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Peter J F Baskett, Jerry P N olan

Hypovolaemic shock is a clinical state in which tissue perfusion is rendered relatively inadequate by loss of blood or plasma. A reduction in blood volume causes a fall in systolic pressure, which triggers a sympathetic catecholamine response. This results in peripheral vasoconstriction, a rise in pulse rate, and a reduction in pulse pressure. The tachycardia and increased cardiac contractility raise the myocardial oxygen requirement. Blood flow to the skin and peripheral tissues is reduced, in an effort to preserve reasonable perfusion of vital organs such as the brain, heart, liver and kidneys. Anaerobic metabolism, with the production of lactate, occurs in tissues that are inadequately perfused.' If blood loss continues, the increasing metabolic acidosis will impair the function of vital organs. Further myocardial depression compounds the development of shock, and pain stimuli add to the sympathetic outburst.

Early symptoms

and signs


The following are early symptoms and signs of hypovolaemic shock. They reflect the underlying pathophysiology. How blood loss can lead to multiorgan tallure . Tachycardia (caused by catecholamine release) Skin pallor (results from vasoconstriction caused by catecholamine release) Hypotension (caused by hypovolaemia, Classification of hypovolaemic shock by blood loss (adult) perhaps followed by myocardial Class III Class IV Class I Class 11 insufficiency) . Confusion, aggression, drowsiness, and Blood loss coma (caused by cerebral hypoxia and 30-40 >40 15-30 <15 Percentage acidosis) 1500-2000 >2000 800-1500 750 Volume (mI) Tachypnoea (caused by hypoxia and Blood pressure acidosis) Reduced Normal Very Iow Unchanged Systolic General weakness (caused by hypoxia Raised Reduced Diastolic Very Iow or Unchanged and acidosis) unrecordable Thirst (caused by hypovolaemia) 100-120 Pulse 120 (thready) 120 (very Slight . Reduced urine output (caused by thready) tachycardia reduced perfusion) (beats/min) Undetectable 'In most cases signs and symptoms can be reNormal Slow (>2 s) Slow (>2 s) Capillary refill lated to the amount of blood loss, which can be Normal Tachypnoea Tachypnoea Tachypnoea Respiratory rate classedin four broad groups (classes I-IV). (>20/min) (>20/min) Generally, losses up to 750 ml (class I) (15% 0-10 10-20 >30 20-30 Urinary flow rate of the circulating blood volume) generate no (ml/h) pronounced signs or symptoms. Further haemPale Pale Colour Pale, clammy, orrhage, up to 1.5 litres (class 11), produces Extremities and cold normal cardiovascular signs of catecholamine release, Ashen Pale Pale Normal thirst, weakness, and tachypnoea. Systolic Complexion pressure begins to fall as blood loss mounts to Anxious or Alert Mental state Anxious, Drowsy, 2 litres (class Ill) and often becomcs unconfused, or aggressIVe aggressIve, recordable after 2.5-3.0 litres (class IV) have unconscIous drowsy been lost.

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ABC of Major Trauma

Previously healthy young adults have remarkable compensatory capabilities and systolic pressure is often preserved in spite of quite appreciable blood loss (1.5-2.0 litres). A narrowed pulse pressure is often the earliest sign. Eventually, however, there is a precipitous fall as the myocardium suddenly fails because of hypoxia and acidosis. Conversely, patients with coronary arterial disease may become hypotensive because of myocardial insufficiency after only modest blood losses of up to 1.5 litres. Factors affecting r~sponse to blood loss Patients receiving certain drugs (for example, ~ blockers) may be unable to prQcl\lce an '1-pJ?ropriate sympathetic response and may also become hypotensive after modest blood loss. Other factors that can modify the response to blood loss include the patient's age, the extent of tissue damage, and the period of time between injury and examination. In children, normal haemodynamic values are maintained until blood loss is relatively great. Tachycardia and skin pallor are the earliest signs, and hypotension indicates uncompensated shock with severe blood loss and inadequate resuscitation. As a rule, a child's systolic blood pressure is 80 mm Hg plus twice the age in years, The diastolic pressure is about two thirds of the systQlic pressure. A systolic pressure of 70 mm Hg or less in a child therefore indicates serious cardiovascular decompensation. In elderly patients, hypotension may be an early sign of blood loss. Their physiological reserves are reduced and they are less able to respond to release of catecholamiQes by tachycardia. The ensuing hypotension may result in early organ failure because of hypoperfusion, and this is exaggerated in normally hypertensive patients. Extensive tissue damage from major limb injuries is associated with early cardiovascular decompensation, not only because of blood loss and haematoma formation but also because of extravasation of fluid while oedema is developing. About a quarter of the volume of oedema fluid is contributed by lost plasma volume, and this may amount to 20-30% of the overt blood loss. Clearly, oedema formation increase with time and this becomes more important as the time between injury and examination increases, The objective of the management of hypovolaemic shock is to maintain tissue oxygenation and restore it to normal values. This entails applying the basic principles of resuscitation of patients with trauma. Resuscitation is followed by definitive treatment (including surgery). Symptoms of hypovolaemia Class I II according to blood 1055*

