38 Table 3.2 Drawing family trees to reveal domi nantly inherited disease Advances in genetics touch all branches of medicine. It is increasingly important for docto rs to identify patients at high risk of genetic disease and to make appropriate referrals. The key skill is drawing a family tree to help you structure a family history as follows: 1 Start with your patient : Draw a square for a male and a circle for a female. Add a small arrow (see below) to show that this person is the propositus (the person through whom the f amily tree is ascertained). 2 Add your patient \200\231s parents, brothers, and sisters: Re cord basic informa- tion only (e.g., age, and if alive and well [a&w]). If dead, note age a nd cause of death, and pass a diagonal line through that person \200\231s symbol. (Continued) s l l i k s Table 3.2 (Continued) 3 Ask the key question \200\234Has anybody else in your family had a similar problem as yo urself ? \200\235 (e.g., heart attack/angina/stroke/cancer). Ask only about the family of d iseases that relate to your patient \200\231s main problem. Do not record a full medical hi story for each family member: Time is too short. l a c i n i l C 4 Extend the family tree upward to include grandparents: If you haven \200\231t revealed a problem by now, go no further \200\224you are unlikely to miss important familial disease. If your patient is elderly, it may be impos- sible to obtain good information about grandpa rents. If so, fill out the family tree with your patient \200\231s uncles and aunts on both the mother \200\231s and father \200\231s sides. 5 Shade those in the family tree affected by the disease: \212= an affected female; \200 = an affected male. This helps to show any genetic problem and, if there is one, will help demonstrate the pattern of inheritance. 6 Extend the tree: If you have identified a famili al susceptibility, or your patient has a recognized genetic disease, extend the family tree down to include children, to identify others who may be at risk and who may benefit from s creening. You must find out who is pregnant in the family, or may soon be, and arrange appr opriate genetic counseling. The family tree in Figure 3.1 shows these ideas at work and indicates that there is evidenc e for genetic risk of colon cancer. 39 \200\234This section owes much to Dr. Helen Firth, whom we thank. \200\235 Review of systems The review of systems is a compendium of medical symptoms, grouped by bod y system. It is an important safety net to identify issues the clinician may have forgotten to ask about or the patient forgot to mention. It is typically presented as a series of cl osed yes-or-no questions, heralded by a transition statement such as, \200\234Now I \200 \231d like to ask you a series of questions about whether you \200\231ve recently experienc ed different types of medical symptoms, and you can simply answer yes or no. \200\235 Obtai n enough detail about posi- tive responses to determine whether positive symptoms are signi ficant or trivial (the more severe and chronic the symptom, the more likely it is to be imp ortant). With increasing experience, the review of systems can often be parsed down and gre atly expedited. Some experienced clinicians systemati- cally review systems as they are per forming the physical examination. Elements of selected system reviews are illustrated below . General questions may be the most significant (e.g., in identifying cancer, endocrine pro blems, or tuberculosis [TB]): \212 \212 \212 \212 \212 \212 \212 \212 \212 Cardior espiratory symptoms Chest pain. Palpitations (awareness of heartbeats). Exertional dyspnea (= breathlessness; quantify exercise toler- ance and how it has changed : E.g., stairs clim bed or distance walked before onset of breathlessness). Paroxysmal nocturnal dyspnea (sensa tion of short- ness of breath, often with coughing/choking, that awakens the patient). Orth opnea (breathlessness on lying flat: Quantify the number of pillows the patient must sleep on to prevent dyspnea). Edema. Intermittent claudication (reproducible leg pain that occurs with exercise and is relieved by rest). Cough. Sputum. Hemoptysis (coughing up blood). Whe ezing. GI symptoms Think of symptoms throughout the GI tract, from mouth to anus: \212 \212 \212 \212 \212 Tenesmus is a feeling of incomplete defecation (e.g., due to rectal inflam- mation or tumor). Hematemesis is vomiting blood. Melena refers to black, tarry, fou l-smelling stools, and hematochezia refers to passage of red blood per rectum, usually in o r with stools. Genitourinary symptoms \212 \212 \212 Weight loss Night sweats Any lumps Fatigue Sleeping pattern Appetite Fevers Itching Recent trauma 40 Swallowing Indigestion Nausea/vomiting Abdominal pain Bowel habit Incontinence (stress or urge) Dysuria (painful micturition) Hematuria (bloody urine) \212 \212 Nocturia (needing to urinate at night) Frequency (frequent urination) or