Show Summary Details
Page of

Systematic assessment 

Systematic assessment
Systematic assessment

Heather Baid

, Fiona Creed

, and Jessica Hargreaves

Page of

PRINTED FROM OXFORD MEDICINE ONLINE ( © Oxford University Press, 2021. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

date: 05 May 2021

Assessment principles and strategies

A systematic assessment of the patient is required in order to optimize patient care and management. At the very minimum a patient assessment should be conducted on admission and at the start of each nursing handover. Additional assessments will be prompted by changes in the patient’s status. Depending on the severity of the patient’s condition, the assessment may need to be conducted rapidly.

The assessment process consists of a review of the patient’s past medical history, the reason for their admission to the critical care unit and/or the problems currently being experienced by the patient, and the findings of the physical assessment of the patient.

Principles of history taking

History taking is an important element of the assessment of a patient, as it identifies contemporary and past illnesses, indicates how the patient and their family are affected by the illness, introduces the patient to the nurse and the care setting, and will inform the clinical diagnosis.

  • Put the patient at ease to enable full disclosure of their health history.

  • Start with broad questions and then move on to system-specific questions.

  • Identify the primary signs and symptoms of the problem that is being experienced by the patient (e.g. chronology, severity, duration, triggers, relievers).

  • Include questions about the patient’s past medical, medication, family, and social history.

Principles of physical assessment

The physical assessment involves a ‘look, listen, and feel’ approach that corresponds to the following more formal medical terms:

  • inspection

  • palpation

  • percussion

  • auscultation.

All assessment findings should be documented in an agreed format and communicated to the multidisciplinary team and the patient as appropriate. Document the resuscitation status of the patient and the maximum level of care offered in the event of further deterioration.

Common assessment strategies include:

  • ABCDE assessment

  • head-to-toe assessment

  • focused assessment (e.g. by body system) (see Chapters 4, 6, 8, 9, and 10).

Further reading

Cox C Physical Assessment for Nurses., 2nd ed. Wiley-Blackwell: Chichester, 2009.Find this resource:

Douglas G, Nicol F and Robertson C (eds). Macleod’s Clinical Examination, 13th ed. Churchill Livingstone: Edinburgh, 2013.Find this resource:

Hogan-Quigley B, Palm ML and Bickley LS. Bates’ Nursing Guide to Physical Examination and History Taking. Lippincott Williams & Wilkins: Philadelphia, PA, 2011.Find this resource:

Ranson M, Abbott H and Braithwaite W (eds). Clinical Examination Skills for Healthcare Professionals. M&K Update: Keswick UK, 2014.Find this resource:

ABCDE assessment

This consists of assessment of Airway, Breathing, Circulation, Disability, and Exposure. This assessment strategy is commonly used in a critical care context, and is particularly suited to the rapid or emergency assessment of a patient.


Indicators of airway compromise (see Box 2.1)

  • Look for altered or increased respiratory effort, use of accessory muscles (sternocleidomastoid, trapezius, and internal intercostals), paradoxical chest and abdominal movements ‘see-saw respiration’, drooling (inability of the patient to swallow their own saliva), and bleeding from the nose, mouth or tracheostomy.

  • Listen for hoarseness, stridor, snoring, gurgling, and inability to speak.

  • Feel for movement of expired air from the mouth or nose, and for sweaty or clammy skin.


Indicators of respiratory compromise

  • Look for altered or increased respiratory effort, use of accessory muscles (sternocleidomastoid, trapezius, and internal intercostals), nasal flaring, pursed-lip breathing, inability to lie flat, central cyanosis, depth of breathing, pattern of breathing, unilateral chest expansion, chest and/or spinal deformity, presence and patency of chest drains, chest surgery (past or present), trauma, bruising, bleeding, and flail chest.

  • Listen for inability to complete full sentences, audible breath sounds, and abnormal breath sounds via auscultation of the anterior, lateral, and posterior surfaces of the chest (unilateral, inspiratory and/or expiratory wheeze, crackles, pleural rub, and bronchial, decreased, or absent breath sounds).

  • Feel for tracheal deviation, subcutaneous emphysema, crepitus, thoracic tenderness, and abnormal resonance via percussion (hyper-resonance or dullness).

  • Record the respiratory rate (normal range, 12–20 breaths/min) and oxygen saturations (normal range, 97–100%).

For specialized respiratory assessment and monitoring, see Chapter 4.


Indicators of circulatory compromise

  • Look for pallor, cyanosis (peripheral and central), chest deformity, jugular venous distension, cardiac devices (pacemaker or implantable defibrillator), bruising, and haemorrhage.

