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Hypovolaemia
Trauma
Hypovolaemia
Common causes of hypovolaemia
Louie Plenderleith
Absolute hypovolaemia Blood loss • Trauma • Surgery • Leaking aortic aneurysm • Haematemesis Plasma loss • Burns • Skin loss
Abstract Hypovolaemia is usually caused by loss of fluid from the body, leading to a lack of adequate circulatory filling, reduced organ blood flow and organ damage. Initially the body responds with arterial and venous constriction and mobilizes fluid from the tissues, followed by tachycardia and oliguria. These mechanisms can maintain blood pressure until about 30% of blood volume is lost, but at the expense of organ perfusion. After this point hypotension occurs. The primary management is to prevent further losses and refill the circulation using appropriate fluids. Colloids and crystalloids appear equivalent for this purpose, and hypertonic saline may be useful in initial resuscitation. For large losses care must be taken to maintain body temperature, haematocrit and coagulation. In situations where there is a large continuing blood loss only limited initial resuscitation is necessary until rapid control of bleeding is achieved. Optimal replacement can be difficult to assess; clinical measures such as peripheral perfusion and urine output can underestimate fluid requirements. Static measurements such as central venous pressure are of little use, but dynamic measures such as stroke volume response to fluid or pulse pressure variation can indicate fluid responsiveness. Monitoring organ perfusion is the ideal assessment of optimal fluid replacement, either directly or with surrogates such as central venous saturation.
Extravascular fluid loss • Vomiting • Diarrhoea • Sweating (exercise, pyrexia) • Ileus • Third-space loss • Excessive renal loss (diuretics, polyuric renal failure) • Dialysis or haemofiltration Relative hypovolaemia • Anaphylaxis • Sepsis • Vasodilator drugs (e.g. nitrates) • Neuraxial local anaesthesia (spinal or epidural) Table 1
which fluid is lost. If the loss has been from the total extracellular fluid (rather than just the circulation) then the total deficit will be approximately 3 times the blood volume loss. The body limits the effects of fluid loss in several ways. Vasoconstriction of both the arterial and venous systems is the immediate response. This reduces the circulatory filling capacity and redistributes blood from the skin and gastrointestinal tract (thus maintaining venous return) but may lead to inadequate perfusion of these organs. Extravascular fluid is mobilized into the circulation. Volume receptors in the heart and great veins, and osmolar receptors in the CNS cause a reduction in urine output and an increase in fluid intake (thirst) (Figure 1).
Keywords blood loss; circulatory volume assessment; resuscitation
Inadequate filling of the circulation (hypovolaemia) is a common problem during perioperative and intensive care management. Absolute hypovolaemia is generally caused by excessive fluid loss, but can also be due to inadequate fluid intake (Table 1). Relative hypovolaemia occurs when the capacity of the circula tion expands, as in sepsis or anaphylactic shock. This article will concentrate on absolute hypovolaemia.
Diagnosis The history and presenting complaint are important in raising the possibility of hypovolaemia because 10% of blood volume can be lost before there are any clinical signs. After this point the physiological responses described above may result in the following: • cold peripheries with poor capillary return and cyanosis • oliguria • dry axillae • increasing heart rate (although bradycardia can occur) • thirst • decreasing pulse pressure (caused by maintained systolic but raised diastolic blood pressure), followed by hypotension after loss of about 30% of blood volume
Pathophysiology After the loss of about 30% of the blood volume (1500–2000 ml) there is insufficient intravascular volume to maintain left vent ricular filling, causing cardiac output and blood pressure to fall. Organ damage occurs before this point because physiological responses cause the restriction of blood flow to some tissues. The total body fluid deficit depends on the compartment from
Louie Plenderleith, FRCA, is Consultant Anaesthetist in Anaesthesia and Intensive Care at the Western Infirmary, Glasgow. He qualified from Edinburgh University and trained in Sheffield and Glasgow.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 8:2
60
© 2007 Elsevier Ltd. All rights reserved.
Trauma
should be cross-matched as soon as possible, and 100% oxygen should be administered.