polyuria (passing excessive amounts of urine) Hesitancy (difficulty starting urination) Terminal dribbling Va ginal discharge Menses: Frequency, regularity, heavy or light, duration, painful First day of last menstrual period (LMP) Number of pregnancies Menarche Menopause Any chance of pregn ancy now? s l l i k s l a c i n \212 \212 \212 \212 \212 \212 \212 \212 \212 Neurological symptoms \212Special se nses: Sight, hearing, smell, and taste \212 \212 \212 \212 \212 \212 \212 The import ant thing is to assess function: What the patient can and cannot do at home, work, etc. Mus culoskeletal symptoms \212 Pain, stiffness, swelling of joints \212 Trauma \212 Function al deficit Thyroid symptoms \212Hyperthyroidism: Prefers cold weather, ill-tempered, sweat y, diarrhea, oli- gomenorrhea, weight loss (although often \206\221 appetite), tremor, pal pita- tions, visual problems i l C Seizures, fainting Headache \200\234Pins and needles \200\235 (paresthesias) or numbness W eakness ( \200\234Do your arms and legs work? \200\235), poor balance Speech problems Sphin cter disturbance Higher mental function and psychiatric symptoms 41 \212Hypothyroidism: Depressed, slow, tired, thin hair, hoarseness, heavy peri- ods, constipation, dry skin, prefers warm weather History-taking may seem deceptively easy, as if the patient knew the hard facts and the onl y problem was extracting them; but what a patient says is a mixture of hearsay ( \200\234sh e said I looked very pale \200\235), innuendo ( \200\234you know, doctor: down below \200 \235), legend ( \200\234I suppose I bit my tongue; it was a real seizure, you know \200\235 ), exaggeration ( \200\234I haven \200\231t slept for 2 weeks \200\235), and improbabilitie s ( \200\234the Pope put a transmitter in my brain \200\235). The great skill (and pleasure ) in taking a history lies not in ignoring these garbled mes- sages, but in making sense of them. Collateral history taken from family members and other caregivers can also be very i mportant in developing the story of a patient \200\231s illness. Physical examination The physical examination is performed to make diagnoses (in most of de r- matology and much of neurology, for instance) and as a tool to generate hypotheses. Pati ents often expect to be examined, and, as such, the physical exam is also a ritual that hel ps affirm the physician \200\231s connection and com- mitment to the patient and helps buil d trust. We must act respectfully and professionally and recognize the vulnerability of pat ients, who are disrobing and allowing touch by a physician who they may have just met. With a few exceptions (e.g., blood pressure [BP]), the physical examination is not a good scree ning test for detecting unsuspected disease. Although you will generally be expected to exa mine all four major systems (cardio- vascular, respiratory, abdominal, and neurological), p lan your examination to emphasize those areas that the history suggests may be abnormal. A few well-directed, problem-oriented minutes can save hours of fruitless, but very thorough, physical examination. It is also very important to com- municate well with patients as you examine them, letting them know what you are doing and commenting on findings. Practice is the key; the physical exam must be explored at the bedside! Look at your patient as a whol e to decide how sick he or she seems to be. Does he or she appear well or in extremis ? Try to decide why you think so. Is he in pain, and does it make him lie still (e.g., peritonit is) or writhe about (e.g., colic)? Is breathing labored and rapid? Is she obese or cachecti c? Is behavior appropriate? Can you detect any unusual smell (e.g., hepatic fetor, ketosis, cigarettes, alcohol)? Specific diagnoses can often be made from the face and body habitus, and these may be missed unless you stop and consider them: E.g., acromeg- aly, thyrotoxico sis, myxedema, Cushing \200\231s syndrome, or hypopituitarism. Is there an abnormal distrib ution of body hair (e.g., bearded \231\200 or hairless \231\202 ) suggestive of endocrine disease? Is there anything to trigger thoughts about Paget \200\231s disease, Marfan \200 \231s syndrome, or Parkinson \200\231s disease? Look at the skin (e.g., the spider telangie ctasia, palmar erythema, dilated abdominal veins of liver disease, and the butterfly facial rash of lupus). Assess the degree of hydration by examining the skin turgor (reliable in p ediat- ric populations), the axillae, and mucus membranes. Check peripheral perfusion. Comp are lying and standing BP to identify postural hypotension, a sign of vol- ume depletion. T he hands and fingernails hold a wealth of clues; see Table 3.3. Check for cyanosis (central and peripheral, p. 72). Is the patient jaun- diced (usually first noticed in the conjuncti va of the eyes)? Pallor is a nonspecific sign and depends in part on the patient \200\231s natural skin pigments. Anemia is assessed from the palmar skin creases and conjunctivae \200\224usually pale if Hb is <9 g/dL. No physical sign convincingly argues against a diagn osis of anemia. Pathological hyperpigmentation is seen in Addison \200\231s disease, hemoch romatosis, and amiodarone, gold, and minocycline therapy. Check vital signs , which can pro vide an early indication that a patient is ill. Weight (and input/output charts) may be hel pful in monitoring patients who are volume-overloaded. The average oral temperature is 36.8 C (98.2 F), and temperature is usually lowest at 6 am and highest at 4 \200\2236 pm ( \200\234diurnal variation \200\235). Rectal temperatures are on average 0.4 to 0.5 C (0. 