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NR302 Exam 3 Study Guide Health Assessment I., Study notes of Nursing

NR302 Exam 3 Study Guide Health Assessment I.

Typology: Study notes

2021/2022

Available from 08/27/2022

Terrie001
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Position and Surface Landmarks Chapter 19 Heart and Neck Vessels o Precordium: area on anterior chest overlying heart and great vessels o During contraction, apex beats against chest wall, producing an apical impulse o Heart has four chambers: atria and ventricles o Great vessels lie bunched above base of heart o Pulmonary veins return freshly oxygenated blood to left side of heart, and aorta carries it out to body Heart Wall, Chambers, and Valves o Heart wall has numerous layers ➢ Pericardium: tough, fibrous, double-walled sac that surrounds and protects heart ➢ Myocardium: muscular wall of heart; it does pumping ➢ Endocardium: thin layer of endothelial tissue that lines inner surface of heart chambers and valves o Heart has two pump systems o Each side of the heart has an atrium and ventricle ➢ Atrium: thin-walled reservoir for holding blood ➢ Ventricle: thick-walled, muscular pumping chamber ➢ Heart Chambers and Valves o Four chambers separated by valves, whose main purpose is to prevent backflow of blood ➢ Valves are unidirectional: can only open one way ➢ Valves open and close passively in response to pressure gradients in moving blood o Four valves in heart ➢ Two atrioventricular (AV) valves ➢ Two semilunar (SL) valves AV Valves o Two AV valves separate atria and ventricles ➢ Tricuspid valve: right AV valve ➢ Bicuspid, or mitral valve: left AV valve

  • Valves’ thin leaflets are anchored by collagenous fibers (chordae tendineae) to papillary muscles embedded in ventricle floor ➢ AV valves open during heart’s filling phase, or diastole, to allow ventricles to fill with blood ➢ During pumping phase, or systole, AV valves close to prevent regurgitation of blood back up into atria SL Valves o SL valves are set between ventricles and arteries ➢ Each valve has three cusps that look like half moons ➢ Pulmonic valve: SL valve in right side of heart ➢ Aortic valve: SL valve in left side of heart
  • Open during pumping, or systole, to allow blood to be ejected from heart ➢ No valves are present between vena cava and right atrium, or between pulmonary veins and left atrium, for this reason
  • Abnormally high pressure in left side of heart gives a person symptoms of pulmonary congestion
  • Abnormally high pressure in right side of heart shows in neck veins and abdomen
  • Chambers and Valves Direction of Blood Flow I Unoxygenated red blood drains into vena cava, follows route of venous blood o From liver to right atrium (RA) through inferior vena cava ➢ Superior vena cava drains venous blood from the head and upper extremities ➢ From RA, venous blood travels through tricuspid valve to right ventricle (RV) o From RV, venous blood flows through pulmonic valve to pulmonary artery ➢ Pulmonary artery delivers unoxygenated blood to lungs Direction of Blood Flow II ➢ Lungs oxygenate blood
  • Pulmonary veins return fresh blood to LA ➢ From LA, arterial blood travels through mitral valve to LV
  • LV ejects blood through aortic valve into aorta ➢ Aorta delivers oxygenated blood to body o Circulation is continuous loop; blood is kept moving by continually shifting pressure gradients ➢ Blood flows from area of higher pressure to area of lower pressure Cardiac Cycle o Rhythmic flow of blood through heart is cardiac cycle ➢ Has two phases, diastole and systole ➢ Diastole: ventricles relax and fill with blood; this takes up two thirds of cardiac cycle ➢ Systole: heart’s contraction, blood pumped from ventricles fills pulmonary and systemic arteries; this is one third of cardiac cycle Cardiac Cycle: Diastole ➢ Ventricles relaxed, and AV valves, tricuspid and mitral, are open; opening of normal valve is silent ➢ Pressure in atria higher than that in ventricles, so blood pours rapidly into ventricles
  • This first passive filling phase called protodiastolic filling ➢ Toward end of diastole, atria contract and push last amount of blood into ventricles
  • This active filling phase called presystole, or atrial systole o Note that atrial systole occurs during ventricular diastole, a confusing but important point

Cardiac Cycle: Systole o Ventricular pressure becomes higher than that in atria, so mitral and tricuspid valves close o Closure of AV valves contributes to first heart sound (S1) and signals beginning of systole ➢ AV valves close to prevent any regurgitation of blood back up into atria during contraction o For a very brief moment, all four valves are closed and ventricular walls contract ➢ Isometric contraction: this contraction against closed system works to build high level pressure in ventricles Events in Right and Left Side of Heart I Systole o Consider left side of heart o When pressure in ventricle finally exceeds pressure in aorta, aortic valve opens and blood is ejected rapidly ➢ After ventricle’s contents are ejected, its pressure falls o When pressure falls below pressure in aorta, some blood flows backward toward ventricle, causing aortic valve to close o This closure of semilunar valves causes second heart sound (S2) and signals end of systole Events in Right and Left Side of Heart II o Diastole again ➢ Now all four valves are closed and ventricles relax