Physiological changes in hypovolaemic shock
Increase
Type of fluid: findings from studies and meta-analyses have failed to show any superiority of crystalloids or colloids for final patient outcome. Generally, crystalloids should be used for mild hypovolaemia, and colloids combined with crystalloids may be used in more severe states to fill the circulation rapidly. Hyper tonic saline seems useful in the acute stage of haemorrhage as it mobilizes fluid from the extravascular space to the circulation; therefore a small volume gives a greater response than another type of fluid. During resuscitation, haematocrit (or haemoglobin concentra tion) and clotting should be monitored and appropriate replace ment given (RBCs, fresh frozen plasma, cryoprecipitate). In cases of severe haemorrhage, administration of blood and clotting factors should not be delayed whilst waiting for confirmation of a low haematocrit or coagulopathy. After infusion of large volumes of blood the complications of massive transfusion should be considered (impaired oxygen delivery, hypocalcaemia, hyperkalaemia, metabolic acidosis and acute lung injury). Generally, resuscitation should occur before surgery, but this may not be possible when bleeding is from major vessels. After major traumatic haemorrhage without head injury, early resus citation to a lower systolic pressure (80 mm Hg, radial pulse just palpable) with rapid control of the source of bleeding may improve patient outcome. In these cases smaller resuscitation volumes are required, thus minimizing haemodilution and clot ting abnormalities. If there is a coexisting head injury, hypoten sion will worsen the outcome and this regimen is inappropriate.
Decrease
Normal values
10%
20%
30%
750 ml
40%
1500 ml
Blood loss in adult Heart rate Blood pressure Cardiac output
Central venous pressure Urine output Skin perfusion
Figure 1
Quantity of fluid: the initial target of resuscitation is the attain ment of an adequate blood pressure and resolution of tachycardia. However, when these are first achieved there is still considerable fluid deficit and fluid administration should continue. Too rapid administration of fluid may overload the circulation, leading to pulmonary oedema despite a continuing extravascular deficit. This is particularly a risk in elderly patients and arises because the resolution of vasoconstriction is not immediate and fluid takes time to diffuse to the tissues. The final aims of treatment for hypovolaemia are the res toration of the blood and extravascular volumes and delivery of sufficient oxygen to the tissues. Fluid administration may con tinue for some time after further losses have been prevented as fluid continues to move into the extravascular space, leading to further fluid requirements. The assessment of blood-volume status is difficult. While clinical measures (i.e. warm peripheries and a urine output of more than 30–50 ml/hour) may be of some use, they generally underestimate deficit. Static pressure measurements such as CVP and pulmonary capillary wedge pressure (PCWP) are also unhelpful as venoconstriction can maintain filling pressures in the presence of volume deficit. This also applies to single mea surements of stroke volume and cardiac output/index. Dynamic measures are more useful in assessing blood-volume status. These measures follow the response to changes in left ventricular filling, usually induced by rapidly administering a relatively small volume of fluid. The simplest method is to fol low the response of the CVP or PCWP to this bolus – if the CVP
• anxiety followed by confusion and a rising respiratory rate appear as the cardiac output falls • central venous pressure (CVP) may be normal or slightly reduced because of venoconstriction • decompensation may present earlier in elderly patients because of reduced physiological reserve. Procedures that result in vasodilation (e.g. sedation or anaes thesia) or reduce the venous return (e.g. mechanical ventilation or a change in posture) may reveal a hidden volume deficit and cause cardiovascular collapse. If severe hypovolaemia is not rapidly corrected then endorgan damage occurs. Hypotension and rapid blood transfusion initiate other responses, which lead to increased capillary leak, and redistributive hypovolaemia develops. Therefore, merely replacing the volume lost is insufficient. Management The management of hypovolaemia requires the prevention of further fluid loss, primarily by control of bleeding, and the replacement of fluid deficit. The initial management of hypovo laemia is fluid replacement; vasopressors have no role. The main aim is to fill the circulation sufficiently to restore the cardiac output and tissue flow. In severe haemorrhage or other large losses this will require the use of large-bore cannulae and fluid warming systems to prevent patient cooling. In small children intraosseous cannulae can be used if access is difficult. Blood
ANAESTHESIA AND INTENSIVE CARE MEDICINE 8:2
61
© 2007 Elsevier Ltd. All rights reserved.