7 \200\2231.0 F) higher than oral measurements, which in turn are 0.4 to 0.7 C (0.7 \200\2231.3 F) higher than axillary temperatures and 0.4 C (0.7 F) higher than tympanic membrane measurements. An oral temperature >37.7 C (99.9 F) constitutes a fever (defined as the 99th percentile of maximum tempera- tures in healthy persons). Do not always believ e the temperature chart \200\224if the patient feels warm and you suspect fever, take the t emperature yourself. Pulse (rate, contour, rhythm), BP , and respiratory rate and breathing pattern are discussed in the next sections. 42 s l l i k s Table 3.3 The hands A wealth of information can be gained from gently shaking hands and then inspecting the han ds of the patient. Are they warm and well-perfused? Warm, sweaty hands may signal hyperthyr oidism, whereas cold, moist hands may be due to anxiety. Are the rings tight with edema? Ar e there any nicotine stains? Does the patient have difficulty shaking your hand (rheumatoid arthritis, p. 413)? Inability to let go of your hand suggests myotonia. Nails Koilonychia (spoon-shaped nails) suggests iron deficiency (also fun- gal infection or Raynaud \200\231s ). Onycholysis (detachment of the nail from the nail bed) is seen with fungal nail infectio n, psoriasis, and hyperthyroidism. Beau \200\231s lines are transverse furrows that signify temporary arrest of nail growth and occur with periods of severe illness. As nails grow at a rate of about 1 mm/week, by measuring distance from the cuticle it may be possible to da te the stress. Mees \200\231 lines are single, white, transverse bands that are also seen i n acute illness (including arsenic poisoning) and grow out during recovery. Muehrcke \200 \231s lines are paired, white, transverse bands sometimes seen in hypoalbuminemia. Terry \200\231s nails: Proximal portion of nail is white/pink, nail tip is red/brown (nonspecific , seen in cirrhosis, chronic renal failure, heart failure, others). Pitting is seen in psor iasis and alopecia areata. Splinter hemorrhages are fine longitudinal hemorrhagic streaks ( under nails), which in the febrile patient may suggest infective endocarditis. They are als o associated with trauma, scleroderma, and other conditions. Nail-fold infarcts are charact eristically seen in vasculitic disorders. Digital clubbing occurs with many disorders (p. 7 2) and is character- ized by enlargement of the terminal segments of the fingers or toes th at results from the proliferation of the connective tissue between the nail matrix and the distal phalanx. There is loss of the angle between the nail and the nail-fold (i.e., no dip ), and the nail feels \200\234boggy. \200\235 Exact patho- genesis is unknown. Chronic par onychia is a chronic infection of the nail folds and presents as a painful swollen nail wit h intermittent discharge. Predisposing fac- tors include diabetes mellitus, nail biting, an d frequent immersion of the hands in water. Changes occur in the hands in many diseases. Pa lmar erythema is asso- ciated with cirrhosis, pregnancy, and polycythemia. Pallor of the pa lmar creases suggests anemia. Pigmentation of the palmar creases is normal in Asians and bl acks but is also seen in Addison \200\231s disease. A symmetrical red, scaly eruption on th e knuckles (Gottron \200\231s sign) with abnormal capil- lary nail bed loops suggests derma tomyositis (p. 404). Dupuytren \200\231s con- tracture (fibrosis and contracture of palmar fascia) increases with age and is associated with repetitive hand use and vibratory trauma, diabetes mel- litus, complex regional pain syndrome, the presence of other localized fibro sing conditions, and cigarette smoking and alcohol consumption. Swollen proximal interphala ngeal (PIP) and metacarpophalangeal (MCP) joints with sparing of the distal (DIP) joints su ggest rheumatoid arthri- tis; swollen DIP joints suggest osteoarthritis, gout, or psoriatic arthri- tis. Look for Heberden \200\231s (bony DIP joint enlargements) and Bouchard \200 \231s (PIP joint enlargements) \200\234nodes \200\235 in osteoarthritis. l a c i n i l C 43 The cardiovascular system History Ask about age, occupation, exercise tolerance, and risk f actors. \200\234Typical \200\235 angina is exertional chest pain relieved by rest. Presenting