Intravascular Volume Deficit

Blood loss may be assessed using the patient’s history and any measured losses, but more commonly the anaesthetist has to rely on clinical evaluation of the patient’s current cardiovascular status. Profound circulatory shock with hypotension, poor peripheral perfusion, oliguria and altered cerebration is easy to recognize. However, a more careful assessment is needed to recognise the early manifestations of haemorrhage, such as tachycardia and cutaneous vasoconstriction. Useful indices include heart rate, arterial pressure (especially pulse pressure), the state of the peripheral circulation, central venous pressure and urine output. Table 37.3 describes approximate correlations among these clinical indices and the extent of haemorrhage, but it should be stressed that these refer to the ‘ideal’ patient. In young, healthy adults, arterial pressure may be an unreliable guide to volume status because compensatory mechanisms can prevent a measurable decrease in arterial pressure until more than 30% of the patient’s blood volume has been lost. In such patients, attention should be directed to pulse rate, skin circulation and a narrowing pulse pressure. Tachycardia in the presence of a normal arterial pressure should never automatically be attributed to pain or anxiety if there is a clinical history consistent with the potential for intravascular volume loss. In elderly patients with widespread arterial disease, limited cardiac reserve and a rigid vascular tree (fixed total peripheral resistance), signs of severe hypovolaemia may become evident when blood volume has been reduced by as little as 15%. However, as baroreceptor sensitivity decreases with age, elderly patients may exhibit less tachycardia for any degree of volume depletion.

In general, hypovolaemia does not become apparent clinically until circulating blood volume has been reduced by at least 20% (approximately 1000 mL). A reduction by more than 30% of blood volume occurs before the classic ‘shock syndrome’ is produced, with hypotension, tachycardia, oliguria and cold, clammy extremities. Haemorrhage greater than 40% of blood volume may be associated with loss of the compensatory mechanisms that maintain cerebral and coronary blood flow, and the patient becomes restless, agitated and eventually comatose. In patients with major trauma, it is valuable to compare the clinical assessment of the extent of haemorrhage with the measured or assumed loss. A marked disparity between these two estimates often leads to a diagnosis of a further concealed source of haemorrhage.

Whilst clinical evaluation remains the most important and most frequently used guide to the management of intravascular volume deficit, the use of non-invasive and minimally-invasive methods of cardiac output measurement in this setting is growing. These techniques may be of particular benefit in guiding the immediate resuscitation of frail or critically ill patients.

Extracellular Volume Deficit

Assessment of extracellular fluid volume deficit is difficult. Guidance may be obtained from the nature of the surgical condition, the duration of impaired fluid intake and the presence and severity of symptoms associated with abnormal losses (e.g. vomiting). At the time of the earliest radiological evidence of intestinal obstruction, there may be 1500 mL of fluid sequestered in the bowel lumen. If the obstruction is well established and vomiting has occurred, the extracellular fluid deficit may exceed 3000 mL. Table 37.4 describes some of the clinical features seen with varying degrees of severity of extracellular fluid losses. It is clear that considerable losses must occur before clinical signs are apparent, and that these signs are often subjective in more minor degrees of extracellular fluid deficit.

In addition to clinical signs, laboratory investigations may also indicate extracellular fluid volume deficit. Haemoconcentration results in an increased haemoglobin concentration and an increased packed cell volume. As dehydration becomes more marked, renal blood flow diminishes, reducing renal clearance of urea and consequently increasing the blood urea concentration. Patients with moderate volume contraction exhibit a ‘pre-renal’ pattern of uraemia characterized by an increase in blood urea out of proportion to any increase in serum creatinine concentration. Under maximal stimulation from ADH and aldosterone, conservation of sodium and water by the kidneys results in excretion of urine of low sodium concentration (0–15 mmol L^–1) and high osmolality (800–1400 mosmol kg^–1).

Once the extent of blood volume or extracellular fluid volume deficit has been estimated, deficits should be corrected with the appropriate intravenous fluid. The overall priority is to maintain adequate tissue perfusion and oxygenation, therefore correction of intravascular deficit takes precedence – hypovolaemia due to blood loss should be treated with either a balanced crystalloid solution (such as Hartmann’s solution) or a suitable colloid until packed red cells are available (see Ch 12: Fluid, electrolyte and acid–base balance). Resuscitation is usually guided by clinical indices of circulating volume status and organ perfusion. Central venous pressure (CVP) measurement has often been used to guide fluid therapy but CVP has limitations when used to predict intravascular volume status and responsiveness to infused fluids. High-risk surgical patients may benefit from the use of (non-invasive) cardiac output measuring devices to direct fluid resuscitation towards predetermined goals for cardiac output and systemic oxygen delivery.

Extracellular fluid deficit is usually corrected after the correction of any intravascular deficit, by adjusting maintenance fluid infusion rates. Losses from vomiting or gastric aspirates are best replaced by crystalloid solutions containing an appropriate potassium supplement. Hartmann’s solution is often used, although hypochloraemia is an indication for saline 0.9% (with additional potassium). Lower GI losses, such as those due to diarrhoea or intestinal obstruction, are normally replaced volume-for-volume with Hartmann’s solution.

 Although not completely effective, insertion of a nasogastric tube to decompress the stomach and to provide a low-pressure vent for regurgitation may be helpful. Aspiration through the tube may be useful if gastric contents are liquid, as in bowel obstruction, but is less effective when contents are solid. Cricoid pressure is still effective at reducing regurgitation even with a nasogastric tube in situ.

 Clear oral antacids (e.g. sodium citrate) may be used to raise the pH of gastric contents immediately before induction. However, this also increases gastric volume. Particulate antacids should not be used, as they may be very damaging to the airway if aspirated. The preoperative administration of H₂-receptor antagonists consistently raises gastric pH and may reduce the chance of chemical pulmonary injury occurring in the event of inhalation. Although this is standard practice in obstetric anaesthesia, few anaesthetists employ these measures for emergency general surgery. The regimens available are described in Chapter 35.

Rapid-Sequence Induction

This is the technique used most frequently for the patient with a full stomach. The phrase ‘rapid-sequence’ hints at one of the fundamental goals of this technique, which is to minimize as much as possible the duration of time between loss of consciousness and tracheal intubation, during which the patient is at greatest risk of aspiration of gastric contents. In achieving this goal, this technique contravenes one of the fundamental rules of anaesthesia, namely that neuromuscular blockers are not injected until control of the airway is assured. The decision to employ the rapid-sequence induction technique balances the risk of losing control of the airway against the risk of aspiration. Therefore it is vital to assess carefully the likelihood of difficult laryngoscopy or tracheal intubation. The anaesthetist must have a contingency plan prepared for patient management should intubation fail. If preoperative evaluation indicates a particularly difficult airway, alternative methods should be considered, e.g. local anaesthetic techniques or ‘awake intubation’ under local anaesthesia.

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