Critical care medicine

Chapter 16 Critical care medicine


Critical care medicine (or ‘intensive care medicine’) is concerned predominantly with the management of patients with acute life-threatening conditions (’the critically ill’) in specialized units. As well as emergency cases, such units admit high-risk patients electively after major surgery (Table 16.1). Intensive care medicine also encompasses the resuscitation and transport of those who become acutely ill, or are injured in the community. Management of seriously ill patients throughout the hospital (e.g. in coronary care units, acute admissions wards, postoperative recovery areas or emergency units), including critically ill patients who have been discharged to the ward (‘outreach care’), is also undertaken. Teamwork and a multidisciplinary approach are central to the provision of intensive care and are most effective when directed and coordinated by committed specialists.

Table 16.1 Some common indications for admission to intensive care

Intensive care units (ICUs) are usually reserved for patients with established or potential organ failure and provide facilities for the diagnosis, prevention and treatment of multiple organ dysfunction. They are fully equipped with monitoring and technical facilities, including an adjacent laboratory (or ‘near patient testing’ devices) for the rapid determination of blood gases and simple biochemical data such as serum potassium, blood glucose and blood lactate levels. Patients receive continuous expert nursing care and the constant attention of appropriately trained medical staff. High dependency units (HDUs) offer a level of care intermediate between that available on the general ward and that provided in an ICU. They provide monitoring and support for patients with acute (or acute-on-chronic) single organ failure and for those who are at risk of developing organ failure. These units are a more comfortable environment for less severely ill patients who are often conscious and alert. They can also provide a ‘step-down’ facility for patients being discharged from intensive care.

The provision of staff and the level of technical support must match the needs of the individual patient and resources are used more efficiently when they are combined in a single critical care facility rather than being divided between physically and managerially separate units.

In the UK, only around 3.4% of hospital beds are designated for intensive care (3.5 ICU beds per 100 000 population), whereas in many other developed economies, the proportion is much higher.

General aspects of managing the critically ill

Recognition and diagnosis of critical illness

Early recognition and immediate resuscitation are fundamental to the successful management of the critically ill. In order to facilitate identification of ‘at risk’ patients on the ward and early referral to the critical care emergency or outreach team a number of early warning systems have been devised (e.g. the Modified Early Warning Score, MEWS; see Box 16.1). These are based primarily on bedside recognition of deteriorating physiological variables and can be used to supplement clinical intuition. A MEWS score of ≥5 is associated with an increased risk of death and warrants immediate admission to ICU. Another example of a system used to trigger referral to a Medical Emergency Team (MET) is also shown in Box 16.1 (see also ‘Management of shock and sepsis’ and ‘Clinical assessment of respiratory failure’, below).

In some of the most seriously ill patients, the precise underlying diagnosis is initially unclear but in all cases, the immediate objective is to preserve life and prevent, reverse or minimize damage to vital organs such as the lungs, brain, kidneys and liver. This involves a rapid assessment of the physiological derangement followed by prompt institution of measures to support cardiovascular and respiratory function in order to restore perfusion of vital organs, improve delivery of oxygen to the tissues and encourage the removal of carbon dioxide and other waste products of metabolism (following the ABC approach: Airway, Breathing, Circulation, see Fig. 16.25, below). The patient’s condition and response to treatment should be closely monitored throughout. The underlying diagnosis may only become clear as the results of investigations become available, a more detailed history is obtained and a more thorough physical examination is performed. In practice resuscitation, assessment and diagnosis usually proceed in parallel.