symptoms Risk factors for coronary artery disease (CAD) Smoking Chest pain Dyspnea \200\224exertional? Hypertension Diabetes orthopnea? Paroxysmal nocturnal dyspnea (PND)? mellitus Ankle swelling Palpitations; dizziness; Hyperlipidemia Family history of premature CAD a blackouts Intermittent claudication Past history Angina or myocardial Past tests and procedures: Electrocardiogram Echocardiography infarction (MI) Rheumatic fever (ECG) Angiograms Angioplasty/stents Stress tests CABG (coronary artery bypass grafts) 44 a First- degree relative <50 yrs (men) or <60 yrs (women) Appearance Ill or well? In pain? Dyspneic? Is the patient pale, cold, and clammy? Is there corneal arcus or xanthelasma (hyperlipidemia)? Are there signs of Graves \200\231 disease ( bulging eyes, goiter; p. 298)? Are there dysmorphic body features suggestive of a genetic d isease (e.g., Down \200\231s, Marfan \200\231s, or Turner \200\231s syndromes, etc.)? Can y ou hear the click of a prosthetic valve? Hands Digital clubbing occurs in congenital cyanot ic heart disease and endocarditis (also seen in lung cancer, pus in the lung, and others). Splinter hemorrhages, Osler \200\231s nodes (tender nodules in finger pulps), and Janeway l esions (red nonpainful macules on palms and soles) are signs of infective endocarditis, as are Roth spots (hemorrhagic lesions of the retina). Pulse See p. 48. Blood pressure See Tab le 3.7 for review of measurement technique. The systolic BP is the pressure at which repeti tive sounds are first heard (Korotkoff phase 1) as the cuff is deflated; the diastolic is w hen the heart sounds disappear (phase 5) or become muffled (phase 4; used in children, and when sounds are heard nearly to a level of 0 mm Hg). The pulse pres- sure is defined as the difference between systolic and diastolic. It is narrow in aortic stenosis and wide in aor tic regurgitation. Examine the fundi for hypertensive changes. Shock may occur if systolic BP is <100 mm Hg. Postural hypotension is defined as a drop in systolic BP of >20 mm Hg or diastolic BP >10 mm Hg on standing. When checking postural vital signs, wait 2 min before m easuring the supine vitals and at least 1 min after stand- ing before measuring the upright vitals. Jugular venous pressure see p. 48. Precordium Inspect for scars : Median sternotomy (CABG or valve replacement). Inspect for a ny implanted device (e.g., pacemaker, defibril- lator). Palpate the apical impulse . Normal position: Fifth intercostal space in the mid-clavicular line. Is it displaced laterally (c ardiomegaly, depressed ejection fraction)? Is the diameter \211 4 cm (dilated heart)? Is it sustained (left ventricular pressure and/or volume overload due to aortic valvular disea se or ventriculo-septal defect (VSD), cardiomyopathy, or ventricular aneurysm)? Feel for le ft parasternal heave (right ventricle [RV] enlargement; e.g., in pulmonary stenosis, cor pu lmonale, atrial septal defect [ASD]) or thrills (transmitted murmurs). Auscultating the hea rt see Figure 3.2. Lungs Examine the lung bases for crackles and pleural effusions (can det ect high left heart pressure in patients with known heart disease). Edema Examine the ankle s, legs, and sacrum for pitting edema (in the con- text of elevated central venous pressure [CVP]; e.g., abnormally distended neck veins; indicates cardiac disease or pulmonary hyper tension). Abdomen Hepatomegaly and ascites may occur in right-sided heart failure. Pulsatil e liver occurs with tricuspid regurgitation. Aortic aneurysm may be palpable in the epigast rium (physical exam is highly sensitive for detect- ing aneurysms >5 cm in diameter; the di ameter usually indicating surgical repair). Peripheral pulses Palpate radial, brachial, car otid, femoral, dorsalis pedis, and posterior tibial pulses. The dorsalis pedis pulse is not palpable in up to 14% of healthy persons, and the posterior tibial is not palpable in up t o 10% of healthy persons (although distal pulses are rarely both missing in the absence of disease). See Table 3.4 for review of diagnosing peripheral vascular disease. Diminished or delayed femoral pulses are also a classic finding in coarctation of the aorta. Auscultate for carotid bruits in patients with stroke or transient ischemic attack (TIA) symptoms (inc reases the like- lihood of an important stenotic lesion, but the absence of a bruit does no t rule out carotid stenosis). A continuous femoral bruit following femoral artery puncture (e.g., for cardiac catheterization) is diagnostic for arterio- venous fistula. s l l i k s l a c i n i l C 45 Figure 3.2 Auscultating the heart \212 The bell is used to detect low-frequency sounds and the diaphragm detects high-frequency so unds. When using the bell, apply it lightly to the body wall with only enough force to crea te an air seal (exces- sive pressure with the bell turns it into a diaphragm).The room shou ld be quiet. Close the door to the examination room