In pr sy
llIlj IT"

Blood loss (ml) <750 Up to 1500

None Cardiovascular signs caused by catecholamine release: thirst, weakness, tachypnoea Systolic pressure falls Systolic pressure becomes unreadable

Up to 2000 >2000



*Assuming a 70 kg patient

Resuscitation of patients (I) Adequate pulmonary (3) Replacement (2) Control of haemorrhage

with traUIIla


of lost volume

(4) Monitoring the effects of (I), (2), and (3) (5) SUpport of myocardial contractiIity (6) Relief of pain



Pulmonary oxygenation in patients with hypovolaemic shock

To ensure optimal pulmonary oxygenation, patients with hypovolaemic shock should have a clear airway and adequate ventilation with oxygen at a high inspired concentration. Unconscious patients with severe shock should be intubated and will require positi,'e pressure ventilation. A pneumothorax, haemothorax, or significant gastric distension will impair ventilation and should be treated immediately.

Ensure a clear airway and adequate ventilation with oxygen at a high inspired concentration

.Intubate patients with severe shock and Use positive pressure ventilation


of haemorrhage

Peripheral Periph"Tal haemorrhage should be controlled with firm pressure and, where possible, by ekvation of the injured part. 28


Control with firm pressure and, where possible, by elevation of the injured part



Replacementof blood loss

In most cases blood loss should be replaced intrayenously in the pre-hospital phase, in response to the patient's clinical signs and symptoms. In all patients with blunt trauma and an anticipated transit time to hospital of more than 15 minutes, intrayenous replacement should be started without delay. Howeyer, in patients with penetrating torso injury, particularly if the anticipated transit time is short, it is reasonable not to infuse fluid in an attempt to maintain normotension.. Aggressi,'e transfusion in such cases may dislodge existing blood clots and will enhance haemorrhage. There will be loss of oxygen carrying capacity and dilution of clotting factors. As there is no prospect of arresting haemorrhage in the field in penetrating torso injury, the priority must be to transport the patient for definitive surgical care without delay. Exceptions to the rule include: the entrapped patient, where efforts must be made to achieye a systolic blood pressure of 80 mm Hg during release, and . patients with head injury, where the priority is to maintain a well oxygenated cerebral perfusion (see chapter 6). In all patients with blunt trauma estimated to haye lost more than 750 ml of blood, the loss should be replaced with intravenous fluid.

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Hypotensive resuscitation
Patients with penetrating torso trauma should be tl'fll1sp()J{ted to de.411itivesuJ{gicfllcare without delay Vigorous fluid infusion to maintain normotension increase bleeding and cause haemodilution may

Intravenous fluid

replacement in haemorrhagic


I haemorrhage

<750 ml (15%) Class IIhaemorrhage 750-1500 m! (15.-30%) Class

III haemorrhage

2.5 I Ringer-lactate solution or 1.0 I gelatin solution (or 0.75 I 6% starch) L5 I g<!latinsolutio!1 (or 1.5 I 6% starch), plus 1.0 I Ringer-lactate solution 1.5 I gelatin solution (or 1.51..6% starch), plus 1.0 I Ringer-lactate solution and red cells 1.5 I gelatin solution (or 1.5 I 6% starch), plus 1.0 I Rifiger-Iactate solution and red cells

lqOO~2000ml (30-40%)