  • Listen for reduced level of consciousness due to poor cardiac output (confusion, drowsiness), complaints of chest pain, and abnormal heart sounds via auscultation (S3, S4, murmurs, pericardial rub).

  • Feel for pulse rhythm and strength, capillary refill time (normal value ≤ 3 s), limb temperature, and sweaty, clammy, warm, or cool skin.

  • Record heart rate (normal range, 60–100 beats/min), blood pressure (normal range, mean arterial pressure ≥ 65 mmHg), central venous pressure (normal range, 2–10 mmHg), urine output (normal range, ≥ 0.5 mL/kg/h), and core temperature (normal range, 36–37.5°C).

For specialized cardiac assessment and monitoring, see Chapter 6.


Indicators of neurological compromise

  • Look for pupil size, equality, and reaction to light, as well as head trauma and cerebrospinal fluid leakage (otorrhoea, rhinorrhoea).

  • Listen for reduced level of consciousness due to poor neurological function (confusion, drowsiness), and complaints of pain.

  • Record the blood glucose concentration (normal range, 4–8 mmol/L), Alert Verbal Pain Unresponsive (AVPU) response (normal response, Alert), and Glasgow Coma Scale (GCS) score (normal score, 15/15) (see Table 2.1).

Table 2.1 Glasgow Coma Scale (GCS)

Eye response

Verbal response

Motor response





Obeys commands


To speech




Localizes to pain


To pain


Inappropriate words


Flexion to pain


No response


Incomprehensible sounds


Abnormal flexion


No response




No response


For specialized neurological assessment and monitoring, see Chapter 8.


Indicators of physiological compromise

  • Look for bleeding, bruising, burns, rashes, swelling, inflammation, infection, and wounds on the body.

  • Listen for complaints of pain, pruritus, heat, and cold.

  • Feel for venous thromboembolism and oedema.

Head-to-toe assessment

This assessment strategy is best used in combination with the ABCDE assessment. It also focuses on physical assessment and observations, but is suitable for the routine assessment of a critically ill patient.


In addition to the Disability section of the ABCDE assessment:

Assess pain

  • Assess every 4 hours or as necessary.

  • If the patient is able to self-report, use a numerical rating scale (e.g. scale of 0 to 10 where 0 = no pain and 10 = worst pain ever experienced). Ask the patient to score their pain from 0 to 10, and ensure that pain is assessed on movement (e.g. when the patient coughs).

  • If the patient is unable to self-report, use the Behavioural Pain Scale (BPS) (score in the range 3–12) (see Table 2.2).

Table 2.2 Behavioural Pain Scale (BPS)




Facial expression



Partially tightened (e.g. brow lowering)


Fully tightened (e.g. eyelid closing)




Upper limbs

No movement


Partially flexed


Fully flexed with finger flexion


Permanently retracted


Compliance with ventilation

Tolerating ventilation


Coughing but tolerating ventilation


Fighting ventilator


Unable to control ventilation


Assess delirium

  • Assess every shift or as necessary (see Box 2.2).

  • Use a delirium screening tool—e.g. the Confusion Assessment Method-ICU (CAM-ICU) (see Figure 2.1) or the Intensive Care Delirium Screening Checklist (ICDSC) (0–12) (see Figure 2.2).

Figure 2.1 Confusion Assessment Method-ICU (CAM-ICU) worksheet.

Figure 2.1 Confusion Assessment Method-ICU (CAM-ICU) worksheet.

(Reproduced with permission from Vanderbilt Medical University. Copyright © 2013, E. Wesley Ely, MD, MPH and Vanderbilt University, all rights reserved.)

Figure 2.2 Intensive Care Delirium Screening Checklist (ICDSC).

Figure 2.2 Intensive Care Delirium Screening Checklist (ICDSC).

(Reproduced with permission from Vanderbilt Medical University. Copyright © 2013, E. Wesley Ely, MD, MPH and Vanderbilt University, all rights reserved.)

Delirium is an acute event that develops over hours or days, and has a medical rather than psychiatric cause. Delirium subtypes are as follows:

  • hypoactive patient—withdrawn, lethargic, apathetic, or may even be unresponsive

  • hyperactive patient—extremely agitated, emotionally labile, exhibiting disruptive behaviours such as refusing care, shouting, violence, removing cannulae, and attempting to self-discharge.

Table 2.3 lists the risk factors that predispose critical care patients to delirium.