and turn off the television. Listen wit h diaphragm and bell at the apex (mitral area). Identify first and second heart sounds : Ar e they normal? Listen for added sounds (p. 51) and murmurs (Figure 3.6, p. 52) during systo le and then during diastole. Repeat at lower left sternal edge and in aortic and pulmonary areas (right and left of manubrium) \200\224and, in patients with systolic mur- murs, liste n in both the left axilla (radiation of mitral regurgitation) and over the carotids and rig ht clavicle (radiation of aortic stenosis). Listen with the patient in three positions: Sup ine, left lateral decubitus, and seated upright. The lateral decubitus position is best for detection of S3 and S4 and the diastolic rumble of mitral stenosis. Upright posi- tioning is necessary to detect some pericardial rubs and the blowing diastolic murmur of aortic reg urgitation. \212 \212 Pulmonary area Aortic area 46 1 Mitral area 2 3 4 5 Tricuspid area Locations for auscultating heart valve murmurs. After N Talley, S O \200\231Connor. Clinica l Examination 4th ed. Blackwell Science, 2002. s l l i k s Table 3.4 Diagnosis of peripheral vascular disease se The ankle brachial index (ABI) is the diagnostic standard for detecting peripheral arterial disease (PAD). The ABI has also been shown to pre- dict mortality and adverse cardiovascul ar events independent of tradi- tional risk factors. l a c i n i l Technique and interpretation: \212 Position patient supine. Measure the highest systolic B P at each ankle (dorsalis pedis and poste- \212 rior tibial arteries) with a hand-held Dop pler device and divide these by the highest BP in the brachial artery to get the ABI for ea ch leg. Normal ABI ranges from 1.0 to 1.2; <0.9 is diagnostic of PAD, and <0.5 indicates se vere disease. C \212 Other signs helpful in detecting peripheral vascular disease in the symp- tomatic leg (alth ough classic intermittent claudication occurs only in the minority of patients with PAD) in clude the absence of both pedal pulses or the femoral pulse, and the presence of wounds or sores on the foot or an asymmetrically cool foot. Findings that are unhelpful include atrop hic skin, hairless lower limbs, and a prolonged capillary refill time. 47 Jugular venous pressure The jugular veins (either the external or internal jugular veins ma y be used, optimally on the right side of the patient \200\231s neck) act as a manometer of right atrial pressure (e.g., CVP). Observe two features: The height (jugular venous pressu re, JVP) and the waveform of the pulse. JVP observations are often difficult, especially in obese patients. Do not be downhearted if the skill seems to elude you. Keep on watching ne cks and the patterns you see will slowly start to make sense. See Table 3.5 for differentia ting between arterial and venous pulses. The height First assess JVP with the patient recli ned to 45 degrees, with his head turned slightly to the left. The patient should be reposit ioned as needed, to whichever angle between the supine and upright position best reveals th e top of the neck veins. The top of the neck veins is indicated by the point above which th e subcutaneous conduit of the external jugular vein disappears or above which the pulsating waveforms of the internal jugular wave become imperceptible. The JVP is the vertical heigh t of the pulse above the sternal angle. It is raised if >3 cm. Pressing firmly over the pat ient \200\231s midabdomen often produces a transient rise in the JVP. If a rise in JVP of \211 4 cm persists throughout a 10 sec compression, it is a positive abdominojugular reflu x sign (also called hepatojugular reflux). Many clinicians recognize a positive test by obs erving the neck veins at the moment the abdominal pressure is released, regarding a fall >4 cm as positive. This is an accurate sign of elevated left atrial pressure (e.g., in patien ts with dyspnea, it indicates that at least some of the dyspnea is due to disease in the le ft side of the heart). The jugular venous waveform See Figure 3.3. To identify individual w aveforms, listen to the heart sounds as you look at the neck veins. The x descent ends just before S 2 , and the y descent begins just after S 2 . The normal venous waveform has a pr ominent x descent and a small or absent y descent. Abnormalities of the jvp Raised jvp with normal waveform: Fluid overload, heart failure (du e to heart or lung disease) Raised jvp with absent pulsation: Superior vena cava (SVC) obst ruction Large a wave: Pulmonary hypertension, pulmonic or tricuspid stenosis Cannon a wave: When the right atrium contracts against a closed tricuspid valve, large \200\234cannon \200\235 a waves result. Causes: Atrioventricular dissociation, ventricular tachycardia, ot her arrhythmias Absent a wave: Atrial fibrillation Large systolic v waves: Coincide with th e carotid pulsation and collapse after S 2 (prominent y descent); seen in tricuspid regurgi tation