*If the patient has COPD or congenital heart disease, cyanosis may be ‘constant’.

COMPREHENSIVE ASSESSMENT OF THE BREATHLESS PATIENT

Occasional breathlessness is a common human experience and may be a normal reaction to exercise or it can be a symptom of serious pathology. A respiratory rate of >24 breaths/min indicates the potential for respiratory failure and is a medical emergency (Jenkins and Johnson 2010).

It is therefore important that a thorough assessment is undertaken to arrive at a comprehensive assessment of the patient’s condition. This includes all other vital sign measurements because the assessment of one system is not to be taken in isolation.

Onset

The onset of the breathlessness provides vital information to the possible aetiology (Jenkins and Johnson 2010). If the onset is rapid (i.e. minutes to hours) it usually indicates speedily evolving pathology, e.g. acute pulmonary oedema (APO), anaphylaxis, acute asthma, pneumothorax, pulmonary embolism or a cardiac arrhythmia (Jenkins and Johnson 2010). A slower onset of breathlessness (i.e. hours to days) may indicate infections or exacerbation of COPD (Jenkins and Johnson 2010).

Severity

It is important to establish what is normal for the patient and the effect of the breathlessness on the patient (Jevon and Ewens 2000). Can the patient talk with ease? How far can the patient walk without having to stop? Can the patient climb the stairs Is the patient orthopnoeic? Is the patient platypnoeic (i.e. sitting up exacerbates the breathlessness, and may be indicative of pulmonary emboli – Jenkins and Johnson 2010)? If orthopnoea is present how many pillows does the patient sleep with? Does breathlessness affect the patient’s daily activities or occupation? Does the patient require oxygen at home?

Timing

Severe asthma and left ventricular failure are more common at night. Occupation-related asthma is worse when the patient is at work and improves when the patient is at home (Jevon and Ewens 2000). Bronchitis is more common in the winter months.

Finger clubbing

Finger clubbing can indicate pulmonary or cardiovascular disease such as pulmonary fibrosis, lung cancer, bronchiectasis; clinical features often include loss of nail bed angle, an increased curvature of the nail and swelling of the terminal part of the digit, this is usually as a result of chronic hypoxaemia but its absence does not exclude disease (Simpson 2006; Jenkins and Johnson 2010).

Shape of the chest

The normal chest is bilaterally symmetrical, although it can be distorted by disease of the ribs or spinal vertebrae as well as by underlying lung disease. In kyphosis (forward bending) or scoliosis (lateral bending) of the vertebral column, lung movement can be severely restricted. A barrel chest is sometimes associated with chronic bronchitis and emphysema (Jevon and Ewens 2000).

Chest percussion

Percussion of the chest wall causes the chest wall and underlying tissues to move (Simpson 2006), which in turn helps to establish whether the underlying tissues are air filled, fluid filled or solid (Bickley and Szilagyi 2009). As a result audible sounds and palpable vibrations are felt. Percussion is performed by placing one hand on the chest with the fingers separated; the other hand is used as a hammer to tap the interphalangeal joint, moving down the chest at 3- to 4-cm intervals (Simpson 2006). Comparison should be made between the left and right sides of the chest.

Hyper-resonance (loud sound) to percussion is caused by an increase in air in the chest, e.g. emphysema or pneumothorax. Dense sound to percussion can be caused by thickening of the chest wall, lung consolidation or pleural effusion.

Auscultation of the chest

Normal breath sounds are categorized as: vesicular, bronchovesicular and bronchial (Moore 2007):

• Vesicular: low pitched or soft, heard through inspiration and expiration without pause, heard over most of the lung fields (Moore 2007; Bickley and Szilagyi 2009).
  
• Bronchovesicular: moderate in pitch, heard in anterior region near the main bronchi and sometimes separated by a silent interval (Moore 2007; Bickley and Szilagyi 2009).
  
• Bronchial: louder and higher in pitch, separated by a pause and longer on expiration (Bickley and Szilagyi 2009).
  
• Adventitious sounds are abnormal breath sounds from the above, including crackles and wheezing (Moore 2007).