Table 2.3 Risk factors for delirium

All critical care patients

Critical care patients over 80 years of age

History of:

  • hypertension

  • smoking

  • sensory impairment

  • malnutrition

History of:

  • depression

  • cognitive impairment

  • dementia

Raised bilirubin level

Raised urea:creatinine ratio


  • epidural, urinary catheter, physical restraint


  • benzodiazepines, opioids

Severity of illness

Assess sedation

  • Assess every 24 h or as necessary.

  • Use a sedation scoring system—for example, the Richmond Agitation Sedation Scale (RASS) (see Box 2.3 for sedation goals).

Respiratory and ventilation

In addition to the Airway and Breathing sections of the ABCDE assessment:

Assess airway adjunct

  • Every shift or as necessary.

  • If an endotracheal tube is in place, note the tube lip level and check that it is fixed securely, and also check the patency of the tubing and the heat and moisture exchanger (HME) filter (if used). Confirm the cuff pressure (normal range, 20–30 cmH2O).

  • For a tracheostomy tube, perform the same checks (except for lip level), and check the patency of the inner cannula. Replace or check 4-hourly or as necessary.

Assess mechanical ventilation

  • Every shift or as necessary.

  • Check the ventilator settings (tidal volume, minute volume, peak and plateau pressures) and alarm limits. Check patient compliance and comfort with mechanical ventilation.

Assess oropharyngeal and tracheal secretions

  • Every shift or as necessary.

  • Check quantity—frequency of suctions, single or multiple passes.

  • Check quality—mucoid or purulent, consistency (normal or loose), colour (clear is normal).

  • Check whether the patient coughs on suctioning.


In addition to the Circulation section of the ABCDE assessment:

Assess cardiac rhythm

  • Every shift and as necessary.

  • Use routine 3- or 5-lead ECG monitoring and a 12-lead ECG to check for ischaemic changes, infarction, or abnormal rhythms.

Assess fluid status

  • Every shift or as necessary.

  • Check blood pressure, heart rate, and urine output ≥ 0.5 mL/kg/h.

  • Calculate and review cumulative fluid balance.

  • Note the use of crystalloid and/or colloid.

  • Note the fluid challenge response.

  • Note insensible losses (e.g. diaphoresis, tachypnoea, diarrhoea).

  • Check the indications, route, risks, benefits, and goals of fluid therapy support.

  • Check the mucous membranes and axillae (note whether moist or dry, and with pink colour or pallor).

  • Check for peripheral and pulmonary oedema, capillary refill, and jugular venous distension.

  • Check the patient’s weight weekly.

  • Review laboratory results (e.g. FBC, U&E, and lactate).

  • Review cardiac output monitoring (see Systematic assessment p. [link]).


In addition to the Exposure section of the ABCDE assessment:

Assess the integument

  • Every shift and as necessary.

  • Check the patient’s pressure areas for pressure ulcers.

  • Note the date of insertion and location of vascular access devices, catheters, and drains.

Abdomen and nutrition

In addition to the ABCDE assessment:

Assess the abdomen

  • Every shift or as necessary.

  • Conduct a physical assessment of the abdomen.

  • If surgical drains are present, note collection volumes.

  • For specialized abdominal assessment and monitoring, see Systematic assessment pp. [link] and[link].

Assess nutrition and elimination

  • Every shift or as necessary.

  • Screen for malnutrition using a recognised screening tool such as the Malnutrition Universal Screening Tool (MUST)1 or the NUTrition Risk in the Critically ill score (NUTRIC)2,3. (see Systematic assessment p. [link]).

  • Consider refeeding syndrome (poor diet before admission) (see Systematic assessment p. [link]).

  • Check nasogastric tube position (see Systematic assessment p. [link]) and gastric residual volume (if using enteral feeding) see Systematic assessment p. [link].

  • Check the indications, route, risks, benefits, and goals of nutrition support (20–30 kcal/kg/day) (see Systematic assessment p. [link]).

  • Check the patient’s weight weekly.

  • Check the swallowing assessment (this may fall within the remit of the speech and language therapist).

  • Document nutritional intake (oral, enteral, and parenteral) (see Systematic assessment p. [link]).

  • Check blood pressure and heart rate, and that urine output is ≥ 0.5mL/kg/h.

  • Check blood glucose and insulin therapy (maintain blood glucose concentration ≤ 10 mmol/L).

  • Review laboratory results (e.g. FBC, U&E, and lactate).

  • Urinalysis.