Intravenous cannulation Two short, large bore intravenous cannulae (14 gauge or larger) should be inserted. Blood samples for full blood count, urea and electrolytes, and cross match can be taken from the first cannula. Easiest access is usually at the antecubital fossa, but anywhere on the upper limb is acceptable. The long saphenous vein at the ankle or the femoral vein in the groin can be used, but these are not ideal if the patient has pelvic or intra-abdominal injuries. If peripheral access is impossible percutaneously, other options include cut down on a peripheral vein, central venous cannulation or the intraosseous route. A cut down has few complications and can be performed quickly with minimal training. Standard large bore cannulae can be inserted by cut down. Possible cut down sites are the antecubital fossa, the saphenous vein at the ankle, and the proximal saphenous vein. Central venous access may not be easy in the hypovolaemic patient and there is a risk of creating a pneumothorax. Successful central venous cannulation will depend largely on the skill and experience of the operator. If the central route is to be used for rapid fluid resuscitation a relatively short large bore catheter (e.g., 8.5 F pulmonary artery introducer sheath) should be used. In the hypovolaemic patient, central venous pressure monitoring will often be required after the initial fluid challenge; this is best displayed continuously, via a transducer. The intraosseous route (usually the proximal tibia) is useful in children but will not allow high enough flow rates for effective fluid resuscitation in adults. A sample for arterial blood gas analysis should be obtained at an early stage. Severely injured patients will have a marked lactic acidosis that will be reflected by a significant base deficit and high plasma lactate (often> 2 mmol per litre). Reversal of the base deficit is an indicator of adequate resuscitation. Insertion of an arterial cannula (radial, brachial, or femoral) will allow continuous direct blood pressure monitoring and is convenient for repeated blood gas sampling. Patients with major injuries are critically ill and warrant invasive monitoring at the earliest opportunity.

Class IV haemorrhage >2000 ml (40%)



z-t--' ...

-Cannulation of the internal jugular vein Remember that the neck should not be turned until injury to the cervical spine has been excluded radiologically and clinically.


ABC of Major 'trauma

Choice of intravenous fluid Principles of fluid management emphasise fast and efficient restoration of intravascular volume. As anaemia is better tolerated than hypovolaemia, fluid resuscitation can initially be with non-blood agents such as a crystalloid (e.g., sodium chloride or Hartmann's solution) or a colloid (e.g., a gelatin or starch solution). Colloids are more efficient, in that equivalent intravascular volume expansion will be achieved with less colloid. However, crystalloids are cheaper than colloids and carry no risk of causing anaphylaxis. Fluid overload is bad far the patient whatever type of fluid is used, and interstitial oedema has several adverse effects (see box). No prospective, randomised trials have clearly shown that colloids are superior to crystalloids for trauma resuscitation, although a recent meta-analysis purports to show increased mortality with colloids. Double blind studies with the power to define the relative merits of colloids and crystalloids in fluid replacement are unlikely to be carried out, given the complexity of trauma cases and difficulty in establishing matched controls. Crystalloid solutions-The American College of Surgeons' ATLS committee recommends the use of Hartmann's solution for the initial resuscitation of severely injured patients. Part of the rationale for using crystalloids is that trauma patients will have sustained considerable interstitial fluid losses as well as intravascular loss. Replacement volumes should be three to four times the estimated intravascular loss. Colloidsolutions-Gelatins are the only cheap colloids available that can be infused in relatively unrestricted volumes. They have no effects on the cross matching of blood' and act as an osmotic diuretic. It has been suggested that bleeding time is prolonged after the use of gelatin solution for fluid resuscitation, compared with that seen after the use of saline. However, the case is far from proven and further study is required. In comparison with that of other colloids, the intravascular half-life of gelatins is relatively short (approximately 2 hours). Hydroxyethyl starch solutions-Hydroxyethyl starch (HES) solutions are synthetic polymers derived from amylopectin. The properties of HES solutions vary according to the degree of substitution of hydroxyethyl groups for glucose. Hetastarch (HES 450/0.7) has an average molecular weight of 450 000 Da. Its high molar substitution ratio (0.7) makes it relatively resistant to breakdown by amylase. This solution has a long half-life (more than 24 hours) and the larger starch molecules tend to accumulate in the reticuloendothelial system. It also causes a coagulopathy via an effect on factor VIII and von Willebrand factor. For these reasons the maximum dose of high molecular weight HES is restricted to 20 ml per kg per day and it cannot be recommended for the resuscitation of trauma patients. The starches of medium molecular weight (200 000 Da), such as Pentastarch or HAES-Steril (HES 200/0.5) have an intravascular half-life of about 6 hours. The maximum recommended dose for these solutions is 33 ml per kg per day. There is some evidence that 10% HES (200/0.5) results in significantly better systemic haemodynamics and splanchnic perfusion than volume replacement with 20% human albumin. The medium molecular weight starches may reduce capillary leak after trauma. Hypertonic saline solutions-Hypertonic crystalloid solutions provide small volume resuscitation and rapid restoration of haemodynamics, with laboratory evidence of improved
30 Pleurevacchest drain system,which allows reinfusionof blood drained from the pleural cavity.