  • Isometric or isovolumic relaxation ➢ Atria have been filling with blood delivered from lungs ➢ Atrial pressure now higher than relaxed ventricular pressure ➢ Mitral valve opens and diastolic filling begins again Events in Right and Left Side of Heart III o Same events happening in right side of heart ➢ But pressures in right side of heart are much lower than those of left side because less energy needed to pump blood to its destination, pulmonary circulation ➢ Events occur just slightly later in right side of heart because of route of myocardial depolarization o Results in two components to each of the heart sounds ➢ In first heart sound, mitral component (M1) closes just before tricuspid component (T1) ➢ With S2, aortic closure (A2) occurs slightly before pulmonic closure (P2) Heart Sounds o Events in cardiac cycle generate sounds that can be heard through a stethoscope over chest wall o These include normal heart sounds and, occasionally, extra heart sounds and murmurs

First Heart Sound (S1) ➢ Occurs with closure of AV valves and thus signals beginning of systole ➢ Mitral component of first sound (M1) slightly precedes tricuspid component (T1)

  • Usually hear these two components fused as one sound
  • Can hear S1 over all precordium, but loudest at apex Second Heart Sound (S2) ➢ Occurs with closure of semilunar valves and signals end of systole ➢ Aortic component of second sound (A2) slightly precedes pulmonic component (P2)
  • Although heard over all precordium, S2 loudest at base Effect of Respiration I o Volume of right and left ventricular systole is just about equal but can be affected by respiration ➢ To learn this, consider the phrase: More to the right heart, less to the left o That means that during inspiration, intrathoracic pressure is decreased o This pushes more blood into vena cava, increasing venous return to right side of heart, which increases right ventricular stroke volume o Increased volume prolongs right ventricular systole and delays pulmonic valve closure Effect of Respiration II ➢ Meanwhile, on left side, greater amount of blood sequestered in lungs during inspiration ➢ This momentarily decreases amount returned to left side of heart, decreasing left ventricular stroke volume ➢ Decreased volume shortens left ventricular systole and allows aortic valve to close a bit earlier ➢ When aortic valve closes significantly earlier than pulmonic valve, you can hear two components separately; this is a split S Extra Heart Sounds (S3) o Third heart sound (S3) ➢ Normally diastole is silent event ➢ However, in some conditions, ventricular filling creates vibrations that can be heard over chest ➢ S3 occurs when ventricles resistant to filling during early rapid filling phase (protodiastole) ➢ Occurs immediately after S2, when AV valves open and atrial blood first pours into ventricles Question The school nurse hears an extra heart sound on a 16-year-old male athlete. The nurse believes this is because: 1. an extra heart sound in a child or young adult is usually considered a physiological S 3 and is (^) considered normal. 2. this patient may have a heart murmur and will need to be checked by a cardiologist. 3. the nurse should assess if the patient has been running because an extra heart sound may be the heart’s reaction to increased activity.

4. the nurse should determine if heart disease runs in the patient’s family and refer him to his primary care physician. Extra Heart Sounds (S4) Fourth heart sound (S4) ➢ Occurs at end of diastole, at presystole, when ventricle resistant to filling ➢ Atria contract and push blood into noncompliant ventricle ➢ This creates vibrations that are heard as S ➢ S4 occurs just before S Extra Heart Sounds: Murmurs o Blood circulating through normal cardiac chambers and valves usually makes no noise o However, some conditions create turbulent blood flow and collision currents o These result in a murmur, much like a pile of stones or a sharp turn in a stream creates a noisy water flow o A murmur is a gentle, blowing, swooshing sound that can be heard on chest wall Conditions Resulting in Murmur o Velocity of blood increases (flow murmur), for example, in exercise, thyrotoxicosis o Viscosity of blood decreases, for example, in anemia o Structural defects in valves, narrowed valve, incompetent valve o Unusual openings occur in chambers, dilated chamber, wall defect Characteristics of Sound o All heart sounds are described by ➢ Frequency or pitch: described as high pitched or low pitched - Although these terms are relative because all are low-frequency sounds and need good stethoscope to hear them ➢ Intensity or loudness: loud or soft ➢ Duration: very short for heart sounds; silent periods are longer ➢ Timing: systole or diastole Conduction I o Heart has unique ability: automaticity ➢ Can contract by itself, independent of any signals or stimulation from body ➢ Contracts in response to an electrical current conveyed by a conduction system ➢ Specialized cells in sinoatrial (SA) node, near superior vena cava initiate an electric impulse Because SA node has intrinsic rhythm, it is called the pacemaker Conduction II o Current flows in orderly sequence, first across atria to AV node low in atrial septum o There, it is delayed slightly so that atria have time to contract before ventricles are stimulated o Then, impulse travels to bundle of His, right and left bundle branches, and then through ventricles

