Pocket Companion. Australian Adapting Editors. Clare Cole Olivia Hill Rosemary Saunders

Transcription

1 Pocket Companion Australian and New Zealand edition Australian Adapting Editors Clare Cole Olivia Hill Rosemary Saunders

2 Contents About the author/s (TBC) 0 Preface 0 Acknowledgments 0 Chapter 1 The health assessment interview and the health history 0 Chapter 2 Physical assessment techniques 0 Chapter 3 The general survey, measurement, vital signs Chapter 4 and pain assessment 0 Peripheral vascular system and lymphatic system 0 Chapter 5 Heart and neck vessels 0 Chapter 6 Nose, mouth and throat 0 Chapter 7 Thorax and lungs 0 Chapter 8 Musculoskeletal system 0 Chapter 9 Skin, hair and nails 0 Chapter 10 Urinary tract function 0 Chapter 11 Abdomen 0 Chapter 12 Bowel function 0 Chapter 13 Mental status examination 0 Chapter 14 Neurological system 0 Chapter 15 Eyes 0 Chapter 16 Ears 0 Chapter 17 Female sexual and reproductive function 0 Chapter 18 Male sexual and reproductive function 0 Chapter 19 Breasts and regional lymphatics 0 Chapter 20 The complete physical examination 0 References 0 Index 0

3 Chapter Five Heart and neck vessels The cardiovascular system consists of the heart, a muscular pump and the blood vessels. The blood vessels are arranged in two continuous loops, the pulmonary circulation and the systemic circulation (see Fig 12.1, JF&W). When the heart contracts, it pumps blood simultaneously into both loops. Anatomy The praecordium is the area on the anterior chest overlying the heart and great vessels. The heart extends from the second to the fifth intercostal space and from the right border of the sternum to the left midclavicular line (see Fig 12.2, JF&W). Think of the heart as an upside-down triangle in the chest. The top of the heart is the broader base, and the bottom is the apex, which points down and to the left. During contraction, the apex beats against the chest wall, producing an apical impulse. The right side of the heart pumps blood into the lungs, and the left side of the heart simultaneously pumps blood into the body. Each side has an atrium and a ventricle (Fig 5.1). The atrium is a thin-walled reservoir for holding blood and the thick-walled ventricle is the muscular pumping chamber. There are four valves in the heart. The two atrioventricular (AV) valves separate the atria and the ventricles. The right AV valve is the tricuspid; the left AV valve is the bicuspid, or mitral, valve. The AV valves open during the heart s filling phase, or diastole, to allow the ventricles to fill with blood. The semilunar (SL) valves are set between the ventricles and the arteries. The semilunar valves are the pulmonic valve in the right side of the heart and the aortic valve in the left side of the heart. They open during pumping, or systole, to allow blood to be ejected from the heart. 59

4 - PROOFS FOR SAMPLE ONLY 60 Clinical companion: health assessment Aorta (arch) Cut edge of pericardium Superior vena cava Pulmonary veins Pulmonary artery Pulmonary veins Left atrium Aortic valve Pulmonic valve Mitral (AV) valve Right atrium Chordae tendineae Left ventricle Tricuspid (AV) valve Papillary muscle Inferior vena cava Right ventricle Endocardium Myocardium Figure 5.1 Heart wall, chambers and valves. Pat Thomas, The cardiac cycle is the rhythmic movement of blood through the heart. It has two phases, diastole and systole (see Fig 12.6, JF&W). In diastole, the ventricles relax and fill with blood. The AV valves, the tricuspid and mitral, are open. During the first rapid filling phase, protodiastolic filling, blood pours rapidly from the atria into the ventricles. Towards the end of diastole, the atria contract and push the last amount of blood into the ventricles, called presystole. The closure of the AV valves contributes to the first heart sound (S1) and signals the beginning of systole. The AV valves close to prevent any regurgitation of blood back up into the atria during contraction. Then the semilunar valves, the aortic and pulmonic, open, and blood is ejected rapidly into the arteries. After the ventricles contents are ejected, the semilunar valves close. This causes the second heart sound (S2) and signals the end of systole. Cardiovascular assessment includes the neck vessels the carotid artery and the jugular veins (see Fig 12.10, JF&W).

