2Department of Anesthesiology, Perioperative Medicine and General Intensive Care, Salzburg University Hospital and Paracelsus Private Medical University, Salzburg, Salzburg Austria
3Medical Intensive Care Unit and Centre of Haemostaseology, University Hospital Leipzig, Leipzig, Germany
4Divisions of Critical Care and Pulmonology, Department of Medicine, Charlotte , Maxeke Johannesburg Academic Hospital and Faculty of Health Sciences University of the Witwatersrand, Johannesburg, South Africa
Martin W. Dünser, Email: ta.ca.dem-i@resneud.nitram.
.
Martin W. Dünser,
Martin W. Dünser
5Department of Anesthesiology and Intensive Care Medicine, Kepler University Hospital, Johannes Kepler University Linz, Linz, Austria
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Daniel Dankl
6Department of Anesthesiology, Perioperative Medicine and General Intensive Care, Salzburg University Hospital and Paracelsus Private Medical University, Salzburg, Austria
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Sirak Petros
7Medical Intensive Care Unit and Centre of Haemostaseology, University Hospital Leipzig, Leipzig, Germany
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Mervyn Mer
8Divisions of Critical Care and Pulmonology, Department of Medicine, Charlotte Maxeke Johannesburg Academic Hospital and Faculty of Health Sciences University of the Witwatersrand, Johannesburg, South Africa
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Disclaimer
5Department of Anesthesiology and Intensive Care Medicine, Kepler University Hospital, Johannes Kepler University Linz, Linz, Austria
6Department of Anesthesiology, Perioperative Medicine and General Intensive Care, Salzburg University Hospital and Paracelsus Private Medical University, Salzburg, Austria
7Medical Intensive Care Unit and Centre of Haemostaseology, University Hospital Leipzig, Leipzig, Germany
8Divisions of Critical Care and Pulmonology, Department of Medicine, Charlotte Maxeke Johannesburg Academic Hospital and Faculty of Health Sciences University of the Witwatersrand, Johannesburg, South Africa
Martin W. Dünser, Email: ta.ca.dem-i@resneud.nitram.
.
Copyright © Springer International Publishing AG, part of Springer Nature 2018
This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization [WHO] declaration of COVID-19 as a global pandemic.
Abstract
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.
Inspection
Body Position
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.
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Fig. 5.1
Critically ill patient with acute heart failure and respiratory distress at admission to the intensive care. Courtesy of Martin W. Dünser, MD. Note the sitting position and the pillows placed under the back of the patient to relieve dyspnoea. Furthermore, note the tanned appearance of the patient [obviously from sunbathing] indicating the patient has been active until before this episode of acute illness
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].
Patients with acute asthma or an exacerbation of chronic obstructive pulmonary disease [COPD] feel most relief from dyspnoea when sitting and leaning forward with their arms stemmed on their knees or the bed [Fig. 5.2]. This position allows maximizing respiratory muscle contraction. Patients with COPD who regularly take this position may develop hyperkeratosis of the skin over the knees and distal thighs [Dahl sign].
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Fig. 5.2
Typical body position taken by a patient with an acute asthma attack. Courtesy of Martin W. Dünser, MD
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.
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.
Patients with multiple rib fractures can present with an unstable chest wall [“flail chest”]. This is particularly common in patients in whom several adjacent ribs of the anterior or lateral chest wall have fractured into one or more free pieces [Fig. 5.3]. This chest wall segment then moves inwards during spontaneous inspiration and outwards during expiration delicately compromising chest wall mechanics and possibly gas exchange [which is usually impaired due to concomitant underlying lung damage or contusion; see Fig. 5.3]. In patients with large freely moving chest wall components, a mediastinal shift [or “flutter”] may occur with changes of intrathoracic pressures over the respiratory cycle and cause additional hemodynamic instability. In most cases, an unstable chest can be recognized by inspection of the [anterior or lateral] chest wall. Palpation with the examiner’s palms placed over the anterior and lateral chest wall helps to detect smaller flail segments. In mechanically ventilated patients, positive airway pressure prevents the free chest wall part from moving inwards during inspiration, thus stabilizing the chest wall. In these patients, freely moving chest wall parts can only be detected by meticulous palpation. Abnormal or paradoxical chest movements may be observed in patients after cardiac surgery with sternal infection and instability. In some of these patients, partial or total sternectomy with muscle flap reconstruction is performed leaving them with a chronic unstable chest which is obvious on clinical inspection, as the muscle flap typically moves inwards during inspiration and outwards during expiration.
