The Airway and Lungs
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Extremely useful and relevant information can be obtained when analysing the position assumed by patients with dyspnoea. Relief of breathlessness in a sitting or standing position compared to the recumbent position is referred to as orthopnoea. While increased venous return in the supine patient is well tolerated in individuals with a preserved heart function, this leads to pulmonary venous congestion, an increase in interstitial lung water and a subsequent reduction of lung capacities with resultant shortness of breath in patients with impaired heart function. Accordingly, patients with heart failure prefer to sit upright (e.g. supporting their back with pillows to achieve a maximum upright position) (Fig. 5.1). Conversely, placing the patient into a supine position may be used as a stress test to exclude respiratory distress due to heart failure or (pulmonary) fluid overload. A history of paroxysmal nocturnal dyspnoea characterized by repeated awakening due to breathlessness while sleeping in the recumbent position is a typical symptom of heart failure.
5.1.1 Body Position
Trepopnea is a phenomenon encountered in patients with heart failure (e.g. in those with right-sided pleural effusion), asymmetrical pulmonary disease (large atelectasis or total lung collapse, pleural effusion, pneumonia, patients post pneumonectomy) or mediastinal/endobronchial tumours. It describes the occurrence of dyspnoea in one lateral position as opposed to the other. As gravity causes blood to be redistributed in the chest, dyspnoea develops in the lateral position with the more diseased side of the lung placed downwards. In clinical practice, this effect can also be used therapeutically (“place the good lung down!” to improve oxygenation).
Platypnea refers to breathlessness which occurs or increases in the upright position but is relieved with recumbency. In these patients, breathlessness is frequently accompanied by deoxygenation (orthodeoxia). This phenomenon can be observed in patients with right-to-left shunts through intra-cardiac or more often intra-pulmonary shunts [e.g. (bi)basal pneumonia, basal emphysema or arteriovenous shunts such as in patients with the hepatopulmonary syndrome or Osler disease]. Pathophysiologically, gravitational redistribution of the blood to more affected basal parts of the lungs can explain the occurrence of dyspnoea in the upright position in these patients.
5.1.2 Chest Form, Chest Wall Expansion and Symmetry
Visual inspection of the chest can reveal important clues about lung function. Chest wall deformities such as kyphosis, scoliosis, kyphoscoliosis, severe funnel (pectus excavatum) or pigeon-shaped (pectus carinatum) chests are associated with reduced lung capacities and resultant restrictive lung disease. A barrel-shaped chest is suggestive of the presence of underlying COPD and/or lung hyperinflation. Similarly, centripetal (abdominal) obesity may be associated with a reduction in chest wall compliance and lung capacities. Scars of previous thoracic surgeries indicate that the patient may have reduced lung capacities (e.g. due to lung resections). In patients with COPD, lung apices may be seen and palpated in the supraclavicular region. Enlarged intercostal spaces with bulging lung tissue are less frequently noted over the lateral chest wall during acute exacerbation in asthenic patients. Significant deformities of the chest due to trauma (e.g. “stove-in chest”) are rare, but, if present, they are associated with life-threatening/fatal lung and/or mediastinal injuries.
The range of chest wall expansion during inspiration is a good clinical marker of tidal volume. Patients with barely visible expansions of the (lower) chest typically have (very) low tidal volumes and are at high risk of respiratory failure. Common causes are reduced pulmonary or chest wall compliance, COPD, respiratory muscle fatigue or neuromuscular diseases. In obese patients, the extent of chest excursions is difficult to assess and making conclusions about the size of tidal volume unreliable.
When assessing the symmetry of chest wall expansions, it is important to make sure that the patient is lying flat so that asymmetry is not due to the patient’s position. Asymmetrical chest wall expansions reflect asymmetrical lung ventilation and can arise from pneumothorax, atelectasis or consolidation (e.g. pneumonia). While a pneumothorax results in elevation of the affected hemithorax, total lung collapse/volume loss leads to reduced chest wall expansion with the affected hemithorax lagging behind the contralateral side. In both pneumothorax and total lung collapse/lung collapse, chest wall expansions of the affected hemithorax are reduced. Rarely and only in asthenic patients result unilateral lung diseases (e.g. pneumonia) in reduced ipsilateral chest wall expansions.
5.1.3 Skin Colour
Chronic cyanosis can be detected more reliably than acute cyanosis as patients commonly have elevated haemoglobin levels. Other signs of chronic hypoxaemia include facial plethora, clubbing of fingers (drumstick fingers) and toes and nail bed cyanosis. Although clubbing is largely seen in patients with lung diseases leading to chronic hypoxaemia [e.g. pulmonary fibrosis, asbestosis, lung cancer (usually absent with small cell carcinoma of the lung), mesothelioma, suppurative lung disease including empyema, lung abscess and bronchiectases and only very rarely with COPD], it can be hereditary or result from non-pulmonary diseases such as cyanotic heart disease, inflammatory bowel disease or chronic liver disease. In some patients, ballotability of the nails or sponginess of the nail beds, an early stage of clubbing, has been observed within as short as 2 weeks after onset of pulmonary disease.