Trauma
or PCWP rises briefly then falls more fluid should be given, if it rises and remains up then fluid should be stopped. More ac curate information can be achieved by monitoring the change in stroke volume (or less satisfactorily cardiac output) to the fluid challenge. Stroke volume can be measured using thermodilution, oesophageal Doppler or pulse contour analysis (PICCO or LIDCO). If stroke volume increases, further boluses should be given until no further increases are seen. Pulse pressure variation (PPV) uses the beat-to-beat varia tions in blood pressure induced by the swings in intrathoracic pressure produced by mechanical ventilation. These variations rapidly alter venous return and cardiac transmural pressure, leading to beat-to-beat changes in ventricular filling and stroke volume, and hence pulse pressure. The greater the variation the more likely there is to be a volume deficit and the effects of fluid boluses can be followed. The best prediction of volume responsiveness occurs when PPV is assessed during controlled mechanical ventilation with large tital volumes (> 8 ml/kg) without spontaneous breathing, and the fall in blood pressure should occur during the early phase of expiration.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 8:2
Maximal stroke volume may not be required to achieve good organ perfusion. Superior vena cava saturation has been used as a measure of tissue oxygenation, and achieving above 70% dur ing the initial resuscitation of severe sepsis has been associated with an improved outcome. There is evidence from several studies that perioperative fluid optimization targeted to dynamic measurements of stroke vol ume improves outcomes, especially if achieved early, even in situations where the deficit is occult. ◆
Further reading Grocott MPW, Mythen MG, Tong JG. Perioperative fluid management and clinical outcomes in adults. Anaesth Analg 2005; 100: 1093–106. Orlinsky M, Shoemaker W, Reis ED, Kernstein MD. Current controversies in shock and resuscitation. Surg Clin North Am 2001; 81: 1217–62. Palazzo M. Circulating volume and clinical assessment of the circulation. Br J Anaesth 2001; 86: 742–6.
62
© 2007 Elsevier Ltd. All rights reserved.
Hypovolaemia
Common causes of hypovolaemia
Louie Plenderleith
Absolute hypovolaemia Blood loss • Trauma • Surgery • Leaking aortic aneurysm • Haematemesis Plasma loss • Burns • Skin loss
Abstract Hypovolaemia is usually caused by loss of fluid from the body, leading to a lack of adequate circulatory filling, reduced organ blood flow and organ damage. Initially the body responds with arterial and venous constriction and mobilizes fluid from the tissues, followed by tachycardia and oliguria. These mechanisms can maintain blood pressure until about 30% of blood volume is lost, but at the expense of organ perfusion. After this point hypotension occurs. The primary management is to prevent further losses and refill the circulation using appropriate fluids. Colloids and crystalloids appear equivalent for this purpose, and hypertonic saline may be useful in initial resuscitation. For large losses care must be taken to maintain body temperature, haematocrit and coagulation. In situations where there is a large continuing blood loss only limited initial resuscitation is necessary until rapid control of bleeding is achieved. Optimal replacement can be difficult to assess; clinical measures such as peripheral perfusion and urine output can underestimate fluid requirements. Static measurements such as central venous pressure are of little use, but dynamic measures such as stroke volume response to fluid or pulse pressure variation can indicate fluid responsiveness. Monitoring organ perfusion is the ideal assessment of optimal fluid replacement, either directly or with surrogates such as central venous saturation.
