Physiotherapists need to be able to analyse the results (Fig. 3.1.1). The procedure itself involves taking an arterial blood sample and is normally carried out only by medical or nursing staff and some extended scope physiotherapists with specialized training.

Fig 3.1.1 Example of a set of arterial blood gas results. As can be seen, a blood gas result may contain more information than blood gases alone.

Findings (Fig. 3.1.2, Table 3.1.1)

You should also consider haemoglobin (Hb) levels when interpreting ABG results (see 3.48 Pulse oximetry). Fig 3.1.2 summarizes the process of interpreting ABG’s in flowchart format.

Fig 3.1.2 Flowchart for arterial blood gas analysis.

Table 3.1.1 Blood gas measurements

pH	Measure of level of acidity or alkalinity of blood Normal range 7.35–7.45

P_aCO₂

Partial pressure of carbon dioxide in arterial blood (plasma)

Normal range 4.7–6 kPa (35–45 mmHg)

P_aO₂

Partial pressure of oxygen in arterial blood (plasma)

Normal range 10.7–13.3 kPa (80–100 mmHg)

S_aO₂

Saturation level of Hb in arterial blood (measures how fully saturated each unit of Hb is, given as a percentage)

Normal range 95–100%

Amount of bicarbonate (base) in the blood

Normal range 22–26 mmol l⁻¹

BE (base excess)

Base excess is a simpler way of expressing bicarbonate levels and gives the amount of above or below the average value of 24 mmol l⁻¹

Normal range −2 to +2

NB. Partial pressure refers to the pressure exerted by one specific gas (e.g. oxygen), which forms part of the total pressure exerted by the mixture of gases (e.g. oxygen, carbon dioxide and nitrogen) in the blood.

Process of Interpreting ABGs.

1. Check pH

a. Decide whether pH is within normal range or whether there is an acidosis (low pH below 7.35) or an alkalosis (high pH above 7.45).

b. Anything outside the normal range can interfere with metabolism and may become critical. Discuss any recent changes with medical or nursing staff.

2. Check P_aCO₂

If there is an acidosis or an alkalosis, you need to decide whether this is due to a respiratory or metabolic problem. Identify any hypercapnia (high P_aCO₂ above 6 kPa) or hypocapnia (low P_aCO₂ below 4.7 kPa) (Box 3.1.1).

i. Respiratory acidosis is when hypercapnia causes the blood to become more acidic (i.e. high P_aCO₂ and low pH).

Hypercapnia suggests that the patient is hypoventilating (underbreathing). This may be due to fatigue or neuromuscular weakness, so the patient may need support with ventilation, e.g. non-invasive ventilation (NIV). Hypercapnia may also be due to insensitivity to high P_aCO₂ levels, as seen in some patients with chronic obstructive pulmonary disease (COPD) (CO₂ retainers).

Hypocapnia suggests that the patient is hyperventilating (overbreathing). This may be due to pain or anxiety. The patient may need reassurance and might benefit from a pain review, or breathing control and relaxation techniques (see 3.55 Respiratory rate).

3. Check (or BE)

Top tip!

If there is a metabolic problem the pH and the move in the same direction as if in an elevator (e.g. if the pH is high the will also be high).

i. Metabolic acidosis is when lower levels of bicarbonate (or BE) cause the pH to become more acidic (both change in the same direction to become lower).

ii. Metabolic alkalosis is when higher levels of bicarbonate (or BE) cause the pH to become more alkaline (both change in the same direction to become higher).

4. Check for compensation

Compensation is the balancing of one system with the other (respiratory and metabolic) to make sure the pH stays within normal limits. This is very important for metabolism. Each system (respiratory or metabolic) can therefore adjust its levels of carbon dioxide or bicarbonates in response to changes in the other system. For example, if there is a respiratory acidosis, the kidneys can start to conserve bicarbonates in the blood (i.e. not pass as many out in the urine). This will raise

levels and make the blood more alkaline, thereby restoring the pH.

Top tip!

If the pH and the P_aCO₂ have moved in the same direction, this suggests that the respiratory system is compensating and the problem is metabolic.

If the pH and the have moved in the opposite direction, this suggests that the metabolic system is compensating and the problem is respiratory.

The respiratory system can react to change quickly (within a couple of hours) but the metabolic system may take approximately 2 days to respond. Any compensation may be full (complete) or partial (Box 3.1.3).

i. Full compensation is seen when both the P_aCO₂ and the

are outside the normal range and the pH is within the normal range.

ii. Partial compensation is when the P_aCO₂ and

are both out of range but the pH is not quite within normal limits.

Note that it may be impossible to distinguish between compensated respiratory acidosis and compensated metabolic alkalosis, or between compensated respiratory alkalosis and compensated metabolic acidosis without looking at other clinical findings or a series of ABGs.