5.1.4 Respiratory Rate
The respiratory rate is determined by counting the number of chest wall expansions over 20–30 s and then multiplying it to attain the number of breaths per minute. A respiratory rate between 10 and 15 breaths per min is physiologically normal in the resting individual. Except in some elderly patients, in whom respiratory rates may physiologically reach 25 breaths per min, any increase >20 breaths per min must be considered abnormal and referred to as tachypnoea. The degree of tachypnoea is a solid but non-specific indicator of disease severity with respiratory rates >30 breaths per min often associated with life-threatening conditions. Tachypnoea is more valid to predict subsequent cardiac arrest in hospitalized patients than tachycardia or abnormal arterial blood pressure. A persistently normal respiratory rate is, conversely, a useful finding that makes certain pathologies (e.g. shock, significant pulmonary embolism) rather unlikely. Physiologically, a rise in respiratory rate increases alveolar ventilation, carbon dioxide elimination and alveolar oxygen tension. Tachypnoea can therefore not only be observed in (acute) lung disease but also in patients with reduced systemic oxygen delivery and metabolic acidosis. Despite this, tachypnoea, in clinical practice, correlates notoriously poorly with the degree of hypoxaemia. Furthermore, ventilation can be stimulated by increased sympathetic tone (e.g. pain), inflammation (e.g. sepsis) and cerebral dysfunction (e.g. cortical or midbrain lesions). Unlike most other patients, patients with metabolic acidosis first increase their alveolar ventilation by an increase in tidal volume and only later by an increase in respiratory rate. This form of tachypnoea is referred to as hyperpnoea and is physiologically the most effective way to eliminate carbon dioxide via the lungs as dead space ventilation is minimized. Although in some cases, an increase in tidal volumes may be evident as “Kussmaul” breathing, increased minute ventilation in patients with metabolic acidosis is difficult to recognize. It often only becomes apparent when surprisingly low pH ranges have been reached. As very low (<7.1–7.2) pH values are most often caused by anion gap acidosis (mostly of diabetic origin), the most common causes of hyperpnoea include ketoacidosis, lactic acidosis, poisoning (e.g. salicylate, toxic alcohols, carbon monoxide, cyanide, isoniazid, paraldehyde, iron) and uraemia.
5.1.5 Respiratory Rhythm
This is in contrast to Biot breathing which resembles Cheyne-Stokes breathing at first sight but differs in that alternating episodes of hyper- and apnoea start and stop more abruptly. Overall, alterations of hyper- and apnoeic spells are less regular than in Cheyne-Stokes breathing. Biot breathing is fairly uncommon but a sensitive indicator of pontine or brainstem pathology. This explains why patients with Biot breathing are at an increased risk of apnoea.
Apneustic or ataxic breathing is characterized by an irregular respiratory rate and tidal volumes. The patient typically holds the breath at the end of each inspiration before the next cycle of expiration starts at an irregular, slow rate. It reflects a preterminal sign (brainstem pathology or severe brain hypoperfusion) and usually precedes gasping and respiratory arrest (see Part I Sect. 4.3).
5.1.6 Breathing Pattern
Four breathing patterns are essential to recognize in the critically ill patient: the physiologic, paradoxical, obstructive and restrictive breathing pattern.
Physiologically, contraction of the diaphragm and intercostal muscles raises both the chest and abdomen during inspiration. Expiration occurs passively with the chest and abdomen descending. The normal time ratio of inspiration to expiration is 1:2.
Paradoxical breathing refers to the inward movement of the chest while the abdomen raises during inspiration. This breathing pattern is seen in patients with an obstructed airway (e.g. comatose patient in the recumbent position) and needs to be recognized without delay. Paradoxical breathing (or abdominal paradox) also occurs in patients with severe respiratory distress or diaphragmatic dysfunction (remember: abdominal respiratory movements indirectly indicate how the diaphragm is moving). In these patients, the abdomen moves inwards while the chest wall raises. It is a highly sensitive and alarming sign of impending respiratory decompensation. Furthermore, paradoxical breathing can be observed in patients with cervical spinal cord injury when only the diaphragm contracts moving the abdomen outwards and the chest inwards during inspiration.
In patients with an obstructive breathing pattern, exhalation of air is impaired. Clinically, this becomes evident by active abdominal contraction during expiration. The chest often descends slowly and incompletely with the abdominal muscles contracting and moving the abdomen down- and outwards. The time used for expiration exceeds the time for inspiration. The most common clinical conditions leading to impaired expiratory airflow and an obstructive breathing pattern are asthma and COPD and pulmonary fluid overload/oedema which cause small airway collapse. Using the lips to generate a positive expiratory pressure (“pursed lip breathing”) is common in patients with an obstructive breathing pattern, particularly those with emphysema. It reduces respiratory rate, increases tidal volume (by up to 500–600 mL) as well as carbon dioxide elimination. Furthermore, the increase in end-expiratory pressure as mediated by “pursed lip breathing” shifts the diaphragm into a better position at the beginning of inspiration and thereby improves diaphragmatic function.