  • Check bowel output, frequency, and type using the Bristol Stool Chart (see Figure 2.3) (see Systematic assessment pp. [link] and [link]).

Figure 2.3 Bristol Stool Chart.

Figure 2.3 Bristol Stool Chart.

(Reproduced by kind permission of Dr K. W. Heaton, Reader in Medicine at the University of Bristol © 2000 Norgine Pharmaceuticals Ltd.)


1 Malnutrition Advsiory Group. Malnutrition Universal Screening Tool. BAPEN, 2011. Systematic assessment

2 Critical Care Nutrition. NUTRIC score. Critical Care Nutrition, 2013. Systematic assessment

3 Heyland DK et al. Identifying critically ill patients who benefit the most from nutrition therapy: the development and initial validation of a novel risk assessment tool. Critical Care. 2011; 15: R268.Find this resource:

Further reading

Barr J et al. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Critical Care Medicine 2013; 41: 263–306.Find this resource:

The 2014 CAM-ICU Training Manual Redesign Team. Confusion assessment method for the ICU (CAM-ICU): the complete training manual. Ely EW and Vanderbilt University, 2014. Systematic assessment

European Society for Parenteral and Enteral Nutrition (ESPEN). ESPEN guidelines on enteral nutrition: intensive care. Clinical Nutrition 2006; 25: 210–23.Find this resource:

European Society for Parenteral and Enteral Nutrition (ESPEN). ESPEN guidelines on parenteral nutrition: intensive care. Clinical Nutrition 2009; 28: 387–400.Find this resource:

Langley-Evans S and King CR. Assessment of nutritional status in clinical settings. Journal of Human Nutrition and Dietetics 2014; 27: 105–6.Find this resource:

National Institute for Health and Care Excellence (NICE). Intravenous Fluid Therapy in Adults in Hospital. CG174. NICE: London, 2013. Systematic assessment this resource:

Schneider A et al. Estimation of fluid status changes in critically ill patients: fluid balance chart or electronic bed weight? Journal of Critical Care 2012; 27: 745e7–12.Find this resource:

Mental health assessment

Assessment of mental health and well-being is integral to the holistic care of a critically ill patient. The assessment has a twofold purpose—first, to identify the impact of physical illness or injury on the patient’s mental health, and second, to establish the effect, if any, of mental ill health on the patient’s physical health and recovery. In addition, nurses should be familiar with the principles and functions of mental capacity assessment.

During the mental health assessment, it may become apparent that the patient is at risk. This should prompt immediate referral to mental health services. Box 2.4 lists the physical signs and symptoms that may be attributable to mental disorders and/or medication prescribed for a mental disorder.

ABC mental health assessment

This involves rapid assessment of mental health status within three domains.

Affective domain

This domain focuses on observation of the patient’s emotional state and expressed feelings. It involves objective interpretation by the nurse of the patient’s non-verbal communication, and documentation of the patient’s mood, which is a subjective finding.

Behaviour domain

This domain focuses on observation of the patient’s behaviour. It involves subjective interpretation by the nurse of the patient’s behaviour and appearance. Caution is needed when interpreting the patient’s behaviour as a sign of mental disorder (e.g. inability to maintain eye contact can be a sign of depression, but this behaviour can also be due to a social or cultural convention).

Cognition domain

This domain focuses on evaluation of the patient’s cognitive function. Within this domain there is overlap with neurological assessment (see Systematic assessment p. [link]). It involves objective interpretation by the nurse of the patient’s orientation to person, place, and time, and observation of any signs of confusion or change in alertness.

Mental capacity assessment

The five key principles

  • Every adult has the right to make their own decisions (i.e. a patient is assumed to have capacity unless proven otherwise).

  • A person must be given as much help as is practicable before anyone treats them as not being able to make their own decisions.

  • If an individual makes what might be seen as an unwise decision, they should not be treated as lacking capacity to make that decision.

  • Anything that is done or any decision that is made on behalf of a person who lacks capacity must be done or decided in their best interests.

  • Anything that is done for or on behalf of a person who lacks capacity should be minimally restrictive of their basic rights and freedoms.

Mental capacity assessment applies to situations where a person may be unable to make a particular decision at a particular time. It does not mean an inability to make general decisions or that a loss of capacity is permanent.

Assessment of mental capacity

  • Identify the specific decision to be made.

    • The assessment of capacity relates to a particular decision made at a particular time, and is not about a range of decisions (see Box 2.5).

  • Functional test of capacity.

    • Is there an impairment of, or disturbance in, the functioning of the person’s mind or brain (this may be either permanent or temporary)?