The chart in Table 3.1.2 assumes that any compensation is complete not partial.

5. Check oxygenation

Hypoxaemia. P_aO₂ reflects the ability of the lungs to allow the transfer of oxygen from the environment to the circulating blood. A reduced P_aO₂, regardless of F_iO₂ (how much oxygen the patient is receiving), is called hypoxaemia. You should always check if a reading has been taken while the patient is receiving oxygen therapy, and, if so, how much they are receiving (see 3.43 Oxygen delivery). A P_aO₂ of 10.7 kPa is normal, but would not be considered normal if the patient is receiving 60% oxygen.

Identify any significant, deteriorating or potentially critical levels of hypoxaemia. In acute respiratory disease, a P_aO₂ <10.7 kPa may be significant and <7.3 kPa may be critical, but chronic respiratory patients may be able to tolerate lower oxygen levels, and hypoxaemia may not be considered significant until it drops below 7.3 kPa. Oxygen therapy should be considered for patients with significant (or worsening) hypoxaemia.

S_aO₂ levels may be used to determine the need for oxygen therapy. Give oxygen when S_aO₂ <90% (see 3.48 Pulse oximetry).

6. Check for respiratory failure

a. Identify whether the patient is in respiratory failure – is it type I or type II?

i. Type I respiratory failure occurs when P_aO₂ is low and P_aCO₂ is normal or slightly reduced.

ii. Type II respiratory failure occurs when P_aO₂ is low and P_aCO₂ is high.

b. Acute or chronic respiratory failure?

Table 3.1.2 Respiratory and metabolic acidosis and alkalosis

Top tip!

Type One failure is when One gas (i.e. Oxygen) is affected – remember they both begin with O!

Type Two is when Two gases (i.e. oxygen and carbon dioxide) are affected.

When respiratory failure is due to acute respiratory disease, there may be little or no compensation from raised

levels because it takes time (e.g. days) for adequate compensation to occur. Therefore, the pH is likely to be low (respiratory acidosis).

When respiratory failure is due to a chronic respiratory disease there may be compensation from raised

levels. Therefore, the pH may be normal, or only slightly lower than normal (compensated respiratory acidosis). Check any current ABG results against any previous or usual results as this will also help to confirm the diagnosis of acute or chronic failure.

It is important to identify the extent to which any respiratory failure is acute or chronic because patients with chronic respiratory disease can tolerate lower levels of hypoxaemia and may not need oxygen therapy until their levels become lower. Additionally, they may be reliant on a ‘hypoxic’ drive to breathe, and if they are given too much oxygen therapy their drive to breathe could be seriously reduced.

Documentation

Record each value together with time and date of test, and any oxygen therapy or ventilation support given at the time of measurement. Record the patient’s position if appropriate.

Clinical examples (answers follow)

Answers to clinical examples

Case 1

This man has a respiratory acidosis (uncompensated). It is an acute condition and may be due to pneumonia or a severe chest infection – note he has type II respiratory failure and may require additional ventilator support.

Case 2

This girl has respiratory alkalosis (uncompensated). This is an acute situation and has been caused by hyperventilation due to anxiety.

Case 3

This man has compensated respiratory acidosis. This is a chronic situation because there has been enough time for to increase and his pH is within the normal range, despite his high P_aCO₂ (remember he is an ex-miner; therefore, respiratory disease would not be uncommon).

Case 4

This man has partially compensated metabolic acidosis. His symptoms suggest diabetes, which can cause a fall in and therefore a fall in pH. There is some compensation because the P_aCO₂ has gone down, suggesting that he is breathing more in order to try and raise the pH. This is only partially successful because his pH is still below the normal range. Physiotherapy is not going to help his breathing at this point as he needs medical attention to stabilize his diabetes.

3.2 Attachments

Definition

These may be any piece of equipment that is attached to the patient, e.g. intravenous (i.v.) lines, central venous line, ECG lines, surgical drains, ventilator tubing, saturations monitor and catheter (Figs 3.2.1 and 3.2.2).

Fig 3.2.1 Example of patient attachments in an intensive therapy unit.

Fig 3.2.2 Example of patient attachments in the ward setting.

Purpose

The purpose of an attachment is specific to what is being monitored – many of these will be discussed throughout this chapter. However, the ultimate aim of attachments can be subdivided as:

• monitoring/assessment of the patient, e.g. saturations monitor, intracranial pressure (ICP) bolt

• provision or drainage of fluids, i.e. what is going in and out, such as drips and drains

• treatment/support of the patient, e.g. renal support, ventilator.

Procedure

Be aware of all attachments and take care not to displace any equipment during your assessment.

Findings

If you do not know what a piece of equipment or fluid running into the patient is, ask the nursing staff. It may be important information that will influence what you can/cannot do with the patient, e.g. changing position.

