pressure/pulse: Systolic BP: 100 to 140 Diastolic BP: 60 to 90 Systolic BP is more responsive to a range of stimuli. Systolic pressure drops and diastolic pressure rises on standing.Pulse rate: Rate is labile, bounding, or increased after exercise; bradycardia may be present in the athlete. Jugular veins: Venous hums are usually not significant.Arterial insufficiency or pulse abnormalities are exhibited. Jugular distention >2 cm suggests ventricular failure. Positive Homans sign indicates venous thrombosis. Positive Trendelenburg sign suggests venous insufficiency. Varicosities are present. Right-left pulse asymmetry suggests impaired circulation.Infants and childrenNewborn blood pressure is 60 to 96 systolic and 30 to 62 diastolic. Blood pressure of children varies with age. Capillary refill occurs in less than 1 second.Venous hums seen in children have no pathologic significance.Purplish plethora in the newborn suggests polycythemia. Hypertension in children may suggest kidney disease. A femoral pulse weaker than a radial pulse suggests coarctation of the aorta. Carotid artery bruits heard in children should be assessed. A bounding pulse is associated with a large left-to-right shunt produced by a patent ductus arteriosus.Pregnant womenBlood pressure readings gradually fall until they reach a nadir at 16 to 20 weeks of gestation and then gradually rise to pre-pregnant levels at term.Increased venous pooling may cause edema of lower extremities and varicosities.Pregnancy may induce hypertension. Hyperreflexia and epigastric pain, facial and abdominal edema, visual changes, and headaches are caused by pregnancy-induced hypertension (PIH).Older adultsBlood pressure increases with age. Surface vessels are more tortuous and distended, and the heart is more transverse with age. Dorsalis pedis and posterior tibial pulses become more difficult to find. Systolic BP may increase. (Hypertension in older adults is defined as greater than 140/90.)The risk of heart disease and cardiovascular problems increase with age. Hypertension in the older adult is defined as a pressure greater than 140/90. See Box 15-2: Comparison of Pain from Vascular Insufficiencies and Musculoskeletal Disorders (p. 473). See Table 15-1: Locations of Palpable Pulses (p. 468); Table 15-2: Arterial Pulse Abnormalities (p. 470); and Box 15-3: Capillary Refill Time (p. 474). See Tables 15-5 (p. 483) and 15-6 (p. 484) on blood pressure levels of boys and girls aged 1 to 17 years. See cultural differences discussed in the Physical Variations box (p. 476). Mosby items and derived items 2006, 2003, 1999, 1995, 1991, 1987 by Mosby, Inc. an affiliate of Elsevier Inc Course Lecture Content: Cardiovascular (CV) System: Heart and Blood Vessels: Advanced assessment of the cardiovascular system - Chest X-Ray - 12-lead EKG Assessment findings of abnormal presentations in the cardiovascular system Differential diagnoses of the cardiovascular system Christopher W. Blackwell, Ph.D., ARNP-C Assistant Professor, School of Nursing College of Health & Public Affairs University of Central Florida NGR 5003: Advanced Health Assessment & Diagnostic Reasoning Advanced Assessment of the CV System Anatomy and Physiology: Heart located between 3rd-6th ICS; base at top, apex at bottom Dextrocardia is when the heart is completely reversed w/ L structures on R and R on L; when stomach on R and liver on L termed Situs Inversus Pericardium surrounds and encases heart, lubricates w/ few ccs pericardial fluid Epicardium surrounds heart and meets vessels Myocardium is thick muscular (middle) layer Endocardium lines 4 chambers of heart and covers valves RA/LA (top) RV/LV (bottom); LA/LV separated from RA/RV via septum RA/LA (top) RV/LV (bottom); LA/LV separated from RA/RV via septum Atria serve as reservoirs of blood returning from veins; ventricles pump blood to lungs and body organs Most ant surface of heart is R ventricle; L ventricle is L border of the heart; contractions responsible for PMI @ 5th ICS, MCL L atrium forms most of posterior heart AV valves separate atria from ventricles (L-Mitral/R-Tricupsid); Semilunar Valves separate ventricles from pulmonary and aorta (R-Pulmonic/L-Aortic) Closure of Mitral and Tricuspid valves (S1) pumps blood into ventricles, prevents backflow into atria; ventricles contract, pumping blood through Pulmonic and Aortic valves, which close (S2) to prevent backflow into ventricles R-sided pressures much < than those of the L SA ( AV ( bundle of His ( L/R bundle branches ( Purkinje fibers Advanced Assessment of the CV System Gross Anatomy Advanced Assessment of the CV System EKG Waveform Advanced Assessment of the CV System Infants and Children: By 1 year, infants L ventricle twice the size of R (as in adult) Heart tends to lie more horizontally than adult, apex @ 4th ICS (not PMI) until age 7 Pregnant Women: Maternal blood vol ! 