Indications

A ‘routine’ preoperative chest x-ray (CXR) is not necessary unless there are specific indications (see NICE Guidelines1). Management is changed as a result of less than 1% of preoperative films, increasing as the American Society of Anaesthesiologists (ASA) score rises. Acute change in cardiac/respiratory signs or symptoms is the only undisputed indication in elective nonthoracic surgery. Similarly there seems to be no clear advantage to a ‘routine’ chest x-ray in the intensive care unit (ICU).

The chest x-ray is an essential part of the trauma series and is considered an important adjunct in the diagnosis of chest wall fractures, pneumothorax, haemothorax, and injuries to the heart and great vessels.

How it is done

The standard view is the posteroanterior (PA) film, with the patient facing the cassette and the x-ray tube 2 m away. An anteroposterior (AP) film is taken when the patient is unable to stand, with the cassette behind the patient. In the AP chest x-ray the heart will be magnified, and it is inappropriate to comment on cardiomegaly (unless it is gross) on this basis. A PA view shows the scapulae clear of the lungs whilst in AP they always overlap.

Interpretation

The chest x-ray (Fig. 2.1) is a two-dimensional representation of a three-dimensional structure. An understanding of chest anatomy is essential to interpretation of plain chest x-ray abnormalities.

Fig. 2.1 Posteroanterior chest x-ray (A) with diagrammatic annotation (B). The hilum is higher on the left but the hemidiaphragm is lower. The carina is at T4 on expiration and T6 on inspiration.

Owing to the routine use of CT scanning, the lateral chest x-ray and decubitus film are now rarely seen. A lateral x-ray may differentiate structures that are unclear on PA chest x-ray. A decubitus film is taken with the patient on his or her side to assess:

Abnormalities of the lung

Consolidation – infiltration of the alveolar space by inflammatory tissue. The classic example is pneumonia – airspace disease and consolidation, which is not usually associated with volume loss. There may be an associated (parapneumonic) effusion.

The silhouette sign – an interface between isodense structures in contact with each other. The radiographic distinction between anatomical borders of lung and soft tissue can be ‘lost’ by abnormalities of the lung, which increase its density.

Air bronchogram – when the air spaces fill with pus or fluid, the alveoli fill first with the bronchi being relatively spared, therefore the bronchi stand out. This is called an air bronchogram and is a sign of airspace disease such as consolidation, pulmonary oedema or atelectasis.

Atelectasis: a linear increased density and volume loss on chest x-ray. Some indirect signs of volume loss include vascular crowding or mediastinal shift towards the collapse. There may be compensatory hyperinflation of adjacent lobes, or hilar elevation (upper lobe collapse) or depression (lower lobe collapse).

Interstitial disease

The interstitial space surrounds bronchi, vessels and groups of alveoli. Disease in the interstitium manifests itself by reticulonodular shadowing (criss cross lines or tiny nodules or both). The main two processes affecting the interstitium are accumulation of fluid (pulmonary oedema) and inflammation leading to fibrosis (Fig. 2.2 and Box 2.1).

Fig. 2.2 Pulmonary oedema: diffuse hazy shadowing in a bat-wing distribution and upper lobe blood diversion.

Pulmonary oedema may be cardiogenic or noncardiogenic. In congestive heart failure, the pulmonary capillary wedge pressure (PCWP) rises and the upper zone veins dilate – this is called upper zone blood diversion. With increasing PCWP, interstitial oedema occurs with the appearance of Kerley B lines and prominence of the interlobar fissures. Increased PCWP above this level causes alveolar oedema, often in a classic perihilar ‘bat wing’ pattern. Pleural effusions also occur. Unusual patterns may be found in patients with chronic obstructive pulmonary disease (COPD) who have predominant upper lobe emphysema.

A helpful mnemonic for noncardiogenic pulmonary oedema is NOT CARDIAC: near-drowning, oxygen therapy, transfusion or trauma, CNS disorder, ARDS, aspiration, or altitude sickness, renal disorder, drugs, inhaled toxins, allergic alveolitis, contrast or contusion.

COPD is often seen on CXR as diffuse hyperinflation with flattening of diaphragms and enlargement of pulmonary arteries and right ventricle (cor pulmonale). In smokers the upper lung zones are commonly diseased.

Abnormalities of the mediastinum

On the PA film, the heart takes up to half of the total thoracic measurement in adults (more in children).

In mediastinal deviation, tension pneumothorax and pleural effusion push the mediastinum away; lung collapse pulls it towards the affected side.

Findings for pneumomediastinum include streaky lucencies over the mediastinum that extend into the neck and elevation of the parietal pleura along the mediastinal borders.

Causes of pneumomediastinum include:

Pericardial effusion causes a globular enlarged heart shadow. More than 400 mL of fluid must be in the pericardium to lead to a detectable change on plain x-ray. If it is chronic then there may be little functional impairment. An echocardiogram is indicated to detect impairment in right ventricular diastolic filling and to guide drainage.

Abnormalities of the hila and pulmonary vessels

Enlarged hila could be due to an abnormality in any of the three structures that lie there:

Pleural abnormalities

Pneumothorax

A pneumothorax is air inside the thoracic cavity but outside the lung. It appears as air without lung markings in the least dependent part of the chest. It is best demonstrated by an expiration film. It can be difficult to see when the patient is in a supine position – air rises to the medial aspect of the lung becoming a lucency along the mediastinum. It may also collect in the inferior sulci causing a deep sulcus sign (Fig. 2.3).

Fig. 2.3 Left-sided pneumothorax with a deep sulcus sign.

Causes of spontaneous pneumothorax include:

• Idiopathic

• Asthma

• COPD

• Pulmonary infection

• Neoplasm

• Marfan syndrome.

A hydropneumothorax is both air and fluid in the pleural space. It is characterized by an air–fluid level on an upright or decubitus film in a patient with a pneumothorax.

Further investigations

Computed tomography (CT) scan, ventilation/perfusion (VQ) scan, etc (see below).

Limitations and complications

Indications

Fig. 2.4 A CT scan consistent with acute lung injury.

How it is done

Limitations and complications

Indications

Fig. 2.5 A ventilation/perfusion scan showing multiple perfusion abnormalities. This is suggestive of several pulmonary emboli.

How it is done

Interpretation

Further investigations

Limitations and complications

Indications

How it is done

Further investigations

Limitations and complications

Indications

Fig. 2.6 Normal spirometry. ERV, expiratory reserve volume; FRC, functional residual capacity; IC, inspiratory capacity; IRV, inspiratory reserve volume; RV, residual volume; VC, vital capacity; TLC, total lung capacity.

How FRC is measured

Interpretation

Further investigations

Limitations and complications

Indications

With flow/volume curves, occasionally used preoperatively to:

Fig. 2.7 Volume/time curves: (A) normal; (B) obstructive; (C) restrictive.

How it is done

Interpretation

Data presented as graphs and numerical data (absolute numbers, % predicted).

Further investigations

Limitations and complications

Indications

How it is done

Interpretation

Data presented as graphs and numerical data (absolute numbers, % predicted).

Normal range/graph

• Normal: Fig. 2.8A.

Fig. 2.8 Flow-volume loops in (A) normal and (B) mild intrathoracic airway obstruction.

Abnormalities

• Intrathoracic airway obstruction

– Airway compression during expiration produces a characteristic ‘curvilinear’ shape (Fig. 2.8B)

– Increasingly severe disease lowers PEFR and FVC

– Common causes: emphysema/bronchitis; asthma; bronchiectasis.

• Extrathoracic obstruction (Fig. 2.9).

Fig. 2.9 Flow-volume loops in (A) fixed and (B) variable extrathoracic obstruction.

A fixed obstruction reduces both peak expiratory and inspiratory flow rates

– On expiration, extrathoracic airway pressures are above atmospheric and hold the airway open: expiration is less affected

– On inspiration, the decreased extrathoracic airway pressures narrow the airway, hence a greater effect on inspiration

– Causes include: tracheal stenosis, laryngeal paralysis, goitre.

A variable obstruction may be held open during expiration by the above atmospheric extrathoracic airway pressures, so expiration is relatively unaffected.

Causes include pharyngeal muscle weakness of Obstructive Sleep Apnoea, laryngeal tumour

• Respiratory muscle weakness (Fig. 2.10). Lower pressure/slower rise of airway pressures cause:

– Lower, later PEFR in expiration and lower flow throughout inspiration

– Loss of large airway flow changes (‘expiratory spikes’) when the patient is asked to cough (a test rarely done clinically).

• Restrictive lung disease

– Reduced vital capacity, PEFR and accelerated emptying.

Fig. 2.10 Flow-volume loop in (A) respiratory muscle weakness and (B) restrictive disease.

