Resuscitation in hypovolaemic shock

What is hypovolaemic shock?

Hypovolaemic shock occurs when the volume of the circulatory system is too depleted to allow adequate circulation to the tissues of the body. The aim of resuscitation is to correct the hypovolaemia and hypoperfusion of vital organs such as the kidneys before irreversible damage occurs.

There are also other causes of shock:

• Cardiogenic - eg, massive myocardial infarction or other cause of primary cardiac (pump) failure.

• Obstructive - eg, massive pulmonary embolism, cardiac tamponade, tension pneumothorax.

• Distributive - vasodilatation +/- leakage from endothelium; with the following subtypes: septic shock, anaphylactic shock, and neurogenic shock. Neurogenic shock is associated with cervical and high thoracic spinal cord injury. It can present as hypotension, bradyarrhythmia, and loss of temperature control.

Risk factors

A healthy adult can withstand the loss of half a litre from a circulation of about five litres without ill effect. However, larger volumes and rapid loss cause progressively greater problems.

The risk is very much related to the degree of hypovolaemia and the speed of correction. In children and young adults tachycardia is one of the earliest signs of hypovolaemia as the circulatory system is much better able to cope with the rigours of fluid loss.

The risk of morbidity and mortality is much greater as age increases. Pre-existing pathology in the cardiovascular, respiratory and renal systems also increases risk.

Hypovolaemic shock symptoms and presentation

Symptoms

• The individual may feel cold, unwell, anxious, faint and short of breath.

• There may be faintness on standing or even on sitting up, due to postural hypotension.

• There may be symptoms related to the cause of the hypovolaemia, such as pain from a bleeding ulcer, dissecting aneurysm, ruptured ectopic pregnancy, trauma or burns.

• Gut ischaemia can lead to nausea and vomiting but the significance is often overlooked.

Signs

• The patient may look pale and sweaty.

• There may be tachypnoea.

• The periphery may be cold from poor perfusion, and capillary refill time may be prolonged. However, this can be a poor indicator of hypovolaemia.

• There may be tachycardia and a fall in blood pressure (BP) or postural hypotension. Tachycardia and cold peripheries from vasoconstriction may occur before a fall in BP, especially in children and young adults.

• Young people may show little rise in pulse rate and no fall in BP despite significant exsanguination. It is very easy to underestimate the severity of loss in a young person.

• Late features include confusion or even coma.

What causes hypovolaemic shock? (Aetiology)

The causes of hypovolaemic shock are:¹

• Haemorrhagic shock: loss of blood, which may be revealed or occult.

  • May be due to visible bleeding or rupture of an internal organ like the spleen or liver.

  • A fractured femur will bleed about half a litre and a fractured pelvis will lose about one litre of blood - note these volumes vary according to age/weight.

  • The volume of haematemesis gives little indication of the degree of bleeding.

  • Bleeding from ectopic pregnancy is also occult with little or no vaginal loss, and 30% of ectopic pregnancies rupture before a menstrual period has been missed. It is important to maintain a high level of clinical suspicion.

• Leakage of plasma and often some blood as seen in burns.

• Severe loss of water and salt:

  • This may occur with vigorous exercise in a hot environment. Exercise in extreme heat can cause serious loss of water and salt. As the rate of sweating rises, the concentration of sodium in the sweat rises, so that the total loss of sodium rises exponentially. Ability to remove sodium from sweat improves with acclimatisation.

  • Poor fluid intake.

  • Fluid loss from diarrhoea and/or vomiting. Severe diarrhoea and vomiting will cause marked loss of electrolytes as well as water.

  • Inappropriate diuresis.

Investigations

• Check Hb, U&E, LFT and, in haemorrhage and burns, group and cross-match.

• Coagulation screen.

• Blood gases (arterial or venous) may show a metabolic acidaemia from poor perfusion; lactate levels particularly reflect hypoperfusion.

• Monitor urine output, which may require a catheter.

• Ultrasound can be useful for differentiating hypovolaemic from cardiogenic shock; the vena cava can be assessed for adequate filling and echocardiogram can show any pump failure.

• Central venous pressure (CVP) monitoring may be useful where there is evidence of shock.

Staging

For adults, the clinical staging relating to loss of blood volume can be classified as:²

• Class 1: 10-15% loss of total blood volume; physiological compensation and no clinical changes appear.

• Class 2: 15-30% blood loss; postural hypotension, generalised vasoconstriction and reduction in urine output to 20-30 ml/hour.

• Class 3: 30-40% blood loss; hypotension, tachycardia over 120, tachypnoea, urine output under 20 ml/hour and the patient is confused.

• Class 4: over 40% blood loss; marked hypotension, tachycardia and tachypnoea. No urine output and the patient is comatose.

The Adult Trauma Life Support guidelines describes a similar classification linking the amount of blood loss with the specific physiological findings - eg, stage 4 hypovolaemic shock results in various clinical changes including a pulse rate >140 bpm, respiratory rate >35 breaths per minute and confusion.² The guidelines are useful in teaching but their role in real clinical scenarios is more limited and caution should be used.^{3 2} For example, women with a ruptured ectopic pregnancy can appear haemodynamically stable at presentation and then suddenly deteriorate.

Physiologically, three stages of hypovolaemic shock are recognised:

• Compensated shock: baroreceptor reflexes result in increase in myocardial contractility, tachycardia and vasoconstriction. They maintain cardiac output and BP and lead to the release of vasopressin, aldosterone and renin.

