Chapter 13 Chest Inspection, Palpation, and Percussion

“According to a German physician, if the chest covered with a simple shirt is struck with the hand, it gives back a dull sound on the side where vomica is, as if one was striking a flesh piece, whereas if the chest opposite side is struck, it gives back a resonant sound, as if one was striking a drum. However, I still doubt that this information is generally correct.”

–Tissot SAAD: Avis au peuple sur sa santé. Paris, 1782.

“A most violent and startling knocking was heard at the door…. The object that presented itself to the eyes of the astonished clerk was a boy—a wonderfully fat boy—standing upright at the mat, with his eyes closed as if in sleep. He had never seen such a fat boy…, and this, coupled with the utter calmness and repose of his appearance, so very different from what was reasonably to have been expected of the inflictor of such knocks, smote him with wonder…. The extraordinary boy spoke not a word; but he nodded once and seemed to the clerk’s imagination to snore feebly.”

Charles Dickens, Pickwick Papers

Generalities

Chest inspection, palpation, and percussion are the foundations of physical exam. Percussion is 15 years older than the United States, the brainchild of an Austrian innkeeper’s son who figured out that patients’ chests could behave like barrels of wine. Although rather “ancient,” these maneuvers retain considerable value. Their skilled use may in fact still provide key pieces to our diagnostic mosaic. Indeed, bedside diagnosis of lung diseases requires all these maneuvers to yield useful information.

Pearl:

In contrast to cardiac diseases, where a bedside diagnosis can often be achieved by auscultation alone, a pulmonary diagnosis usually requires a comprehensive and competent performance of all parts of the exam, starting with inspection, palpation, and percussion.

1 What are the main components of the chest exam?

They are the same as for any other section of the exam: inspection, palpation, percussion, auscultation, and … contemplation. This last (but not least) component was added by William Osler, as the necessary pondering of information garnered through the four preceding stages. Pondering was so important for Sir William that several portraits actually depict him at the bedside, deeply engrossed in his own contemplative thoughts. Yet, with the fading of bedside rounds, contemplation took a hit, becoming the latest casualty in the never-ending feud between science and art for the soul of medicine.

2 What is the usual sequence in a typical pulmonary exam?

The patient usually remains seated, with the physician moving from front to back and sides. Initial assessment includes an evaluation of effort, rate, and depth of respiration. It also should identify any wheeze, or grunt, or noisy sound that might be audible without the need of a stethoscope. Sequential inspection of the anterior, posterior, and lateral chest should then be carried out. Finally, palpation, percussion, and auscultation complete the exam. The examination should be thorough and go from the chest surface toward the inner structures (Fig. 13-1).

Figure 13-1 Algorithm for the nonauscultatory pulmonary examination.

A. Chest Inspection

4 What are the most common abnormalities of respiration?

Mostly the ones related to the vital signs of the respiratory pump, such as pattern of breathing and its three main components: (1) rate, (2) depth, and (3) rhythm. Each of them may be abnormal, and all may be evaluated by simply observing the patient during the interview. In addition, grunting, nasal flaring, and pursed-lip respiration also can be detected through bedside observation (see later).

5 What are the abnormalities of posture?

These, too, can be detected by simple observation, even before the patient undresses. They are mostly related to compensatory postures, designed to improve the efficiency of the respiratory “pump.” Patients with chronic obstructive pulmonary disease (COPD), for example, usually sit up and lean forward, so that they can better tense the accessory respiratory muscles and improve their contractility. Patients may lean so much forward to eventually have to prop themselves up by their resting elbows against the thighs. With time, the protracted pressure on the thighs leads to hyperpigmented calluses immediately above the knees (Dahl’s sign).

6 What are the main abnormalities in the use of respiratory muscles?

In addition to recruitment of accessory muscles of respiration, the main abnormality is an asynchronous contraction of the diaphragm and intercostals (paradoxical respiration), an important sign of impending respiratory failure.

7 What about asymmetry in thoracic expansion?

This, too, can be detected by simple inspection, even though it is usually best evaluated by palpation.

8 What abnormalities of the chest cage can be detected by inspection?

Abnormalities of the spine, ribs, and sternum. All may adversely affect lung mechanics and thus lead to compensatory postures.

9 And what about abnormalities of the chest surface?

They are pallor or cyanosis, hyperpigmentation or hypopigmentation, expiratory bulges, collateral circulations, dermatomic lesions, and chest wall fistulas. All are detectable by astute observation.