Constrictive pericarditis: High plateau of JVP (which rises on inspiration \200\224 Kussmaul \200\231s sign) with deep x and y descents Pulses Assess the radial pulse to determine rate and rhythm . Contour may be best assessed at the brachials or carotids. Rate Count the pulse for 30 sec and double the result. Is the pulse tachy- cardic (>100 bpm) or bradycardic (<50 bpm)? Rhythm An irregularly irregular p ulse occurs in AF or multiple ectopics. A regularly irregular pulse occurs in second-degree heart block and ven- tricular bigeminy. Volume and contour Normal carotid volume is easily felt with light palpation, whereas reduced carotid volume is difficult to feel even with f irm palpation. Normal carotid upstroke feels like a sharp tap, whereas reduced/delayed caro tid upstroke feels like a nudge. Pulsus parvus et tardus (carotid pulse with small volume a nd reduced/ delayed upstroke) is a finding of aortic stenosis. Palpable femoral pulse indic ates a systolic BP of >60 mm Hg (presence or absence of femoral pulse can help determine se verity of shock). Collapsing pulses (also called water hammer pulses ; felt at the radial a rtery when the patient \200\231s wrist is elevated above the heart) occur most commonly in chronic aortic regurgitation but are seen in many conditions associated with increased stro ke volume. Pulsus bisferiens (two beats per cardiac cycle, both in systole) can occur in he modynamically significant aortic regurgitation (also in combined aortic stenosis and regurg itation). See Figure 3.4. Dicrotic pulses (two beats per cardiac cycle, one in systole and one in dias- tole) occur in younger patients with severe myocardial dysfunction, low stroke volumes, and high systemic resistance. Pulsus alternans (alternating strong and weak beats ) indicates severe left ventricular dysfunction. Pulsus paradoxus (inspiratory fall in syst olic BP of >10 \200\22312 mm Hg) is a common finding in cardiac tamponade and acute asthma. See Table 3.5 for review of technique. 48 s l l i k s Table 3.5 Distinguishing arterial and venous pulses In distinguishing venous from arterial pulses in the neck, note that the venous pulse: \212 l a c i n Has a prominent have a prominent ascending or outward movement. Is not usually palpable. Is obliterated by finger pressure on the vein. Rises transiently following pressure on the ab domen ( reflux ). Drops lower in the neck as the patient sits up (and becomes more prominen t when you lower the head of the bed). Becomes more prominent during inspiration (but also drops lower in the neck). Usually has a double pulse for every arterial pulse (flicking lik e a snake \200\231s tongue). descending movement, versus arterial pulsations that i l \212 \212 \212 C abdominojugular \212 \212 \212 Figure 3.3 The jugular venous pressure wave 49 The jugular venous pressure wave. After Macleod, ed., Clinical Examination, 4th ed. New Yor k: Churchill Livingstone. Table 3.6 Pulsus paradoxus \212 Have the patient breathe normally (vigorous respirations can induce a pulsus paradoxus). Be gin checking the BP in the usual way. As you slowly deflate the cuff, note the BP at which you first hear Korotkoff sounds. Sounds will disappear during inspiration and then reappear , corresponding to the higher systemic BP occurring during expiration. Keep slowly deflatin g the cuff until you hear Korotkoff sounds with every heartbeat. Note the BP at this point. The difference between the two BP recordings is the pulsus paradoxus. It is considered sig nificant if it is >10 \200\22312 mm Hg. \212 \212 \212 Figure 3.4 Arterial pulse waveforms Normal Bisferiens Collapsing Anacrotic Typical arterial pulse waveforms. After J Burton. Aids to Undergraduate Medicine, 6th ed. N ew York: Churchill Livingstone. Table 3.7 Measuring blood pressure \212 Patients should be seated quietly for 5 min in a chair, with their feet on the floor and th e arm supported at heart level. Use the correct size cuff (a too small cuff will overestima te BP). The blood pressure cuff \200\231s bladder should encircle at least 80% of the arm. The bladder should be centered over the brachial artery, and the cuff applied snugly. Infla te the cuff while palpating the brachial artery until the pulse disap- pears. This provides an estimate of systolic pressure. Inflate the cuff until 20 \200\22330 mm Hg above systoli c pressure, then place stethoscope over the brachial artery. Deflate the cuff at 2 mm Hg/se c. \212Systolic pressure: The appearance of repetitive sounds (Korotkoff \212 50 \212 \212 phase 1). \212Diastolic pressure: Usually the disappearance of sounds (phase 5). However, in some in dividuals (e.g., pregnant women), sounds are pres- ent until the zero point. In this case, the muffling of sounds, Korotkoff phase 4, should be used. Record pressure, patient positio n (e.g., seated), arm, and cuff size. Obtain two readings, separated by at least 30 sec, an d average them. \212 Heart sounds