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Fig. 5.3
Flail chest in a patient with serial lateral rib fractures with a large mobile chest wall segment and corresponding chest computer tomography scan. Courtesy of Martin W. Dünser, MD
Skin Colour
Central cyanosis characteristically affects the lips, oral/sublingual mucosa and tongue [Fig. 5.4]. It reflects severe hypoxaemia but can also be seen in patients with meth- [>1.5 g/dL, brownish hue or “chocolate” cyanosis] or sulfhaemoglobinemia [>0.5 g/dL]. Central cyanosis becomes visible if the absolute quantity of capillary/venular blood in the lips or oral mucosa exceeds 4.25 g/dL [>2.38 g/dL in the arterial blood] of deoxygenated haemoglobin. In non-anaemic patients, this corresponds to an arterial oxygen saturation of approximately 80%. Clinical recognition of central cyanosis can be tricky with false-positive and false-negative results. In anaemic patients, hypoxaemia must be more profound before central cyanosis develops. For example, in patients with a haemoglobin concentration of 7.5 g/dL [e.g. as may occur in patients in the intensive care unit], central cyanosis only becomes detectable when oxygen saturation drops to values 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 [ 80–90 mmHg or >10–12 kPa] and/or hypoxia [PaO2 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.
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.
Palpation
Chest palpation can reveal important additional information. A common palpation technique in critically ill mechanically ventilated patients is to place the examiner’s palm on the upper sternum [Fig. 5.17]. When large enough in amount, tracheobronchial secretions cause bubbling vibrations that can be felt through the chest wall, particularly during expiration. Less frequently and mostly only in asthenic patients can the much finer vibrations of lung oedema be felt when the palm is placed over the lower lateral chest wall [Fig. 5.18]. Palpation is also useful to evaluate the symmetry of chest wall expansions. This can be done by placing both hands around the chest or over the subcostal angle [Fig. 5.19]. Tactile fremitus refers to vibrations felt by the examiner with both palms placed over the chest as the patient speaks [e.g. saying “99”]. As non-aerated lung tissue transmits vibrations better than aerated lung parts, tactile fremitus is more pronounced over consolidated as compared to aerated lung fields. Tactile fremitus is absent over areas of pleural effusion or pneumothorax. This examination technique only detects large consolidations and is rarely applicable in critical care.
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Fig. 5.17
Palpation for the presence of large amounts of tracheobronchial secretions. Courtesy of Martin W. Dünser, MD
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Fig. 5.18
Palpation for the presence of alveolar lung oedema. Courtesy of Martin W. Dünser, MD
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Fig. 5.19
Assessing the symmetry of chest wall expansions by palpation. Courtesy of Martin W. Dünser, MD. [a] Palpating both lateral chest walls with the examiner’s hands; [b] placing the examiner’s hands over the subcostal angle
Palpation of subcutaneous air is a unique sensation and often generates a distinctive sound [“crepitus”]. In severe forms of subcutaneous [or surgical] emphysema, this “crepitus” may lack as subcutaneous tissue layers are splinted too far apart. It is specific for the presence of subcutaneous emphysema which may accompany pulmonary barotrauma. Significant amounts of air have already collected in the subcutaneous tissues, once it can be palpated first. Subcutaneous emphysema can develop rapidly, occasionally even within only a few minutes. Development of subcutaneous emphysema in trauma patients [e.g. already at scene] or after surgery is often caused by a bronchial injury and significant air leak. Extensive subcutaneous emphysema is an obvious clinical diagnosis as air commonly distributes to areas of the body where there is soft subcutaneous tissue [e.g. the face and in particular the eyelids—Fig. 5.20]. Pneumomediastinum can be felt by palpation of the jugulum and supraclavicular tissue. In clinical practice, it is most frequently encountered in postoperative cardiac or thoracic surgical patients. Usually, subcutaneous emphysema subsides within a few hours to days following pleural or mediastinal drainage. Persistence or progression must always be considered as a sign of an ongoing air leak.