5 Developmental considerations Chapter 5 Heart and neck vessels 61 Infants and children The fetal heart functions early; it begins to beat at the end of 3 weeks gestation. The lungs are nonfunctional, but the fetal circulation compensates for this (see Fig 12.13, JF&W). Oxygenation takes place at the placenta, and the arterial blood is returned to the right side of the heart. There is no point in pumping all this freshly oxygenated blood through the lungs, so it is rerouted in two ways. First, about two-thirds of it is shunted through an opening in the atrial septum, the foramen ovale, into the left side of the heart, where it is pumped out through the aorta. Second, the rest of the oxygenated blood is pumped by the right side of the heart out through the pulmonary artery, but it is detoured through the ductus arteriosus to the aorta. Because they are both pumping into the systemic circulation, the right and left ventricles are equal in weight and muscle wall thickness. Inflation and aeration of the lungs at birth produces circulatory changes. Now the blood is oxygenated through the lungs rather than through the placenta. The foramen ovale closes within the first hour because of the new pressure in the right side of the heart which is lower than that in the left side. The ductus arteriosus closes later, usually within 10 to 15 hours of birth. Now, the left ventricle has the greater workload of pumping into the systemic circulation, so that when the baby has reached 1 year of age, the left ventricle s mass increases to reach the adult ratio of 2:1, left ventricle to right ventricle. The heart s position in the chest is more horizontal in the infant than in the adult; thus the apex is higher, located at the fourth left intercostal space (see Fig 12.14, JF&W). It reaches the adult position when the child reaches age 7 years. The pregnant female Blood volume increases by 30% to 40% during pregnancy, with the most rapid expansion occurring during the second trimester. This creates an increase in stroke volume and cardiac output and an increased pulse rate of 10 to 15 beats per minute. Despite the increased cardiac output, arterial blood pressure decreases in pregnancy as a result of peripheral vasodilatation. The blood pressure drops to its lowest point during the second trimester then rises after that. The blood pressure varies with the person s position, as described in the Objective data section below.

6 62 Clinical companion: health assessment Late adulthood (65+ years) It is difficult to isolate the ageing process of the cardiovascular system per se because it is so closely interrelated with lifestyle, habits and diseases. We now know that lifestyle is a modifying factor in the development of cardiovascular disease; smoking, diet, alcohol use, exercise patterns, and stress have an influence on coronary artery disease. Lifestyle also affects the ageing process; cardiac changes once thought to be due to ageing are partially due to the sedentary lifestyle accompanying ageing (see Fig 12.15, JF&W). What is left to be attributed to the ageing process alone? Haemodynamic changes 1 From age 20 to 60 years, systolic blood pressure increases by about 20 mmhg, and by another 20 mmhg between ages 60 and 80 years (Wei, 1992). This is due to stiffening of the large arteries, which, in turn is due to calcification of vessel walls (arterio sclerosis). This stiffening creates an increase in pulse wave velocity because the less compliant arteries cannot store the volume ejected. 2 The overall size of the heart does not increase with age, but left ventricular wall thickness increases. This is an adaptive mechanism to accommodate the vascular stiffening mentioned earlier that creates an increased workload on the heart. 3 No significant change in diastolic pressure occurs with age. A rising systolic pressure with a relatively constant diastolic pressure increases the pulse pressure (the difference between the two). 4 No change in resting heart rate occurs with ageing. 5 Cardiac output at rest is not changed with ageing. 6 There is a decreased ability of the heart to augment cardiac output with exercise. This is shown by a decreased maximum heart rate with exercise and diminished sympathetic response. Noncardiac factors also cause a decrease in maximum work performance with ageing: decrease in skeletal muscle performance, increase in muscle fatigue, increased sense of dyspnoea. Chronic exercise conditioning will modify many of the ageing changes in cardiovascular function (Zipes et al, 2005). Arrhythmias. The presence of supraventricular and ventricular arrhythmias increases with age. Ectopic beats are common in ageing people; although these are usually asymptomatic in healthy