o Electric impulse stimulates heart to do its work, which is to contract o Small amount of electricity spreads to body surface and can be measured and recorded on electrocardiograph (ECG) Electrocardiograph (ECG) o ECG waves arbitrarily labeled PQRST, which stand for o P wave: depolarization of atria o P-R interval: from beginning of P wave to beginning of ➢ QRS complex (time necessary for atrial depolarization plus time for impulse to travel through AV node to ventricles) o QRS complex: depolarization of ventricles o T wave: repolarization of ventricles o Electrical events slightly precede mechanical events in heart Pumping Ability o In resting adult, heart normally pumps between 4 and 6 L of blood per minute throughout body ➢ This cardiac output equals volume of blood in each systole (called stroke volume) times number of beats per minute (rate) ➢ Heart can alter its cardiac output to adapt to metabolic needs of body ➢ Preload and afterload affect heart’s ability to increase cardiac output Preload o Preload: venous return that builds during diastole ➢ Length to which ventricular muscle stretched at end of diastole just before contraction ➢ When volume of blood returned to ventricles increased

  • Muscle bundles stretched beyond normal resting state
  • Force of this switch is preload ➢ According to Frank-Starling law, greater the stretch, the stronger the heart’s contraction ➢ This increased contractility results in an increased volume of blood ejected, increased stroke volume Afterload o Afterload: opposing pressure ventricle must generate to open aortic valve against higher aortic pressure ➢ Resistance against which ventricle must pump its blood ➢ Once ventricle is filled with blood, ventricular end diastolic pressure is 5 to 10 mm Hg, whereas that in aorta is 70 to 80 mm Hg.
  • To overcome this difference, ventricular muscle tenses, isovolumic contraction
  • After aortic valve opens, rapid ejection occurs Neck Vessels: Carotid Artery Pulse Carotid artery is a central artery o Close to heart; timing closely coincides with ventricular systole o Located in groove between trachea and sternomastoid muscle, medial to and along- side that muscle

o Note characteristics of its waveform ➢ Smooth rapid upstroke ➢ Summit rounded and smooth ➢ Downstroke more gradual and has a dicrotic notch caused by closure of aortic valve Neck Vessels: Jugular Venous Pulse and Pressure I o Jugular veins empty unoxygenated blood directly into superior vena cava ➢ Because no cardiac valve exists to separate superior vena cava from right atrium, jugular veins give information about activity on right side of heart ➢ Specifically reflect filling pressure and volume changes ➢ Jugular veins expose this because volume and pressure increase when right side of heart fails to pump efficiently Neck Vessels: Jugular Venous Pulse and Pressure II o Two jugular veins present in each side of neck ➢ Larger internal jugular lies deep and medial to sternomastoid muscle ➢ Usually not visible, although diffuse pulsations may be seen in sternal notch when person is supine ➢ External jugular vein is more superficial; lies lateral to sternomastoid muscle, above clavicle Jugular Pulse: 5 Components o The A wave reflects atrial contraction because some blood flows backward to vena cava during right atrial contraction o The C wave, or ventricular contraction, is backflow from bulging upward of tricuspid valve when it closes at beginning of ventricular systole o The X wave descent shows atrial relaxation when right ventricle contracts during systole and pulls bottom of atria downward o The V wave occurs with passive atrial filling because of increasing volume in right atria and increased pressure o Finally, the Y descent reflects passive ventricular filling when tricuspid valve opens and blood flows from RA to RV o Developmental Competence: Infants and Children o Fetal heart begins to beat after 3 weeks’ gestation o Right and left ventricles equal in weight and muscle wall thickness and both pumping into systemic circulation o Inflation and aeration of lungs at birth produces circulatory changes o Now blood is oxygenated through lungs rather than through placenta o Now left ventricle has greater workload of pumping into systemic circulation Developmental Competence: Pregnant Woman Blood volume increases by 30% to 40% during pregnancy o Most rapid expansion occurs during second trimester o Creates an increase in stroke volume and cardiac output and an increased pulse rate of 10 to 15 beats per minute