A restrictive breathing pattern is characterized by a prolonged and strenuous inspiration. Expiration usually follows a normal pattern. In contrast to obstructive breathing, the time required for inspiration exceeds that for expiration. Clinically, restrictive breathing is recognized by inspecting the upper chest wall. The most common clinical conditions leading to a restrictive breathing pattern are pulmonary diseases with a reduced lung or chest wall compliance (e.g. lung fibrosis, ARDS, early interstitial lung oedema). If expiratory flow limitation is severe and air trapping occurs in patients with asthma/COPD, restrictive and obstructive breathing pattern can be observed at the same time.
5.1.7 Work of Breathing
Dyspnoea is the subjective feeling of breathlessness and cannot be clinically assessed but only relayed by the patient. On the other hand, the work of breathing can be assessed by inspection. Although clinical signs of an increased work of breathing usually correlate well with the degree of dyspnoea, some patients (e.g. those with COPD) surprisingly do not feel dyspnoea despite of an obvious increase in the work of breathing.
Clinical signs of an increased work of breathing
• Sitting/upright position (see Fig. 5.1)
• Inability to speak in full sentences
• Forced or laboured inspiratory and/or expiratory efforts
• (Twitchy) use of accessory respiratory muscles (e.g. scalene, sternocleidomastoid and trapezius muscles; Fig. 5.8)
• Arms stemmed on knees/thighs (tripod stance) (see Fig. 5.1)
• Intercostal, suprasternal or supraclavicular retractions (Fig. 5.8)
• Nose flaring (ala nasal flaring)
• Elevation of the shoulders and/or movements of the head synchronous with inspiration (Fig. 5.9)
• Elevation of eyebrows and eyelids synchronous with inspiration
• Inspiratory (downward) retractions of the trachea and larynx during inspiration
• Upward motion of the clavicles and shoulders during inspiration
• Backward movement of the head during inspiration
• Sucking sound during inspiration in intubated patients who breath spontaneously (DD: cuff pressure too low)
• Diaphoresis, profuse (cold) sweating
• Tremor or jerks (in hypercapnia)
• Anxiety, fear of death
• Reduced sensorium (e.g. talking/praying without responding to voice)
• Depressed mental statea
Indirectly, respiratory distress and by that the work of breathing can be determined whether the patient can speak in full sentences. Patients with an increased work of breathing can only speak single words or speak in a staccato fashion (e.g. few words spoken with each breath). Assessment of the work of breathing and indirectly the vital capacity is particularly important in patients with acute neuromuscular diseases, first of all the Guillain–Barré syndrome. In these patients, inability to count to more than ten in a single breath is highly indicative of a critically reduced (forced) vital capacity (e.g. <1 L) and the need for endotracheal intubation. Conversely, patients who can count to 20 or higher with one breath usually have forced vital capacities within the safe range. Rapid progression of muscular weakness, particularly if it involves facial, neck and proximal extremity muscles, can highlight critical drops in vital capacity. A reduction in the volume of the voice and the inability to lift the head or elbow are further danger signs of impending respiratory failure.
In patients with a pleural drainage and a water seal in place, the swing of the water level (in the container) over the respiratory cycle reflects changes in pleural pressure. In patients with an increased work of breathing, typically large swings of the water level can be seen during inspiration and expiration.
5.1.8 Patient-Ventilator Dyssynchrony
Distinct patterns of patient-ventilator dyssynchrony with corresponding clinical findings and possible underlying problems
Type of patient-ventilator dyssynchrony
Minimal chest wall expansions between breaths with greater chest wall expansion
Wrong ventilatory mode (e.g. controlled, unassisted), trigger sensitivity too low, dynamic hyperinflation
Delayed chest wall expansion during inspiration, in severe cases can resemble the picture of an obstructed airway
Inspiratory flow rate is too low, inspiratory time is too long
Tachypnoea without signs of increased work of breathing
Trigger sensitivity too high, water/secretions in ventilator tubings
Two inspirations following each other without sufficient expiration in between
Too low pressure support, too short inspiration
Coughing, fighting, repeated inspiratory pressure alarms
Coughing or fighting the ventilator at the end of inspiration
Pressure support or inspiratory flow too high (e.g. leak around the mask during non-invasive ventilation), inspiratory time too long
5.1.9 Tracheobronchial Secretions
While the amount of tracheobronchial secretions correlates with the severity of pulmonary oedema, it is rather the appearance which is of relevance for clinical interpretation in other pulmonary conditions. In rare cases, tracheal secretions may appear normal despite the presence of pneumonia or even diffuse alveolar haemorrhage. Sometimes tracheal secretions only increase during the resolution of pulmonary infections. It is, however, a rule of thumb that the longer an infectious process in the lungs persists (e.g. chronic bronchitis or bronchiectasis), the more unlikely it is that tracheal secretions will remain unaltered. Large amounts of normally appearing rather liquid tracheal secretions can occasionally be seen in intubated or tracheotomized critically ill patients with no obvious lung pathology and may reflect a hypersecretory response to the tracheal foreign body.
