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Hypovolaemic
shock
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
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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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Symptoms
None Cardiovascular signs caused by catecholamine release: thirst, weakness, tachypnoea Systolic pressure falls Systolic pressure becomes unreadable
Up to 2000 >2000
III
IV
*Assuming a 70 kg patient
Resuscitation of patients (I) Adequate pulmonary (3) Replacement (2) Control of haemorrhage
with traUIIla
oxygenation
of lost volume
(4) Monitoring the effects of (I), (2), and (3) (5) SUpport of myocardial contractiIity (6) Relief of pain
Pulmonary
oxygenation
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
Control
of haemorrhage
Peripheral Periph"Tal haemorrhage should be controlled with firm pressure and, where possible, by ekvation of the injured part. 28
haemorrhage
Control with firm pressure and, where possible, by elevation of the injured part
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Hypovolaemic
loss*
shoe
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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
shock
Class
I 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.
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-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.
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VISCO
globir volaer signifi tissue TI signifi resusc haem under condi1 conce are a severe
Fluid All in capac Sims cope' a trau ISa se The c transf infusic severa indept
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Hypovolaemic
shock
!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.
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Monitoring
progress
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
31
L
Variables
to monitor
during
fluid replacement
. . . . . . . . .
.
Respira~i()n rattJ
Pulse rate
ul c;J r~ hJ c c
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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.
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Patient receiving
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.
Summary
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
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