10 What about assessment of extremities and neck veins?

Although often carried out separately, examination of neck veins and extremities is an important aspect of respiratory evaluation. Finding clubbing, for example, or asterixis may provide valuable information toward the recognition of an underlying respiratory disease. The same can be said for the detection of either nicotine stains (usually on fingers) or a smoker’s face (deep and premature wrinkles coupled with skin coarsening), both indications of unrepentant smoking even before a social history is obtained. Finally, distended neck veins in patients with either cor pulmonale or pulmonary embolism also can be a very important diagnostic sign.

(1) Abnormalities of Respiration

Abnormalities in the Rate of Inspiration

11 What are the main abnormalities in respiratory rate?

The major ones are an increase and a decrease. The normal respiratory rate in an adult should be around 20 ± 5 breaths a minute. Hence, tachypnea indicates a rate faster than 25/minute, whereas bradypnea usually indicates a rate slower than 8/minute, as observed in narcotic-induced respiratory depression.

12 Can tachypnea be considered normal?

Probably not. Still, a respiratory rate >20 breaths/minute is often seen in elderly nursing home residents with chronic medical conditions but no active disease.

13 What is the clinical significance of true tachypnea?

It usually indicates moderate to severe cardiorespiratory disease, requiring a compensatory increase in the work of breathing. In hospitalized patients, it carries a bad prognosis. In fact, on internal medicine wards, it predicts cardiorespiratory arrest. It also argues in favor of pneumonia, both in the inpatient and outpatient settings. In hospitalized pneumonia patients, it can even predict death, thus providing a far more accurate prognostic indicator than either tachycardia or abnormal blood pressure. It also predicts failure to wean from mechanical ventilation.

14 Can absence of tachypnea be helpful?

Yes, because tachypnea is so common in chest diseases that its presence adds relatively little, whereas its absence challenges a cardiac or respiratory diagnosis. For example, tachypnea is so frequent in pulmonary emboli (92% of patients) that a normal respiratory rate argues strongly against the diagnosis. The same can be said for tamponade, where tachypnea is a must. Conversely, in an acute abdomen, tachypnea directs attention to a supradiaphragmatic rather than subdiaphragmatic process.

15 Does tachypnea predict hypoxemia?

Not necessarily. In fact, some patients might actually be hypoxic as a result of hypoventilation (and therefore of bradypnea). Others might use instead tachypnea to fully compensate for hypoxemia. Hence, the need for monitoring not only the respiratory rate, but also oxygen saturation.

16 What is the clinical significance of bradypnea?

It should prompt consideration of hypothyroidism, but it also may suggest a central nervous system disease, or, as indicated before, the use of narcotics and sedatives.

17 What is apnea?

It is the absence of respiration for at least 20 seconds while awake or 30 seconds while asleep. It is often seen in patients with either neuromuscular dysfunction (central apnea) or airway obstruction induced by rapid eye movement (REM) sleep (obstructive sleep apnea). Note that apnea also remains the final event of all respiratory failures, whether due to pulmonary or neuromuscular disease.

Abnormalities in the Depth of Respiration

18 What are the main abnormalities in the depth of respiration?

Hyperpnea and hypopnea (Fig. 13-2).

Figure 13-2 Patterns of respiration. The horizontal axis indicates the relative rates of these patterns. The vertical swings of the lines indicate the relative depth of inspiration.

(Adapted from Seidel HM, Ball JW, Dains JE, Benedict GW: Mosby’s Guide to Physical Examination, 3rd ed. St. Louis, Mosby, 1995.)

19 What is hyperpnea?

It is an increase in tidal volume, usually accompanied (but not necessarily) by an increase in rate. In other words, hyperpnea is a rapid and deep respiration. The classic form was first described by Kussmaul in patients with diabetic ketoacidosis, who attempt to compensate by hyperventilating. This compensation also can be observed in any of the other anion gap metabolic acidoses, which can be recalled with the mnemonic make up a list: methanol poisoning, aspirin intoxication, ketoacidosis, ethylene glycol ingestion, uremia, paraldehyde administration, and lactic acidosis.

20 Is there a difference between hyperpnea and the hyperventilation of cardiorespiratory disease?

Yes. In cardiorespiratory disease, vital capacity is typically compromised, and thus breaths are shallow, with the increase in ventilation due primarily to a faster rate. In contrast, true hyperpnea relies more on increased tidal volume. Since this does not rebreathe dead space as much, it is a better CO₂ controller. Hence, hyperpnea rather than tachypnea is the compensation of choice in metabolic acidosis.