Critically ill patients require multidisciplinary care with:

image Intensive skilled nursing care (usually 1 : 1 or 1 : 2 nurse/patient ratio in the UK).

image Specialized physiotherapy including mobilization and rehabilitation.

image Management of pain and distress with judicious administration of analgesics and sedatives (see p. 893).

image Constant reassurance and support (critically ill patients easily become disorientated and delirium is common.

image H2-receptor antagonists or proton pump inhibitors in selected cases to prevent stress-induced ulceration.

image Compression stockings (full-length and graduated), pneumatic compression devices and subcutaneous low-molecular-weight heparin to prevent venous thrombosis.

image Care of the mouth, prevention of constipation and of pressure sores.

image Nutritional support (see p. 222). Protein energy malnutrition is common in critically ill patients and is associated with muscle wasting, weakness, delayed mobilization, difficulty weaning from ventilation, immune compromise and impaired wound healing. There is also an association between malnutrition and increased mortality. It is therefore recommended that nutritional support should be instituted as soon as is practicable in those unable to meet their nutritional needs orally, ideally within 1–2 days of the acute episode. Enteral nutrition, which is less expensive, preserves gut mucosal integrity, is more physiological and is associated with fewer complications, is preferred. Recently, the value of early feeding has been questioned, apart from giving small amounts to ensure gut viability. Parenteral nutrition is sometimes indicated at a later stage for those unable to tolerate or absorb enteral nutrition and should be initiated without delay, at least within 3 days. Persistent attempts at enteral nutrition in those with gastrointestinal intolerance leads to underfeeding and malnutrition.

image Critically ill patients commonly require intravenous insulin infusions, often in high doses, to combat hyperglycaemia and insulin resistance (see p. 1006). Although the use of intensive insulin therapy to achieve ‘tight glycaemic control’ (blood glucose level between 4.4 and 6.1 mmol/L) was shown to improve outcome (at least when combined with aggressive nutritional support), more recent studies have failed to confirm this finding and have indicated that this approach is associated with an unacceptably high incidence of hypoglycaemia, and possibly an increase in mortality. Current recommendations suggest that blood glucose levels should be maintained at <8–10 mmol/L.

Discharge of patients from intensive care should normally be planned in advance and should ideally take place during normal working hours. Planned discharge often involves a period in a ‘step-down’ intermediate care area. Premature or unplanned discharge, especially during the night, has been associated with higher hospital mortality rates. A summary including ‘points to review’ should be included in the clinical notes and there should be a detailed handover to the receiving team (medical and nursing). The intensive care team should continue to review the patient, who might deteriorate following discharge, on the ward and should be available at all times for advice on further management (e.g. tracheostomy care, nutritional support). In this way, deterioration and readmission to intensive care (which is associated with a particularly poor outcome) or even cardiorespiratory arrest might be avoided.

This chapter concentrates on cardiovascular and respiratory problems. Many patients also have failure of other organs such as the kidney and liver; treatment of these is dealt with in more detail in the relevant chapters.

Applied cardiorespiratory physiology

Oxygen delivery and consumption

Oxygen delivery (DO2) (Fig. 16.1) is defined as the total amount of oxygen delivered to the tissues per unit time. It is dependent on the volume of blood flowing through the microcirculation per minute (i.e. the total cardiac output, image) and the amount of oxygen contained in that blood (i.e. the arterial oxygen content, CaO2). Oxygen is transported both in combination with haemoglobin and dissolved in plasma. The amount combined with haemoglobin is determined by the oxygen capacity of haemoglobin (usually taken as 1.34 mL of oxygen per gram of haemoglobin) and its percentage saturation with oxygen (SO2), while the volume dissolved in plasma depends on the partial pressure of oxygen (PO2). Except when hyperbaric oxygen is administered, the amount of dissolved oxygen in plasma is insignificant.

Clinically, however, the utility of this global concept of oxygen delivery is limited because it fails to account for changes in the relative flow to individual organs and the distribution of flow through the microcirculation (i.e. the efficiency with which oxygen delivery is matched to the metabolic requirements of individual tissues or cells). Furthermore, some organs (such as the heart) have high oxygen requirements relative to their blood flow and will receive insufficient oxygen, even if the overall oxygen delivery is apparently adequate. Lastly, microcirculatory flow is influenced by blood viscosity.

