Chest Inspection, Palpation, and Percussion

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 breaths per minute, as observed in narcotic-induced respiratory depression.

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.

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.

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 supra diaphragmatic rather than subdiaphragmatic process.

Does tachypnea predict hypoxemia ?

Not necessarily. In fact, some patients might actually be hypoxic as a result of hypo ventilation (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.

What is the clinical significance of bradypnea ?

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

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.

What are the main abnormalities in the depth of respiration?

Hyperpnea and hypopnea ( Fig. 11.2 ).

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.

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 carbon dioxide (CO ₂ ) controller. Hence, hyperpnea rather than tachypnea is the compensation of choice in metabolic acidosis.

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 poliarteritis 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 107–110). 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).

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).

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. 11.2 ). 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.

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.

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 .

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 CO ₂ 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 CO ₂ and the arterial CO ₂ delivered to the medulla. Hence, low alveolar CO ₂ 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 CO ₂ , 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 CO ₂ blood levels leads to excessive hyperventilation, until the CO ₂ bottoms out and respiration ceases completely. Eventually, the apnea-induced increase in CO ₂ leads to another phase of hyperpnea, and the cycle starts anew.

What are the therapeutic implications of Cheyne-Stokes?

Given its major swings in ventilation (and O ₂ blood levels), patients with Cheyne-Stokes respiration may require administration of supplemental oxygen and, overall, have a worse prognosis.

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 10 , Question 146).

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 hypoventilation, 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 .

What is a grunting respiration?

It is another abnormal respiratory pattern. A typical grunting respiration is the râle de la mort , a preterminal 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.

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 later, 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 CO ₂ . An increased intraalveolar 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.

What is pursed-lip respiration?

Another respiratory pattern, typically seen in obstructive lung disease – usually emphysema ( Fig. 11.3 ). 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 intraairway pressure, thus inducing auto-PEEP (positive end-expiratory pressure). It is often accompanied by an expiratory wheeze or grunt .

What is the physiologic impact of pursed-lip respiration?

It increases arterial O ₂ while decreasing CO ₂ . It does so by behaving as an expiratory positive airway pressure in a Bi-PAP (bilevel positive airway pressure) machine. It also slows respiratory rate (by as much as 40%), improves tidal volume, and decreases dyspnea. The mechanism for the latter is unclear, although it probably involves an effect on interstitial J-receptors as well as an overall reduction in the work of breathing.

What is nasal flaring ?

It is the outward inspiratory motion of the nostrils – a valuable sign of respiratory distress. Often associated with the use of accessory muscles.