Extravascular fluid loss • Vomiting • Diarrhoea • Sweating (exercise, pyrexia) • Ileus • Third-space loss • Excessive renal loss (diuretics, polyuric renal failure) • Dialysis or haemofiltration Relative hypovolaemia • Anaphylaxis • Sepsis • Vasodilator drugs (e.g. nitrates) • Neuraxial local anaesthesia (spinal or epidural) Table 1
which fluid is lost. If the loss has been from the total extracellular fluid (rather than just the circulation) then the total deficit will be approximately 3 times the blood volume loss. The body limits the effects of fluid loss in several ways. Vasoconstriction of both the arterial and venous systems is the immediate response. This reduces the circulatory filling capacity and redistributes blood from the skin and gastrointestinal tract (thus maintaining venous return) but may lead to inadequate perfusion of these organs. Extravascular fluid is mobilized into the circulation. Volume receptors in the heart and great veins, and osmolar receptors in the CNS cause a reduction in urine output and an increase in fluid intake (thirst) (Figure 1).
Keywords blood loss; circulatory volume assessment; resuscitation
Inadequate filling of the circulation (hypovolaemia) is a common problem during perioperative and intensive care management. Absolute hypovolaemia is generally caused by excessive fluid loss, but can also be due to inadequate fluid intake (Table 1). Relative hypovolaemia occurs when the capacity of the circula tion expands, as in sepsis or anaphylactic shock. This article will concentrate on absolute hypovolaemia.
Diagnosis The history and presenting complaint are important in raising the possibility of hypovolaemia because 10% of blood volume can be lost before there are any clinical signs. After this point the physiological responses described above may result in the following: • cold peripheries with poor capillary return and cyanosis • oliguria • dry axillae • increasing heart rate (although bradycardia can occur) • thirst • decreasing pulse pressure (caused by maintained systolic but raised diastolic blood pressure), followed by hypotension after loss of about 30% of blood volume
Pathophysiology After the loss of about 30% of the blood volume (1500–2000 ml) there is insufficient intravascular volume to maintain left vent ricular filling, causing cardiac output and blood pressure to fall. Organ damage occurs before this point because physiological responses cause the restriction of blood flow to some tissues. The total body fluid deficit depends on the compartment from
Louie Plenderleith, FRCA, is Consultant Anaesthetist in Anaesthesia and Intensive Care at the Western Infirmary, Glasgow. He qualified from Edinburgh University and trained in Sheffield and Glasgow.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 8:2
60
© 2007 Elsevier Ltd. All rights reserved.
Trauma
should be cross-matched as soon as possible, and 100% oxygen should be administered.
Physiological changes in hypovolaemic shock
Increase
Type of fluid: findings from studies and meta-analyses have failed to show any superiority of crystalloids or colloids for final patient outcome. Generally, crystalloids should be used for mild hypovolaemia, and colloids combined with crystalloids may be used in more severe states to fill the circulation rapidly. Hyper tonic saline seems useful in the acute stage of haemorrhage as it mobilizes fluid from the extravascular space to the circulation; therefore a small volume gives a greater response than another type of fluid. During resuscitation, haematocrit (or haemoglobin concentra tion) and clotting should be monitored and appropriate replace ment given (RBCs, fresh frozen plasma, cryoprecipitate). In cases of severe haemorrhage, administration of blood and clotting factors should not be delayed whilst waiting for confirmation of a low haematocrit or coagulopathy. After infusion of large volumes of blood the complications of massive transfusion should be considered (impaired oxygen delivery, hypocalcaemia, hyperkalaemia, metabolic acidosis and acute lung injury). Generally, resuscitation should occur before surgery, but this may not be possible when bleeding is from major vessels. After major traumatic haemorrhage without head injury, early resus citation to a lower systolic pressure (80 mm Hg, radial pulse just palpable) with rapid control of the source of bleeding may improve patient outcome. In these cases smaller resuscitation volumes are required, thus minimizing haemodilution and clot ting abnormalities. If there is a coexisting head injury, hypoten sion will worsen the outcome and this regimen is inappropriate.