Oxygenation of the blood

Oxyhaemoglobin dissociation curve

The saturation of haemoglobin with oxygen is determined by the partial pressure of oxygen (PO2) in the blood, the relationship between the two being described by the oxyhaemoglobin dissociation curve (Fig. 16.2). The sigmoid shape of this curve is significant for a number of reasons:

The PaO2 is in turn influenced by the alveolar oxygen tension (PAO2), the efficiency of pulmonary gas exchange, and the partial pressure of oxygen in mixed venous blood image.

Pulmonary gas exchange

In normal subjects there is a small alveolar-arterial oxygen difference (PA–aO2). This is due to:

Pathologically, there are three possible causes of an increased PA–aO2 difference:

image Diffusion defect. This is not a major cause of hypoxaemia even in conditions such as lung fibrosis, in which the alveolar-capillary membrane is considerably thickened. Carbon dioxide is also not affected, as it is more soluble than oxygen.

image Right-to-left shunts. In certain congenital cardiac lesions or when a segment of lung is completely collapsed, a proportion of venous blood passes to the left side of the heart without taking part in gas exchange, causing arterial hypoxaemia. This hypoxaemia cannot be corrected by administering oxygen to increase the PAO2, because blood leaving normal alveoli is already fully saturated; further increases in PO2 will not, therefore, significantly affect its oxygen content. On the other hand, because of the shape of the carbon dioxide dissociation curve (Fig. 16.4), the high PCO2 of the shunted blood can be compensated for by over-ventilating patent alveoli, thus lowering the CO2 content of the effluent blood. Indeed, many patients with acute right-to-left shunts hyperventilate in response to the hypoxia and/or to stimulation of mechanoreceptors in the lung, so that their PaCO2 is normal or low.

image Ventilation/perfusion mismatch (see p. 796). Diseases of the lung parenchyma (e.g. pulmonary oedema, acute lung injury) result in image mismatch, producing an increase in alveolar deadspace and hypoxaemia. The increased deadspace can be compensated for by increasing overall ventilation. In contrast to the hypoxia resulting from a true right-to-left shunt, that due to areas of low image can be partially corrected by administering oxygen and thereby increasing the PAO2 even in poorly ventilated areas of lung.

Stroke volume

The volume of blood ejected by the ventricle in a single contraction is the difference between the ventricular end-diastolic volume (VEDV) and end-systolic volume (VESV) (i.e. stroke volume = VEDV – VESV). The ejection fraction describes the stroke volume as a percentage of VEDV (i.e. ejection fraction = (VEDV − VESV)/VEDV × 100%) and is an indicator of myocardial performance.

Three interdependent factors determine the stroke volume (see p. 671).

Monitoring critically ill patients

As well as allowing immediate recognition of changes in the patient’s condition, monitoring can also be used to establish or confirm a diagnosis, to gauge the severity of the condition, to follow the evolution of the illness, to guide interventions and to assess the response to treatment. Invasive monitoring is generally indicated in the more seriously ill patients and in those who fail to respond to initial treatment. These techniques are, however, associated with a significant risk of complications, as well as additional costs and patient discomfort and should therefore only be used when the potential benefits outweigh the dangers. Likewise, invasive devices should be removed as soon as possible.

Blood pressure

Alterations in blood pressure are often interpreted as reflecting changes in cardiac output. However, if there is vasoconstriction with a high peripheral resistance, the blood pressure may be normal, even when the cardiac output is reduced. Conversely, the vasodilated patient may be hypotensive, despite a very high cardiac output.