Further investigations

Limitations and complications

Indications

How it is done

Interpretation

Further investigations

Limitations and complications

Indications

Pulse oximetry is a minimum monitoring standard for anyone undergoing anaesthesia or sedation. It is used in recovery, any high dependency or intensive care situation, anyone with respiratory or cardiovascular compromise, or any patient considered likely to deteriorate. Pulse oximeters also measure pulse rate and estimate pulse regularity; thus they are used as an intermittent observation for any hospital inpatient. It is also used after plastic or orthopaedic surgery distal to the affected site, as a surrogate marker of perfusion.

Physiological principles

Oxyhaemoglobin absorbs different light wavelengths compared to deoxyhaemoglobin. The wavelength of light absorbed corresponds to the degree of oxygenation of the haemoglobin.

How it is done

A source of light comes from a probe (on the finger or ear) at two wavelengths (usually 650 nm and 805 nm). The light is partially absorbed by haemoglobin, by amounts which differ depending on how much saturated with oxygen it is. By calculating the absorption at the two wavelengths, a processor can display the proportion of haemoglobin that is oxygenated. The processor subtracts the non-pulsatile part, leaving only the arterial component.

Interpretation

Oxygen saturation is expressed as a percentage of oxygen content of haemoglobin, as a proportion of oxygen capacity of haemoglobin. Normal ranges are 97–100% for a healthy subject breathing room air. Any form of cardiac or respiratory disease may reduce it.

Management principles

A low SpO₂ in the absence of artefact indicates that the oxygen saturation of arterial blood is poor. This should be corrected depending upon the underlying cause; increasing the fractional inspired oxygen concentration (FiO₂) may be helpful in the absence of shunt.

Limitations and complications

Pulse oximetry is subject to inaccuracies. Artefact may be caused by flickering overhead lights, shivering, poor arterial pulsation, certain nail varnishes or inks, and the presence of carbon monoxide (carboxyhaemoglobin tends towards an oximeter reading of 100%) and methaemoglobinaemia (tends towards 85%). A venous pulsation due to tricuspid regurgitation will cause low readings.

Oxygen saturation is not a marker of ventilation, especially if supplemental oxygen is being administered. Similarly, one cannot comment on oxygen delivery to the tissues, which is also affected by haemoglobin concentration and cardiac output. Because the calibration is carried out on healthy volunteers, readings below 70% are inaccurate.

Indications

A requirement of minimum monitoring standards for patients undergoing general anaesthesia. It gives useful information on:

How it is done

Most commonly measured by infrared (IR) spectography. Expired CO₂ is a polyatomic gas and absorbs IR rays (specific wavelengths around 4.8 μm).

Interpretation

The amount absorbed is proportional to the concentration of the absorbing gas present. Concentration of CO₂ can be determined by comparing the measured absorbance with the absorbance of a known standard.

Data presented as

End tidal CO₂ (P_ETCO₂), expressed as partial pressure, measured in kPa or mmHg.

Physiological principles

During the respiratory cycle exhaled CO₂ produces a display of instantaneous CO₂ concentration versus time. In the healthy patient, end-tidal CO₂ (P_ETCO₂) closely approximates to arterial CO₂ (PaCO₂). CO₂ in exhaled gas is dependent on its carriage from site of production in the tissues to the lungs via the right heart (Table 2.1). Thus capnography also provides limited but useful information on cardiac output, pulmonary blood flow and the diffusion of pulmonary capillary gases. A mismatch between P_ETCO₂ and PaCO₂ may occur due to both physiological and pathological processes.

Table 2.1 Conditions affecting arterial – end-tidal CO₂ gradient

Normal range

In the healthy patient P_ETCO₂ approximates PaCO₂ (5–5.6 kPa). Figure 2.11 shows four phases of a normal capnograph trace:

Fig. 2.11 Four phases of a normal capnograph trace.

Abnormalities and management principles

See Fig. 2.12.

Fig. 2.12 (A) Baseline elevated suggests CO₂ re-breathing. Check anaesthetic circuitry and gas flow rate. (B) Slow upstroke phase 2 suggests obstruction to expiratory gas flow (e.g. asthma, bronchospasm, COPD and kinked endotracheal tube or in the presence of leaks in the breathing system). Examine patient and anaesthetic circuit. (C) Loss of plateau in phase 3 suggests differing time constants in the lung seen with COPD and emphysema. Examine and optimize patient treatment. (D) Cleft signifies return of respiratory effort during mechanical ventilation or artefact associated with abdominal movement during surgery. Check adequacy of muscle paralysis.

Indications

Hypoxaemia may be the result of shunting. Understanding its basis allows a rational approach to its correction.

How it is done

The total physiological shunt fraction can be calculated using the shunt equation, which allows calculation of the amount of venous blood bypassing ventilated alveoli and mixing with pulmonary end-capillary blood:

where CcO₂ = end-capillary O₂ content, CaO₂ = arterial O₂ content and CvO₂ = mixed venous O₂ content.