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Fig. 5.20
Typical features of subcutaneous/surgical emphysema in a patient with chest trauma and pulmonary barotrauma. Courtesy of Martin W. Dünser, MD
Another feature that may be detected by chest wall palpation is a warmer skin over a pleural empyema. In patients with chest pain, palpation of the costal cartilages may reveal the costochondral junction or Tietze syndrome as an important differential diagnosis in patients with acute chest pain. Finally, palpation of the trachea and its position can assist in the recognition and assessment of severe barotrauma [Fig. 5.21]. In patients with tension pneumothorax or large pleural effusion, the trachea can be deviated to the contralateral side; in patients with total lung collapse/volume loss/atelectasis, or fibrosis, to the ipsilateral side.
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Fig. 5.21
Palpation of the position of the trachea. Courtesy of Martin W. Dünser, MD
Palpation is one of the key techniques to examine the chest in patients sustaining severe trauma. In order to detect rib and sternal fractures, the chest wall is palpated for bony crepitus over both infraclavicular areas and the sternum [Fig. 5.22]. Bimanual lateral compression of the mid- and lower chest induces localized pain in awake patients with rib fractures [Fig. 5.23]. In unconscious or sedated patients, fractures of single ribs are difficult to diagnose, particularly if fractures are posterior. In spontaneously breathing patients, flail chest wall segments are discerned by placing the examiner’s hands over the lateral and anterior chest wall while feeling for paradoxically moving segments [Fig. 5.24]. In patients who are mechanically ventilated, flail chest wall segments cannot be palpated since flail segments do not move paradoxically as pleural pressure remains positive over the respiratory cycle. In these patients, all areas of the chest wall need to be meticulously examined by digital compression. Flail segments are identified by mobility and inward movement on compression. In case a mini-thoracotomy/thoracostomy is performed [Fig. 5.25], the lung can be palpated with the finger that enters the pleural cavity. The first information obtained is whether the lung is up or down [e.g. confirming the presence of pneumothorax]. Although taking into account that only a very small area of the lung is palpated, the texture of the lung can give the examiner a rough idea of the lung injury. An uninjured or mildly traumatized lung feels tense like a balloon and quickly expands upon release of the pneumothorax. A severely contused lung feels slippery and has the consistency of a blood clot. Despite release of air from the pleural cavity, it does not expand at all or only incompletely and with a significant delay.
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Fig. 5.22
Palpation of the sternum to detect sternal fracture and/or instability. Courtesy of Martin W. Dünser, MD
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Fig. 5.23
Lateral chest compression to screen for rib fractures and/or a flail chest. Courtesy of Martin W. Dünser, MD
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Fig. 5.24
Palpation techniques to detect a flail chest in the spontaneously breathing [a] and mechanically ventilated patient [b] Courtesy of Martin W. Dünser, MD
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Fig. 5.25
Digital palpation of the lung in a patient with severe chest trauma during thoracostomy and placement of a chest drain. Courtesy of Martin W. Dünser, MD
Percussion
Percussion of the chest is only a meaningful examination technique when it can be performed in an acceptably quiet setting. It requires experience to correctly interpret its findings. Percussion is performed by placing the [second or] third finger of the examiner on the anterior chest wall and firmly [=firmly!] tapping its distal segment with one finger of the other hand [Fig. 5.26]. The sound produced by this can be classified as normal, hyperresonant or dull. A hyperresonant sound is higher in pitch, somehow “hollow” [tympanic] and can be heard over a pneumothorax, large bullae or in patients with COPD. It is extremely helpful to confirm hyperresonance by comparing it to the percussion sound of the contralateral hemithorax. Percussion over pleural effusions or large lung consolidations results in a dull and short resonance. A “stony dull” percussion note typically implies a pleural effusion. While percussion to test for pneumothorax or total lung atelectasis is performed over the anterior chest wall, the posterior or lateral chest wall [in the sitting position] is percussed in case a pleural effusion or lung consolidation is suspected. Percussion sounds in patients with lung emphysema and/or large anterior bullae are equally hyperresonant but less tympanic than in patients with a [large] pneumothorax.
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Fig. 5.26
Percussion of the anterior chest wall to differentiate between a pneumothorax and [total] lung collapse. Courtesy of Martin W. Dünser, MD
The Physical Examination in Relation to Intubation and Extubation
Recognition of the Anatomically Difficult Airway: The LEMON Approach
There are multiple reasons why establishing a safe airway [anatomical, physiologic, process-related] can be [terrifyingly] difficult. The clinical examination is crucial to recognize the anatomically and physiologically difficult airway and thus induce appropriate subsequent preparations. No clinical sign alone is sensitive or specific enough though. A reliable prediction of an anatomically difficult airway can be achieved by using the LEMON approach. This mnemonic stands for Look, Evaluate, Mallampati, Obstruction and Neck mobility. Clinical signs to be looked for are summarized in Table 5.4. Evaluation includes the 3-3-2 examination technique [Table 5.5 and Fig. 5.27]. Although the Mallampati score was first described in the sitting patient during preoperative evaluation and has not been validated in critically ill patients, it is worthwhile assessing. The patient is asked to protrude the tongue as far as possible while saying “aah”. The visibility of the soft palate and uvula is then inspected and graded into four classes [Fig. 5.28]. While the chances for uncomplicated laryngoscopy and intubation are high in class one, the risk of a difficult laryngoscopy is significant in classes three and four. Neck mobility must only be assessed in patients without cervical spine instability and thus not in all critically ill patients, particularly not those in the pre-hospital setting or emergency department. The simplest way to confirm adequate neck mobility for laryngoscopy is to passively move the patient’s head. Alternatively in awake patients, the patient can be asked to bend his head so that his/her chin touches the chest wall.
Table 5.4
Anatomical signs suggestive of a potentially difficult airway
Difficult mask ventilationDifficult 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
• Pregnancy
• Craniofacial syndromes
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Table 5.5
The 3-3-2 examination technique
Examination stepAssessment ofQuestionInterpretation if “no”1Mouth openingDo THREE [patient-sized] fingers fit between the incisors?Insertion of laryngoscope and laryngoscopy likely difficult2Volume of submandibular spaceDo THREE [patient-sized] fingers fit between the mentum and hyoid bone?Laryngoscopy likely difficult3Location of the larynxDo TWO [patient-sized] fingers fit between the hyoid bone and thyroid cartilage?Laryngoscopy and intubation likely difficult
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Be aware that the 3-3-2 rule has been developed to predict difficult laryngoscopy and intubation with the use of a conventional laryngoscope. With the advent of video laryngoscopes, new challenges arose. While visualization of the vocal cords [laryngoscopy] became easier, intubation [passing the tube through the vocal cords] can remain a challenge [remember: visualization is not intubation, S. Seidl, 2015]
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Fig. 5.27
Examination steps of the 3-3-2 examination technique to recognize the anatomically difficult airway. Courtesy of Sirak Petros, MD. See Table 5.5 for explanations
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Fig. 5.28
Mallampati classification
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.
Bilateral chest wall expansion and/or auscultation of bilateral breath sounds in synchrony with mechanical ventilation usually indicates correct endotracheal tube position in the non-breathing patient but is unreliable if the patient maintains spontaneous breathing over the intubation process. In the latter patient, expiratory airflow can be felt at the end of the tube to confirm endotracheal tube position. A fast screening method involves firmly placing the examiner’s fingers into one anterior intercostal space of the left hemithorax [Fig. 5.29]. Delivery of a firm breath with a ventilation bag results in synchronous lung expansion which can be felt with the finger tips [yellow arrow].
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Fig. 5.29
Rapid screening technique to assess endotracheal tube placement at the first breath with the ventilation bag [see yellow arrow and text for explanation]. Courtesy of Martin W. Dünser, MD
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.
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