o Despite increased cardiac output, arterial blood pressure decreases in pregnancy as a result of peripheral vasodilation o Blood pressure drops to lowest point during second trimester, then rises after that o Blood pressure varies with person’s position Developmental Competence: Aging Adult It is difficult to isolate “aging process” of cardiovascular system, per se, because it is so closely interrelated with lifestyle, habits, and diseases o Lifestyle, smoking, diet, alcohol use, exercise patterns, and stress have an influence on coronary artery disease o Lifestyle also affects aging process; cardiac changes once thought to be due to aging are partially due to sedentary lifestyle accompanying aging o What is left to be attributed to aging process alone? Hemodynamic Changes with Aging o With aging, there is an increase in systolic BP due to thickening and stiffening of the arteries o Left ventricular wall becomes thicker but the overall size of the heart does not change o Pulse pressure increases o No change in resting heart rate or cardiac output at rest o Ability of heart to augment cardiac output with exercise is decreased Arrhythmias o Presence of supraventricular and ventricular arrhythmias increases with age o Ectopic beats common in aging people; usually asymptomatic in healthy older people, may compromise cardiac output and blood pressure when disease present o Tachyarrhythmias may not be tolerated as well in older people ➢ Myocardium thicker and less compliant, and early diastolic filling impaired at rest ➢ Thus, may not tolerate a tachycardia as well because of shortened diastole Age-Related Changes in ECG o Occur as result of histologic changes in conduction system; these changes include ➢ Prolonged P-R interval (first-degree AV block) and prolonged Q-T interval, but the QRS interval is unchanged ➢ Left axis deviation from age-related mild LV hypertrophy and fibrosis in left bundle branch ➢ Increased incidence of bundle branch block o Although hemodynamic changes associated with aging alone do not seem severe or portentous, incidence of cardiovascular disease increases with age Cardiac Disease and Aging Adult

o Incidence of coronary artery disease increases sharply with advancing age and accounts for about half of deaths of older people ➢ Hypertension and heart failure also increase with age ➢ Lifestyle habits play a significant role in the acquisition of heart disease o Also, increasing physical activity of older adults associated with a reduced risk of death from cardiovascular diseases and respiratory illnesses ➢ Both points underscore need for health teaching as an important treatment parameter Culture and Genetics I Prevalence is an estimate of how many people in a stated geographic location have a disease at a given time ➢ In the U.S., more than 1 in 3 have one or more forms of cardiovascular heart disease (CVD)

  • Annual rates of first CVD event increase with age
  • For women, comparable rates occur 10 years later in life than for men, but this gap narrows with advancing age ➢ Causes of CVD: interaction of genetic, environmental, and lifestyle factors ➢ Evidence shows potentially modifiable risk factors contribute to overwhelming majority of cardiac risk Culture and Genetics II o Although all adults have some potential CVD risk, some groups, defined by race, ethnicity, gender, socioeconomic status, and educational level carry an excess burden of CVD ➢ Higher percent of men than women have hypertension until 45 years, after which the percentages are similar
  • After 64 years, women have much higher percentage than men ➢ Hypertension is 2 to 3 times more common among women taking oral contraceptives, especially obese and older women ➢ Hypertension in Blacks is among highest in world and is rising Culture and Genetics: Hypertension o Prevalence of hypertension is 41.4% Blacks o 25.8% for American Indians or Alaska Natives o 28.1% for Whites o 22.2% for Hispanics and 18.7% for Asians o Compared with Whites, Blacks develop hypertension earlier in life, and their average BP is much higher ➢ Thus, Blacks have greater rate of stroke, death due from heart disease and end- stage kidney disease Culture and Genetics: Smoking o In the 45+ years from 1965 to 2010, U.S. smoking rates declined by 54% among adults over 18

o In 2010, 21.2% of men and 17.5% of women were smokers o Nicotine increases risk of myocardial infarction (MI) and stroke by causing ➢ Increase in oxygen demand with a concomitant decrease in oxygen supply ➢ Activation of platelets, activation of fibrinogen; and an adverse change in lipid profile Culture and Genetics: Serum Cholesterol o High levels of low density lipoprotein gradually add to lipid core of thrombus formation in arteries, which results in MI and stroke o Age-adjusted prevalence of LDL cholesterol levels over 130 mg/dL include ➢ 39.9% of Mexican American men and 30.4% of Mexican American women ➢ 30.1% of white men and 29.3% of white women ➢ 33.1% of black men and 31.2% of black women Culture and Genetics: Obesity o Epidemic of obesity in U.S. is well known ➢ Among Americans age 20 or older, prevalence of overweight or obesity

  • Overall 68% are overweight or obese
  • Of which 73% are men and 64% are women
  • Obesity increases the risk of comorbid conditions, such as but not limited to HTN, hyperlipidemia, type II diabetes Culture and Genetics: Type II Diabetes Mellitus (DM) o Risk of CVD is twofold greater among persons with DM ➢ Increased prevalence of DM in U.S. is being followed by an increasing prevalence of CVD morbidity and mortality ➢ Diabetes causes damage to large blood vessels that nourish brain, heart and extremities; this results in stroke, coronary artery disease, and peripheral vascular disease ➢ About 12.6% of Blacks over age 20 have DM ➢ 11.8% of Hispanic Americans have DM, compared to 7.1% of Whites Culture and Genetics: Sex Differences o Regardless of ethnicity, CVD is the leading cause of death in women ➢ Within the first year following an MI, women age 45 and older are 26% more likely to die than their male counterparts (19%) ➢ Women may report different symptoms than the typical “chest pain” experienced by men, thus clinical diagnosis may be delayed Subjective Data o Chest pain o Dyspnea o Orthopnea o Cough o Fatigue o Cyanosis or pallor