Pink or blood-stained tracheal secretions (haemoptysis) reflect haemorrhage in the tracheobronchial tree, distal airways or alveoli, but sometimes result from aspiration of the blood from the upper airways (nose, pharynx) or gastrointestinal tract. While small amounts of blood suctioned from the trachea of patients intubated for several days frequently arise from minor tracheobronchial tears (e.g. due to repeated suctioning, particularly when coagulation is impaired), it may indicate sentinel bleeding from a serious underlying lesion (e.g. tumour, pulmonary artery erosion, arteriovenous fistula). Fresh, bright red blood produced or suctioned from the airways is always an emergency and requires immediate attention. When compared to bleeding from other organs or tissues, pulmonary haemorrhage can rapidly result in death (due to suffocation) even with minor to moderate amounts of blood lost (e.g. >250–500 mL). In addition to the aforementioned pathologies, a myriad of clinical conditions can cause haemoptysis (e.g. pulmonary embolism, bronchitis, pneumonia, tuberculosis, lung abscess, bronchiectasis, bronchial carcinoma, bronchial adenoma, mycetomas, diffuse alveolar haemorrhage, trauma, recreational drugs such as crack or cocaine, congestive heart failure, mitral stenosis).
5.2.1 Without the Stethoscope
In some patients, especially those with severe respiratory dysfunction, a few distinct breathing sounds may be readily audible with the “naked” ear.
An expiratory, high-pitched sound may be heard without a stethoscope in patients with severe intrathoracic (e.g. foreign body), mostly distal airway obstruction. Loud expiratory wheezing is a symptom of an asthmatic attack or COPD exacerbation. Identical to inspiratory stridor, the volume of the expiratory stridor does not correlate with the degree of airway obstruction. Impending respiratory decompensation is heralded by a decrease in the volume of expiratory wheezing. A “silent chest” describes the condition when airflow has decreased to such an extent that expiratory wheezing is not audible even with a stethoscope. Occasionally, a monophonic wheeze is heard during inspiration and expiration (mostly only with the stethoscope). This is caused by partial obstruction of the distal trachea or tracheal bifurcation (e.g. by a tumour, mediastinal mass or foreign body). Polyphonic wheezing (differing tones of wheeze) is heard in patients with varying reductions in airway diameter or calibre.
In patients with severe, life-threatening pulmonary oedema, usually of cardiogenic origin, crackles may be heard without a stethoscope. Crackles are then heard during expiration and resemble the sound heard when air is blown through a straw into a glass of water. This is in contrast to auscultation using the stethoscope when crackles are primarily heard during inspiration. Only when oedema floods the alveoli and reaches the distal airways can crackles be heard during expiration as well. The more oedema fluid enters small and larger airways, the louder the crackles become until they can be heard with the “naked” ear. Another sound which can occasionally be heard in patients with pulmonary oedema is grunting. Grunting arises from vocal cord closure during expiration followed by their sudden and short opening. Physiologically, vocal cord closure increases end-expiratory pressure and by that functional residual capacity and oxygenation. Although grunting has been reported as a sign of respiratory muscle fatigue, grunting breathing is usually associated with a rather low respiratory rate (approximately 20 breaths per minute).
A sound which is heard more commonly is that of airway secretions. They result in coarse, loud crackly and gurgling sounds during inspiration and especially expiration. While secretions in the trachea and bronchi sound more muffled and distant (like small water bubbles in a closed container), secretions in the pharynx and glottis generate a louder, less muffled and “closer” sound. One study found that the presence of gurgling breath sounds during quiet breathing or speech in hospitalized patients was independently associated with hospital-acquired pneumonia . In dying patients, inspiratory and expiratory sounds due to airway secretions are often heard and have been referred to as the “death rattle”.
Partial airway obstruction is typically associated with gurgling and/or snoring sounds (see Part I Sect. 3.1). Gurgling sounds can be heard during inspiration and sometimes also expiration. They indicate that secretions or semi-solid materials are obstructing the larynx or pharynx. Snoring, on the other hand, is heard only during inspiration and results from partial occlusion of the pharynx by the tongue, soft palate and/or epiglottis. The absence of any breathing sounds is not helpful to verify airway patency as both complete obstruction and full airway patency produce no breathing sounds.
Cough is a common but non-specific symptom of pulmonary disease. Only in exceedingly rare cases are the characteristics of a cough specific enough to allow diagnosis of a certain pulmonary disorder (e.g. whooping cough). Barking or croupy cough is suggestive but not specific for viral upper airway disease. Productive or “chesty” coughs allow for inspection and interpretation of tracheobronchial secretions. Although commonly associated with pulmonary infection, a relevant number of patients with chest infection may present with non-productive cough. This appears to be more common in atypical or nonbacterial pulmonary infections. The history is essential to interpret cough in subjects with community-acquired critical illness. For example, cough accompanied by fever, sweats and productive sputum makes acute pulmonary infection likely. Increased coughing in a patient with a history of smoking, prior cough, productive sputum and wheezing is highly suggestive of a COPD exacerbation. A personal/family history of atopic disease together with new or worsening cough (particularly nocturnal) and wheezing is strongly indicative of an acute asthma attack. A drug history should also always be taken to exclude drug-induced coughing in patients with persistent cough (angiotensin-converting enzyme inhibitors, beta blockers including topical usage of these agents, e.g. in glaucoma). Symptoms of dyspepsia, particularly gastro-oesophageal reflux disease, should also be inquired about in such patients.