Physiological principles

When blood flow and oxygen content is known, the amount of shunt flow and its impact on systemic arterial oxygenation can be calculated. The shunt is described as a percentage of the cardiac output. Anatomical shunt exists with normal anatomy, e.g. thebesian and bronchial veins contribute a small degree of shunt in all humans by emptying into the left heart.

Abnormal anatomical shunts are best divided into pulmonary and/or extrapulmonary, e.g. pulmonary arteriovenous fistula or an atrial septal defect:

Abnormalities and management principles

In clinical practice a degree of shunting may be seen due to altered VQ matching associated with anaesthetic agent use, intermittent positive pressure ventilation (IPPV), patient positioning and hydration status. However, shunt is commonly the result of pulmonary pathology including pneumonia, atelectasis and pulmonary oedema, which during anaesthesia may prove difficult to treat. True shunts respond poorly to increased oxygen concentration, but improvement in oxygenation may be seen with attention to the conduct of anaesthesia and optimizing cardiac output, ventilatory settings including positive end expiratory pressure (PEEP) and patient positioning, thus correcting VQ inequalities.

Further investigations

Data presented as

Compliance is defined as the volume change per unit pressure change (ΔV/ΔP) (mL/cmH₂O), a measure of lung distensibility.

Physiological principles

Many diseases result in altered pulmonary elasticity, which can be measured by changes in compliance (ΔV/ΔP), or elastance (ΔP/ΔV).

During spontaneous ventilation the total compliance of the chest wall and lungs is approximately 100 mL/cmH₂O. The lung compliance is approximately 200 mL/cmH₂O. During ventilated anaesthesia, total compliance of the respiratory system is approximately 70–80 mL/cmH₂O.

Indications for measurement

How it is done

Interpretation

The lung at residual volume requires an opening pressure before inflation takes place. A lower inflection point indicates the pressure at which many collapsed alveoli are opening at the same time. Application of PEEP that is equal to or greater than the pressure corresponding to the lower inflection point results in significant alveolar recruitment and decrease in pulmonary shunt. This approach may avoid mechanical ventilation-induced lung injury resulting from the repeated opening and closure of the terminal bronchioles during each respiratory cycle.

The P-V relationship is linear around FRC until total lung capacity (TLC) is approached as denoted by an upper inflection point (UIP) (Fig. 2.13). Above UIP overdistension of alveolar units occurs and no more recruitment is achieved. On the P/V curve this point is situated around 30 cmH₂O. A stiff lung (e.g. ARDS) has a low compliance, whereas a highly distensible lung (e.g. emphysema) has a high compliance.

Fig. 2.13 Pressure–volume curve used to measure compliance. FRC, functional residual capacity; RV, residual volume;TLC, total lung capacity.

Compliance is affected by posture, and will be increased with age and emphysematous lung disease. Increases in extravascular lung water, consolidation, poorly adjusted mechanical ventilation and fibrosis are common causes of reduced compliance.

Limitations of technique

May require a patient to be paralyzed and disconnected from the ventilator. Inspiratory hold techniques are also time consuming and may be subject to error when intrinsic PEEP is present. The quasi-static technique may be of limited use where high gas flow rates result in high airway resistance as a source of error.

Indications

How it is done

Interpretation

See Table 2.3.

Table 2.3 Definitions and normal ranges of measured and calculated acid-base parameters breathing room air at sea level

Abnormalities

• The disorder can be calculated by working through Fig. 2.14 (below).

• Respiratory compensation for metabolic disorder: the minute volume will change in minutes to alter CO₂.

• Metabolic compensation for a respiratory disorder: renal bicarbonate reabsorption will change within 12 hours, but complete correction takes some days.

Fig. 2.14 Flow diagram for interpretation of acid-base abnormalities. ¹with attempted respiratory compensation (either acute or chronic); ²with attempted metabolic compensation (i.e. treated with bicarbonate or longer than ∼6 hours); ³with no respiratory compensation; ⁴with no metabolic compensation; ⁵mixed respiratory/metabolic acidosis if CO₂ high and HCO₃/BEx low; ⁶mixed respiratory/metabolic alkalosis if CO₂ low and HCO₃/BEx high; ⁷acid-base disturbances are rarely fully compensated by the patient’s natural mechanisms.

Management principles

Further investigations

Strictly, it refers to the venous electrolyte concentrations.

In the context of a metabolic acidosis:

Limitations and complications