o Edema o Nocturia o Past cardiac history o Family cardiac history o Personal habits (cardiac risk factors) Chest Pain Questions I o Any chest pain or tightness? ➢ Onset: When did it start? How long have you had it this time? Had this type of pain before? How often? ➢ Location: Where did the pain start? Does the pain radiate to any other spot? ➢ Character: How would you describe it? Is it crushing, stabbing, burning, or viselike? (Allow the person to offer adjectives before you suggest them.) (Note if uses clenched fist to describe pain.) ➢ Is pain brought on by activity (what type), rest, emotional upset, eating, sexual intercourse, or cold weather? Chest Pain Questions II o Any associated symptoms, such as sweating, ashen gray or pale skin, heart skipping a beat, shortness of breath, nausea or vomiting, or racing of heart? ➢ Is the pain made worse by moving the arms or neck, breathing, or lying flat? ➢ Is the pain relieved by rest or nitroglycerin? How many tablets? Dyspnea Questions o Any shortness of breath? ➢ What type of activity, and how much brings on shortness of breath? How much activity brought it on 6 months ago? ➢ Onset: Does the shortness of breath come on unexpectedly? ➢ Duration: Is it constant or does it come and go? ➢ Does it seem to be affected by position, such as lying down? ➢ Does it awaken you from sleep at night? ➢ Does the shortness of breath interfere with activities of daily living? Cough Questions o Do you have a cough? ➢ Duration: How long have you had it? ➢ Frequency: Is it related to time of day? ➢ Type: Is it dry, hacking, barky, hoarse, or congested? ➢ Do you cough up mucus? What color is it? Does it have any odor? Is it blood- tinged? ➢ Associated with activity, position (lying down), anxiety, or talking? ➢ Does activity make it better or worse (sit, walk, exercise)? ➢ Is it relieved by rest or medication? Fatigue Questions

o Do you seem to tire easily? Able to keep up with your family or co-workers? ➢ Onset: When did it start? Sudden or gradual? Any recent change in energy level? ➢ Fatigue related to time of day? All day? Morning, evening? Assorted Subjective History Questions Orthopnea o How many pillows do you use when sleeping or lying down? Cyanosis or pallor o Have you ever noticed your facial skin turn blue or ashen? Nocturia o Do you awaken at night with an urgent need to void? How long has this been occurring? o Edema Questions o Do you have any swelling of your feet and legs? ➢ Onset: When did you first notice this? Any recent change? ➢ What time of day does the swelling occur? Do your shoes feel tight at the end of day? ➢ How much swelling would you say there is? Are both legs equally swollen? ➢ Does swelling go away with rest, elevation, or after a night’s sleep? ➢ Do you have any associated symptoms, such as shortness of breath? If so, does shortness of breath occur before leg swelling or after? Cardiac History Questions o Do you have a history of hypertension, elevated cholesterol or triglycerides, heart murmur, congenital heart disease, rheumatic fever or unexplained joint pains as child or youth, recurrent tonsillitis, or anemia? o Have you ever had heart disease? When was this? Was it treated by medication or heart surgery? o When was your last ECG, stress ECG, serum cholesterol measurement, or other heart tests? o Any family history of hypertension, obesity, diabetes, coronary artery disease (CAD), sudden death at younger age? Personal Habits (Cardiac Risk Factors) I o Nutrition ➢ Please describe your usual daily diet (Note if this diet is representative of the basic food groups, the amount of calories, cholesterol, and any additives such as salt) ➢ What is your usual weight? Has there been any recent change? o Smoking ➢ Do you smoke cigarettes or use other tobacco products? At what age did you start? How many packs per day? For how many years have you smoked this amount? Have you ever tried quitting? If so, how did this go? (Cardiac Risk Factors) II