• Progressive or uncompensated shock: occurs with myocardial depression, failure of vasomotor reflexes and failure of the microcirculation, with increase in capillary permeability, sludging and thrombosis, resulting in cellular dysfunction and lactic acidosis.

• Irreversible shock: failure of vital organs with inability to recover.

These stages are also applicable to children but their period of compensated shock may be relatively longer than in adults. However, their cardiac reserve is less, so that the shift to uncompensated shock can progress more rapidly to the irreversible stage.

Hypovolaemic shock treatment and management

The resuscitation of traumatic haemorrhagic shock has undergone a shift in the last 20 years with the advent of damage control resuscitation. Major principles include minimisation of crystalloid, permissive hypotension, transfusion of a balanced ratio of blood products, and goal-directed correction of coagulopathy. In particular, plasma has replaced crystalloid as the primary means for volume expansion for traumatic haemorrhagic shock.^{4 5}

General measures

• Oxygen should be given.

• Venous access must be secured early. Maintaining adequate perfusion of vital organs is essential.

• For initial fluid resuscitation, using starches, dextrans, albumin or fresh frozen plasma, or gelatins, versus crystalloids probably makes little or no difference to mortality.⁶

• For haemorrhage, blood should be given as soon as possible. Rapid infusion devices and autologous blood transfusion may be employed if blood loss is massive and fast.⁷

• There is some debate around fluid replacement where haemorrhage is ongoing. Modern ideas include avoiding excessive crystalloid fluid resuscitation by allowing hypotension and early use of blood and massive transfusion protocols with damage control surgery to combat the lethal triad of hypothermia, coagulopathy and acidosis.⁸

• One meta-analysis found significant benefits of hypotensive resuscitation relative to mortality in traumatic haemorrhagic shock patients. It not only reduced the need for blood transfusions and the incidences of ARDS and multiple organ dysfunction, but it caused a non-significant acute kidney injury incidence.⁹

• A central venous pressure (CVP) line may be required. CVP is far more sensitive to the balance between loss and replacement than pulse or BP and, in the elderly, it can prevent over-transfusion and pulmonary oedema.

Pharmacological

• Initial goal-directed resuscitation for hypotensive shock usually includes administration of intravenous fluids, followed by initiation of vasopressors. Despite obvious immediate effects of vasopressors on haemodynamics, their effect on patient-relevant outcomes remains controversial. A Cochrane review found no evidence of substantial differences in total mortality between several vasopressors, including dopamine, norepinephrine, epinephrine, phenylephrine, vasopressin, and terlipressin.¹⁰

• If there is pain, analgesia must be given by the IV route, as any other route will be ineffective. Pain increases metabolic rate and so aggravates tissue ischaemia.

Surgical

• If bleeding continues, surgery may be needed to stem the flow. It is usual to resuscitate first to reduce the risk, especially as induction of anaesthesia can lead to collapse of a fragile circulation. In some cases like ruptured ectopic pregnancy and placenta praevia, the rate of bleeding cannot be matched by transfusion and the cause must be treated before resuscitation can be effective.

• In trauma, first aid measures may help stem blood loss. In gunshot wounds look for not just the entrance but also the exit wound. The latter may be significantly larger than the former. If a high-powered weapon was used, primary closure of the wound should not be attempted.

Resuscitative endovascular balloon occlusion of the aorta (REBOA)

• REBOA has been used in hypovolaemic shock as a result of haemorrhage.¹¹

• It involves introducing a balloon via the femoral artery into the aorta, which is then inflated and in effect cuts off blood supply above the haemorrhaging point.

• It has been used in various settings, including postpartum haemorrhage, trauma, upper gastrointestinal bleeding and ruptured aortic aneurysm.

• It is only a temporary measure until more definitive treatment to halt the haemorrhage can take place.

• The evidence base is currently limited.^{12 13}

Complications

• Blood is directed away from the kidneys and gut. This can produce acute kidney injury and complications of gut ischaemia.

• Acute tubular necrosis can occur.

• Inadequate perfusion leads to hypoxia and metabolic acidosis.

• About 75% of the blood flow to the right ventricle and 100% to the left ventricle occurs in diastole. A fall in diastolic pressure will predispose to cardiac arrhythmias and even arrest. Upset of acid-base balance, hypoxia and disturbance of electrolytes will aggravate the problem.

• In those who are susceptible, dehydration may lead to haemoconcentration and sludging of the circulation with such complications as venous sinus thrombosis.

Prognosis

Prognosis is worse in the elderly than in the young. Physical fitness improves outcome. Rapid and adequate replacement of the circulating volume may prevent the complications of hypoperfusion, including acute kidney injury, renal failure, ischaemic damage to the gut, brain damage and cardiac arrest.

Hypovolaemic shock prevention

• Loss of circulating volume must be diagnosed and treated before the condition becomes critical. This is often difficult when bleeding is internal and hence occult. It is often poorly done.

• Where the loss is simply salt and water, oral replacement will be adequate in the early stages.

• In other cases, venous access and adequate replacement are required at an early stage.

• Small children are very susceptible to dehydration, as are the elderly.

• Nowadays sportsmen are very much more aware of the problems of dehydration. Even slight dehydration has a marked adverse effect on fitness.