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!llicrocirculatory haemodynamics. They exert their effect by recruitment of interstitial volume, thus increasing circulating volume and increasing blood pressure. However, raising the blood pressure may not always be an ideal goal, and the role of hypertonic solutions in trauma resuscitation has yet to be defined. Head-injured patients with a score of less than 9 on the Glasgow Coma Scale may benefit from hypertonic saline. Bloodand haemoglobin solutions--Once a patient has lost more than 30-40% of his or her blood volume a resuscitation fluid with good oxygen-carrying capability will become necessary. Currently, this implies the need for a blood transfusion, which unfortunately has several disadvantages (see box). Several haemoglobin solutions are at an advanced stage of development; problems related to toxic stroma, short intravascular half-life, and high colloid osmotic pressure have been overcome. An increase in mean arterial pressure (an effect related partly to binding of nitric oxide), and decreased viscosity of the haemoglobin solutions, may result in significantly better oxygen delivery to vital organs. However, some clinical studies of haemoglobin solutions have been stopped prematurely because of side effects in the study group. Furthermore, the long term safety of massive transfusion with haemoglobin solutions in humans has yet to be demonstrated. What is the optima~ haematocrit in the acute trauma patient? Hypovolaemia is tolerated considerably less well than anaemia. Traditional teaching is that all patients require a haematocrit of 30% or a haemoglobin of 109 per dl for optimal oxygen delivery. However, normovolaemic patients with good cardiopulmonary function will tolerate haemoglobin levels down to at least 7 g per dl. As long as normovolaemia is achieved the reduction in viscosity results in a significant increase in cardiac output and tends to improve tissue oxygenation. The problem is that a history of ischaemic heart disease or significant respiratory disease may not be available during resuscitation of the acute trauma patient. Furthermore, the haemoglobin concentration of a haemorrhaging patient undergoing resuscitation will be changing rapidly. Under these conditions the margin of safety is small if the haemoglobin concentration is reduced as low as 7 g per dl. Until more data are available, the target haemoglobin concentration of a severely injured patient should be around 109 per dl. Fluid warming All intravenous fluids should be properly warmed. A high capacity fluid warmer, such as the Level 1 (Level 1 HIOOO, Sims Level 1 Inc, Rockland, MA, USA), will be required to cope with the rapid infusion rates used during resuscitation of a trauma patient. Hypothermia (core temperature below 35C) is a serious complication of severe trauma and haemorrhage. The causes of hypothermia in a patient requiring massive transfusion include exposure, tissue hypoperfusion, and infusion of inadequately warmed fluids. Hypothermia has several adverse effects (see box), and in trauma patients is an independent predictor of survival.

Disadvantages of blood transfusion

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Intravenous infusion in military surgery.