    • If the answer is yes, does the impairment or disturbance result in the person being unable to make the particular decision?

The person will be unable to make the particular decision if, after all appropriate help and support has been given to them, they cannot:

    • understand the information relevant to that decision, including the likely consequences of making or not making the decision

    • retain that information

    • use or weigh that information as part of the decision-making process

    • communicate their decision (either verbally or non-verbally).

Mental capacity terminology

  • Lasting power of attorney (LPA)—a legal document that allows decisions to be made by an identified person (the attorney) on behalf of a person who lacks mental capacity (the donor). The document is only considered legal if it is registered with the Office of the Public Guardian.

  • Court of Protection— a specialist court that arbitrates over issues specifically related to mental capacity. The Court of Protection will appoint a Deputy when decisions need to be made on behalf of a person who lacks mental capacity.

  • Deprivation of liberty safeguards (DOLS)—decision making on behalf of a person who lacks capacity can potentially deprive them of their personal freedom and choice (deprivation of liberty). Safeguards now exist to ensure that decisions are made in the best interests of the person, and that the process is legal and open to challenge.

  • Independent Mental Capacity Advocate (IMCA)—an IMCA is appointed if a person who lacks capacity has no one other than paid staff to assist them with decision making about serious medical treatment.

  • Advance decisions—an advance decision allows a person to refuse pre-specified medical treatment at a time when they may no longer be capable of consenting to or refusing treatment. The person must have capacity at the time of making the decision, and must clearly identify which treatments would be refused and under what circumstances. Until an advance decision has been identified and confirmed as valid, the healthcare professionals must continue to act in the person’s best interests.

Factors that affect the mental health and well-being of critically ill patients

  • Communication barriers:

    • endotracheal tube or tracheostomy

    • sedation

    • cognitive dysfunction

    • muscle weakness.

  • Confusion:

    • may be linked to the patient’s past medical history (e.g. mental disorder, dementia)

    • may be the reason for their admission (e.g. neurological injury, sepsis)

    • may be caused by their treatment (e.g. post-sedation delirium).

  • Environment:

    • noise levels

    • activity levels and intensity

    • privacy and dignity

    • unfamiliar surroundings

    • transfer and discharge.

Further reading

Crews M et al. Deprivation of liberty in intensive care. Journal of the Intensive Care Society 2014; 15: 320–4.Find this resource:

Menon DK and Chatfield DA. A guide for critical care settings: Mental Capacity Act 2005. Version 6. Intensive Care Society: London, 2011.Find this resource:

Mental Capacity Act 2005.

White SM and Baldwin TJ. 2006. The Mental Capacity Act 2005—implications for anaesthesia and critical care. Anaesthesia 61 (4): 381–389.Find this resource:

Blood gas analysis

Blood gas analysis is used to direct ventilation and oxygenation strategies and act as a guide to the acid–base balance of the patient. Normal arterial and venous blood gas values are listed in Table 2.4.

Table 2.4 Normal arterial and venous blood gas values

Normal arterial values

Normal venous values

pH  7.35–7.45

pH  7.35–7.45

PaCO2  4.6–6.0 kPa

PvCO2  4.5–6.0 kPa

HCO3  22–26 mmol/L

HCO3  22–28 mmol/L

Base excess  +2 to –2 mmol/L

Base excess  +2 to –2 mmol/L

Lactate  0.5–1.5 mmol/L

Lactate  0.5–2.2 mmol/L

PaO2  10.0–13.3 kPa

PvO2  11–13 kPa

SaO2  > 95%

SvO2  65–75%

  • pH—this is a measure of how acid or alkaline the blood is in the presence of H+ ions. A low pH is acidotic (more H+ ions), whereas a high pH is alkalotic (fewer H+ ions).

  • PaCO 2—partial pressure of arterial carbon dioxide (CO2), which is the primary metabolite of cellular respiration. CO2 dissolves in water (H2O) to form carbonic acid, which dissociates into H+ and HCO3 ions. This process is speeded up in the presence of the enzyme carbonic anhydrase.

  • HCO 3 —bicarbonate is a buffer found in the plasma, which resists changes in pH by retaining or releasing H+ ions. If there are more HCO3 ions than H+ ions, the blood is more alkalotic. Bicarbonate is produced in the liver and kidneys.

  • Buffering is the first line of correction of pH, but the HCO3 supply will fall, so H+ ion elimination is also required. Excess H+ ions are removed from the circulation by the kidneys, which excrete H+ ions in the urine and reabsorb HCO3 ions in the proximal tubule of the nephron, or by the lungs, which excrete H+ ions in H2O. Removal from the lungs occurs within minutes or hours, whereas removal from the kidneys occurs over a period of days.

  • Base excess (BE)—this refers to the amount of acid required to return 1 L of blood to pH 7.4 at a PCO2 of 5.3 kPa. It reflects the metabolic component of a pH imbalance.

    • Negative BE indicates the amount of acid that needs to be removed in order to return the pH to normal (i.e. as a result of a metabolic acidosis).

    • Positive BE indicates the amount of acid that needs to be retained or added in order to return the pH to normal (i.e. as a result of a metabolic alkalosis).

  • Lactate (or lactic acid)—this chemical is produced in anaerobic metabolism, and it is an indicator that increased metabolic demand is exceeding the supply of oxygen available. A raised lactate concentration is associated with acidosis.

  • PaO 2—partial pressure of arterial oxygen. Oxygen is the primary substrate for cellular respiration. It binds to haemoglobin to form oxyhaemoglobin. Different physical conditions will affect the affinity of haemoglobin for oxygen. These include pH, PCO2, temperature, and 2,3-diphosphoglycerate (2,3-DPG).

  • SaO 2—Oxygen saturation is a measure of how much oxygen is bound to haemoglobin. The higher the partial pressure of oxygen (PO2), the higher the oxygen saturation will be.

Values are corrected for the patient’s specific body temperature, and fractionated inspired oxygen concentration (FiO2) is entered. The standard bicarbonate (stdHCO3 ) and the standard base excess (stdBE) values are given with the respiratory component of the acid–base disturbance removed. Therefore if the stdHCO3 is lower than HCO3 , the acidosis is metabolic in origin.

Arterial blood gas analysis

Check whether the pH is within the normal range

  • If the pH is below the normal range this is acidosis.

  • If the pH is above the normal range this is alkalosis.

  • If the pH is within the normal range, check whether the PCO2 and the HCO3 are also within the normal range.

Check the cause of the acidosis (low pH)

  • If the PCO2 is above the normal range this is respiratory acidosis.

  • If the HCO3 is below the normal range this is metabolic acidosis.

  • If the PCO2 is above the normal range and the HCO3 is below the normal range this is mixed acidosis.

Check the cause of the alkalosis (high pH)

  • If the PCO2 is below the normal range this is respiratory alkalosis.

  • If the HCO3 is above the normal range this is metabolic alkalosis.

  • If the PCO2 is below the normal range and the HCO3 is above the normal range this is mixed alkalosis.

Check for compensation

  • If the pH is not within the normal range this is not compensated.

  • If the pH is within the normal range and the PCO2 and the HCO3 are outside the normal range but in opposite directions (i.e. either high PCO2 and low HCO3 , or low PCO2 and high HCO3 ) this is compensated.

Check whether the PO2 is within the normal range

  • If the PO2 is below the normal range this is hypoxaemia.

  • If the PO2 is above the normal range this is hyperoxaemia.

Table 2.5 summarizes the different arterial blood gas results.

Table 2.5 Representation of acidosis and alkalosis values




Respiratory acidosis


Respiratory alkalosis


Metabolic acidosis


Metabolic alkalosis


Respiratory and metabolic acidosis

Respiratory and metabolic alkalosis

Acid–base disturbances

  • Respiratory acidosis—increased production and/or decreased excretion of CO2. Causes include:

    • obstructive lung disease

    • respiratory depression (over-sedation, brain injury, neuromuscular disorders)

    • hypoventilation (error in non-invasive or mechanical ventilation, chest deformities, or pain restricting ventilation).

  • Respiratory alkalosis—increased excretion of CO2. Causes include:

    • restrictive lung disease

    • pulmonary embolus

    • hyperventilation (error in non-invasive or mechanical ventilation, hypoxia, anxiety).

  • Metabolic acidosis—increased production or retention of acid and/or increased excretion of base/alkali. Causes include:

    • uraemia

    • acid ingestion (aspirin, ethylene glycol)

    • acid from abnormal metabolism (ketoacidosis)

    • hyperchloraemia (due to excess intravenous infusions)

    • lactic acidosis (due to exercise, shock, hypoxia, liver failure, or trauma)

    • loss of alkali (due to diarrhoea, bowel fistula, or renal tubular necrosis).