Diminished breath sounds can be caused by poor ventilation, e.g. airway obstruction or respiratory depression, or by increased separation of the stethoscope from the bronchial tree, e.g. obesity, pleural effusion, pneumothorax or bronchial tumour. Fine late inspiratory crackles may be heard, e.g. pulmonary oedema; coarse early inspiratory crackles are heard in bronchitis and bronchiectasis (Simpson 2006); a coarse rubbing sound indicates pleural inflammation.

Medications

Medications that the patient is currently taking may be significant, e.g. beta blockers can exacerbate asthma and left ventricular failure. Drugs such as amiodarone and methotrexate can cause pneumonitis or pulmonary fibrosis (Jenkins and Johnson 2010).

Halitosis

This may indicate poor oral hygiene or could be a sign of an infection of the upper respiratory tract.

Patient’s position and emotional state

Does the patient need to sit in a particular position, e.g. supported by a bed table to facilitate breathing? Is the patient orthopnoeic? A breathless patient will be anxious.

Past medical history and family medical history

All previous illnesses, operations, hospital admissions and investigations, particularly those that are respiratory related, e.g. COPD, should be noted (Booker 2004). Has the patient been prescribed any respiratory-related medication, e.g. inhalers or oxygen? If so the frequency and effectiveness of its use should be noted. Any respiratory disease in the patient’s family should be noted.

Occupational and social history

When assessing respiratory disease, both past and present occupations together with any exposure to dust, asbestos, coal or animals could be significant. Smoking history, past and present consumption, should be noted, together with any exposure to infection, e.g. tuberculosis. The type of living accommodation may be significant, e.g. stairs, damp environment, lack of a working lift in a block of flats.

Patient’s age

Certain respiratory diseases are more likely to occur at particular times of life: <30 years – asthma, pneumothorax, cystic fibrosis, congenital heart disease; >50 years – chronic bronchitis, COPD, carcinoma of the lung, pneumoconiosis, ischaemic heart disease.

Recent travel

Patients who have recently arrived from the Asian subcontinent may have been exposed to tuberculosis or recently identified viruses such as avian influenza.

Allergies

Any allergies should be recorded both in the patient’s medical and nursing notes and on the prescription administration chart. It is also relevant to ascertain in what form the allergy manifests, e.g. tongue swelling or pruritus, and whether the patient carries an adrenaline injection for self-administration (e.g. EpiPen). Dependent on individual hospital policy the patient may be required to wear a red armband in addition to the above precautions.

ASSOCIATED SYMPTOMS OF DYSPNOEA

Chest pain

Respiratory-related chest pain or pleuritic pain is usually sharp in nature and aggravated by deep breathing, coughing or movement of the trunk and can be intermittent or transient (Bickley and Szilagyi 2009; Jenkins and Johnson 2010). It is often localised to one particular area (Jevon and Ewens 2000) and may be present in pneumonia, pleuritis or systemic inflammatory disease (Jenkins and Johnson 2010).

Cough

A cough is a common respiratory symptom. It occurs when deep inspiration is followed by an explosive expiration. A cough that is worse at night is suggestive of asthma or heart failure, while a cough that is worse after eating is suggestive of oesophageal reflux. The timing and duration of the cough is important (Bickley and Szilagyi 2009; Jenkins and Johnson 2010):

• Dry cough: laryngitis, left ventricular failure or mitral stenosis
  
• Dry cough may become productive: tracheobronchitis, viral pneumonia, bacterial pneumonia, pulmonary tuberculosis, lung cancer, pulmonary emboli may be due to a chest infection
  
• Chronic cough: asthma, post nasal drip, chronic bronchitis, lung abscess
  
• Irritating chronic dry cough: may be due to oesophageal reflux
  
• Chronic cough with production of large volumes of purulent sputum: may be due to bronchiectasis
  
• Change in the character of a chronic cough: may be due to a serious underlying pathology, e.g. carcinoma of the lung
  
• Cough with haemoptysis (streaked with blood or bloody): bacterial pneumonia, chronic bronchitis, pulmonary tuberculosis, bronchiectasis.

