5 - hypovolaemic shock

8/13/2019 5 - Hypovolaemic Shock

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5 Hypovolaemic shock

Peter J F Baskett, Jerry P N olan

Hypovolaemic shock is a clinical state in which tissue perfusion

isrendered 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 areduction 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.

. Tachycardia (caused by catecholamine release).Skin pallor (results from vasoconstrictioncaused by catecholamine release).Hypotension (caused by hypovolaemia,perhaps followed by myocardial

insufficiency)

. Confusion, aggression, drowsiness, andcoma (caused by cerebral hypoxia and

acidosis)

.. Tachypnoea (caused by hypoxia andacidosis)

.General weakness (caused by hypoxia

and acidosis).Thirst (caused by hypovolaemia). Reduced urine output (caused by

reduced perfusion)

'In most cases signs and symptoms can be re-lated to the amount of blood loss, which can be

classedin four broad groups (classes I-IV).

Generally, losses up to 750 ml (class I) (15%

of the circulating blood volume) generate no

pronounced signs or symptoms. Further haem-

orrhage, up to 1.5 litres (class 11), produces Extremities

cardiovascular signs of catecholamine release,

thirst, weakness, and tachypnoea. Systolic

pressure begins to fall as blood loss mounts to2 litres (class Ill) and often becomcs un-

recordable after 2.5-3.0 litres (class IV) havebeen lost.

How blood loss can lead to multiorgan tallure

Classification of hypovolaemic shock by blood loss (adult)

Blood loss

Percentage

Volume (mI)

Blood pressure

Systolic

Diastolic

Pulse

(beats/min)

Capillary refill

Respiratory rate

Urinary flow rate

(ml/h)

Complexion

Mental state

Class I Class 11 Class III Class IV

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750 800-1500 1500-2000 >2000

Unchanged Normal Reduced Very Iow

Unchanged Raised Reduced Very Iow orunrecordable

Slight 100-120 120 (thready) 120 (very

tachycardia thready)

Normal Slow (>2 s) Slow (>2 s) Undetectable

Normal Tachypnoea Tachypnoea Tachypnoea

(>20/min) (>20/min)

>30 20-30 10-20 0-10

Colour Pale Pale Pale, clammy,

normal and cold

Normal Pale Pale Ashen

Alert Anxious or Anxious, Drowsy,aggressIVe aggressIve, confused, or

drowsy unconscIous

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ABC of Major Trauma

Previously healthy young adults have remarkable com-

pensatory 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 modestblood 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 uncompen-

sated shock with severe blood loss and inadequate resusci-

tation. As a rule, a child's systolic blood pressure is 80 mm Hgplus twice the age in years, The diastolic pressure is about two

thirds of the systQlic pressure. A systolic pressure of 70 mm Hgor 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 tachy-

cardia. 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 onlybecause 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 injuryand 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).

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.

Control of haemorrhage

Periph"Tal haemorrhage should be controlled with firm

pressure and, where possible, by ekvation of the injuredpart.

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Symptoms of hypovolaemia according to blood 1055* RBlood loss (ml)


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r*

Replacementof blood loss

Inmost 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, intrayenousreplacement 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 tothe rule include:.the entrapped patient, where efforts must be made toachieye a systolic blood pressure of 80 mm Hg duringrelease, and

. patients with head injury, where the priority is to maintaina 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 withintravenous fluid.

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 thefirstcannula.

Easiest access is usually at the antecubital fossa, butanywhere 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 foreffective 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 deficitand 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

Hypovolaemic sho

Hypotensiveresuscitation.Patients with penetrating torso trauma should betl'fll1sp()J{tedto de.411itivesuJ{gicfllcare without delay.Vigorous fluid infusion to maintain normotension mayincrease bleeding and cause haemodilution

Intravenous fluid replacement in haemorrhagicshock

Class I haemorrhage

(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 solutionand red cells

1.5 I gelatin solution

(or 1.5 I 6% starch),

plus 1.0 I Rifiger-Iactate solutionand red cells

Class IIhaemorrhage

750-1500 m! (15.-30%)

Class III haemorrhage

lqOO~2000ml (30-40%)

Class IV haemorrhage

>2000 ml (40%)

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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


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ABC of Major 'trauma

Choice of intravenous fluid

Principles of fluid management emphasise fast and efficientrestoration 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 equivalentintravascular 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 todefine the relative merits of colloids and crystalloids in fluid

replacement are unlikely to be carried out, given the complexityof 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 willhave sustained considerable interstitial fluid losses as well as

intravascular loss. Replacement volumes should be three tofour 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 resusci-

tation, 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 (approx-imately 2 hours).

Hydroxyethyl starch solutions-Hydroxyethyl starch (HES)

solutions are synthetic polymers derived from amylopectin.

The properties of HES solutions vary according to the degreeof 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 largerstarch molecules tend to accumulate in the reticuloendothelial

system. It also causes a coagulopathy via an effect on factorVIII and von Willebrand factor. For these reasons the

maximum dose of high molecular weight HES is restricted to20 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 anintravascular half-life of about 6 hours. The maximum recom-

mended 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 thanvolume replacement with 20% human albumin. The medium

molecular weight starches may reduce capillary leak aftertrauma.

Hypertonic saline solutions-Hypertonic crystalloid solutions

provide small volume resuscitation and rapid restoration of

haemodynamics, with laboratory evidence of improved

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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 onthe Glasgow Coma Scale may benefit from hypertonic saline.

Bloodandhaemoglobinsolutions--Once a patient has lost morethan 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 tobe 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 haemo-globin levels down to at least 7 g per dl. As long as normo-volaemia is achieved the reduction in viscosity results in a

significant increase in cardiac output and tends to improve

tissueoxygenation.

The problem is that a history of ischaemic heart disease or

significant respiratory disease may not be available duringresuscitation 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.

Monitoring progress and treatment

The volume status of the patient is best determined by

observing the vital signs and other monitoredyariables (see

b ) ft bl l fl id h ll ( h 2 lit f

Hypovolaemic shock

Disadvantagesof blood transfusion

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Intravenous infusion in military surgery.

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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 (associatedwith 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 Iowblood 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 asuitable 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.

Pain relief

Pain relief is essential, not only for compassionate reasons butalso 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.

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 earliestopportunity, so that priorities can be assessed and arrange-

ments made for definitive care. Chest radiograph, abdominal

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Variables to monitor during fluid replacement

. Peripheral oxygen saturation

. Respira~i()n rattJ.Pulse rate

.Arterial pressure

.Pulse pressure

c

c

..Urinary output.Base deficit or lactate

.Temperature

. End tidal carbon dioxide levels.Mentalsfate

. Changes in the electrocardiogram

/.:?

Needle pericardiocentesis.

ott..,~

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Resuscitative

thoracotomyfor cardiac

tamponade

caused by astab wound.

Patient receiving Entonox on the way to hospital.


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ultrasound or diagnostic peritoneal lavage, urinary or gastric

catheterisation, computed tomography or arterial angiog-

raphy, 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.

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

Hypovolaemic shock

pathophysiological changes to be established. Early, aggressivetreatment 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 thanthe choice of intravenous fluid. Fluid resuscitation should be

guided by haemodynamic variables, urine output, and serumlactate 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 haemorrhageis arrested.

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5 - hypovolaemic shock

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