In critically ill patients with a cough of new onset, it is important to exclude lung infection and pulmonary oedema. Acute pulmonary oedema is, in its early stages, often associated with a quite distinctive non-productive, superficial, staccato-like cough. With increasing severity of pulmonary oedema, coughing occurs following almost each inspiration. Physiologically, cough in patients with pulmonary oedema is thought to arise from stimulation of interstitial juxtacapillary receptors (J-receptors) by increased lung water. These receptors may also be involved in the coughing response to pulmonary embolism, barotrauma/pneumothorax, lung hyperinflation (e.g. recruitment manoeuvre) or re-expansion of atelectasis (e.g. after drainage of a large pleural effusion). A similar cough as with early pulmonary oedema can be heard in patients with dysphagia who aspirate saliva or liquids (e.g. during the water swallow test). In patients with shock, particularly heart failure, the haemodynamic response to coughing can be used as an indicator of the underlying cardiovascular pathology. Prolonged arterial hypotension or even cardiovascular collapse in response to coughing or more frequently “fighting the ventilator” in a patient on catecholamine support is highly suggestive of right heart failure. Less commonly, patients with severe left heart failure or hypovolaemia may experience aggravation of haemodynamic instability following coughing or “fighting the ventilator”.
5.2.2 Auscultation: Listening with the Stethoscope
188.8.131.52 Normal Breath Sounds
Summary of abnormal breath sounds
Bronchial breath sounds over lung periphery
Harsh and loud breath sounds instead of normal vesicular breathing
Inspiration and expiration
Fluid-filled lung such as in pneumonia/consolidation, ARDS or fluid overload
Diminished or absent breath sounds
Breath sounds diminished in volume or completely absent
Inspiration and expiration
Bilateral: shallow breathing, lung protective ventilation, emphysema, dynamic hyperinflation (“silent chest” in asthma or COPD), bilateral pneumothorax (rare), thick chest wall (e.g. obesity)
Unilateral: bronchial intubation, atelectasis, pleural effusion, pneumothorax
High-pitched, clicking or crackling
Bronchopneumonia, bronchitis, COPD or bronchiectasis (typically coarse)
Like Velcro being pulled apart
Pan- or late inspiratory
Lung fibrosis, interstitial lung disorders
Like strands of hair being rolled between the fingers
Pan- or late inspiratory
Bilateral (from base to top): lung oedema (typically fine and late inspiratory)
Unilateral or localized: pneumonia
Rhonchi (retained secretions)
Low-pitched (coarse), snoring, vibrating and sometimes gurgling
Inspiration and expiration
Liquid or semi-solid materials in the tracheobronchial tree (e.g. tracheobronchial secretions)
Continuous musical, squeaking or whistle-like sound
Localized and monophonic: tumour, mucus plug, foreign body
generalized and polyphonic: asthma, COPD, fluid overload, pulmonary congestion
Inspiration and expiration
Partial obstruction of the distal trachea or tracheal bifurcation (e.g. by a tumour or foreign body)
Pleural friction rub
Brushing sound like walking on snow
Inspiration and expiration
Inflammation or irritation of the pleura
184.108.40.206 Bronchial Breath Sounds Auscultated over the Lung Peripheries
Bronchial breath sounds are present when sounds are heard during inspiration and expiration and are of the same intensity and duration. It is distinctly abnormal to hear bronchial breath sounds instead of vesicular breathing over the lung peripheries. Bronchial breathing occurs when patent airways are surrounded by fluid-filled or consolidated adjacent lung tissue, thus allowing for better transmission of breath sounds from the large bronchi to the lung peripheries. Common conditions in which vesicular breath sounds are replaced by bronchial breath sounds are pneumonia, the acute respiratory distress syndrome (ARDS) or fluid overload states.
220.127.116.11 Diminished or Absent Breath Sounds
The volume or intensity of breath sounds physiologically depends on several factors including the thickness of the chest wall as well as the velocity and amount of air entering the lungs. This explains, for example, why only diminished breath sounds may be heard in obese patients or those with a small tidal volume [e.g. during shallow breathing or (lung protective) mechanical ventilation]. As often painfully experienced, the quality and type of the stethoscope can dramatically influence the perceived volume of breath sounds, too. When auscultating patients in the recumbent position, it is physiologic that less air enters the basal versus the upper parts of the lung physiologically, resulting in diminished breath sounds in dependent lung fields. This is especially pronounced during controlled mechanical ventilation where inspiratory airflow is generated by positive instead of negative pressure and air is mostly distributed to non-dependent lung areas.
Furthermore, several pathologic conditions (e.g. emphysema) can reduce the volume of breath sounds. As no air enters collapsed lung tissues (atelectasis), (bronchial) breath sounds over these lung areas are diminished. As the breath sounds heard are transmitted from adjacent lung segments, substantial parts of the lungs (e.g. large parts of a lobe) need to be collapsed and unaerated before breath sounds cannot be heard anymore. Air or fluid in the pleural space also diminishes the intensity of breath sounds. In the majority of patients with a pneumothorax, pleural air evenly encases (and compresses) the lung. This leads to diminished and distant or, in a large pneumothorax, absent breath sounds over the affected hemithorax. Due to the aforementioned fact that breath sounds are transmitted from adjacent lung segments, breath sounds from the contralateral lung can be heard over the parasternal chest wall even in patients with a pneumothorax. Another important cause for absent breath sounds over one hemithorax is (unnoted) bronchial intubation and one-lung ventilation. Even though the amount of pleural fluid collections may be massive (e.g. in severe haemothorax), it is unusual that breath sounds are diminished or absent over the entire hemithorax. As fluid collects in the dependent areas of the pleural cavity, breath sounds are typically diminished or absent over these parts. Compression atelectasis commonly accompanies pleural effusions. In some patients, fine crackles are heard over the transition zone between compressed and aerated lungs and are indicative of the lung segments which open and collapse during each respiratory cycle. Differentiating between pleural effusion and atelectasis by auscultation alone is difficult. In awake and cooperative patients, it may help to test for transmission of voice. If the patient says “eee” and the examiner hears “aaa” over the affected lung part, atelectasis rather than effusion is likely present. This phenomenon is referred to as aegophony and results from enhanced transmission of sound through consolidated or non-aerated lung tissue, in contrast to pleural fluid (may also be heard where fibrotic lung is present).
Crackles have formerly been referred to as crepitations or rales. Currently, the term crackle is the preferred terminology. Crackles refer to high-pitched, clicking or crackling non-musical breath sounds which are heard during inspiration. Depending on their occurrence during inspiration, they are divided into early or late crackles. Generally, crackles are produced by explosive opening of alveoli or distal airways during inspiration. Crackles heard during early inspiration result from the popping open of airways >2 mm in diameter and are lower-pitched than late or pan-inspiratory crackles. Early inspiratory crackles sound coarse and are encountered in patients with bronchopneumonia, bronchitis, COPD or bronchiectasis. Late- or pan-inspiratory crackles are finer, higher-pitched and result from opening of collapsed alveoli during inspiration. Alveolar diseases such as pneumonia, lung oedema or interstitial lung disease/fibrosis are characteristic pathologies resulting in late- or pan-inspiratory crackles. In contrast to lung oedema and interstitial lung disease/fibrosis, pneumonia results in localized crackles often accompanied by rhonchi (or retained secretions). While crackles resulting from alveolar pulmonary oedema have been compared to the sound of a strand of hair being rolled between the fingers, crackles in patients with interstitial lung diseases/fibrosis (e.g. idiopathic pulmonary fibrosis) have been compared to the sound made by Velcro being pulled apart. Interestingly, crackles cannot be heard in all patients with pulmonary fibrosis. This seems to depend on the underlying pathology of fibrosis, as crackles are heard in almost every patient with idiopathic pulmonary fibrosis (which causes fibrotic changes of the terminal bronchioli and alveoli) but only a minority of those with pulmonary fibrosis from sarcoidosis (which causes fibrotic changes alongside the bronchovascular bundle but not the terminal small airways).
Rhonchi are low-pitched (coarse), snoring, vibrating and sometimes gurgling breath sounds. They are typically heard during both inspiration and expiration but are usually louder during expiration. Partial obstruction of medium-sized and large airways by liquids or semi-solid materials (mostly thick secretions) is the most common pathology resulting in rhonchi. These sounds are sometimes also referred to as retained secretions.
A wheeze is a highly characteristic continuous musical, squeaking or whistle-like breath sound heard during expiration. Wheezing results from significant (>50%) narrowing of smaller airways. It can be localized or heard over both lungs. A localized wheeze is commonly monophonic (produced by a single tone) and results from the obstruction of a single (larger) airway, for example, by a tumour, mucus plug, foreign body or compression by a mediastinal mass. In few but notable cases, the distal opening of the endotracheal tube (without a Murphy’s eye) directly faces the posterior wall of the trachea which intermittently obstructs the tube during expiration resulting in severe prolongation of expiratory airflow and a monophonic wheeze. Similarly, a monophonic wheeze can be heard over both lungs in patients with vocal cord dysfunction who present with asthma-like symptoms. A wheeze that can be heard over both lungs is usually polyphonic as it results from several tones due to narrowing of different sized and located airways (“concertus asthmaticus”). Multiple conditions can cause airway narrowing, of which the archetypical is bronchoconstriction due to asthma or anaphylaxis. In critically ill patients, the most common conditions associated with a wheeze are COPD, pulmonary fluid overload and left heart failure. It is important to note that in severe small airway obstruction (e.g. severe asthma attack or COPD exacerbation) or with very low airflows (e.g. low tidal volumes in respiratory decompensation or (ultra)lung-protective ventilation), the volume of wheezing is reduced or even absent (“silent chest”). However, pitch and length of the wheeze correlate with the severity of expiratory airflow obstruction.
18.104.22.168 Pleural Friction Rub
The pleural friction rub is a characteristic brushing sound which resembles the sound that occurs when walking on snow or rubbing two pieces of leather together. It is caused by inflammation (pleuritic) or irritation of the visceral and/or parietal pleura. In contrast to crackles, the pleural friction rub is heard during both inspiration and expiration and usually localized to a rather small area. A pleural friction rub is rarely encountered in critically ill patients but can occasionally be heard in patients with pneumonia or those with a recent pulmonary embolism. In patients with pleural drains of larger size (>20 Charrière) and under negative pressure, a squeaking friction rub may be heard. In patients with bronchopleural fistula and a chest drain in place, the bubbling of the air exiting over the water seal is often heard distally on auscultation.