Hypotension jeopardizes perfusion of vital organs. The adequacy of blood pressure in an individual patient must always be assessed in relation to the premorbid value. Blood pressure is traditionally measured using a sphygmomanometer but if rapid alterations are anticipated, continuous monitoring using an intra-arterial cannula is indicated (Practical Box 16.1; Fig. 16.8).

image Practical Box 16.1

Radial artery cannulation

Central venous pressure (CVP)

This provides a fairly simple, but approximate method of gauging the adequacy of a patient’s circulating volume and the contractile state of the myocardium. The absolute value of the CVP is not as useful as its response to a fluid challenge (the infusion of 100–200 mL of fluid over a few minutes) (Fig. 16.9). The hypovolaemic patient will initially respond to transfusion with little or no change in CVP, together with some improvement in cardiovascular function (falling heart rate, rising blood pressure, increased peripheral temperature and urine output). As the normovolaemic state is approached, the CVP usually rises slightly and reaches a plateau, while other cardiovascular values begin to stabilize. At this stage, volume replacement should be slowed, or even stopped, in order to avoid overtransfusion (indicated by an abrupt and sustained rise in CVP, often accompanied by some deterioration in the patient’s condition). In cardiac failure, the venous pressure is usually high; the patient will not improve in response to volume replacement, which will cause a further, sometimes dramatic, rise in CVP.

Central venous catheters are usually inserted via a percutaneous puncture of the subclavian or internal jugular vein using a guidewire technique (Practical Box 16.2; Figs 16.10, 16.11). The guidewire techniques can also be used in conjunction with a vein dilator for inserting multilumen catheters, double lumen cannulae for haemofiltration or pulmonary artery catheter introducers. The routine use of ultrasound to guide central venous cannulation reduces complication rates.

image Practical Box 16.2

Internal jugular vein cannulation

The CVP should be read intermittently using a manometer system or continuously using a transducer and bedside monitor. It is essential that the pressure recorded always be related to the level of the right atrium. Various landmarks are advocated (e.g. sternal notch with the patient supine, sternal angle or mid-axilla when the patient is at 45°), but which is chosen is largely immaterial provided it is used consistently in an individual patient. Pressure measurements should be obtained at end-expiration.

The following are common pitfalls in interpreting central venous pressure readings:

Pulmonary artery pressure

A ‘balloon flotation catheter’ enables reliable catheterization of the pulmonary artery. These ‘Swan–Ganz’ catheters can be inserted centrally (Fig. 16.10) or through the femoral vein, or via a vein in the antecubital fossa. Passage of the catheter from the major veins, through the chambers of the heart, into the pulmonary artery and into the wedged position is monitored and guided by the pressure waveforms recorded from the distal lumen (Practical Box 16.3; Fig. 16.13). A chest X-ray should always be obtained to check the final position of the catheter. In difficult cases, screening with an image intensifier may be required.

Once in place, the balloon is deflated and the pulmonary artery mean, systolic and end-diastolic pressures (PAEDP) can be recorded. The pulmonary artery occlusion pressure (PAOP, previously referred to as the pulmonary artery or capillary ‘wedge’ pressure) is measured by reinflating the balloon, thereby propelling the catheter distally until it impacts in a medium-sized pulmonary artery. In this position there is a continuous column of fluid between the distal lumen of the catheter and the left atrium, so that PAOP is usually a reasonable reflection of left atrial pressure.

The technique is generally safe – the majority of complications such as ‘knotting’, valve trauma and pulmonary artery rupture (which can be fatal) are related to user inexperience. Pulmonary artery catheters should preferably be removed within 72 h, since the incidence of complications, especially infection, then increases progressively

Less invasive techniques for assessing cardiac function and guiding volume replacement

Disturbances of acid–base balance

The physiology of acid–base control is discussed on page 660. Acid–base disturbances can be described in relation to the diagram illustrated in Figure 13.13, p. 663 (which shows PaCO2 plotted against arterial [H+]).

Both acidosis and alkalosis can occur, each of which are either metabolic (primarily affecting the bicarbonate component of the system) or respiratory (primarily affecting PaCO2). Compensatory changes may also be apparent. In clinical practice, arterial [H+] values outside the range 18–126 nmol/L (pH 6.9–7.7) are rarely encountered.

Blood gas and acid–base values (normal ranges) are shown in Table 16.2. (For blood gas analysis, see p. 891.)