Listen systematically: Sounds then murmurs. While listening, palpate the carot id artery: S 1 is synchronous with the upstroke. The heart sounds The first and second soun ds are usually clear. Confident pronouncements about other sounds and soft murmurs may be d ifficult. Even senior colleagues disagree with one another about the more difficult sounds and murmurs. The first heart sound (S1) is usually loudest at the apex and represents clo- sure of mitral and tricuspid valves. See Figure 3.5. Abnormally loud S 1 can occur because of delayed closure of the mitral valve (as in mitral stenosis) or due to vigorous ventricul ar contractions (as in fever, thyrotoxicosis). Faint or absent S 1 occurs due to weak ventr icular contractions (MI, left bundle branch block [LBBB]) or due to early closure of the mi tral valve (when PR interval is >0.20 sec or in acute aortic regur- gitation). Varying inte nsity of S 1 (assuming the rhythm is regular ) indicates atrioventricular dissociation. Prominent splitting of S 1 can occur in patients with RBBB o r paced beats. The second heart sound (S 2 ) represents aortic (A 2 ) and pulmonary valve ( P 2 ) closure. The most important diagnostic feature of S 2 is the \200\234splitting \200 \235 of its A 2 and P 2 components; intensity of S 2 has less diagnostic importance (despit e traditional teachings, no evidence supports a loud P 2 as a sign of pulmonary hypertensio n). Splitting in inspiration is normal and is mainly due to the variation with respiration of right heart venous return, causing P 2 to be further delayed. Splitting is usually heard only in the pulmonary area (second left interspace; see p. 46), because P 2 is too faint e lsewhere. Wide physiologic splitting (A 2 P 2 interval widens further during inspiration) o ccurs most commonly in right bundle branch block (RBBB). Wide fixed splitting (A 2 P 2 inte rval remains constant during inspiration and expiration) occurs in ASD. Paradoxic ( \200 \234 reversed \200\235) splitting (i.e., splitting \206\221 on expiration) occurs in LBBB, RV pac- ing, aortic stenosis, and ischemic heart disease. A third heart sound (S 3 ) may o ccur just after S 2 and represents exaggerated early diastolic filling. It is low-pitched a nd best heard with the bell of the stethoscope. S 3 can be physiologic in individuals young er than 40 yrs. An S 3 is an important finding indicating depressed ejection fraction and e levated left atrial pressures (associated with heart failure, aortic valve disease). A four th heart sound (S 4 ) occurs just before S 1 and represents atrial con- traction against a ventricle made stiff by any cause; for example, due to hypertension, other cardiomyopathy, or aortic stenosis. S 4 has less diagnos- tic value (does not predict ejection fraction, le ft heart filling pressures, or severity of aortic stenosis). \200\234Gallop \200\235 rhyth ms: Third and fourth heart sounds are also called gallops , as they can give the impression of galloping hooves. An S 3 gallop sounds like \200\234Ken-tucky, \200\235 whereas an S 4 gallop sounds like \200\234Tenne-ssee. \200\235 When S 3 and S 4 occur during tachycardia , they may appear together as a single loud sound, a summation gallop . An aortic ejection sound is heard early in systole with bicuspid aortic valves, aortic stenosis, or a dilated aortic root. The right heart equivalent lesions may also cause clicks (e.g., pulmonary ejec tion sound). Mid-systolic clicks occur in mitral valve prolapse. An opening snap precedes t he mid-diastolic murmur of mitral stenosis. A pericardial knock is a loud early diastolic s ound that can occur in constric- tive pericarditis (higher frequency than S 3 and heard ove r a wider area). Prosthetic sounds are caused by mechanical valves. Prosthetic mitral valve clicks occur in time with S 1 , and aortic valve clicks are timed with S 2 . s l l i k s l a c i n i l C 51 Figure 3.5 The cardiac cycle QRS P T ECG 4th 1st 2nd 3rd Heart sounds A P 110 ) g H m m Aortic pressure ( 50 e r u s s e r P Left atrial pressure Left ventricular pressure 0 End-diastolic volume Left ventricular volume 52 130 ) L m ( e m u o v l 65 r a l u c End-systolic volume Position of atrioventricular valves Position of aortic and pulmonary valves i r t n e v Open Open Open Systole 3 2 t f e L Diastole 1 Diastole 1 Phase of cardiac cycle 4 1 = Ventricular filling 2 = Isovolumetric ventricular contraction 3 = Ventricular ejection 4 = Isovolumetric ventricular relaxation After P . Paolini. Heart murmurs Always consider other symptoms and signs before auscultation and think: What do I expect to hear? However, don \200\231t let your expectations determine what you hear. Use the stethoscope correctly. Remember that the bell is used to detect low-pitched sounds (e.g., mitral stenosis) and should be applied gently to the skin (a bell applied tightly to the skin becomes a diaphragm). The dia- phragm is used to detect higher-pitched sounds (e. g., aortic regurgitation). Consider any murmur in terms of timing (systolic, diastolic, or continuous), intensity (see Table 3.8 and Figure 3.6), pitch , and location (where the mur- mur is loudest and where it radiates). An innocent systolic murmur (also called functional murmur ) is soft (grade 1 or 2), early in systole, and heard along the left sternal border . Anything beyond this description (including all diastolic murmurs) could indicate underlying structu ral heart disease and may need an echocardiogram to further evaluate. Timing and quality A systolic-ejection murmur ( SEM , crescendo \200\223decre- scendo) usually originates from a bnormal flow over an outflow tract and waxes and wanes with the intraventricular pressures. SEMs may be innocent and are common in children and high-output states (e.g., tachycardia, preg- nancy). Pathologic causes include aortic stenosis and sclerosis, pulmonary stenosis, and hypertrophic obstructive cardiomyopathy (HOCM). A holosystolic murmur ( HSM ) is of un iform intensity and obscures both S 1 and S 2 . It occurs due to regurgitation from a ventr icle into a low-pressure chamber (e.g., mitral or tricuspid regurgitation, VSD). Mitral val ve prolapse may produce a late systolic murmur and a midsystolic click. Early diastolic mur murs are high-pitched, blowing, and decrescendo. These occur in aortic and, although rare, pulmonary regurgitation. Mid-diastolic murmurs are low-pitched and rumbling. They occur in mitral stenosis (often accentuated presystolically also) and are easily missed: Listen for the \200\234absence of silence \200\235 in diastole. Also often seen in moderate or severe aortic regurgitation (Austin Flint murmur). Continuous murmurs begin in systole and contin ue into diastole and may occur with a patent ductus arteriosus, arteriovenous fistula, or c oarctation of the aorta. Intensity Intensity is generally a poor guide to the severity of a lesion (exceptions include aortic and mitral regurgitation, where murmurs of grade \211 3 indicate more severe disease). Many patients with right-sided val- vular lesions (such as tricuspid regurgitation), and many with mild mitral or aortic regurgitation, do not have a udible murmurs. To help distinguish the etiology of a systolic murmur, observe how its inte nsity changes with changing cardiac cycle lengths (as in atrial fibrillation): Mitral regur gitation does not change in intensity, but aortic stenosis becomes louder after a longer du ration diastole (HOCM responds unpredictably to changing cycle lengths). See Table 3.8. Are a where loudest The location (and timing) of a systolic murmur does not reliably distinguis h aortic stenosis from mitral regurgitation. However, highest intensity of murmur at second right intercostal space (among sys- tolic murmurs radiating to the right clavicle) can hel p determine likelihood of severe aortic stenosis. Radiation The SEM of aortic stenosis clas sically radiates to the right clavicle and carotids (if the murmur over the right clavicle is absent, then aortic stenosis is considerably less likely), in contrast to the HSM of mit ral regurgitation, which classically radiates to the axilla. Accentuating maneuvers Movemen ts that bring the relevant part of the heart closer to the stethoscope accentuate murmurs ( e.g., leaning forward for aortic regurgitation, left lateral decubitus position for mitral stenosis). Right-sided murmurs characteristically intensify during normal inspiration (insp iration increases venous return to the right side of the heart and decreases it to the left side of the heart). The Valsalva maneuver (forced expiration against a closed glottis) dec reases systemic venous return, accen- tuating the systolic murmur of HOCM. Squatting-to-sta nding also decreases venous return and may also intensify mitral valve prolapse. Increasing afterload (via isometric handgrip exercise or transient arterial occlusion) will intensify murmurs of mitral regurgitation and VSD. Nonvalvular murmurs A pericardial friction rub ma y be heard in pericardi- tis. It is a superficial scratching sound, not confined to systole or diastole. s l l i k s l a c i n i l C 53 Figure 3.6 Common heart murmurs \200\223Ejection-systolic e.g., aortic stenosis \200\223Early diastolic e.g., aortic regurgitation S1 S2 S1 S1 S2 S1 \200\223Pansystolic e.g., mitral regurgitation \200\223Mid-diastolic murmur e.g., mitral stenosis S1 S2 S1 S1 S2 S1 Opening snap Presystolic accentuation Table 3.8 Grading intensity of heart murmurs The intensity of murmurs is graded on a 1 \200\2236 scale: Grade 1/6: Grade 2/6: Grade 3/6: Grade 4/6: Grade 5/6: Grade 6/6: 54 Very soft, only heard after listening for a while Soft, but detectable immediately Clearly audible, but no thrill palpable Clearly audible, palpable thrill Audible with stethoscope p artially touching chest Can be heard without placing stethoscope on chest The respiratory system Presenting symptoms