5.5 The Physical Examination in Relation to Intubation and Extubation
5.5.1 Recognition of the Anatomically Difficult Airway: The LEMON Approach
Anatomical signs suggestive of a potentially difficult airway
Difficult mask ventilation
Difficult laryngoscopy and intubation
• Age > 55 years
• Body mass index >26
• Lack of teeth
• Presence of beard
• History of snoring
• Airway obstruction
• Prominent upper incisors
• Large tongue (Fig. 5.25)
• Short and thick neck
• Facial trauma or burn
• Previous tracheostomy
• Previous airway surgery/radiation
• Upper airway obstruction (stridor!)
• Oropharyngeal or neck masses
• Craniofacial syndromes
The 3-3-2 examination technique
Interpretation if “no”
Do THREE (patient-sized) fingers fit between the incisors?
Insertion of laryngoscope and laryngoscopy likely difficult
Volume of submandibular space
Do THREE (patient-sized) fingers fit between the mentum and hyoid bone?
Laryngoscopy likely difficult
Location of the larynx
Do TWO (patient-sized) fingers fit between the hyoid bone and thyroid cartilage?
Laryngoscopy and intubation likely difficult
5.5.2 Clinical Indicators of Endotracheal Tube Position
The only reliable methods to confirm correct endotracheal tube position are direct visualization (bronchoscopy or direct laryngoscopy) and end-tidal carbon dioxide measurement. The clinical examination can only suggest correct and more importantly incorrect tube placement. It can be used in addition to or in the event that the aforementioned techniques are not available or have not yet been installed.
If the endotracheal tube is advanced too far, its tip usually enters the right main stem bronchus resulting in hypoventilation of the left lung. It is difficult to determine the endobronchial position of the tip of the tube by clinical examination alone. As a small air leak between the inflated balloon and the tracheal bifurcation often exists despite of the tube’s tip being positioned in the right bronchus, diminished breath sounds can often be heard over the contralateral (mostly left) lung on auscultation. Only in rare instances, when the tube is advanced far enough for the balloon to obliterate the entire right or left main stem bronchus, are contralateral breath sounds absent. In addition to observation of chest movements and bilateral auscultation, verifying the insertion depth of the tube as 20–21 cm in females and 22–23 cm in males rendered the highest sensitivity and specificity to detect endobronchial intubation .
Importantly, the clinical examination can help to recognize oesophageal tube misplacement. Unless spontaneous ventilation is maintained during intubation, absence of chest movements and development or worsening of cyanosis despite ventilation must primarily be considered a sign of oesophageal tube misplacement. While delivery of breaths to the oesophagus with a ventilation bag can feel similar to delivery of breaths to the lungs, air is not expired or only at a much slower rate from the stomach/oesophagus than from the lungs. This is then typically associated with gurgling sounds. Entrance of gastric juice into the tube (be sure not to mistake it for lung oedema!) during expiration is another sign that is highly suggestive of oesophageal intubation (unless tracheal aspiration of gastric content has occurred before). Expiratory misting of the tube is usually absent in oesophageal intubation but has anecdotally been observed after large amounts of gastric air exit through the tube during release of positive pressure.
5.5.3 Assessing Preparedness for Extubation
Certain absolute and relative criteria need to be present so that a patient can be extubated safely. The absolute criteria include sufficient spontaneous gas exchange, the presence of upper airway reflexes and adequate cough strength. Although several scores and cut-off values have been suggested to predict successful extubation, it is clinically difficult to apply single values to all patients. While it is fairly easy to assess adequate oxygenation with the use of arterial oxygen saturation and/or blood gas analysis on reasonable ventilator settings (FiO2 < 0.45(−0.5), PEEP < 7 cm H2O), evaluation of adequate spontaneous ventilation primarily relies on clinical skills. In clinical practice, this is achieved by close observation of the patient for signs of respiratory distress, an increased work of breathing or a pathologic breathing pattern either during a spontaneous breathing trial or on an augmented spontaneous ventilation mode. It is advisable to take at least 1 min or longer to observe the patient, particularly those who have been ventilated for several days. Although a respiratory rate < 25 breaths per minute on reasonable ventilatory support should be present in the majority of patients, some individuals can be extubated successfully at higher respiratory rates. These subjects are typically alert and have a poor tube tolerance or an underlying restrictive lung process necessitating higher respiratory rates. Finally, the patient’s own estimation whether he or she can breathe without the tube often helps to predict whether the extubation will be successful or not.
Although it is preferable to have the patient alert and cooperative at extubation, this is—against common belief—no absolute criterion for extubation. In some patients with a rapidly reversible neurological condition (e.g. mild or moderate brain trauma, intoxication, delirium) and well-maintained upper airway reflexes, prolonged sedation and ventilation may carry higher risks than early extubation. However, this must be individually evaluated and a risk-benefit assessment considered.