7 Chapter 5 Heart and neck vessels 63 older people, they may compromise cardiac output and blood pressure when disease is present. Tachyarrhythmias may not be tolerated as well in older people. The myocardium is thicker and less compliant, and early diastolic filling is impaired at rest (Wei, 1992). Thus, it may not tolerate a tachycardia as well because of shortened diastole. Also, tachyarrhythmias may further compromise a vital organ whose function has already been affected by ageing or disease. For example, a ventricular tachycardia produces a 40% to 70% decrease in cerebral blood flow. Although a younger person may tolerate this, an older person with cerebrovascular disease may experience syncope (Cheitlin and Zipes, 2001). ECG. Age-related changes in the ECG occur as a result of histological changes in the 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. Other considerations Risk factors Hypertension. Untreated hypertension risks organ damage to heart, main blood vessels, brain and kidneys. The most accurate means of BP monitoring is 24hr ambulatory monitoring (Clement et al, 2003). Smoking. In adults, 20% Australians smoke daily (AIHW, 2004). There are mixed reports about the incidence by age, gender and ethnicity. Regardless of these variables all persons need to be reminded to quit smoking for the sake of their health on each presentation to a health service. Quit services are government funded and printed information is available in most languages. High cholesterol. In a study to characterise the lipid profile of Indigenous Australians and Torres Strait Islanders a significantly lower high density lipoprotein (HDL) level was recorded when compared to non-indigenous Australians independent of age, sex and diabetic status (O Neal et al, 2008). This observational data supports the need for ongoing attention to reduce the deleterious effects of dyslipidaemia on heart health, with intensive efforts required to assist those most susceptible.

8 64 Clinical companion: health assessment Obesity. A body mass index (BMI) of 25 kg/m 2 or higher is considered to be overweight and a BMI of 30 kg/m 2 or higher is considered to be obese. The World Health Organization (WHO) has reported that obesity is reaching epidemic proportions. Obesity compounds any health problem. Census data has identified that excess weight is directly attributed to some 7% of cardiac deaths (AIHW, 2002). Diabetes. The incidence of diabetes is rising internationally. This is attributed to increasing rates of obesity, physical inactivity and an ageing population (AIHW, 2009). It is known that there is a higher incidence of diabetes in indigenous populations, those living in lower socioeconomic areas, those born overseas or living in regional or remote areas. Type 2 diabetes increases the risk of heart disease two to four fold and abolishes the protectiveness of female sex in the non-diabetic population (Bate and Jerums, 2003). The complications of diabetes are well recognised and include cardiovascular and renal disease and blindness (Bate and Jerums, 2003). Subjective data An accurate assessment requires the nurse to obtain a careful history from the patient of the symptoms they experience and to then undertake the clinical 1 Chest pain 2 Dyspnoea 3 Orthopnoea 4 Cough 5 Fatigue 6 Cyanosis or pallor examination that correlates with what the patient has reported. These have been grouped under the following headings: 7 Oedema 8 Nocturia 9 Past cardiac history 10 Family cardiac history 11 Personal habits (cardiac risk factors)

9 Chapter 5 Heart and neck vessels 65 Objective data Preparation When performing an assessment of the carotid arteries, the person can be sitting up. To assess the jugular veins and the praecordium, the person should be supine with the head and chest slightly elevated. Stand on the person s right side; this will facilitate your hand placement and auscultation of the praecordium. The room must be warm chilling makes the person uncomfortable and shivering interferes with heart sounds. Take scrupulous care to ensure quiet; heart sounds are very soft, and any ambient room noise masks them. Ensure the female s privacy by keeping her breasts draped. The female s left breast overrides part of the area you will need to examine. Gently displace the breast upwards, or ask the woman to hold it out of the way. When performing a regional cardiovascular assessment, use this order: 1 Pulse and blood pressure (see Ch 9, JF&W) 2 Extremities (see Ch 11, JF&W) 3 Neck vessels 4 Praecordium The logic of this order is that you will begin observations peripherally and move in towards the heart. Equipment needed Marking pen Small centimetre ruler Stethoscope with diaphragm and bell endpieces Alcohol wipe (to clean endpiece)