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and treatment

The volume status of the patient is best determined by observing the vital signs and other monitoredyariables (see box) after a reasonably large fluid challenge (such as 2 litres of


ABC of Major Trauma

Hartmann's solution or 1 litre of gelatin solution). Fluid resuscitation should be continued to produce an adequate arterial pressure, a urine flow of at least I ml per kg per min, and a central venous pressure that responds to a rapid infusion of 200 ml by a sustained rise of more than 3 cm H2O over the previous value. Lack of improvement in the patient's vital signs after fluid replacement suggests exsanguinating haemorrhage (associated with major thoracic, abdominal, or pelvic in,iuries) and the need for immediate surgical intervention and transfusion of blood. Group 0 blood can be obtained immediately in the emergency room, group confirmed blood can be issued in 10 min, and a full cross match will take 45 min. A transient response to the initial fluid challenge suggests that the patient may have lost 20-40% of his or her circulating blood volume and has ongoing bleeding; immediate surgical assessment is required and the patient is likely to need blood. A sustained reduction in heart rate and increase in blood pressure suggests only moderate blood loss Oessthan 20% of the circulating volume). In the absence of ongoing bleeding, such patients can be effectively resuscitated with clear fluids only. A rising central venous pressure associated with a Iow blood pressure, tachycardia, and a reduced urine output indicates tension pneumothorax, cardiac tamponade, or cardiac failure (secondary to cardiac contusion or ischaemic heart disease). Cardiac tamponade is treated by thoracotomy, sometimes preceded by rapid needle pericardiocentesis. Cardiac failure can be confirmed by echocardiography, which will demonstrate a poorly contracting myocardium. The insertion of a pulmonary artery catheter may help to optimise volume replacement. These patients may requite inotropic drugs such as dobutamine or adrenaline. Resuscitation end-points Some investigators have questioned whether the return to normal of heart rate, blood pressure, and urine output is a suitable resuscitation end-point for the trauma patient. Once bleeding has been controlled and the patient admitted to an intensive care unit, goal directed therapy (increasing oxygen delivery and oxygen consumption to empirically derived values) might increase survival following severe trauma. This approach is highly controversial and requires the early insertion of a pulmonary artery floatation catheter. Most intensive care specialists will use the serum lactate or base deficit as an indicator of adequate oxygen delivery.


to monitor


fluid replacement

. Peripheral oxygen saturation

. . . . . . . . .

Respira~i()n rattJ
Pulse rate

ul c;J r~ hJ c c

Arterial pressure Pulse pressure Urinary output

Base deficit or lactate


End tidal carbon dioxide levels


Changes in the electrocardiogram


Needle pericardiocentesis.

Pain relief
Pain relief is essential, not only for compassionate reasons but also because it influences the pathophysiology of hypovolaemic shock by reducing catecholamine secretion. Giving a mixture of 50% nitrous oxide and 50% oxygen (Entonox) before the patient reaches hospital is of value. This should be supplemented with intravenous opioid given in increments (e.g., morphine 5 mg or fentanyl 50 micrograms) and titrated to effect. An antiemetic drug should be given intravenously if an opioid is given.





C r:.di/R-'

Resuscitative thoracotomy for cardiac tamponade caused by a stab wound.

Communication with the specialist

Most patients with hypovolaemic shock will require surgical control of bleeding. It is good practice to call the surgical specialist(s) to the emergency department at the earliest opportunity, so that priorities can be assessed and arrangements made for definitive care. Chest radiograph, abdominal 32

Patient receiving

Entonox on the way to hospital.

Hypovolaemic shock
ultrasound or diagnostic peritoneal lavage, urinary or gastric catheterisation, computed tomography or arterial angiography, as indicated, may help to determine the likely source of haemorrhage. However, patients with severe haemodynamic compromise require immediate surgical intervention on clinical grounds alone. pathophysiological changes to be established. Early, aggressive treatment offers the best results in most cases. Reliable intravenous access should be established in accordance with the expertise and experience of the attending clinician. Achieving restoration of tissue perfusion and oxygenation using an appropriate volume of fluid is more important than the choice of intravenous fluid. Fluid resuscitation should be guided by haemodynamic variables, urine output, and serum lactate or base deficit or both. Early surgery offers the best chance to control ongoing bleeding and an opportunity to correct abnormal physiology. This is particularly important in penetrating torso trauma, where controlled hypotension is acceptable until haemorrhage is arrested.

Many patients die of hypovolaemic shock, e.ven though the principles of management and treatment are well known and understood. Too often, however, too little clinical treatment is given too late, allowing a malignant, irreversible cycle of