  • Metabolic alkalosis—increased production or retention of base/alkali and/or increased excretion of acid. Causes include:

    • alkali ingestion

    • excess bicarbonate or buffer infusions

    • renal disorders

    • hypokalaemia

    • drugs (diuretics, ingestion of alkali)

    • loss of acid (due to gastric aspirates or vomiting).


This is defined as a low oxygen concentration in the blood:

  • < 8.0 kPa when breathing air

  • < 11.0 kPa when breathing > 0.4 FiO2.

Acute compensation can occur to avoid tissue hypoxia (e.g. increasing cardiac output or increasing oxygen extraction by the tissues).

Chronic compensation by increasing red blood cell numbers and haemoglobin levels is seen in chronic obstructive pulmonary disease (COPD) and in populations who live at high altitudes.

Causes of hypoxaemia

  • Ventilatory inadequacy—for example, mechanical defects (including airway obstruction), neuromuscular dysfunction, central nervous system depression.

  • Ventilation/perfusion mismatch—for example, pulmonary embolus, poor right cardiac function, acute respiratory distress syndrome (ARDS).

  • Shunt—for example, atelectasis, pneumonia.

  • Diffusion limitation—for example, ARDS, fibrosing alveolitis, pulmonary oedema.

Tissue hypoxia

This is defined as inadequate oxygen to support cell metabolism. It is extremely difficult to monitor directly, and hypoxaemia is commonly used as a marker of possible hypoxia.

There are four categories of hypoxia.

  • Hypoxic hypoxia—hypoxaemia results in inadequate oxygen delivery to the cells.

  • Anaemic hypoxia—arterial oxygen is normal, but oxygen-carrying capacity is inadequate due to either low Hb or dysfunctional Hb (e.g. in carbon monoxide poisoning).

  • Circulatory hypoxia—oxygen delivery is insufficient to meet cell needs or does not reach the cells due to shunt.

  • Histotoxic hypoxia—the ability of the cells to utilize oxygen is impaired (e.g. in cyanide poisoning, which blocks mitochondrial electron transport).

Laboratory investigations

Critical care patients require ongoing measurement of renal function, electrolytes, and haematology indices. Blood cultures and other microbiology samples should be taken as required (in the event of inflammation, infection, or pyrexia) (see Table 2.6).

Table 2.6 Normal values for common blood tests. (Reproduced from Longmore M, Wilkinson I, Baldwin A and Wallin E, Oxford Handbook of Clinical Medicine, Ninth Edition, 2014, with permission from Oxford University Press.)


Reference interval

Your hospital

White cell count (WCC)

4.0–11.0 × 109/L

Red cell count

  • ♂ 4.5–6.5 × 1012/L

  • ♀ 3.9–5.6 × 1012/L


  • ♂ 130–180 g/L

  • ♀ 115–160 g/L

Packed red cell volume (PCV) or haematocrit

  • ♂ 0.4–0.54 L/L

  • ♀ 0.37–0.47 L/L

Mean cell volume (MCV)

76–96 fL

Mean cell haemoglobin (MCH)

27–32 pg

Mean cell haemoglobin concentration (MCHC)

300–360 g/L

Red cell distribution width (RCDW, RDW)



  • 2.0–7.5 × 109/L;

  • 40–75% WCC


  • 1.3–3.5 × 109/L;

  • 20–45% WCC


  • 0.04–0.44 × 109/L;

  • 1–6% WCC


  • 0.0-0.10 × 109/L;

  • 0–1% WCC


  • 0.2–0.8 × 109/L;

  • 2–10% WCC

Platelet count

150–400 × 109/L

Reticulocyte count

0.8–2.0%1 25–100 × 109/L

Erythrocyte sedimentation rate

Depends on age

Prothrombin time (citrated bottle) (factors I, II, VII, X)

10–14 s

Activated partial thromboplastin time (VIII, IX, XI, XII)

35–45 s

D-dimer1 (citrated bottle, as for INR)

< 0.5 mg/L

Drugs (and other substances) may interfere with any chemical method; as these effects may be method dependent, it is difficult for the clinician to be aware of all the possibilities. If in doubt, discuss with the lab.