10 66 Clinical companion: health assessment Procedures and normal findings The neck vessels Palpate the carotid artery Located central to the heart, the carotid artery yields important information on cardiac function. Palpate each carotid artery medial to the sternocleidomastoid muscle in the neck (see Fig 12.16, JF&W.) Avoid excessive pressure on the carotid sinus area higher in the neck; excessive vagal stimulation here could slow down the heart rate. Take care to palpate gently. Palpate only one carotid artery at a time to avoid compromising arterial blood to the brain. Feel the contour and amplitude of the pulse. Normally the contour is smooth with a rapid upstroke and slower downstroke, and the normal strength is 2+ or moderate (see Ch 11, JF&W). Your findings should be the same bilaterally. Inspect the jugular venous pulse From the jugular veins you can assess the central venous pressure (CVP) and thus judge the heart s efficiency as a pump. Although the external jugular vein is easier to see, the internal (especially the right) jugular vein is attached more directly to the superior vena cava and thus is more reliable for assessment. You cannot see the internal jugular vein itself, but you can see its pulsation. Abnormal findings and clinical alerts Carotid sinus hypersensitivity is the condition in which pressure over the carotid sinus leads to a decreased heart rate, decreased BP, and cerebral ischaemia with syncope. Diminished pulse feels small and weak (decreased stroke volume). Increased pulse feels full and strong (hyperkinetic states) (see Table 11.1, JF&W).

11 Chapter 5 Heart and neck vessels 67 Procedures and normal findings The person should be placed in the supine position anywhere from a 30- to a 45-degree angle, wherever you can best see the pulsations. In general, the higher the venous pressure is, the higher the position you need. Remove the pillow to avoid flexing the neck; the head should be in the same plane as the trunk. Turn the person s head slightly away from the examined side, and direct a strong light tangentially onto the neck to highlight pulsations and shadows. Note the external jugular veins overlying the sternocleidomastoid muscle. In some persons, the veins are not visible at all, whereas in others they are full in the supine position. As the person is raised to a sitting position, these external jugulars flatten and disappear, usually at 45 degrees. Now look for pulsations of the internal jugular veins in the area of the suprasternal notch or around the origin of the sternocleidomastoid muscle around the clavicle. You must be able to distinguish internal jugular vein pulsation from that of the carotid artery. It is easy to confuse them because they lie close together. Use the guidelines shown in Table 12.1, JF&W. The praecordium Inspect the anterior chest Arrange tangential lighting to accentuate any flicker of movement. Abnormal findings and clinical alerts Unilateral distension of external jugular veins is due to local cause (kinking or aneurysm). Full distended external jugular veins above 45 degrees signify increased CVP as with heart failure.

12 68 Clinical companion: health assessment Procedures and normal findings Pulsations. You may or may not see the apical impulse, the pulsation created as the left ventricle rotates against the chest wall during systole. When visible, it occupies the fourth or fifth intercostal space, at or inside the midclavicular line. Palpate the apical impulse Localise the apical impulse precisely by using one finger pad (see Fig 12.17, A, JF&W). Asking the person to exhale and then hold it aids the examiner in locating the pulsation. You may need to roll the person midway to the left to find it; note that this also displaces the apical impulse further to the left (See Fig 12.17, B, JF&W). Note: Location The apical impulse should occupy only one interspace, the fourth or fifth, and be at or medial to the midclavicular line Size Normally 1 cm 2 cm Amplitude Normally a short, gentle tap Duration Short, normally occupies only first half of systole Abnormal findings and clinical alerts A heave or lift is a sustained forceful thrusting of the ventricle during systole. It occurs with ventricular hypertrophy as a result of increased workload. A right ventricular heave is seen at the sternal border; a left ventricular heave is seen at the apex (see Table12.8, JF&W). The point at which you can palpate the apical impulse is the point at which you place your stethoscope to auscultate the apical heart sounds. Cardiac enlargement: Left ventricular dilatation (volume overload) displaces impulse down and to left and increases size more than one space. Increased force and duration but no change in location occurs with left ventricular

13 Chapter 5 Heart and neck vessels 69 Procedures and normal findings The apical impulse is easily palpated in most adults. It is not palpable in obese persons or in persons with thick chest walls. With high cardiac output states (anxiety, fever, hyperthyroidism, anaemia), the apical impulse increases in amplitude and duration. Auscultate the apical (mitral) area In most situations the registered nurse will only need to perform the skill of auscultation of the two heart sounds at the apex of the heart. To do this you will use both endpieces of your stethoscope when auscultating heart sounds. Although all heart sounds are low frequency, the diaphragm is for relatively higher pitched sounds, and the bell is for relatively lower pitched ones. Locate the fifth intercostal space at the left midclavicular line mitral valve area. Before you begin, alert the person: I always listen to the heart in a number of places on the chest. Just because I am listening a long time does not necessarily mean that something is wrong. After you place the stethoscope, try closing your eyes briefly to tune out any distractions. 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 Abnormal findings and clinical alerts hypertrophy and no dilatation (pressure overload) (see Table 12.8, JF&W). Not palpable with chronic obstructive pulmonary disease due to hyperinflated lungs.