21 Who was Kussmaul?

Adolf Kussmaul (1822–1902) was a graduate of Heidelberg and Würzburg (where he studied under Virchow) and a part-time German Army surgeon. He was the first to describe periarteritis nodosa and progressive bulbar paralysis. He also was the first to attempt gastroesophagoscopy, pleural tapping, and peritoneal lavage. His name is linked to the respiration of patients with metabolic acidosis, the clinical description of pericarditis, pulsus paradoxus, aphasia, and, of course, Kussmaul’s sign, the inspiratory increase in jugular venous pressure (and distention) seen in patients with obstruction to right-sided venous return (see Chapter 10, questions 115–118). A meticulous and precise man famous for complaining that none of his colleagues could write good German, Kussmaul contributed satirical poems to a weekly magazine under the pseudonym of Gottlieb Biedermeier, an imaginary and unsophisticated poet who eventually came to symbolize the values and tastes of the early 19th-century German bourgeois: reliable, hard-working, but boringly unimaginative (like in the Biedermeier style of furniture. “Bieder” is German for “everyday, plain” while “Meier,” or Meyer, is a common German last name).

22 What is hypopnea?

It is shallow respiration, usually indicative of impending respiratory failure or obesity-hypoventilation (Pickwickian syndrome). In this regard, hypopnea is often associated with periods of apnea (see question 17).

Abnormalities in Rhythm and Pattern of Respiration

23 What are the main abnormalities in respiratory rhythm?

They are many, and usually the result of disruption in the neurogenic control of the respiratory pump. Hence, they are often seen in comatose patients. Thus, they are valuable to recognize because they may help localizing the site of the neurologic lesion (see Fig. 13-2). Moving downward in a rostrocaudal fashion, from the uppermost to the lowermost neurologic center, the most common abnormalities of respiratory rhythm are (1) Cheyne-Stokes respiration, (2) Biot’s respiration, (3) apneustic breathing, (4) central hyperventilation, and (5) ataxic (agonal) respiration.

24 What is Cheyne-Stokes respiration?

It is a form of periodic breathing (i.e., a regularly irregular pattern consisting of a series of cycles). Each “cycle” has a constant respiratory rate but variable depth, insofar as it progressively increases in amplitude (crescendo), eventually culminating in a peak followed by a decrescendo period. This fades into complete apnea, from which another cycle restarts. The crescendo-decrescendo phase lasts approximately 30 seconds, whereas the apneic period is usually just a little shorter.

25 What is the physiologic repercussion of Cheyne-Stokes?

Mostly a swing in cerebral blood flow, caused by alternating hyperpnea (higher cerebral flow) and hypopnea (lower cerebral flow). These are probably responsible for some of the mental status changes described in these patients, such as alertness, agitation, and increased muscle tone during hyperpnea, followed by sleepiness, motionlessness, and decreased tone during apnea.

26 What is the clinical significance of Cheyne-Stokes?

It may be encountered in normal people as a result of aging or simply sleep.

It also can be seen in normal individuals who recently moved to high altitudes, where environmental hypoxia leads to a heightened CO₂ response of the respiratory centers.

The classic association, however, is with congestive heart failure, where Cheyne-Stokes is found in as many as one third of cases, reflecting worse function and prognosis. The reduced cardiac output of these patients leads to a lag between alveolar CO₂ and the arterial CO₂ delivered to the medulla. Hence, low alveolar CO₂ is reflected much later in the blood that bathes the medulla. This asynchrony between alveoli and medulla, coupled to higher sensitivity of the respiratory centers to CO₂, eventually leads to the hyperpnea-hypopnea-apnea cycle.

Cheyne-Stokes also can be seen in various neurologic disorders (such as meningitis, bilateral or unilateral cerebral infarctions/hemorrhage, and traumatic brain stem or supratentorial damage) in which the underlying mechanism is heightened sensitivity of the respiratory centers to carbon dioxide stimulations. As a result, any increase in CO₂ blood levels leads to excessive hyperventilation, until the CO₂ bottoms out and respiration ceases completely. Eventually, the apnea-induced increase in CO₂ leads to another phase of hyperpnea, and the cycle starts anew.

27 What are the therapeutic implications of Cheyne-Stokes?

Given its major swings in ventilation (and O₂ blood levels), patients with Cheyne-Stokes respiration may require administration of supplemental oxygen and, overall, have a worse prognosis.

28 Who were Cheyne and Stokes?

John Cheyne (1777–1836) was a Scot and himself the son of a surgeon, often helping his father to care for patients by bleeding and dressing them. After graduating at age 18 from the University of Edinburgh, he served in the army for 4 years. During this time, he took part in the battle of Vinegar Hill, which broke Irish resistance to British rule. In 1809, he went to Dublin, where he was eventually appointed Physician-in-General for Ireland, becoming the founder of modern Irish medicine.