40-50% (from 3-5L to approx 4.5-7.5L); returns to normal 3-4 weeks s/p delivery L ventricle ! in thickness and mass CO (HR x SV) ! 30-40%; returns to normal 2 weeks s/p delivery Slight axis deviation as uterus enlarges, shifting heart horizontally Older Adults: Heart size tends to ! w/ age in absence of CVD/HTN L ventricular wall thickens (! likelihood for CHF) and valves tend to fibrose and calcify CO during exercise ! 30-40% Myocardium becoomes more rigid and more susceptible to irritability (dysrhythmias) Fibrosis and sclerosis in the SA and valves, ! baroreceptor sensitivity and ! vagal tone; conduction system scleroses, leading to dysrhythmias (1st degree AV block, bundle branch block, ST-T wave abnormalities, premature atria/ventricular contractions, L ant hemiblock, L ventricular hypertrophy, and A-fib most common) Advanced Assessment of the CV System Review of Related Hx: Hx of Present Illness: Chest Pain: Onset: sudden, gradual, vague onset, length of episode; cyclic nature; r/t exertion, rest, emotion, eating, coughing, temperature extremes, exposure to trauma, awakens from sleep Character: Aching, sharp, tingling, burning, pressure, stabbing, crushing, clenched fist sign Location: radiation to arms/jaw/teeth/scapula; relief w/ rest or position change Severity: interference w/ activities-- need to stop until pain subsides; disrupts sleep; 1-10 rating Associated S/S: anxiety, dyspnea, diaphroesis, dizziness, nausea, vomiting, faintness, cold, clammy skin, cyanosis, pallor; edema (where noted and what time of day) Tx: rest, position change, exercise, NTG, Dig, diuretics, beta-blockers, ACE-I, Ca-channel blockers, NSAIDs, anti-HTNives Other Rx: Non/Rx, alternative Tx; prophylactic use of PCN Fatigue: Unusual/persistent, inability to keep up w. cohorts; inability to maintain usual activities; DOE, CP, palpitations, orthopnea, paroxysmal nocturnal dyspnea (PND), A/N/V Cough: Onset and duration; character (dry/wet; qhs; worse by lying down) SOB: aggravated by exertion?; on level ground, climbing stairs, worse or remaining stable us and number of pillows; PND Syncope: associated w/ palpitation, dysrhythmia, exertion, sudden turn of neck (carotid sinus effect), looking up (vertebral artery occlusion); change in posture Differential Dx: Chest Pain Advanced Assessment of the CV System Past Medical Hx: Cardiac surgery or related hospitalization: course of Tx/ recovery; Dysrhythmias (when diagnosed, S/S, how treated) Acute rheumatic fever, unexplained fever, swollen joints, inflammatory rheumatism, St. Vitus dance Chronic Illness: HTN, bleeding disorders, hyperlipidemia, DM, thryoid dsfunction, CAD, obesity, congenital heart defects Family Hx: DM, CAD, hyperlipidemia, HTN, obesity, congenital heart defects (ventricular septal defectsgreatly ! w/ fam Hx) Sudden deaths in middle/young-aged relatives Family members, morbidity/mortality r/t CV Dz, age at time of death Personal and Social Hx: Employment: physical demands, environmental hazards (heat, chemicals, dust, stress) Tobacco use: cigarettes, cigars, pipes, chewing tobacco, snuff; duration of use, amt. age started and (potentially) stopped; pack-years Nutritional Status: Usual diet, proportion of fat, food preference, Hx of dieting; wt loss/gain, amt and rate; ETOH consumption (amt/ frequency/ duration of current intake) High-Risk Personality Type (A or D) Relaxation: Hobbies, exercise (type, amt. frequency, sexual practices, # of partners Use of illegal Rx: amyl nitrate (poppers), cocaine Advanced Assessment of the CV System Infants: Tiring easily during feeding Breathing changes (more heavily, rapidly during feeding or defecating) Cyanosis (perioral during eating, more widespread/persistent, r/t crying) Wt gain as expected? Knee-chest position or other position favored? Pregnancy Hx: rubella in 1st trimester, unexplained fever, Rx use Children: Tiring during play: amount of time to tire, activities that tire, inability to keep up w/ cohorts, reluctance to play Naps: longer than usual (1-2h) Positions: prefers to squat instead of sit during play/TV HAs, Epistaxis, unexplained joint pain/fever, expected physical and cognitive growth and development Pregnant Women: Hx of cardiac Dz/surgery Dizziness/Syncope on standing Indications of cardiac Dz during pregnancy: progressive/severe dyspnea, progressive orthopnea, PND, hemoptysis, syncope on exertion, CP r/t effort/emotion Older Adults: Common S/S of CV Dz: Confusion, dizziness, palpitations, coughs/wheezes, hemoptysis, SOB, CP, impotence, fatigue, lower EXT edema (pattern, frequency, time of day worst); If cardiac Dz Diagnosed: Rx reactions (hyperkalemia = weakness, bradycardia, hypotension, confusion; hypokalemia = weakness, fatigue, cramps, dysrhythmias); DIG toxicity (A/N/V/D, HA, confusion, dysrhythmia, haloed/yellow vision) Inteferference w/ ADLs; perceived/actual coping of family/pt.; orthostatic hypotension Advanced Assessment of the CV System Examination and Findings: Inspection: Noticeable palpation when sitting-up @ PMI is expected; supine, could indicate pathology Absence of PMI w/ faint heart sounds (especially L-lateral position) could indicate extracardiac problem (pleural/ pericardial fluid) Assess entire body for S/S of cardiac compromise (cyanosis, pallor, venous distension, edema, cap refill time) Palpation: Move hand from apex, to L sternal border, to base, to R sternal border, into epigastrum assessing for warmth, thrill (indicative of aortic or pulmonic stenosis, pulm HTN, or atrial septal defect), or physical deformitydocument via ICS, MCL, or MAL Feel for the PMI, it should extend to 5th ICS, MCL, 1 cm in radius, be gentle and brief if > than this, it is a heave/lift Forceful, widely distributed, systole-filling, lateral-downwardly displaced PMI may indicate ! CO or LVH Decreased PMI thrust could indicate overlying fluid or air (pericarditis, PTX) Displacement of PMI to R w/o loss or gain in thrust suggests dextrocardia, dipahragmatic hernia, distended stomach, or pulm abnormality Assess carotid pulse for intensityshould match PMI pulsation Advanced Assessment of the CV System Palpation Techniques Advanced Assessment of the CV System Percussion: CXR (see unit 7) more helpful for structure Percuss from ant axillary line, moving medial to the ICS towards the sternal border mark where resonance turns to dullness to map cardiac size; measure from PMI to midsternal line at each ICS and record distance Auscultation: Environment needs to be as quiet as possible Assess for rate and rhythm, if irregular compare w/ radius for pulse deficit Note carotid pulsation at same time as S1 Listen for extra heart sounds (murmurs) Assess for longer diastole than systolecarefully assess for diastolic murmurs Note for splitting of S1 on expiration, S2 on inspiration; splitting is when relative valves do not close synchronously, producing 2 sounds instead of 1 If S3 and S4 are intense and easy to hear, it is a gallop (easier to hear w/ leg raised) All Physicians Earn Too Much Aortic: 2nd R ICS, R sternal border (S2 > S1) Pulmonic: 2nd L ICS, L sternal border (S2 > S1) Erbs: 3rd L ICS, L sternal border (S2 = S1) Tricuspid: 4th L ICS, L sternal border (S1 > S2) Mitral: 5th L ICS, MCL (S1 > S2) Advanced Assessment of the CV System Auscultation Areas Advanced Assessment of the CV System Pericardial friction rub heard during entire cardiac cycle; heard more distinctly @ PMI Prosthetic mitral valve gives clear click in early diastole, loudest @ PMI, transmitted precordially Prosthetic aortic valve gives clear click in early systole Murmurs are caused by: incompetent valve closures, resulting in regurgitation; needs additional tests to confirm either pathologic or functional (benign) ! CO demands which ! velocity of blood (thyrotoxicosis/anemia) Structure defects, allowing blood flow through inappropriate paths Diminished myocardial contraction Altered blood flow in major vessels near heart Transmitted from valvular aortic stenosis, ruptured chordae tendeinae, or severe aortic regurgitation Vigorous L ventricular ejection Obstructive Dz in cervical arteries (atherosclerotic carotid arteris, fibromuscular hyperplasia, or arteritis Grade I-II: Audible only doppler Grade III-IV: APNs own judgment based on velocity Grade V: Stethoscope held above chest wall Grade VI: APNs ear held above chest wall Advanced Assessment of the CV System Irregular HR occurring in a cyclic pattern w/ variation in breathing may indicate sinus dysrhythmia; Infants: Stagger cardiac exam in 1st 24h of life, then day 2-3 Infants w/ R-CHF have large, firm livers w/ inferior edge up to 6 cm below R costal margin Purplish plethora = polycythemia, ashy white = shock; central cyanosis (mucous membranes of face/ upper body) = congenital heart defect; Acrocyanosis is of little concern as it usually disappears Cyanosis shortly after birth strongly suggests transpositon of the great vessels, tetralogy of Fallot, tricuspid atresia, severe septal defect, or severe pulmonic stenosis Cyanosis occurring after neonatal period suggests pure pulmonic stenosis, Eisenmenger complex, tetralogy of Fallot, or large septal defects PMI of the newborn @ 4th-5th ICS, MCL Take special note of heart position if dyspnea also present PTX shifts PMI away from area of PTX; diaphragmatic hernias shift heart to R; R-shift of PMI seen in dextrocardia Increased intensity of S3 or S4 is always suspect; murmurs common in 1st 48h of life due to pulmonic pressure shifting If a murmur persists beyond day 2 or 3, is intense, fills systole, occupies diastole, or radiates widely, investigate! Pressing upward on liver L to R shunting through septal defect disappears whereas R to L intensifies Advanced Assessment of the CV System Children: Most heart dysrhythmias in children are not serious; sinus dysrhythmia occurs when the HR speeds and slows corresponding to respiration Organic murmurs in infants likely from congenital defect; rheumatic Dz most frequent cause in acquired Stills murmur, results from rapid blood expulsion through L ventricle into aorta w/ ! activity & ! when child quiet, is innocent When examining child w/ known Dz, note wt. gain, developmental delays, cyanosis, and clubbing HR more variable in children: Newborn: 120-170 1: 80-160 3: 80-120 6: 75-115 10: 70-110 Pregnant Women: HR ! 10-30% during pregnancy; no change on EKG PMI more upward and lateral by 1-1.5 cm 90% of pregnant women have a < grade II systolic murmur Cyanosis, clubbing, neck vein distension, or development of diastolic murmur always an abnormality Older Adults: Transition position changes slowly; occasional ectopic beats common; HR can range from low 40s to > 100 BPM; S4 more common due to ! L ventricular compliance Differential Dx: Heart Murmurs Mitral Stenosis: Narrowed valve restricts forward flow; often occurs w/ mitral regurgitation; often caused by rheumatic fever Heard w/ bell @ apex; L-lateral decubitus position Low-frequency, diastolic rumble; more intense in early/late diastole, does not radiate; systole usually quiet, thrill @ apex in late diastole; S1 ! and often palpable @ L sternal border Differential Dx: Heart Murmurs Aortic Stenosis: Calcification of valve cusps; forceful injection of blood into aorta; caused by congenital bicuspid valve, rheumatic heart Dz, atherosclerosis SERIOUS CONDITION can lead to sudden death Heard over aortic areaejection sound @ 2nd R ICS Midsystolic ejection murmur, medium pitch, coarse, radiates to L sternal border to carotid w/ thrill; S1 disappears in severe cases; soft or absent S2; PMI shifts down if w/ LVH Differential Dx: Heart Murmurs Subaortic Stenosis: Fibrous ring 4mm below aortic valve, progressively worsens, forceful injection into aorta Heard @ apex and along L sternal border Murmur fills systole, medium pitch, coarse, thrill @ apex, double wave felt in carotid, prominent jugular pulsation; S2 usually split w/ audible S3 and S4 Differential Dx: Heart Murmurs Pulmonic Stenosis: Valve restricts forward flow( forceful ejection from ventricle into pulmonary circuit; congenital cause Heard over pulmonic area radiating to L and into neck; thrill in 2nd/3rd ICS Systolic ejection murmur, medium pitch, coarse; thrill; S1 followed by quick click; S2 diminished Differential Dx: Heart Murmurs Tricuspid Stenosis: Calcification of valve cusps restricts forward flow, foreceful ejection into ventricles; usually w/ mitral stenosis; caused by rheumatic fever, endocardial fibreolastosis, R atrial myxoma, or congenital Dz Heard w/ bell over Tricuspid Diastolic rumble accentuated early and late in diastole; thrill over R ventricle; arterial pulse !, prominent venous pulse Differential Dx: Heart Murmurs Mitral Regurgitation: Valve incompetence allows backflow from ventricles to atria; caused by rheumatic fever, MI, myxoma, chordae tendinae rupture Heard best @ apex; transmits to L axilla Holosystolic, high-pitch/harsh; quite loud, obliterates S2, radiates from apex to L axilla; thrill @ apex during systole Differential Dx: Heart Murmurs Mitral Valve Prolapse: Valve is competent in early systole but prolapses into atrium in late systole; progressively worses Heard @ apex & L sternal border; audible only when pt upright Typically late systolic murmur, preceded by midsystolic clicks; variable in intensity and timing Differential Dx: Heart Murmurs Aortic Regurgitation: Valve incompetence allows backflow from aorta to ventricle; caused by rheumatic heart Dz, endocarditis, aortic Dz (Marfan syndrome, medial necrosis), syphilis, ankylosing spondylitis, dissection, cardiac trauma Heard w/ diaphragm w/ pt. sitting down, leaning forward Early diastolic, high pitch, blowing, midsystolic murmur, sounds often not prominent, low=pitched, rumbling murmur @ apex (Flint murmur), early ejection click, often intensified S3-S4 Differential Dx: Heart Murmurs Pulmonic Regurgitation: Valve incompetence allows backflow from pulm artery to ventricle; caused by pulm HTN or SBE Findings similar to aortic regurgitation Differential Dx: Heart Murmurs Tricuspid Regurgitation: Valve incompetence allows backflow from ventricle to atrium; caused by congenital defects, SBE, pulm HTN, cardiac trauma Heard in L lower sternum, radiation to few cms to L Holosystolic murmur over R ventricle; ! on inspiration; S3 and thrill common over tricuspid area Cardiac Abnormalities LVH: Caused by conditions that cause LV to work harder and hypertrophy (aortic stenosis, HTN, ! SVR); PMI displaces downward and lateral to MCL (crackles in lung fields); 3-D Echo RVH: Caused by conditions that cause RV to work harder and hypertrophy; LV displaced posteriorly due to enlarged RV; palpable thrill on L sternal border (peripheral edema); 3-D Echo Sick sinus syndrome: HTN, atherosclerosis, cardiac/rheumatic Dz causes SA node dysfunction w/ dysrthythmia, syncope, dizziness, seizures, palpitations, angina-like symptoms, CHF SBE: Bacterial infection of endocardium prolonged fever, S/S of neurological dysfunction, sudden CHF; IV Rx users highly susceptible; assess for Janeway lesions (small hemorrhagic macules on palms/soles) and Osler nodes (dots on the finger/toenails) CHF: Pump failure results in congestion in pulmonic and systemic circuits; systolic w/ narrow pulse pressure; diastolic widened pulse pressure; diastolic caused by stiffening of ventricle as a result of glucose insult (DM); 3-D Echo; ! JVD, S3. crackles, hepatojugular reflux, dyspnea, orthopnea, tachycardia Cardiac Abnormalities Pericarditis: Sharp, stabbing CP w/ fever, friction rub scratchy, grating, and easily heard Cardiac tamponade: Excess fluid collects between pericardium and heart, suppressing function, resulting in systemic venous congestion (edema, ascites, dyspnea) Becks Triad Cor pulmonale: Symptoms of RVH R-sided CHF Hyperlipidemia: Major risk factor for MI; LDL < 70 mg/dL; total cholesterol: < 200 mg/dL Myocarditis: Focal or diffuse inflammation of the myocardiumfever, sweats, chills, dyspnea, fatigue, palpitations Differential Dx: Dysrhythmias Occur due to disturbed electricity in heart due to MI, Rx, or other cardiac Dz; weakness, syncope, strokelike episodes, palpitations all symptoms Atrial Flutter: Atrial contractions > 200/min; results from heart block (disrupted atrial( ventricular conduction) Differential Dx: Dysrhythmias Sinus Bradycardia: Conduction not altered; < 60 BPM Atrial Fibrillation: Irregular spasms of atria; iregular irregular heart sounds Differential Dx: Dysrhythmias Heart Block: Caused by disruption of conduction between atria ( ventricles 1st Degree: PR interval > .20; overall rate 25-45 BPM 2nd Degree: Mobits Type I: PR interval > .20; QRS dropped throughout EKG Differential Dx: Dysrhythmias Mobitz Type II: PR > .20; pattern to P waves: QRS 3rd Degree Heart Block: Complete SA( AV discommunication Differential Dx: Dysrhythmias Atrial Tachycardia: Rapid regular HR > 200; conduction begins in atrium, but not from SA Ventricular Tachycardia: Grave prognosis; ventricular rate > 200 BPM Ventricular Fibrillation: Grave prognosis; rapid, weak ventricular contraction Pediatric Cardiac Abnormalities Tetralogy of Fallot: Comination of ventricular septal defect, pulmonic stenosis, dextraposition of the aorta, RVH: paroxysmal dyspnea w/ loss of consciousness, and central cyanosis; systolic murmur over 3rd ICSradiates to L neck Ventricular septal defect: Opening between L & R ventricles; arterial pulse small while jugular unaffectedloud, coarse, high-pitched murmur @ L sternal border and apical area no radiation to neck Patent ductus arteriosus: ductus doesnt close, resulting in ! workload of R ventricle; neck vessels dilated w/ wise pulse pressure harsh, loud continuous murmur @ 1st-3rd ICS and lower sternal border Atrial septal defect: Congenital defect allowing mixing of R and L atrial blood; loud, high-pitched systolic murmur over pulmonic arearadiation to back marks this as serious Dextrocardia: R sternal placement of heartas child matures, ABD contents can compress heart and cause parodoxical R arm pain in an MI; 3-D Echo Acute Rheumatic Fever: Occurs as a result of strep skin or pharyngeal infectionmay lead to serious cardiac valvular involvement; murmurs of mitral regurgitation/aortic insufficiency; friction rub, CHF, polyarthritis, painless SQ nodules on elbows, knees, and wrists Geriatric Cardiac Abnormalities Atherosclerotic heart Dx: Thickening and narrowing of coronary arteries due to lipid deposition leads to MI, CHF, angina, dysrhythmias Mitral insufficiency: silent/ painless until sudden CHF, CVA, or dysrhythmia; 3-D Echo; occurs after MI that affects chordae tendinae; tachycardia, pallor, variations in heart sounds Angina: Pain from ischemia due to atherosclerosis; CP radiates to L arm/ jaw; SOB, fatigue, diaphoresis, syncope Senile cardiac amyloidosis: Amyloid (fibrillary proteins released by systemic inflammation or CA) deposit into heart and reduce overall CO by thickening ventricles Aortic sclerosis: thickening and calcification of the aortic valves; may lead to significant obstruction to outflow of aorta; midsystolic murmur Advanced Assessment: Blood Vessels Anatomy and Physiology: Great vessels include aorta, superior/inferior vena cava, pulmonary arteries, and pulmonary veins Pulmonary circuit: deoxygenated blood arrives at superior/ inferior vena cava ( R atrium ( pulmonic valve ( pulmonic artery ( arteries ( arterioles ( capillaries ( alveoli Oxygenated blood returns via pulmonary veins ( L atrium ( aortic valve ( aorta ( arterial system ( Capillaries CO = HR x SV Arteries higher pressure w/ more tensible strength than more passive veins Carotid pulses are greatest pulses of the body Strength of pulses vary with stroke volume, distensibility of aorta and large arteries, blood viscosity, and SVR Jugular veins reflect activity of the R heart; externals more readily accessible than internals In pregnancy, vascular resistance !, resulting in palmar erythema and spider telangiectases; supine hypotension common due to vena cava compression; uterine occlusion of pelvic veins and inferior vena cava results in edema, leg/vulvar varicosities, and hemorrhoids In older adults, vessels become more tortuous as a result of loss of elasticity and vasomotor tone; overall ! SVR results in ! BP. Advanced Assessment: Blood Vessels Review of Related Hx: Leg pain or cramps: Onset and duration: w/ acticity/rest; w/ elevation of legs; recent injury/ immobilization Character: continuous burning in toes; pain when touching toes, thigh/buttock pain, charley horses, aching pain over specific location; induced by activity/amt?; skin changes: cold skin, hair loss, redness or warmth over vein, visible veins, darkening skinbecoming black or odorous Dizziness: Fatigue or limping; improves w/ walking; wake up @ night Severe HAs: Onset and duration: upon awakening, !/! as day progresses, disappearing in the PM Location: frontal/occiput/band over head Character: stabbing, throbbing, dull Known Hx of HTN Ankle Edema: Onset and duration: present in AM; appears as day progresses, sudden vs. insidious onset Related to: recent long air travel, recent high elevations Associated S/S: onset of nocturia, ! urination, SOB Tx attempted: rest, massage, heat, elevation, Rx (Coumadin, anti-HTNives, NSAIDs, Non/Rx, complementary Tx Advanced Assessment: Blood Vessels Past Medical Hx: Cardiac surgery/ hospitalization for evaluation, congenital heart defects, surgeries to correct vascular Dz Acute rheumatic fever, unexplained fever, joint edema, inflammatory rheumatism, St. Vitus dance Chronic illness: HTN and studies to determine cause, coagulopathies, hyperlipidemia, DM, thyroid dysfunction, CAD, A-fib, dysrhythmias, DVT Family Hx: DM, CAD, hyperlipidemia, HTN, risk factors among family members (morbidity/ mortality r/t CV system, HTN, PVD, ages when illness Dx/death) Personal and Social Hx Employment: physical demands, heat, chemicals, dust, sources of stress Tobacco: type (cigs, cigars, smokeless), duration of use, amt. age started/ possibly stopped, pack-years Nutritional status: BMI, usual diet (proportion of fat, food preference, Hx of diet); wt. loss/gain, amt/rate; known hypercholesterolemia/triglyceridiemia Personality assessment: intensity, hostility, inability to relax, compulsions Relaxation: hobbies, frequency of intercourse, sexual practices, # of partners Use of ETOH: CAGE, amt consumed, frequency, duration of current intake Use of ilegal Rx: cocaine/poppers Use of Non/RX, complementary Tx Advanced Assessment: Blood Vessels Infants and Children: Hx of hemophilia, renal Dz, coarctation of the aorta, leg pains during activity Pregnant Women: BP: Pre-preg levels, ! BP during preg, associated S/S: HA, visual changes, N/V, epigastric pain, RUQ pain, oliguria, rapid onset of edema, hyperreflexia, unusual bruising/bleeding EXT: edema, varicosities, pain, discomfort Use of Non/Rx, complementary Tx; ask specifically about Ca supplementation, particularly during 2nd trimester could ! risk of HTN in mom/infant Older Adults: Leg edema: pattern, frequency, time of day most pronounced Interference w/ ADLs Perceived and actual coping ability of pt/fam Claudication: location (uni/bilateral), distance walked until pain, sensation, length of rest time needed for relief Rx used for relief; efficacy of Rx Advanced Assessment: Blood Vessels Examination and Findings: Peripheral Pulses Advanced Assessment: Blood Vessels Auscultation: Assess for bruits using bell (low-pitched) over temporal, carotid (hold breath), subclavian, ABD aorta, renal, iliac, and femoral arteries May also be able to hear radiating murmurs of aortic stenosis/ regurgitation, ruptured chordae tendinae of mitral valve Arterial Occlusion and Insufficiency: S/S r/t: site, degree of occlusion, collateral circulation, rapidity with which problem develops 1st symptom usually pain from muscle ischemia (claudication); 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2nd Trimester: systolic pressure > 125 mm Hg or diastolic > 75 mm Hg indicates pathology 3rd Trimester: systolic pressure > 130 mm Hg or diastolic > 80 mm Hg indicates pathology BP shouldn t ! > 30 mm Hg systolic or 15 mm Hg diastolic from baseline after 1st trimester BP > 140/90 indicates HTN in pregnancy Older Adults: dorsalis pedis and tibial pulses harder to locate; HTN ( BP > 140/90) common Common Vascular Disorders Vessel Disorders: Cranial Arteritis: inflammatory Dz of aortic arch branches: Temporal arteritis seen w/ low-grade, fever, malaise, anorexia, polymyalgia, severe HA w/ red, swollen, tenderness, and nodular; D-Dimer significantly ! Arterial Aneurysm: localized diltation and weakness of artery wall; HTN usually culprit bruits often heard A:V Vistula: pathologic communication between an artery and vein; bruit often heard; located in brain (cause of ICH), GI (cause of GI bleed) and rarely in lungs Peripheral atherosclerotic Dz: Intermittent claudication: plaque significantly builds up in veins and occludes blood flow to muscle, resulting in ischemic pain Raynaud Phenomenon: Bilateral idiopathic, intermittent spasms of microcirculation of hands-- assess for sudden, ice-cold, blanched phalanges, smooth, shiny and tight digital skin; ! risk in smokers; also w/ connective tissue Dz, neurogenic lesions, Rx intoxication, pulm HTN, and trauma Common Vascular Disorders Cerebral Aneurysm and Raynaud Phenomenon Common Vascular Disorders Arterial Embolic Dz: A-fib caused by dilation of L atrium due to mitral regurgitation results in thrombus formation, embolizes to arterial system, causing ischemia Venous thrombosis: redness, thickening, tenderness along involved segment; trauma, prolonged stasis; assess for ankle edema, low-grade fever, tachycardia, +M Homann/s sign; diagnose via doppler flow US Common Vascular Disorders JVP Disorders: A-Fib: See previous slide Cardiac Tamponade: JVP markedly WPWHXXYZZ8[9[][g[[\Y\\/]o]]N^__5`\`````!a ' & F^gdS-'gdS-T^'`)```ddfff g\g^g`gg7i8i9iSijpppjulunuuv vhvjv@|B|v||||||||||||||||||||||||||||||ĺẴẴh&0JmHnHuhS-0JmHnHu hS-0JjhS-0JUhni`jhni`U h Lh&hS-hS-H*UhS-h&hS-hS->*hS-hS-H* hS-hS->!abbd.dddff g^g`gggnh8i9iSibi|itppDqXqtlunuu ' & F^gdS-'gdS-! > 15-25 cm H20; S/S of severe R-sided CHF; Beck s triad Tricuspid regurgitation: Holosystolic murmur in tricuspid region, pulsatile liver, and peripheral edema Children: Coarctation of the aorta: congenital narrowing and stenosis of descending aortic arch femoral pulse felt slightly before radial; diminished or absent femoral pulses also major diagnostic clue; BP much ! in arms than legs; precordium systolic murmur radiates to back; look for prominent figure 3 sign on CXR of older children; surgical intervention ASAP Kawasaki Dz: idiopathic; longstanding fever, systemic vasculitis, strawberry tongue, EXT edema, rashes; aneurysm of coronary arteries may develop and lead to rupture/MI Common Vascular Disorders Pregnant Women: Chronic HTN: BP > 140/90 before 20th week gestation not resolving early postpartum Pre/eclampsia: HTN after 20 weeks gestation w/ proteinuria (or visual changes, HA, ABD pain, abnormal labs) w/ seizure = eclampsia Preeclampsia superimposed on Chronic HTN: All of above (before 20 weeks), but occurs in women w/ previously controlled HTN Gestational HTN: No proteinuria or symptoms; develops during preg but returns to normal by 12 weeks postpartrum Older Adults: Arteriosclerosis obliterans of the EXTs: intermittent claudication, pain, spasm or weakness in muscles, immediately relieved w/ rest; follows age-related pathology of atherosclerosis Venous Ulcers: Found on medial or lateral aspects of lower EXT; iniduration, edema, hyperpigmentation common; CHF, hypoalbuminemia, nutritional deficiency, DM all predisposing factors Common Vascular Disorders Venous Ulcers     PAGE 1 PAGE 6 PAGE 34 uuhvpwfxFybyz@|B|v||||||||||||||||&`h]h&` ' & F^gdS-'gdS-||||||}}'gdS-&` hh]h`h|||}} h Lh&hni`hS- hS-0J,1h/ =!"#$% Dd\  c 8AHorseUnivb%B UDnB UPNG  IHDR!gAMA|Q pHYs.#.#x?vӊIDATx^]uGߜ+wr[CKTQEJ)RwqwIMIvgVff7e˳˛7o P(܁G0ZIP:,P(rTQC)3@5SE Ptym01Q'6zC@1o3@z6<]| ,!(4cȇfV(a=Iu#*QzZC}Pr7a )ңBj=BP)E"+ +م{GebY0))E"+pud,m@JK\ax,"@52^w+\˾*<"@=ÊyKCm_9O-Pp=G#Zpl&@*\a%C|x-?>Pr尢@SQdvĘy "@UdrͱdيfK("sg(7C]b@B !S6ƮigI"P(@N9m#W2>_̭IHt"@5dUX \"kk1F?jQI)E";p?|sR+QaYlyQ(g8O֒dv&pJȠ]LM )܀AX:%wF9m&R(F+~!_ +O 8r*:cwWYY(%E"8aEcj3H'dϡȜ ֚i|zR(.cfM`O׌Ȭb'܂l"@pq갞|?8f '"{43)JSP)eP\ G:m/1=8u:ѿ}Y)+CaYZ'&UL(Bq+vEmNO6rߡ3C9鉑.<<x(נ` =ihE)Epz4~+T_Q6Ͽ'Eb,س2%[4NjP\9,&l{C ?^P1> P?H|%~ֿKufCP(9cVRgXۨ"g yKCFmCR8aE{^ad,Zq>_0OP\ G8}S1NM$OlsWlv@(t_2*ϴIr?;%2\ɣfQ=/)a)Lޤ)E"hҧvc)vOkpA3rI/&Te 9W_} 0pZAP_M#vA&հS^EЬ!_m~XH]h=fP!64q"@>evOqQxJ#a=xsàvGj}Q"@ȣhiWwfb܆%f@D@uo GV-yw(+ 8af?H,2R(yU$T}E?A,b(#E /#axgO 6&ƭSibVHaT8fC=t8:4 VՐަ+#b[M]b"@pqBx-$go2(E" uXٿ}ѻoeU)'P6k'0S9z !PH tX+ԶmuWE۬ސEjQAz9)t" qX~mpPsxVGO)Aa"pg-a&#Xߏ2R(y|ii3y;yp:<ElqD\["Ǔ)eO>(IM_Rm!1Xui1v"uXM`8l`$>ÔKR(`:I(7EJv^"XeP(x+k%)*O^&ܔ|ΣE@ _$uV_$0ز*;H`9WH"RAbLjJC8K$8^l_ŋ4DCH4:JE%8 i ׷}LdVCb"@ȳ`8y0}m]"F+2R(ne lOvwj`t)Br.VI),)9|@ECȍBSW"@㈈ "@p'!@&ӥlk~p|#kZJnPփ/Sej[=zIHVb9xgrTs:"@}6_.U$,T܈l{_=ɍS)ZQ C+V5]伬;gϸ+LY#ˮY.Rlc{i)1sp"V :o?G%-8zwbG/ f%gLu/0ȧgjׯ\¯߰_vMnP@sXQ}WLֲԞUdNwXWW?TB}t(/~T?)#E"{yok%וք9fk@ɹ8TIEt_*lgy3"@TA"@ Fa]PA5V]SX"&cSOƦqy Tgm1w<,JM @_1 U89`ڌ]_1' l8fA<$4BpWPVQEt췟Tx,L>AS߾_wg1R(VۊhVp?uj,CGZv6s{%.2@jE /#b)G>kr\_z^dĽzk7 f$"@Ca픺(GTnwL'wVÝ}VdJ0CH"b`N2س;vMu[=`3IPvX.bAE- 6 U|{z1o%b Ö {i &y9LJN`#n ]ڥM={ف_ӏnWDHą (E"\ְi!uG(*·41O^ v`&UA(EXhڵqX ne;k4-v J*" : ;m&tWe4"PrXnE IUl1Nܛ9+d:B@#5 㨢qi@{/5(рjK͗WNWdW*nA8C ͠ <{1,D=c2጖j]j%P~E@y!]trCаG~x''N\~Ii(yy( qĩmjVu/)`mh]D5#8]TE ﰎ۩{Q^$`cy/Is0Lzr5VAH(4dVrodѤjW v*mb(E"# "Xw38|Uok K|:=PuXѫ n[*Ҡ#W0Ќzf E@Yu6)CL-MqMuN9,6$t#Kp[V2B?f[6$~l&ktGV_{Jㆭ2PaݼϋiVP[\n&97WPꭥ;_ _9N52?+c*2+cU3`GѶ*O=?.^tm_)f FGB/#B{P0|{GVvG+Bя[/siՀSG@谢5My[{PltU~% D%|\V4CTw."!%P:K3!SL Ƀ77~@E71 Ma=9PP݂ؕl}dVH~Ou磱"2k R"@aN)֓>_f0d3d<_]b"7hu(d"@E@7{ >KVĕ'g{U!<FTx ~OO~6vlpPnLfEifa1.:g*?^E cy2ZvҫHG V JԘA ,e*sot@[',g"fb4N>w oR1cLuT$JA @ﰌ\bDf_/>}АH%GEE8t2)E;S+:`!Kfte4 XL^X3p2& zE@4*6}S~jpZ҈*(E" sX;XKl S04fGMxGX^֪mp'MZ_}Lf$դ䣢>Sg-XjD (E- q%AQ3xbB~o޺ jdu$7$ uD)Cw} E(•(PsȊ$;H526|M."~(_9:ҭwa60P)Dlo;@7^t^ESg^5M!h>ڤI-FugUA2XI'^稑*ڔ"sX?.q7W;փvT<Ǟ6KtHNmFn VOy?Z,ȜR?r.ၣcAZ- e0!;*_ /kxTg<\_z@^IU = Y%=qz{~vXAQ^)5KCz̴gX1rOB1u ȔTW4"ŏn\Z^lkR(&xka7[^ u=_`!oSjo<NXsU?:P&}_2}P,=}ʘU[-+O6q a5Y"XN M}=Fzp,82"#ն?+9ٝx-O'2<>TϺjmnCV`MNYw)'$VM`v܈l)0)1E W"-":EFPk7^rG`; 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