o Alcohol ➢ How much alcohol do you usually drink each day or week? When was your last drink? What was the number of drinks that episode? Have you ever been told you had a drinking problem? o Exercise ➢ What is your usual amount of exercise each day or week? What type of exercise (state type or sport)? If a sport, what is your usual activity level (light, moderate, heavy)? o Drugs ➢ Do you take any antihypertensives, beta-blockers, calcium channel blockers, digoxin, diuretics, aspirin/anticoagulants, over-the-counter, or street drugs? ➢ Additional History for Infants o How was mother’s health during pregnancy? Was there any unexplained fever, rubella during first trimester, other infection, hypertension, or drugs taken? ➢ Have you noted any cyanosis while nursing or crying? Is baby able to eat, nurse, or finish bottle without tiring? ➢ Growth: Has this baby grown as expected by growth charts and about same as siblings or peers? ➢ Activity: Were this baby’s motor milestones achieved as expected? Is baby able to play without tiring? How many naps does baby take each day? How long does a nap last? Additional History for Children o Growth: Has this child grown as expected by growth charts? o Activity: Is this child able to keep up with siblings or age mates? o Has the child had any unexplained joint pains or unexplained fever? o Does the child have frequent headaches or nosebleeds? o Does the child have frequent respiratory infections? How many per year? How are they treated? Have any of these been streptococcal infections? o Does child have a sibling with heart defect? Is anyone in child’s family known to have chromosomal abnormalities, such as Down syndrome? Additional History for Pregnant Woman o Have you had any high blood pressure during this or earlier pregnancies? ➢ What was your usual blood pressure level before pregnancy? How has your blood pressure been monitored during the pregnancy? ➢ If high blood pressure, what treatment has been started? ➢ Do you have any associated symptoms, such as weight gain, protein in urine, or swelling in feet, legs, or face? o Have you had any faintness or dizziness with this pregnancy? Additional History for Aging Adult o Do you have any known heart or lung disease, such as hypertension, CAD, chronic emphysema, or bronchitis? o Do you take any medications for your illness, such as digitalis? Are you aware of side effects? Have you recently stopped taking your medication? Why?

Environment ➢ Does your home have any stairs? How often do you need to climb them? Does this have any effect on activities of daily living? Preparation and Equipment Preparation o To evaluate carotid arteries, person can be sitting o To assess jugular veins and precordium, person should be supine with head and chest slightly elevated o Ensure woman’s privacy by keeping her breasts draped Equipment o Marking pen o Small centimeter ruler o Stethoscope with diaphragm and bell endpieces o Alcohol wipe to clean endpiece Neck Vessels: Palpation o Palpate carotid artery ➢ Yields important information on cardiac function ➢ Palpate each carotid artery medial to sternomastoid muscle in neck; palpate gently ➢ Palpate only one carotid artery at a time to avoid compromising arterial blood to brain ➢ Feel contour and amplitude of pulse ➢ Normally contour is smooth with a rapid upstroke and slower downstroke, and the normal strength is 2+ or moderate ➢ Findings should be same bilaterally Neck Vessels: Auscultation I Auscultate carotid artery o For persons middle-aged or older, or who show symptoms or signs of cardiovascular disease, auscultate each carotid artery for presence of a bruit ➢ This is a blowing, swishing sound indicating blood flow turbulence; normally none is present o Lightly apply bell of stethoscope over carotid artery at three levels: ➢ Angle of jaw ➢ Midcervical area ➢ Base of neck Neck Vessels: Auscultation II Auscultate carotid artery ➢ Avoid compressing artery because this could create an artificial bruit and could compromise circulation if carotid artery is already narrowed by atherosclerosis ➢ Ask person to take a breath, exhale, and hold it briefly while you listen so that tracheal breath sounds do not mask or mimic a carotid artery bruit

  • Holding breath on inhalation will also tense levator scapulae muscles, which makes it hard to hear carotids

➢ Sometimes you can hear normal heart sounds transmitted to neck; do not confuse these with a bruit Neck Vessels: Inspection I Inspect jugular venous pulse ➢ From jugular veins you can assess central venous pressure (CVP) and judge heart’s efficiency as a pump

  • Although external jugular vein is easier to see, internal (especially the right) jugular vein is attached more directly to superior vena cava and more reliable for assessment
  • You cannot see internal jugular vein itself, but you can see its pulsation ➢ Position person supine anywhere from a 30- to a 45-degree angle, wherever you can best see pulsations ➢ In general, the higher the venous pressure, the higher the position you need Neck Vessels: Inspection II Inspect jugular venous pulse ➢ Look for pulsations of internal jugular veins in area of suprasternal notch or around origin of sternomastoid muscle around clavicle ➢ You must be able to distinguish internal jugular vein pulsation from that of carotid artery ➢ It is easy to confuse them because they lie close together Jugular Venous Pressure I Estimate jugular venous pressure ➢ Use angle of Louis as arbitrary reference point, and compare it with highest level of venous pulsation ➢ Hold a vertical ruler on sternal angle ➢ Align a straight edge on ruler like a T-square, and adjust level of horizontal straight edge to level of pulsation ➢ Read level of intersection on vertical ruler; normal jugular venous pulsation is 2 cm or less above sternal angle ➢ State person’s position, for example, “internal jugular vein pulsations 3 cm above sternal angle when elevated 30 degrees” Jugular Venous Pressure II Estimate jugular venous pressure ➢ If you cannot find internal jugular veins, use external jugular veins and note point where they look collapsed ➢ If venous pressure is elevated, or if you suspect heart failure, perform hepatojugular reflux
  • Position person comfortably supine and instruct him or her to breathe quietly through open mouth ➢ Hold your right hand on right upper quadrant of person’s abdomen just below rib cage ➢ Watch level of jugular pulsation as you push in with your hand