William Stokes (1804–1878) was instead a bona-fide Irishman and the son of the anatomy professor who had succeeded John Cheyne at the College of Surgeons School in Ireland. Although lacking in formal education (his father wanted to protect him from a society that did not abide by the scriptures), Stokes eventually went to Edinburgh, where he received his doctor of medicine in 1825. In Scotland, he learned of Laënnec and his recent invention, the “cylinder.” He soon became so enamored of this little tool that he even wrote an introductory book about it, the first of its kind in the English language. In fact, Stokes was such a vocal advocate for the use of stethoscopy that he provoked quite a few reactions (and even some sarcasm) among his colleagues. Still, he was a well-liked physician, who worked among the poor during the Dublin typhus epidemic in 1826 (he even contracted the disease but survived) and then again during the subsequent cholera epidemic. His name is linked not only to the eponymous pattern of respiration but also to Stokes-Adams syncope, which the Irish surgeon Robert Adams had described in 1827 and which Stokes included in his 1854 book, Diseases of the Heart and Aorta. Of course, the Italian Morgagni had preceded them both by describing the condition almost 100 years before (see Chapter 11, question 14).

29 What other abnormalities in rhythm are worthy of recognition? What is their significance?

Biot’s respiration is a variant of Cheyne-Stokes, insofar as it is a succession of hyperpneas/hyperventilations and apneas, but without the typical crescendo-decrescendo pattern, the abrupt beginning, and the regularity. It is also less common than Cheyne-Stokes. Biot’s is usually observed in patients with either meningitis or medullary compression. Hence, it carries a worse prognosis, usually resulting in complete apnea and cardiac arrest.

Apneustic breathing is a peculiar pattern of respiration, characterized by a deep inspiratory phase followed by a breath-holding period and a rapid exhalation. It is typical of brain stem (pons) lesions.

Central hyperventilation is often encountered in patients with midbrain/upper pontine lesions. It is an ongoing pattern of hyperpnea and tachypnea (i.e., deep and rapid respirations), which tends to be different from Kussmaul’s respiration, insofar as it is not as fast, but usually deeper.

Ataxic ventilation: From the Greek a- (lack of) and taxis (order), this is a totally anarchic respiratory rhythm—a sort of fibrillation of the respiratory centers, with back-and-forth shifts from hyper- to hypo-ventilation, and from hyperpnea to hypopnea, all intermingled with periods of apnea. It is seen in patients with damage to the medulla, typically preceding death. Hence the term, agonal respiration.

30 What is a grunting respiration?

It is another abnormal respiratory pattern. A typical grunting respiration is the râle de la mort, a pre-terminal gurgling-and-grunting sound produced by patients too ill to clear secretions. The expression translates as “death rattle” (râle is rattle in French), and in the olden days, it used to be a sign of severe pneumonia with impending respiratory muscle fatigue and death. The râle de la mort also is the main cause of Laënnec’s botched nomenclature, insofar as the inventor of the stethoscope became so sensitive to the emotional overtones of the term râle to eventually prefer at the bedside its Latin equivalent rhonchus. This triggered a tremendous (and ongoing) confusion in lung sound terminology.

31 What is the clinical significance of a grunting respiration?

Very much the same as in Laënnec’s days. It can still be heard in adults with respiratory muscle fatigue (and impending arrest), but nowadays it is much more frequent in children, where it usually presents as a short and low-pitched noise produced by forced expiration against a closed glottis. The “grunt” is due to the sudden opening of the glottis and the loud rush of air from the larynx. Its physiology (and significance) is akin to pursed-lip respiration (see below, questions 32 and 33), insofar as it leads to an increase in expiratory airway pressure, which then acts as a mechanical splint against alveolar collapse, increasing tidal volume and oxygenation while decreasing respiratory rate and CO₂. An increased intra-alveolar pressure also has a positive effect against transudation of fluid in patients with pulmonary edema, and thus it is often observed during acute episodes of left ventricular failure.

32 What is pursed-lip respiration?

Another respiratory pattern, typically seen in obstructive lung disease—usually emphysema (Fig. 13-3). Given the alveolar hyperinflation (and reduced lung elasticity) of COPD, patients are at risk for expiratory airway closure and air-trapping. Hence, they resort to pursed lip exhalation, as if they were inflating a balloon. This increases intra-airway pressure, thus inducing auto-PEEP (positive end-expiratory pressure). It is often accompanied by an expiratory wheeze or grunt.