Table 16.2 Arterial blood gas and acid–base values (normal ranges)


35–45 nmol/L

pH 7.35–7.45

PO2 (breathing room air)

10.6–13.3 kPa

(80–100 mmHg)


4.8–6.1 kPa

(36–46 mmHg)

Base deficit



Plasma HCO3

22–26 mmol/L


O2 saturation



Respiratory acidosis. This is caused by retention of carbon dioxide. The PaCO2 and [H+] rise. A chronically raised PaCO2 is compensated by renal retention of bicarbonate, and the [H+] returns towards normal. A constant arterial bicarbonate concentration is then usually established within 2–5 days. This represents a primary respiratory acidosis with a compensatory metabolic alkalosis (see p. 666). Common causes of respiratory acidosis include ventilatory failure and COPD (type II respiratory failure where there is a high PaCO2 and a low PaO2, see p. 814).

Respiratory alkalosis. In this case, the reverse occurs and there is a fall in PaCO2 and [H+], often with a small reduction in bicarbonate concentration. If hypocarbia persists, some degree of renal compensation may occur, producing a metabolic acidosis, although in practice this is unusual. A respiratory alkalosis may be produced, intentionally or unintentionally, when patients are mechanically ventilated; it may also be seen with hypoxaemic (type I) respiratory failure (see Ch. 15, p. 817), spontaneous hyperventilation and in those living at high altitudes.

Metabolic acidosis (p. 664). This may be due to excessive acid production, most commonly lactate and H+ (lactic acidosis) as a consequence of anaerobic metabolism during an episode of shock or following cardiac arrest. A metabolic acidosis may also develop in chronic renal failure or in diabetic ketoacidosis. It can also follow the loss of bicarbonate from the gut or from the kidney in renal tubular acidosis. Respiratory compensation for a metabolic acidosis is usually slightly delayed because the blood–brain barrier initially prevents the respiratory centre from sensing the increased blood [H+]. Following this short delay, however, the patient hyperventilates and ‘blows off’ carbon dioxide to produce a compensatory respiratory alkalosis. There is a limit to this respiratory compensation, since in practice values for PaCO2 less than about 1.4 kPa (11 mmHg) are rarely achieved. Spontaneous respiratory compensation cannot occur if the patient’s ventilation is controlled or if the respiratory centre is depressed, for example by drugs or head injury.

Metabolic alkalosis. This can be caused by loss of acid, for example from the stomach with nasogastric suction, or in high intestinal obstruction, or excessive administration of absorbable alkali. Overzealous treatment with intravenous sodium bicarbonate is sometimes implicated. Respiratory compensation for a metabolic alkalosis is often slight, and it is rare to encounter a PaCO2 above 6.5 kPa (50 mmHg), even with severe alkalosis.

Shock, sepsis and acute disturbances of haemodynamic function

Shock is the term used to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia and/or an inability of the cells to utilize oxygen.


Release of pro- and anti-inflammatory mediators

Severe infection (often with bacteraemia or endotoxaemia), the presence of large areas of damaged tissue (e.g. following trauma or extensive surgery), hypoxia or prolonged/repeated episodes of hypoperfusion can trigger an exaggerated inflammatory response with systemic activation of leucocytes and release of a variety of potentially damaging ‘mediators’ (see also Ch. 3). Although beneficial when targeted against local areas of infection or necrotic tissue, dissemination of this ‘innate immune’ response can produce shock and widespread tissue damage. Characteristically the initial episode of overwhelming inflammation is followed by a period of immune suppression, which in some cases may be profound and during which the patient is at increased risk of developing secondary infections. It also seems that pro- and anti-inflammatory elements of the host response may co-exist.

Microorganisms and their toxic products (Fig. 16.17)

In sepsis/septic shock the innate immune response and inflammatory cascade are triggered by the recognition of pathogen-associated molecular patterns (PAMPs), including cell wall components (e.g. endotoxin) and/or exotoxins (antigenic proteins produced by bacteria such as staphylococci, streptococci and Pseudomonas).

Mar 31, 2017 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Critical care medicine
Premium Wordpress Themes by UFO Themes
%d bloggers like this: