Chapter 16 Critical care medicine
Introduction
Table 16.1 Some common indications for admission to intensive care
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).
Box 16.1
Early warning systems for referral of ‘at risk’ patients to the critical care team
Medical emergency team-calling criteria
Airway | If threatened |
Breathing | All respiratory arrests |
Respiratory rate | <5 breaths/min |
Respiratory rate | >36 breaths/min |
Circulation | All cardiac arrests |
Pulse rate | <40 beats/min |
Pulse rate | >140 beats/min |
Systolic blood pressure | <90 mmHg |
Neurology | Sudden fall in level of consciousness (fall in Glasgow Coma Scale of >2 points) |
| Repeated or prolonged seizures |
Other | Any patient who does not fit the criteria above, but about whom you are seriously worried |
From Hillman K, Chen J, Cretikos M et al. Introduction of the medical emergency team (MET) system: a cluster-randomized controlled trial. Lancet 2005; 365:2091–2097, with permission.
Critically ill patients require multidisciplinary care with:
Intensive skilled nursing care (usually 1 : 1 or 1 : 2 nurse/patient ratio in the UK).
Specialized physiotherapy including mobilization and rehabilitation.
Management of pain and distress with judicious administration of analgesics and sedatives (see p. 893).
Constant reassurance and support (critically ill patients easily become disorientated and delirium is common.
H2-receptor antagonists or proton pump inhibitors in selected cases to prevent stress-induced ulceration.
Compression stockings (full-length and graduated), pneumatic compression devices and subcutaneous low-molecular-weight heparin to prevent venous thrombosis.
Care of the mouth, prevention of constipation and of pressure sores.
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.
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.
FURTHER READING
Casaer MP, Mesotten O, Hermans G et al. Early versus late parenteral nutrition in critically ill adults. N Engl J Med 2011; 365:506–517.
The NICE-SUGAR Study Investigators. Intensive versus conventional glucose control in critically ill patients. N Engl J Med 2009; 360:1293–1297.
Ziegler TR. Parenteral nutrition in the critically ill patient. N Engl J Med 2009; 361:1088–1097.
Applied cardiorespiratory physiology
Oxygenation of the blood
Oxyhaemoglobin dissociation curve
Modest falls in the partial pressure of oxygen in the arterial blood (PaO2) may be tolerated (since oxygen content is relatively unaffected) provided that the percentage saturation remains above 92%.
Increasing the PaO2 to above normal has only a minimal effect on oxygen content unless hyperbaric oxygen is administered (when the amount of oxygen in solution in plasma becomes significant).
Once on the steep ‘slippery slope’ of the curve (percentage saturation below about 90%), a small decrease in PaO2 can cause large falls in oxygen content, whereas increasing PaO2 only slightly, e.g. by administering 28% oxygen to a patient with chronic obstructive pulmonary disease (COPD), can lead to a useful increase in oxygen saturation and content.
Alveolar oxygen tension (PAO2)
The clinician can influence PAO2 by administering oxygen or by increasing the barometric pressure.
Pulmonary gas exchange
In normal subjects there is a small alveolar-arterial oxygen difference (PA–aO2). This is due to:
a small (0.133 kPa, 1 mmHg) pressure gradient across the alveolar membrane
a small amount of blood (2% of total cardiac output) bypassing the lungs via the bronchial and thebesian veins
Pathologically, there are three possible causes of an increased PA–aO2 difference:
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.
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.
Ventilation/perfusion mismatch (see p. 796). Diseases of the lung parenchyma (e.g. pulmonary oedema, acute lung injury) result in
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
can be partially corrected by administering oxygen and thereby increasing the PAO2 even in poorly ventilated areas of lung.
Stroke volume
Three interdependent factors determine the stroke volume (see p. 671).
Myocardial contractility
This refers to the ability of the heart to perform work, independent of changes in preload and afterload. The state of myocardial contractility determines the response of the ventricles to changes in preload and afterload. Contractility is often reduced in critically ill patients, as a result of either pre-existing myocardial damage (e.g. ischaemic heart disease), or the acute disease process itself (e.g. sepsis). Changes in myocardial contractility alter the slope and position of the Starling curve; worsening ventricular performance is manifested as a depressed, flattened curve (Fig. 16.6 and Fig. 14.5). Inotropic drugs can be used to increase myocardial contractility (see below).
Monitoring critically ill patients
Assessment of tissue perfusion
Pale, cold skin, delayed capillary refill and the absence of visible veins in the hands and feet indicate poor perfusion. Although peripheral skin temperature measurements can help clinical evaluation, the earliest compensatory response to hypovolaemia or a low cardiac output, and the last to resolve after resuscitation is vasoconstriction in the splanchnic region.
Metabolic acidosis with raised lactate concentration suggests that tissue perfusion is sufficiently compromised to cause cellular hypoxia and anaerobic glycolysis. Persistent, severe lactic acidosis is associated with a very poor prognosis. In many critically ill patients, especially those with sepsis, however, lactic acidosis can also be caused by metabolic disorders unrelated to tissue hypoxia and can be exacerbated by reduced clearance owing to hepatic or renal dysfunction as well as the administration of adrenaline (epinephrine).
Urinary flow is a sensitive indicator of renal perfusion and haemodynamic performance.
Blood pressure
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).
Practical Box 16.1
Radial artery cannulation
Technique
1. The procedure is explained to the patient and, if possible, consent obtained.
2. The arm is supported, with the wrist extended, by an assistant. (Gloves should be worn.)
3. The skin should be cleaned with chlorhexidine.
4. The radial artery is palpated where it arches over the head of the radius.
5. In conscious patients, local anaesthetic is injected to raise a weal over the artery, taking care not to puncture the vessel or obscure its pulsation.
6. A small skin incision is made over the proposed puncture site.
7. A small parallel-sided cannula (20 gauge for adults, 22 gauge for children) is used in order to allow blood flow to continue past the cannula.
8. The cannula is inserted over the point of maximal pulsation and advanced in line with the direction of the vessel at an angle of approximately 30°.
9. ‘Flashback’ of blood into the cannula indicates that the radial artery has been punctured.
10. To ensure that the shoulder of the cannula enters the vessel, the needle and cannula are lowered and advanced a few millimetres into the vessel.
11. The cannula is threaded off the needle into the vessel and the needle withdrawn.
12. The cannula is connected to a non-compliant manometer line filled with saline. This is then connected via a transducer and continuous flush device to a monitor, which records the arterial pressure.
Central venous pressure (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.
Practical Box 16.2
Internal jugular vein cannulation
Technique
1. The procedure is explained to the patient and, if possible, consent obtained.
2. The patient is placed head-down to distend the central veins (this facilitates cannulation and minimizes the risk of air embolism but may exacerbate respiratory distress and is dangerous in those with raised intracranial pressure).
3. The skin is cleaned with an antiseptic solution such as chlorhexidine. Sterile precautions are taken throughout the procedure.
4. Local anaesthetic (1% plain lidocaine) is injected intradermally to raise a weal at the apex of a triangle formed by the two heads of sternomastoid with the clavicle at its base.
5. A small incision is made through the weal.
6. The cannula or needle is inserted through the incision and directed laterally downwards and backwards in the direction of the nipple until the vein is punctured just beneath the skin and deep to the lateral head of sternomastoid.
Ultrasound-guided puncture is recommended to reduce the incidence of complications.
7. Check that venous blood is easily aspirated.
8. The cannula is threaded off the needle into the vein or the guidewire is passed through the needle (see Fig. 16.11).
9. The CVP manometer line is connected to a manometer/transducer.
10. A chest X-ray should be taken to verify that the tip of the catheter is in the superior vena cava and to exclude pneumothorax.
The following are common pitfalls in interpreting central venous pressure readings:
Blocked catheter. This results in a sustained high reading, with a damped or absent waveform, which often does not correlate with clinical assessment.
Transducer wrongly positioned. Failure to level the system is a common cause of erroneous readings.
Catheter tip in right ventricle. If the catheter is advanced too far, an unexpectedly high pressure with pronounced oscillations is recorded. This is easily recognized when the waveform is displayed.
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.
Practical Box 16.3
Passage of a pulmonary artery balloon flotation catheter through the chambers of the heart into the ‘wedged’ position
Consent should be obtained if possible from the patient after explanation of the procedure.
Note: (a), (b), (c), (d) refer to Figure 16.13.
1. A balloon flotation catheter is inserted through a large vein (see text).
2. Once in the thorax, respiratory oscillations are seen. The catheter should be advanced further towards the lower superior vena cava/right atrium (a), where pressure oscillations become more pronounced. The balloon should then be inflated and the catheter advanced.
3. When the catheter is in the right ventricle (b), there is no dicrotic notch and the diastolic pressure is close to zero. The patient should be returned to the horizontal, or slightly head-up, position before advancing the catheter further.
4. When the catheter reaches the pulmonary artery (c) a dicrotic notch appears and there is elevation of the diastolic pressure. The catheter should be advanced further with the balloon inflated.
5. Reappearance of a venous waveform indicates that the catheter is ‘wedged’. The balloon is deflated to obtain the pulmonary artery pressure. The balloon is inflated intermittently to obtain the pulmonary artery occlusion (also known as pulmonary artery, or capillary, ‘wedge’) pressure (d).
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+]).
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)
H+ | 35–45 nmol/L | pH 7.35–7.45 |
PO2 (breathing room air) | 10.6–13.3 kPa | (80–100 mmHg) |
PCO2 | 4.8–6.1 kPa | (36–46 mmHg) |
Base deficit | ±2.5 |
|
Plasma HCO3– | 22–26 mmol/L |
|
O2 saturation | 95–100% |
|
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.
Shock, sepsis and acute disturbances of haemodynamic function
Pathophysiology
The sympatho-adrenal response to shock (Fig. 16.16)
Reduction in perfusion of the renal cortex stimulates the juxtaglomerular apparatus to release renin. This converts angiotensinogen to angiotensin I, which in turn is converted in the lungs and by the vascular endothelium to the potent vasoconstrictor angiotensin II. Angiotensin II also stimulates secretion of aldosterone by the adrenal cortex, causing sodium and water retention (p. 566). This helps to restore the circulating volume (see p. 639).
Neuroendocrine response
There is release of pituitary hormones such as adrenocorticotrophic hormone (ACTH), vasopressin (antidiuretic hormone, ADH) and endogenous opioid peptides. (In septic shock there may be a relative deficiency of vasopressin.)
There is release of cortisol, which causes fluid retention and antagonizes insulin.
There is release of glucagon, which raises the blood sugar level.