Sputum

Sputum is a key clinical feature of respiratory disease and can provide valuable information for the assessment of a breathless patient, including evaluation of care (Bickley and Szilagyi 2009). If sputum is produced, its colour and consistency should be noted:

• White mucoid sputum: seen in asthma and chronic bronchitis
  
• Purulent green or yellow sputum: may indicate respiratory infection
  
• Blood present: may indicate carcinoma of the lung, pulmonary embolism, recent upper airway trauma or coagulation disorder
  
• Frothy white or pink sputum: seen in pulmonary oedema
  
• Thick, mucoid sputum: feature of asthma, usually at the end of an attack (Bickley and Szilagyi 2009)
  
• Frothy white, sometimes blood-stained sputum: associated with acute pulmonary oedema (Moore 2007)
  
• Foul–smelling sputum: indication of respiratory tract infection
  
• Black specks: common causes include smoking, smoke inhalation and coal dust (Moore 2007).

The patient’s history is important when determining the significance of sputum production at a particular time of day, e.g. chronic expectoration in the morning over a number of years may be suggestive of smoking-induced bronchitis whereas variable morning or nocturnal expectoration may be suggestive of asthma (Law 2000).

Important coexisting clinical features

A number of important coexisting clinical features may be associated with respiratory problems, including (Jevon and Ewens 2000):

• Fever: respiratory infection
  
• Poor appetite and weight loss: carcinoma of the lung, chronic infection
  
• Swollen and painful calf: deep vein thrombosis and pulmonary embolism
  
• Ankle swelling: congestive cardiac failure, deep vein thrombosis
  
• Palpitations: cardiac arrhythmias

MEASUREMENT OF PEAK EXPIRATORY FLOW RATE

Peak expiratory flow rate (PEF) or peak flow is the maximum flow rate, in litres per minute, attained on forced expiration from a position of full inspiration and is a useful baseline measurement of airflow obstruction (Jenkins and Johnson 2010). It is a simple test to ascertain the severity of a patient’s asthma and can provide the practitioner with a guide to the level of airflow resistance within the bronchioles. This resistance can be caused by inflammation and/or bronchospasm. PEF measurement is expressed as a percentage of the patient’s previous best value or of a predicted best value, if this is not available (British Thoracic Society Scottish Collegiate Guidelines Network 2009). Peak flow is not a measure of fitness or the strength of the patient’s chest muscles.

Indications

Recordings should be undertaken four times a day (best of three attempts – Booker 2007), both before and after the administration of bronchodilators (Booker 2004). The results are crucial to the patient’s treatment and are an aid to asthma diagnosis (Miller 2005), an indicator of how well the patient’s asthma is responding to treatment and an aid to measuring the recovery from an asthma attack (Booker 2007).

Normal range for PEF measurement

The reference range for PEF is dependent on age, gender and height (Booker 2007). PEF measurements are not a stand-alone reading during an exacerbation of asthma, but are taken into account with other observations such as respiratory rate, SpO₂, arterial blood gas analysis, work of breathing and ability to complete sentences. However, during a severe exacerbation of asthma the recording of PEF may not be possible and may even worsen a patient’s condition, whereupon other clinical signs and symptoms are sufficient to aid management decisions:

• PEF >50–75% of best predicted: moderate exacerbation
  
• PEF 33–50% of best predicted: acute severe attack
  
• PEF <33% of best predicted: life-threatening attack.

Procedure

PULSE OXIMETRY

Pulse oximetry is widely regarded as one of the greatest advances in clinical monitoring (Giuliano and Higgins 2005) since the invention of the ECG (Fox 2002) and is an essential monitoring and diagnostic tool in both critical care and ward areas (Mathews 2005). It is a simple, non-invasive bedside method of measuring arterial oxygen saturation in peripheral blood vessels (Booker 2008), expressed as SpO₂ (Welch 2005). Pulse oximetry was developed in the 1980s; before this time oxygenation assessment relied on subjective and unreliable physical assessment of the skin for cyanosis (Giuliano and Higgins 2005), which when present is an indicator of advanced hypoxaemia (Giuliano 2006).

Pulse oximetry measures only the extent to which haemoglobin is saturated with oxygen and does not provide information on oxygen delivery to the tissues or ventilatory function (Higgins 2005). Nevertheless, it is an invaluable monitoring tool in a variety of clinical settings, as long as its uses and limitations are fully understood (Jevon and Ewens 2000; Giuliano 2006).

Role of pulse oximetry

Hypoxaemia is common in all aspects of medical practice and without appropriate treatment will lead to cellular death and organ dysfunction.