14 70 Clinical companion: health assessment Procedures and normal findings cannot process everything at once. Begin with the diaphragm endpiece and use the following routine: (1) Note the rate and rhythm, (2) identify S 1 and S 2, and (3) assess S 1 and S 2 separately. Note the rate and rhythm. The rate ranges normally from 60 to 100 beats per minute. (Review the full discussion of the pulse in Ch 9, JF&W and the normal rates across age groups.) The rhythm should be regular. With sinus arrhythmia, the rhythm varies with the person s breathing, increasing at the peak of inspiration and slowing with expiration. Note any other irregular rhythm. If one occurs, check if it has any pattern, or if it is totally irregular. When you notice any irregularity, check for a pulse deficit by auscultating the apical beat while simultaneously palpating the radial pulse. Count a serial measurement (one after the other) of apical beat and radial pulse. Normally, every beat you hear at the apex should perfuse to the periphery and be palpable. The two counts should be identical. When different, subtract the radial rate from the apical and record the remainder as the pulse deficit. S 1 is louder than S 2 at the apex; S 2 is louder than S 1 at the base. S 1 coincides with the carotid artery pulse. Feel the carotid gently as you auscultate at the apex; the sound you hear as you feel each pulse is S 1 (Fig 12.18, JF&W). Abnormal findings and clinical alerts Premature beat an isolated beat is early or a pattern occurs in which every third or fourth beat sounds early. Irregularly irregular no pattern to the sounds; beats come rapidly and at random intervals. A pulse deficit signals a weak contraction of the ventricles; it occurs with atrial fibrillation, premature beats, and heart failure.

15 Chapter 5 Heart and neck vessels 71 Procedures and normal findings S 1 coincides with the R wave (the upstroke of the QRS complex) if the person is on an ECG monitor. Listen to S 1 and S 2 separately. Note whether each heart sound is normal, accentuated, diminished or split. Inch your diaphragm across the chest as you do this. First Heart Sound (S 1). Caused by closure of the AV valves, S 1 signals the beginning of systole. You can hear it over the entire praecordium, although it is loudest at the apex (see Fig 12.19, JF&W). (Sometimes the two sounds are equally loud at the apex, because S 1 is lower pitched than S 2.) You can hear S 1 with the diaphragm with the person in any position and equally well in inspiration and expiration. Second Heart Sound (S 2). The S 2 is associated with closure of the semilunar valves. You can hear it with the diaphragm, over the entire praecordium, although S 2 is loudest at the base (see Fig 12.20, JF&W). Abnormal findings and clinical alerts Causes of accentuated or diminished S 1 (see Table12.3, JF&W). Both heart sounds are diminished with conditions that place an increased amount of tissue between the heart and your stethoscope: chronic obstructive pulmonary disease (hyperinflated lungs), obesity, pericardial fluid. Accentuated or diminished S 2 (see Table 12.5, JF&W). Further objective assessment skills for advanced practice can be found in Chapter 12, JF&W.

16 72 Clinical companion: health assessment Summary checklist Neck 1 Carotid pulse: Observe and palpate 2 Observe jugular venous pulse Praecordium 1 Inspection and palpation: Describe location of apical impulse 2 Auscultation: Identify anatomical areas where you listen Note rate and rhythm of heartbeat Identify S 1 and S 2, and note any variation Additional areas for advance practice nurses Praecordium Palpate for thrills Estimate jugular venous pressure Percussion cardiac borders Auscultation: split S 1, split S 2, murmurs Neck Abnormal findings TABLE 5.1 Diastolic extra sounds (continued) Early diastole Mid-diastole Late diastole Opening snap Third heart sound Fourth heart sound Mitral prosthetic Summation sound Pacemaker-induced valve sound (S 3 + S 4) sound Opening snap Normally the opening of the AV valves is silent. In the presence of stenosis, increasingly higher atrial pressure is required to open the valve. The deformed valve opens with a noise: the opening snap. It is sharp and high pitched, with a snapping quality. It sounds after S 2 and is best heard with the diaphragm at the third or fourth left interspace at the sternal border, less well at the apex. The opening snap usually is not an isolated sound. As a sign of mitral stenosis, the opening snap usually ushers in the low-pitched diastolic rumbling murmur of that condition. Mitral prosthetic valve sound An iatrogenic sound, the opening of a ball-in-cage mitral prosthesis gives an early diastolic sound: an opening click just after S 2. It is loud, is heard over the whole praecordium and is loudest at the apex and left lower sternal border.