Reference interval (labs vary, so a guide only)

Your hospital

Adrenocorticotrophic hormone

< 80 ng/L

Alanine aminotransferase (ALT)

5–35 U/L


35–50 g/L


100–500 pmol/L

Alkaline phosphatase

30–150 U/L (adults)


0–180 Somogyi U/dL


< 10 kU/L

Angiotensin II

5–35 pmol/L

Antidiuretic hormone (ADH)

0.9–4.6 pmol/L

Aspartate transaminase

5–35 U/L


24–30 mmol/L


3–17 μ‎mol/L


< 50 ng/L


< 0.1 μ‎g/L

Calcium (ionized)

1.0–1.25 mmol/L

Calcium (total)

2.12–2.65 mmol/L


95–105 mmol/L


< 5.0 mmol/L

  • VLDL

0.128–0.645 mmol/L

  • LDL

< 2.0 mmol/L

  • HDL

0.9–1.93 mmol/L


  • AM 450–700 nmol/L

  • midnight 80–280 nmol/L

Creatine kinase (CK)

  • ♂ 25–195 U/L

  • ♀ 25–170 U/L

Creatinine (∝ to lean body mass)

70–150 μ‎mol/L

CRP C-reactive protein

< 10 mg/L


12–200 μ‎g/L


2.1 μ‎g/L

Follicle-stimulating hormone (FSH)

  • 2–8 U/L in ♀ (luteal);

  • > 25 U/L in menopause

Gamma-glutamyl transpeptidase

  • ♂ 11–51 U/L

  • ♀ 7–33 U/L

Glucose (fasting)

3.5–5.5 mmol/L

Growth hormone

< 20 mu/L

HbA1c = glycosylated Hb (DCCT)

4–6%. 7% ≈ good DM control

HbA1c IFCC (more specific than DCCT)

  • 20–42 mmol/mol; 53 ≈ good

  • DM control


  • ♂ 14–31 μ‎mol/L

  • ♀ 11–30 μ‎mol/L


  • Venous 0.6–2.4 mmol/L

  • Arterial 0.6–1.8 mmol/L

Lactate dehydrogenase (LDH)

70–250 U/L


< 1.8 mmol/L

Luteinizing hormone (LH) (premenopausal)

3–16 U/L (luteal)


0.75–1.05 mmol/L


278–305 mosmol/kg

Parathyroid hormone (PTH)

< 0.8–8.5 pmol/L


3.5–5.0 mmol/L


  • ♂ < 450 U/L

  • ♀ < 600 U/L

Prostate specific antigen (PSA)

0–4 μ‎g/mL, age specific, see Systematic assessment p. [link]

Protein (total)

60–80 g/L

Red cell folate

  • 0.36–1.44 μ‎mol/L

  • (160–640 μ‎g/L)

Renin (erect/recumbent)

  • 2.8–4.5/

  • 1.1–2.7 pmol/mL/h


135–145 mmol/L

Thyroid-binding globulin (TBG)

7–17 mg/L

Thyroid-stimulating hormone (TSH)

  • 0.5–5.7 mU/L

  • widens with age, [link]

  • assays vary;

  • 4–5 is a grey area

Thyroxine (T4)

70–140 nmol/L

Thyroxine (free)

9–22 pmol/L

Total iron-binding capacity

54–75 μ‎mol/L


0.55–1.90 mmol/L

Triiodothyronine (T3)

1.2–3.0 nmol/L

Troponin T (see [link])

<0.1 μ‎g/L


  • ♂ 210–480 μ‎mol/L

  • ♀ 150–390 μ‎mol/L


2.5–6.7 mmol/L

Vitamin B12

  • 0.13–0.68 nmol/L

  • (>150 ng/L)

Vitamin D

60–105 nmol/L

Urine reference intervals

Reference interval

Your hospital

Cortisol (free)

< 280 nmol/24h

Hydroxyindole acetic acid

16–73 μ‎mol/24h

Hydroxymethylmandelic acid (HMMA, VMA)

16–48 μ‎mol/24h


  • 0.03–0.69 μ‎mol/mmol creatinine (or < 5.5 μ‎mol/day)


350–1000 mosmol/kg

17-oxogenic steroids

  • ♂ 28–30 μ‎mol/24h

  • ♀ 21–66 μ‎mol/24h

17-oxosteroids (neutral)

  • ♂ 17–76 μ‎mol/24h

  • ♀ 14–59 μ‎mol/24h

Phosphate (inorganic)

15–50 mmol/24h


14–120 mmol/24h


< 150 mg/24h


creatinine ratio < 3 mg/mmol


100–250 mmol/24h

1 D-dimer assay is useful for excluding thromboembolic disease if the assay is normal. The D-dimer is non-specific, therefore a raised level is unhelpful and should only be requested if the probability of thromboembolic disease is low (eg Wells score). It needs to get to the lab quickly.

2 Desired upper limit of cholesterol would be < 6 mmol/L. In some populations, 7.8 mmol/L is the top end of the distribution.