Cyanosis is a late sign of hypoxaemia and the oxygen saturation must decrease to 80–85% before any changes in skin colour become apparent (Giuliano and Higgins 2005). In addition, manifestations of hypoxaemia, including restlessness, confusion, agitation, cyanosis, combative behaviour and tachycardia (McEnroe Ayres and Stucky Lappin 2004), may be missed or wrongly interpreted.

Pulse oximetry will immediately alert the practitioner to a fall in arterial oxygen saturations and the development of hypoxaemia, before visual recognition of cyanosis, which is not always present (Jenkins and Johnson 2010). In clinical practice an oxygen saturation of less than 90% is of grave concern.

The mechanics of pulse oximetry

Pulse oximetry (Fig. 3.1) is a differential measurement based on the spectrophotometric absorption method using the Beer–Lambert law for optical absorption (Welch 2005).

Fig. 3.1 Pulse oximeter.

The pulse oximeter probe consists of two light-emitting diodes (one red and one infrared) on one side of the probe. These emit red and infrared light via a relatively translucent area of the body and detect the amount of light passing through the capillary bed (Booker 2008). The ratio of infrared light absorbed by oxyhaemoglobin and the red light absorbed by haemoglobin provides the data used to calculate the SpO₂ (Booker 2008). The more oxygenated the blood, the more red light and the less infrared light pass through (Giuliano 2006). By calculating the ratios of red to infrared light over time, oxygen saturation is calculated (Giuliano 2006).

Uses of pulse oximetry

Pulse oximetry is known as the fifth vital sign (British Thoracic Society 2008) and has become an integral component of standard vital sign recording, along with respiratory rate, blood pressure, pulse rate and temperature in all acute settings.

Advantages of pulse oximetry

Pulse oximetry is an inexpensive, non-invasive and portable method of continuous measurement of arterial oxygen saturation which facilitates the early detection of hypoxaemia and reduces the need for arterial blood gas sampling (Booker 2008).

Normal values for oxygen saturation

All critically ill patients require immediate administration of high concentration oxygen. When stable, oxygen should be titrated against arterial blood gases (British Thoracic Society 2008). Oxygen saturation targets in the acutely ill patient should be 94–98% or 88–92% in those patients at risk of hypercapnia, e.g. COPD or morbid obesity (British Thoracic Society 2008). However, low oxygen saturation levels, i.e. <94%, may be normal in some patients and do not need oxygen therapy if their condition is stable (British Thoracic Society 2008).

Procedure for pulse oximetry

The following preliminary points should be observed:

• Wash and dry hands
  
• Ensure that the probe is clean
  
• Remove nail varnish or artificial nails
  
• Select a probe appropriate for the sensor site, duration of monitoring and patient activity levels (Pullen 2010)
  
• Explain the procedure to the patient.

Select an appropriate site with an adequate pulsating vascular bed. Sites include finger (most popular), ear lobe, toe, nose and forehead, and avoid areas of oedema or on an extremity where non-invasive blood pressure monitoring is being taken (Pullen 2010). The probe should be secured, but without the use of restrictive tape, to ensure blood flow and reduce the risk of pressure sores (Booker 2008). The following precautions must be taken during the procedure:

• Ensure that the trace is reliable and corresponds to pulse rate, i.e. oxygen saturation measurements are accurate (Fig. 3.2).
  
• Ensure careful positioning to ensure that the sensor is opposite the probe (Booker 2008).
  
• Ensure that the alarms on the pulse oximeter are set within locally agreed limits and according to the patient’s condition.
  
• Regularly monitor the probe site for complications, e.g. burns and joint stiffness, and regularly vary the site.
  
• Ensure that the patient’s pulse rate correlates with the pulse oximetry display (Pullen 2010).
  
• Regularly monitor the patient’s vital signs as per monitoring plan.
  
• Document the readings on a track-and-trigger system (British Thoracic Society 2008) and escalate as appropriate.

Fig. 3.2 SpO₂ waveform.

Interpreting plethysmographic waveforms

The quality of the pulse and circulation at the point where SpO₂ is being measured is reflected in the plethysmographic waveform (Fig. 3.2); the strength of the pulse is proportional to the amplitude of the waveform (Booker 2008).

Causes of inaccuracy

Inaccurate readings can be caused by any of the factors listed below:

• Carbon monoxide poisoning: false high readings (British Thoracic Society 2008).
  
• Methaemoglobinaemia (changes in the structure of iron in haemoglobin) and carboxyhaemoglobin (in carbon monoxide exposure) present in high doses can give false high or low readings (Pullen 2010).
  
• Poor vascular perfusion: pulse oximeter requires pulsatile blood flow to evaluate oxygen saturation.
  
• Venous pulsation: e.g. tricuspid valve failure, securing the probe too tightly (Booker 2008) heart failure, inflating blood pressure cuff distal to the probe, resulting in a false low reading.
  
• Poor vascular perfusion: e.g. in hypovolaemia, hypotension, septicaemia, hypothermia, cardiogenic shock or peripheral vascular disease, resulting in a false low reading.
  
• Cardiac arrhythmias such as atrial fibrillation can cause inadequate and irregular perfusion, resulting in a false low reading (Pullen 2010).
  
• Factors that affect light absorption: skin pigmentation, dried blood, high levels of bilirubin , nail polish with a blue pigment in and intravenous dyes, e.g. indocyanine green (Booker 2008).
  
• Bright external light, particularly fluorescent lighting can give a false high reading (Booker 2008).
  
• Low oxygen saturations (Booker 2008).
  
• Patient movement, e.g. shivering; although modern pulse oximeters can minimise the interference from patient movement (Gwinnutt 2006).

Limitations

Although pulse oximetry measures oxygen saturation and can detect hypoxaemia, it does not provide an indication of the adequacy of ventilation and carbon dioxide retention.

Davidson and Hosie (1993) reported a case of a postoperative patient who had a normal oxygen saturation (95%), but had abnormally high carbon dioxide levels causing a life-threatening respiratory acidosis. Failure to detect hypoventilation in such a patient is an example of a false sense of security generated by a single physiological variable being within safe limits (Hutton and Clutton-Brock 1993). If hypercapnia is suspected arterial blood gas analysis should always be performed.

Troubleshooting

It is important to ensure a reliable trace at all times. If it is difficult to secure an acceptable trace:

• Warm and rub the skin to improve circulation
  
• Try a different probe site, e.g. ear lobe
  
• Try a different probe/different pulse oximeter.

Complications

Pulse oximetry is very safe; complications are uncommon and are rarely serious if they do occur. Nevertheless complications have been reported:

• Ischaemic pressure necrosis (Fox 2002): in the reported case the patient was septic, hypotensive and had pre-existing arterial disease. In addition an arterial line was in situ in the radial artery, which may have further compromised the distal circulation.
  
• Blister injuries at the probe site: caused by a faulty probe cable; intermittent shortening resulted in excess electrical current supply to the light-emitting diode causing overheating.
  
• Mechanical injury: if the patient is unable to flex his or her finger; in unconscious or semiconscious patients the probe may inhibit voluntary use of the finger, resulting in stiffness. Changing the probe site regularly is therefore advocated (Booker 2008). This is potentially a problem for patients on intensive care units (ICUs) where prolonged monitoring occurs.

ARTERIAL BLOOD GAS ANALYSIS

Arterial blood gas (ABG) analysis is one of the most common tests performed in the critically ill patient and has become an essential skill for all health-care practitioners (Simpson 2004). It provides clinicians with valuable information about a patient’s respiratory function and metabolic state (Simpson 2004; Allen 2005) and as such forms an integral component of monitoring the critically ill patient. It is important to remember that, as with all assessment methods, ABG interpretation should not be taken in isolation (Simpson 2004).

Procedure for arterial blood sampling

There are two methods of arterial blood sampling, from either a one-off arterial puncture or ‘stab’ or an arterial cannula. An arterial ‘stab’ is usually taken from the radial artery (Woodrow 2004), because it is most accessible. The femoral artery is also sometimes used.

The following procedure for arterial blood sampling is based on recommendations by Driscoll et al. (1997):

Fig. 3.3 Arterial blood sampling.

Fig. 3.4 Blood gas machine.

Indications for ABG analysis

Indications for ABG analysis include:

• respiratory compromise
  
• post cardiopulmonary arrest
  
• metabolic conditions, e.g. diabetic ketoacidosis (DKA)
  
• sudden or unexplained deterioration
  
• evaluation of interventions, e.g. changes in invasive ventilation settings
  
• titration of non-invasive ventilation
  
• before major surgery as a baseline to facilitate postoperative comparison
  
• major trauma.

Principles of ABG analysis

Oxygen supply to the tissues is dependent on how oxygen disassociates itself from the haemoglobin (Hb) molecule to be made available for the tissues. This, in turn, is dependent on blood pH, body temperature and partial pressure of carbon dioxide (PaCO₂) of the blood (Foxall 2008). As the blood becomes more acidotic, warmer and with a higher PaCO₂, the oxygen dissociation curve shifts to the right and reduces the oxygen-carrying capacity of Hb (Elliott et al. 2007). Although less oxygen can be picked up by the lungs, more can be released to the tissues (Elliott et al. 2007). Conversely, a shift to the left results in the Hb molecule having a greater affinity to oxygen but less can be released to the tissues. Therefore this may result in poor oxygenation despite an adequate PaO₂.

When a sample of arterial blood is processed by a blood gas analyser it provides not only an invaluable and accurate insight into the patient’s respiratory function but also a window into their metabolic status.

The levels of blood gases are dependent on three variables: blood supply, ventilation and diffusion. Therefore if there is a poor blood supply to the alveoli but adequate ventilation, insufficient diffusion will lead to retention of PCO₂, e.g. pulmonary embolus. Conversely if there is a good blood supply to the alveoli but poor ventilation, gaseous exchange will also be compromised, e.g. COPD, pneumonia and asthma. Both of these imbalances will lead to a perfusion–ventilation (V/Q) mismatch or a ‘shunt’ (Smyth 2005). Blood gas units of measurement are kilopascals (kPa) or millimetres of mercury (mmHg). Both units are currently in use (to convert kPa to mmHg: kPa × 7.5 = mmHg and to convert mmHg to kPa: mmHg ÷ 7.5 = kPa).

Parameters measured by a blood gas analyser

• The pH: 7.35–7.45. Measures overall acid–base balance of the blood sample and is affected by both respiratory and metabolic function (Foxall 2008). Acid–base balance is the maintenance of hydrogen ion (H⁺) balance that enables normal cell function (Foxall 2008). H⁺ and pH levels have an inverse ratio, i.e. one increases as the other decreases (Simpson 2004). Small changes in pH are life threatening (Allen 2005) so the body relies on compensatory mechanisms to counteract dramatic changes in pH. Buffers in the body act as chemical sponges, which absorb excess alkali or acid (Allen 2005).
  
• PaO₂: 10–12.0 kPa (75–90 mmHg). This is the measurement of partial pressure of oxygen dissolved in the blood sample, not how much oxygen is in the blood (Foxall 2008). Arterial PO₂ (PaO₂) is dependent on the alveolar PO₂ (PAO₂) (Resuscitation Council UK 2011). PaO₂ is always less than PAO2 and the extent of this difference is dependent on the incidence of lung disease. Increases in the difference indicate V/Q mismatch (Simpson 2004). A person with normal lungs breathing air (FiO₂ 0.21) at sea level should have a PaO₂ >11 kPa (80 mmHg) and breathing an oxygen concentration of 50% (FiO₂ 0.5) at sea level will result in a PaO₂ of approximately 40 kPa (300 mmHg) (Resuscitation Council UK 2011). When a patient is receiving supplementary oxygen, a normal PaO₂ will not necessarily indicate adequate ventilation as small increases in FiO₂ will overcome any hypoxaemia caused by under-ventilation (Resuscitation Council UK 2011). A PaO₂ level <8 kPa (60 mmHg) is considered a diagnosis of hypoxaemia (British Thoracic Society 2008). Critically ill patients have increased oxygen demands because of the pathological demands of the body. It is critical that these increased oxygen demands are met to maintain adequate tissue oxygenation and prevent cell death.
  
• PaCO₂: 4.5–6.0 kPa (34–45 mmHg). This is the measurement of partial pressure of dissolved carbon dioxide in the blood (more soluble than oxygen). To be carried to the lungs to be exhaled carbon dioxide is transported in a plasma solution as carbonic acid (H₂CO₃). If the patient has too little or too much carbon dioxide this will have an effect on the acidity or alkalinity of the blood (Foxall 2008). Carbon dioxide concentration provides information about the adequacy of ventilation (Foxall 2008). Carbon dioxide is a waste product of tissue metabolism and the respiratory centres in the brain stem are stimulated in a response to high levels of carbon dioxide (Foxall 2008). The respiratory centres in the brain stem are sensitive to H⁺ concentration (Resuscitation Council UK 2011). Therefore, as the carbon dioxide rises the respiratory centres are stimulated to increase respiratory rate and depth and reduce carbon dioxide levels, and conversely, when there is hyperventilation and carbon dioxide reduces, the respiratory centres are stimulated to reduce respiratory rate and depth:
  
  
  
• Bicarbonate (HCO₃⁻) (22–26 mmol/l): the major buffering systems in the body involve bicarbonate, protein and phosphate; however, bicarbonate is the most important. Buffers have two qualities: they bind free hydrogen ions when they are in excess (acidosis) and donate hydrogen ions when they are too low (alkalosis) (Foxall 2008).
  
• Base excess (BE) (−2 mmol to +2 mmol): base excess is the quantity of acid or base required to restore the blood to a pH of 7.4 (Woodrow 2004; Resuscitation Council UK 2011). A negative value indicates a deficit of base (or excess of acid) and a positive value indicates an excess of base (or deficit of acid) (Resuscitation Council UK 2011).
  
• SaO₂ (92–99%): arterial oxygen saturation is the percentage of oxygen that has combined with the Hb molecule. Oxygen combines with Hb in sufficient amounts to meet the needs of the body, while at the same time releasing oxygen to meet tissue demands (Foxall 2008).
  
• Other values: most analysers measure electrolytes, e.g. sodium (Na⁺), potassium (K⁺), calcium (Ca²⁺) and chloride (Cl⁻), Hb and lactate, which can be useful for a ‘quick check’. In most ICUs these values are accepted as accurate and treatment is titrated according to them. However, if aberrant values are obtained it will be necessary to obtain laboratory analysis for comparison.

Normal ranges for ABG analysis are shown in Table 3.3.

Table 3.3 Normal ranges for arterial blood gas results

(Foxall, 2008)

Systematic analysis of ABG results

Foxall (2008) recommends three principles in analysing ABG results:

• Consider the patient’s clinical history and physical examination.
  
• Systematically analyse the results.
  
• Integrate the clinical findings with interpretation of the data.

A systematic approach for the analysis of ABGs is a prerequisite for objective assessment and the Resuscitation Council UK suggest a five-step approach, as follows

Step I: assess oxygenation

• Is the patient hypoxic?
  
• What supplementary oxygen are they receiving?

Step 2: determine pH level

Is there an acidosis (pH < 7.35) or alkalosis (pH > 7.45) present?

Step 3: determine the respiratory component

Is the PaCO₂ low (<4.7 kPa, <35 mmHg) or high (>6.0 kPa, >45 mmHg)? If the carbon dioxide is low this may indicate either a primary respiratory alkalosis or a secondary respiratory compensation for a metabolic acidosis. If the carbon dioxide is high this may indicate either a primary respiratory acidosis or a secondary compensation for a metabolic alkalosis.

Step 4: determine metabolic component

Is the bicarbonate low (<22 mmol/l) or high (>26 mmol/l)? If the bicarbonate is low this may indicate a primary metabolic acidosis or a secondary renal compensation for a respiratory alkalosis. If the bicarbonate is high this may indicate a primary metabolic alkalosis or a secondary metabolic compensation for a respiratory acidosis. It is not necessary to evaluate BE because the level of BE and bicarbonate mirror each other.

Step 5

Combine the findings from steps 2, 3 and 4 and determine what the primary disturbance is and whether there are any compensatory mechanisms evident.

Best Practice – Arterial Blood Gas Analysis

Consider the patient’s clinical history and physical examination

Systematically analyse the results

Integrate the clinical findings with interpretation of the data

Never remove supplementary oxygen when taking an arterial blood sample for analysis. It is important to assess the patient’s response to supplementary oxygen and the withholding of oxygen in the compromised patient is dangerous practice

The changes in acid–base disorders are summarised in Table 3.4

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