17 Chapter 5 Heart and neck vessels 73 TABLE 5.1 Diastolic extra sounds (continued) Third heart sound The S 3 is a ventricular filling sound. It occurs in early diastole during the rapid filling phase. Your hearing quickly accommodates to the S 3, so it is best heard when you listen initially. It sounds after S 2 but later than an opening snap would be. It is a dull, soft sound and it is low pitched, like distant thunder. It is heard best in a quiet room, at the apex, with the bell held lightly (just enough to form a seal), and with the person in the left lateral position. The S 3 can be confused with a split S 2. Use these guidelines to distinguish the S 3: Location The S 3 is heard at the apex or left lower sternal border; the split S 2 at the base. Respiratory variation The S 3 does not vary in timing with respirations; the split S 2 does. Pitch The S 3 is lower pitched; the pitch of the split S 2 stays the same. The S 3 may be normal (physiological) or abnormal (pathological). The physiological S 3 is heard frequently in children and young adults; it occasionally may persist after age 40 years, especially in women. The normal S 3 usually disappears when the person sits up. In adults, the S 3 is usually abnormal. The pathological S 3 is also called a ventricular gallop or an S 3 gallop, and it persists when sitting up. The S 3 indicates decreased compliance of the ventricles, as in heart failure. The S 3 may be the earliest sign of heart failure. The S 3 may originate from either the left or the right ventricle; a left-sided S 3 is heard at the apex in the left lateral position and a right-sided S 3 is heard at the left lower sternal border with the person supine and is louder in inspiration. The S 3 occurs also with conditions of volume overload, such as mitral regurgitation and aortic or tricuspid regurgitation. The S 3 is also found in high cardiac output states in the absence of heart disease, such as hyperthyroidism, anaemia and pregnancy. When the primary condition is corrected, the gallop disappears.

18 74 Clinical companion: health assessment TABLE 5.1 Diastolic extra sounds (continued) Fourth heart sound The S 4 is a ventricular filling sound. It occurs when the atria contract late in diastole. It is heard immediately before S 1. This is a very soft sound, of very low pitch. You need a good bell, and you must listen for it. It is heard best at the apex, with the person in left lateral position. A physiological S 4 may occur in adults older than 40 or 50 years with no evidence of cardiovascular disease, especially after exercise. A pathological S 4 is termed an atrial gallop or an S 4 gallop. It occurs with decreased compliance of the ventricle (e.g. coronary artery disease, cardiomyopathy) and with systolic overload (afterload), including outflow obstruction to the ventricle (aortic stenosis) and systemic hypertension. A left-sided S 4 occurs with these conditions. It is heard best at the apex, in the left lateral position. A right-sided S 4 is less common. It is heard at the left lower sternal border and may increase with inspiration. It occurs with pulmonary stenosis or pulmonary hypertension. Summation sound When both the pathological S 3 and S 4 are present, a quadruple rhythm is heard. Often, in cases of cardiac stress, one response is tachycardia. During rapid rates, the diastolic filling time shortens and the S 3 and S 4 move closer together. They sound superimposed in mid-diastole, and you hear one loud, prolonged, summated sound, often louder than either S 1 or S 2. Extracardiac sounds Pericardial friction rub Inflammation of the praecordium gives rise to a friction rub. The sound is high pitched and scratchy, like sandpaper being rubbed. It is best heard with the diaphragm, with the person sitting up and leaning forwards, and with the breath held in expiration. A friction rub can be heard any place on the praecordium but usually is best heard at the apex and left lower sternal border, places where the pericardium comes in close contact with the chest wall. Timing may be systolic and diastolic. The friction rub of pericarditis is common during the 1st week after a myocardial infarction and may last only a few hours.