Jugular Venous Pressure III Estimate jugular venous pressure ➢ Exert firm sustained pressure for 30 seconds ➢ This empties venous blood out of liver sinusoids and adds its volume to venous system ➢ If heart is able to pump this additional volume (i.e., if no elevated CVP is present), jugular veins will rise for a few seconds, then recede back to previous level Neck Vessels Precordium I Inspect anterior chest ➢ Arrange tangential lighting to accentuate any flicker of movement ➢ Pulsations: you may or may not see apical impulse, pulsation created as left ventricle rotates against chest wall during systole

  • When visible, it occupies the fourth or fifth intercostal space, at or inside midclavicular line
  • Easier to see in children and in those with thinner chest walls Precordium II Palpate apical impulse ➢ Localize apical impulse precisely by using one finger pad ➢ Asking person to “exhale and then hold it” aids examiner in locating pulsation; may need to roll person midway to left to find it; note that this also displaces apical impulse farther to left ➢ Palpable in about half of adults; is not palpable in obese persons or in persons with thick chest walls ➢ With high cardiac output states (anxiety, fever, hyperthyroidism, anemia), apical impulse increases in amplitude and duration Precordium III Palpate across precordium ➢ Using palmar aspects of your four fingers, gently palpate apex, left sternal border, and base, searching for any other pulsations ➢ Normally none occur ➢ If any are present, note timing ➢ Use carotid artery pulsation as a guide, or auscultate as you palpate Precordium Percussion I ➢ Used to outline heart’s borders, but its use has often been displaced by chest x- ray or echocardiogram ➢ Much more accurate in detecting heart enlargement ➢ When right ventricle enlarges, it does so in anteroposterior diameter, which is better seen on x-ray film ➢ Also, percussion is of limited usefulness with female breast tissue or in an obese person or a person with a muscular chest wall Precordium Percussion II There are times when your percussing hands are only tools you have with you

When you need to search for cardiac enlargement, place your stationary finger in person’s fifth intercostal space over on left side of chest near anterior axillary line Slide your stationary hand toward yourself, percussing as you go, and note change of sound from resonance over lung to dull over heart Precordium Percussion III Normally left border of cardiac dullness at midclavicular line in fifth interspace and slopes in toward sternum as you progress upward, so that by second interspace border of dullness coincides with the left sternal border Right border of dullness normally matches sternal border Precordium Auscultation I Auscultation ➢ Identify auscultatory areas where you will listen; these include four traditional valve “areas”

  • Valve areas are not over actual anatomic locations of valves but sites on chest wall where sounds produced by valves are best heard ➢ Sound radiates with blood flow direction; valve areas are
  • Second right interspace: aortic valve area
  • Second left interspace: pulmonic valve area
  • Left lower sternal border: tricuspid valve area
  • Fifth interspace at around left midclavicular line: mitral valve area Auscultatory Areas Precordium Auscultation II Auscultation ➢ Do not limit your auscultation to only four locations ➢ Sounds produced by valves may be heard all over precordium ➢ Thus, learn to inch your stethoscope in a rough Z pattern, from base of heart across and down, then over to apex; or start at apex and work your way up ➢ Although all heart sounds are low frequency, diaphragm is for relatively higher pitched sounds, and bell is for relatively lower pitched ones Precordium Auscultation III Auscultation ➢ Before you begin, alert person that you always listen to heart in a number of places on chest, and just because you are listening a long time does not necessarily mean that something is wrong ➢ After you place stethoscope, try closing your eyes briefly to tune out any distractions Precordium Auscultation IV Auscultation ➢ Concentrate, and listen selectively to one sound at a time

➢ Consider that at least two, and perhaps three or four sounds may be happening in less than 1 second ➢ You cannot process everything at once ➢ Begin with diaphragm endpiece and use following routine

  • Note rate and rhythm
  • Identify S1 and S
  • Assess S1 and S2 separately
  • Listen for extra heart sounds
  • Listen for murmurs Developmental Competence: Infants Transition from fetal to pulmonic circulation occurs in immediate newborn period Normally the liver is not enlarged, and respirations are not labored Heart rate may range from 100 to 180 beats per minute (bpm) immediately after birth Rapid rates make it more challenging to evaluate heart sounds Developmental Competence: Infant Murmurs These murmurs are usually grade I or II ➢ They are systolic and accompany no other signs of cardiac disease, and they disappear in 2 to 3 days ➢ Murmur of patent ductus arteriosis is continuous machinery murmur, which disappears by 2 to 3 days ➢ On other hand, absence of a murmur in immediate newborn period does not ensure a perfect heart ➢ Congenital defects can be present that are not signaled by an early murmur ➢ Best to listen frequently and to note and describe any murmur according to characteristics Developmental Competence: Children I Note any extracardiac or cardiac signs that may indicate heart disease ➢ Poor weight gain, developmental delay, persistent tachycardia, tachypnea, dyspnea on exertion, cyanosis, and clubbing ➢ Note that clubbing of fingers and toes usually does not appear until late in first year, even with severe cyanotic defects ➢ Apical impulse sometimes visible in children with thin chest walls ➢ Note any obvious bulge or any heave; these are not normal Developmental Competence: Children II Palpate apical impulse ➢ Up to age 4: in fourth intercostal space to left of midclavicular line ➢ Age 4 to 6: at fourth interspace at midclavicular line ➢ Age 7: in fifth interspace to right of midclavicular line ➢ Average heart rate slows as child grows older, although it is still variable with rest or activity ➢ Rhythm remains characterized by sinus arrhythmia ➢ Physiologic S3 is common in children