Documentation

As part of your assessment, all attachments should be noted within your documentation.

3.3 Auscultation

Definition

Auscultation is the process of using a stethoscope to listen to and interpret the lung/breath sounds generated by airflow through the airways.

Purpose

This assessment technique can help identify sputum retention in the airways, or areas of atelectasis. It may be used as an outcome measure before and after physiotherapy. It can also help identify deterioration or more serious pathology such as a pneumothorax that may need further medical investigation.

Procedure

• Equipment

– Good quality stethoscope (Fig. 3.3.1).

– Sterilizing wipes.

• Method

– Clean the diaphragm and earpieces with wipes.

– Place earpieces in your ears (earpieces should face forwards in order to fit into your auditory canals).

– Check that the stethoscope is tuned to the diaphragm (tap the diaphragm lightly – can you hear this clearly? If not twist the metal connector until you can hear the tapping sound most clearly).

– Ask the patient if they would be willing to remove any items of clothing in order to expose the chest area, providing this is appropriate and you can maintain their dignity and comfort.

– Position the patient so you can access anterior and posterior aspects of the chest, e.g. sitting up over the edge of the bed or sitting forwards in a chair. If they are confined to bed, you may need help to sit them forwards slightly when listening posteriorly or help them to roll into side lying. Note that you may have to access the posterior segments by moving your stethoscope under the patient if they are very unwell and unable to move.

– Warn the patient to inform you if they start to feel dizzy.

– Place the stethoscope firmly on the chest wall in the positions described in Fig. 3.3.2 and Table 3.3.1.

– Listen during both inspiration and expiration. Listen to each zone of the lungs on alternate sides of the chest to compare your findings.

– Make sure you listen to one or two full breaths in AND out at each point.

– Allow the patient a period of rest or normal breathing between zones or if they become dizzy.

– When you have finished, note your findings and clean your stethoscope.

Fig 3.3.1 Labelled diagram of a stethoscope.

Fig 3.3.2 Auscultation points.

H, horizontal fissure; LLL, left lower lobe; LUL, left upper lobe; RLL, right lower lobe; RUL, right upper lobe; RML, right middle lobe.

Reproduced and modified with kind permission from Pryor JA, Prasad SA. 2008 Physiotherapy for Respiratory and Cardiac Problems, 4th Edn. Edinburgh, UK: Churchill Livingstone.

Table 3.3.1 Auscultation zones

Mid-axillary Left and right Posterior

Findings

For each zone, record whether breath sounds are normal or bronchial, loud or quiet, and then identify any added sounds.

Breath sounds (Table 3.3.2) arise in the trachea and bronchi and are caused by the turbulence of the air as it flows in and out of these large airways. If you listen over the trachea (just below the cricoid cartilage or Adam’s apple) you will hear what they sound like at the source.You will notice that they are very loud here and also quite harsh sounding. Inspiration and expiration are heard clearly (both are loud) and there is a very slight pause between them. These sounds are known as bronchial breath sounds because they are generated in the bronchi (and trachea).

• Normal breath sounds. If you listen anywhere over the lung fields (including all of the zones shown in Fig. 3.3.2) the sounds are much quieter because you are over lung parenchyma and the air in the lungs has absorbed a lot of the sound. This attenuates the sound, making it smoother, gentler and more continuous, so it is harder to tell when inspiration changes to expiration. Since we expect to hear these sounds when auscultating over the lungs we call them ‘normal breath sounds’.

• Bronchial breathing (bronchial breath sounds heard over lung fields). If you are listening over the lungs and what you hear sounds loud, harsh and discontinuous (i.e. like bronchial breath sounds), it is not ‘normal’ and suggests that these sounds have not been dampened down by the air in the lungs – usually because in that area of lung the air has been replaced by something solid (consolidated). A solid area transmits sound very well because it vibrates more than air (ask the patient to say ‘99’ while auscultating and the sound will be very clear over consolidated lung tissue). These sounds may occur over an area of lobar pneumonia where the alveoli fill with clotted inflammatory exudate, or over collapsed lung tissue (occurring without a sputum plug), or at the lip of a pleural effusion.

• Breath sounds quieter than normal. If the breath sounds are very quiet it might be because the patient is very large and therefore the sounds have been dampened down by excess soft tissue. Make sure you press the stethoscope firmly to the chest wall and press through the adipose tissue to get the best sound transmission. It might, however, be because the breaths were quite small and not generating much turbulence. Perhaps the patient is not breathing very deeply? Does this fit with your observation and palpation? Is one side of the chest moving more than the other side?

Table 3.3.2 Breath sounds

Normal breath sounds

Soft, muffled, louder on inspiration, fade in expiration, ratio 1:2

Turbulence in the large airways

Bronchial breathing

Expiration louder and longer with pause between inspiration and expiration (sounds like Darth Vader)

Heard normally over trachea

If heard over lung fields, suggests:

• Consolidation

• Collapse without a plug

• May also be heard at the lip of a pleural effusion

Breath sounds quiet or absent?

May be due to:

• Collapse with complete obstruction of airway

• Sounds filtered by air (hyperinflation)

• Sounds filtered by pleura, chest wall (obese or muscular patients, pleural effusion, pneumothorax, haemothorax)

• Pneumothorax

Top tip!

Think! If a patient is not breathing very deeply – what possible implications might this have and what problems might this cause?

• Absent breath sounds. A pleural effusion, sputum plugging or pneumothorax could prevent sounds from being heard by absorbing the sound completely before it can be transmitted to the chest wall.

Top tip!

If you auscultate and hear a ‘silent’ chest, it may mean that the patient is in extremis and is unable to move air at all (check airway and stethoscope). This is a medical emergency and you need to seek expert medical assistance straight away!

• Breath sounds louder than normal. Loud breath sounds suggest more turbulence in the large airways. This is usually due to obstruction or narrowing of these airways, e.g. due to COPD. Narrower airways are harder to breathe through, so the patient may be working harder in order to breathe.

• Other added sounds.

– Crackles (Table 3.3.3)

– Fine crackles. Sound like rubbing a hair next to your ear. They may be due to pulmonary oedema or sputum but are often caused by the sudden opening of small airways when lung volumes are low, suggesting atelectasis. If it is the latter, they often resolve after some deep breathing exercises.

– Coarse crackles. Sound like rice crispies crackling as you add the milk. They may be caused by sputum, particularly if you notice that they reduce or change after coughing.

Table 3.3.3 Added sounds: crackles

Crackles	Short, non-musical, popping sounds, fine or coarse
*Fine crackles* Reopening of airways sounds like rubbing hair next to your ear	Atelectasis	• Short, explosive • Periphery lung • Reduce with deep breath
	Intra-alveolar oedema	• ‘Tissue paper’ • Do not resolve with deep breath or cough • Late inspiration (NB: interstitial fibrosis)
	Secretions small airways	• High pitched • Peripheral • Clear with cough
*Coarse crackles* Sounds like pouring milk on rice crispies	Obstruction more proximal and larger airways with sputum. May be inspiratory as well as expiratory	• Early expiratory: central airways • Late expiratory: more peripheral airways • Large deep sound • Changes/clears with coughing

Top tip!

Remember crackles are only heard if the velocity of airflow is adequate and breath sounds are audible. Coarse crackles move/disappear when the patient coughs, whereas fine crackles remain the same after coughing.

– Wheezes (Table 3.3.4). Whistling sounds due to narrowed airway walls vibrating against each other, indicating airway obstruction. High-pitched wheeze indicates bronchospasm or oedema in the walls of conducting airways. Low-pitched wheeze indicates sputum.

You should identify whether wheezes or crackles are heard during inspiration or expiration and whether they are heard early or late during the breath. Louder sounds heard early in the breath are more likely to be generated centrally (in the larger airways).

– Pleural rub (Table 3.3.5). A sound like boots crunching on snow suggests that the pleura are inflamed.

– Stridor (Table 3.3.5). This is a sound like a loud ‘barking’ noise. Occurs during both inspiration and expiration and is usually caused by significant upper airway obstruction, which could be a foreign body or tumour. If stridor is heard as a new/recent symptom, alert the medical staff immediately as the patient’s airway could be compromised.

Table 3.3.4 Added sounds: wheezes

*Wheezes*	Musical sounds due to vibration of wall of narrowed airway
*High pitched*	Bronchospasm	• Potential increased work of breathing
*Low pitched*	Sputum	• Disrupted turbulent flow • Change with coughing
*Localized*	TumourForeign body	• Limited to a local area on auscultation

Table 3.3.5 Other sounds

	Sounds like	Cause
*Pleural rub*	• Creaking/rubbing (like boots on snow) • Localized/generalized • Soft/loud • Equal inspiration to expiration	• Inflammation of pleura • Infection • Tumour
*Stridor*	• Constant pitch on inspiration and expiration • Produced in upper airways	• Croup • Laryngeal tumour • Upper airway obstruction ! Alert medical staff as the patient’s airway is at great risk of compromise

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3.1 Arterial blood gases (ABGs)

Definition

Purpose

Procedure

Findings (Fig. 3.1.2, Table 3.1.1)

Example of respiratory acidosis

Example of respiratory alkalosis

Example of metabolic acidosis

Example of metabolic alkalosis

Example of a fully compensated respiratory acidosis

Example of a partially compensated metabolic acidosis

Documentation