While “overhang” of opioids or sedatives is indicated by a depressed mental state or a distinct breathing pattern (opioids: delayed onset of spontaneous breathing followed by bradypnea with high tidal volumes), it is more difficult to recognize residual neuromuscular blockade. Recognition of the latter is essential as it commonly results in immediate respiratory decompensation after extubation or impaired airway control with an increased risk of delayed tracheal (micro)aspiration and pneumonia. The population at highest risk for residual neuromuscular blockade is critically ill patients after surgery. Important determinants are timing, type and dosage of the neuromuscular blockade agent administered. Hepatic and renal dysfunction can delicately impair the clearance of neuromuscular blocking agents and lead to a prolonged time to full recovery of neuromuscular capacity. Similarly, obesity is a clinical risk factor as patients typically receive higher doses although their muscle mass is only slightly increased. In addition, obese patients are specifically sensitive to any degree of residual neuromuscular blockade. Before extubation, an in-depth physical evaluation alone is not sensitive enough to detect mild degrees of residual neuromuscular blockade. This can only be achieved by quantitative neuromuscular monitoring (e.g. the train-of-four testing). When assessing the patient’s muscular force, it needs to be taken into account that the diaphragm and pharyngeal musculature are exclusively sensitive to neuromuscular blockade and recover last. Therefore, recovery of full peripheral muscle strength (e.g. strong hand squeeze or ability to move extremities particularly in response to external stimuli such as suctioning) must not be used to exclude residual neuromuscular blockade. Similarly, an adequate tidal volume is a highly unreliable marker of full neuromuscular recovery. The best clinical method appears to be the ability to lift the head off the cushion or pillow for at least 5 s. If the patient is extubated despite (unrecognized) residual neuromuscular blockade, a typical clinical picture is seen. Patients immediately obstruct their airways or take shallow breaths which can only be elicited by twitchy movements of the accessory respiratory muscles. This often leads to synchronous small forward movements of the head and chin. Patients are awake, typically frightened and unable to speak.
If upper airway obstruction is considered a risk, the cuff leak test can be performed with the patient still intubated. Given the high odds of false-negative results and the associated risk of unnecessarily prolonging mechanical ventilation, the cuff leak test should only be performed in a highly selected group of critically ill patients. During positive pressure ventilation, the cuff of the endotracheal tube is deflated and the examiner listens for gurgling sounds of air exiting next to the tube. It is important to make sure that the patient’s head is placed in a neutral position as otherwise the position of the head can obstruct the upper airway, particularly in obese patients. An air leak should be audible at peak inspiratory pressures of 20 mbar or lower. The absence of an audible air leak during a correctly performed cuff leak test is a sensible indicator of upper airway compromise or obstruction. If an air leak can only be heard when the patient coughs (which is frequent after deflating the cuff) but not during assisted breathing, the cuff leak test must be considered negative. It should be noted, however, that if an air leak is present, it cannot be safely assumed that the upper airway will be uncompromised after extubation. Performance of the tube occlusion test can increase the predictive value of a positive cuff leak test. During this test, the tube is occluded while the balloon of the tube is still deflated. The patient is then asked to take a deep breath. If inspiration results in visible chest wall expansion, the risk that the upper airways are unobstructed is minimal.
5.5.4 Screening for (Post-extubation) Dysphagia
Oropharyngeal dysphagia is frequent in critically ill patients, particularly after long-term (>48 h) intubation, in the elderly or those with a neurological disease (e.g. stroke) or neuromuscular disease. It is an important contributor to morbidity (hospital-acquired pneumonia) and mortality in these patients. Early recognition of dysphagia is essential. The clinical examination plays a crucial role as a screening tool to trigger definite diagnostic procedures typically including fiberoptic endoscopic evaluation of swallowing or barium swallow. Inability of the patient to swallow resulting in retained oral saliva and secretions is a straightforward diagnosis. However, in the majority of patients with swallowing disorders, symptoms are more subtle. The water swallow test is a valid method with a moderate sensitivity but an acceptable specificity to diagnose dysphagia. The alert patient is placed in the sitting position and offered one or more sips (<20–30 mL) of water to drink. The swallowing process is closely observed for obvious dysfunction (e.g. multiple swallow attempts, water drooling from mouth, non-elevation of larynx) and the patient monitored for coughing, choking, change in voice or throat clearing. Any of these signs strongly suggests the presence of dysphagia and should lead to definite diagnostic tests. In patients with a tracheostomy, the water-swallowing test can be modified. The balloon of the tracheal tube is deflated and the patient offered coloured (e.g. with methylene blue) water to drink. The same observation as described with the standard water-swallowing test is then performed. At the end of the test, the patient is suctioned endotracheally and secretions inspected for the presence of coloured secretions. Sometimes the coloured water also exits from the tracheostoma site and confirms the diagnosis dysphagia.
5.6 Clinical Evaluation of the ECMO Circuit
Inspection and palpation are important techniques to monitor the extracorporeal membrane oxygenation (ECMO) circuit. A detailed daily inspection of all circuit components for integrity and adequate function is obligatory. Similarly, dressings and wounds must be inspected for signs of oozing or bleeding as indicators of (acquired) coagulopathy. Relevant haemolysis can rapidly be recognized at the bedside by checking whether the urine or haemofiltrate are rose coloured. Even though the ECMO circuit may be looked after by a dedicated perfusionist, the (intensive care) physician must be able to perform this examination, too.
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