➢ Occurs in early diastole, just after S2, and is a dull soft sound that is best heard at apex Developmental Competence: Children III Palpate apical impulse ➢ Venous hum, due to turbulence of blood flow in jugular venous system, common in healthy children and has no pathologic significance

  • Continuous, low-pitched, soft hum heard throughout cycle, although loudest in diastole
  • Listen with bell over the supraclavicular fossa at medial third of clavicle, especially on right, or over upper anterior chest ➢ Venous hum is usually not affected by respiration, may sound louder when the child stands, and is easily obliterated by occluding jugular veins in neck with fingers Developmental Competence: Children IV Palpate apical impulse ➢ Heart murmurs that are innocent (or functional) in origin are very common through childhood ➢ Some say they have 30% occurrence, and some say nearly all children may demonstrate murmur ➢ Most innocent murmurs have these characteristics
  • Soft, relatively short systolic ejection murmur
  • Medium pitch; vibratory
  • Best heard at left lower sternal or midsternal border, with no radiation to apex, base, or back Developmental Competence: Children V Palpate apical impulse ➢ For child whose murmur has been shown to be innocent, it is very important that parents understand completely ➢ They need to believe that this murmur is just a “noise” and has no pathologic significance ➢ Otherwise, parents may become overprotective and limit activity for child, which may result in child developing a negative self-concept Developmental Competence: Pregnant Woman Vital signs usually yield an increase in resting pulse rate of 10 to 15 bpm and drop in BP from normal prepregnancy level Palpation of apical impulse is higher and lateral compared with normal position ➢ Heart sounds
  • Exaggerated splitting of S1 and increased loudness of S
  • A loud, easily heard S Developmental Competence: Aging Adult o Gradual rise in systolic blood pressure common with aging

o Overall size of the heart does not change but left ventricular wall thickness increases o Presence of supraventricular and ventricular dysrhythmias increases with age o Age-related ECG changes occur as a result of histologic changes in the conduction system o Incidence of CVD increases with age Culture and Genetics o Causes of CVD include an interaction of genetic, environmental, and lifestyle factors o Increased risk factors for CVD attributed to hypertension in terms of certain ethnic, racial, gender groups o Even though smoking has declined, it is still the leading cause of preventable disease, disability, and death in the U.S. o High levels of LDL lead to an increased risk of CVD and are associated with certain ethnic groups o Obesity is also an associated risk factor for CVD as well as other comorbidities o CVD risk is increased twofold greater in those patients who have diabetes o Sex differences still place women with CVD with the highest death rate Sample Charting: Objective and Assessment Abnormal Findings: Systolic Extra Sounds o Ejection click o Aortic prosthetic valve sounds o Midsystolic click Abnormal Findings: Diastolic Extra Sounds o Opening snap o Mitral prosthetic valve sound o Third heart sound o Fourth heart sound o Summation sound o Pericardial friction rub Abnormal Findings: Abnormal Pulsations: Precordium o Thrill at the base o Lift (heave) at the sternal border o Volume overload at the apex o Pressure overload at the apex Abnormal Findings: Congenital Heart Defects o Patent ductus arteriosus o Atrial septal defect o Ventricular septal defect o Tetralogy of Fallot o Coarctation of the aorta Abnormal Findings: Murmurs Due to Valvular Defects o Midsystolic ejection murmurs o Aortic stenosis o Pulmonic stenosis

o Pansystolic regurgitant murmurs o Mitral regurgitation o Tricuspid regurgitation Abnormal Findings: Murmurs Due to Valvular Defects o Diastolic rumbles of atrioventricular valves o Mitral stenosis o Tricuspid stenosis o Early diastolic murmurs o Aortic regurgitation o Pulmonic regurgitation Summary Checklist: Heart and Neck Vessels Examination o Neck o Carotid pulse – observe and palpate o Observe jugular venous pulse o Estimate jugular venous pressure o Precordium o Inspection and palpation ➢ Describe location of apical pulse ➢ Note any heave (lift) or thrill o Auscultation ➢ Identify anatomic areas noting rate and rhythm ➢ Listen in systole and diastole for murmurs ➢ Repeat with bell ➢ Listen at apex and base