Decrease
Normal values
10%
20%
30%
750 ml
40%
1500 ml
Blood loss in adult Heart rate Blood pressure Cardiac output
Central venous pressure Urine output Skin perfusion
Figure 1
Quantity of fluid: the initial target of resuscitation is the attain ment of an adequate blood pressure and resolution of tachycardia. However, when these are first achieved there is still considerable fluid deficit and fluid administration should continue. Too rapid administration of fluid may overload the circulation, leading to pulmonary oedema despite a continuing extravascular deficit. This is particularly a risk in elderly patients and arises because the resolution of vasoconstriction is not immediate and fluid takes time to diffuse to the tissues. The final aims of treatment for hypovolaemia are the res toration of the blood and extravascular volumes and delivery of sufficient oxygen to the tissues. Fluid administration may con tinue for some time after further losses have been prevented as fluid continues to move into the extravascular space, leading to further fluid requirements. The assessment of blood-volume status is difficult. While clinical measures (i.e. warm peripheries and a urine output of more than 30–50 ml/hour) may be of some use, they generally underestimate deficit. Static pressure measurements such as CVP and pulmonary capillary wedge pressure (PCWP) are also unhelpful as venoconstriction can maintain filling pressures in the presence of volume deficit. This also applies to single mea surements of stroke volume and cardiac output/index. Dynamic measures are more useful in assessing blood-volume status. These measures follow the response to changes in left ventricular filling, usually induced by rapidly administering a relatively small volume of fluid. The simplest method is to fol low the response of the CVP or PCWP to this bolus – if the CVP
• anxiety followed by confusion and a rising respiratory rate appear as the cardiac output falls • central venous pressure (CVP) may be normal or slightly reduced because of venoconstriction • decompensation may present earlier in elderly patients because of reduced physiological reserve. Procedures that result in vasodilation (e.g. sedation or anaes thesia) or reduce the venous return (e.g. mechanical ventilation or a change in posture) may reveal a hidden volume deficit and cause cardiovascular collapse. If severe hypovolaemia is not rapidly corrected then endorgan damage occurs. Hypotension and rapid blood transfusion initiate other responses, which lead to increased capillary leak, and redistributive hypovolaemia develops. Therefore, merely replacing the volume lost is insufficient. Management The management of hypovolaemia requires the prevention of further fluid loss, primarily by control of bleeding, and the replacement of fluid deficit. The initial management of hypovo laemia is fluid replacement; vasopressors have no role. The main aim is to fill the circulation sufficiently to restore the cardiac output and tissue flow. In severe haemorrhage or other large losses this will require the use of large-bore cannulae and fluid warming systems to prevent patient cooling. In small children intraosseous cannulae can be used if access is difficult. Blood
ANAESTHESIA AND INTENSIVE CARE MEDICINE 8:2
61
© 2007 Elsevier Ltd. All rights reserved.
Trauma
or PCWP rises briefly then falls more fluid should be given, if it rises and remains up then fluid should be stopped. More ac curate information can be achieved by monitoring the change in stroke volume (or less satisfactorily cardiac output) to the fluid challenge. Stroke volume can be measured using thermodilution, oesophageal Doppler or pulse contour analysis (PICCO or LIDCO). If stroke volume increases, further boluses should be given until no further increases are seen. Pulse pressure variation (PPV) uses the beat-to-beat varia tions in blood pressure induced by the swings in intrathoracic pressure produced by mechanical ventilation. These variations rapidly alter venous return and cardiac transmural pressure, leading to beat-to-beat changes in ventricular filling and stroke volume, and hence pulse pressure. The greater the variation the more likely there is to be a volume deficit and the effects of fluid boluses can be followed. The best prediction of volume responsiveness occurs when PPV is assessed during controlled mechanical ventilation with large tital volumes (> 8 ml/kg) without spontaneous breathing, and the fall in blood pressure should occur during the early phase of expiration.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 8:2
Maximal stroke volume may not be required to achieve good organ perfusion. Superior vena cava saturation has been used as a measure of tissue oxygenation, and achieving above 70% dur ing the initial resuscitation of severe sepsis has been associated with an improved outcome. There is evidence from several studies that perioperative fluid optimization targeted to dynamic measurements of stroke vol ume improves outcomes, especially if achieved early, even in situations where the deficit is occult. ◆
Further reading Grocott MPW, Mythen MG, Tong JG. Perioperative fluid management and clinical outcomes in adults. Anaesth Analg 2005; 100: 1093–106. Orlinsky M, Shoemaker W, Reis ED, Kernstein MD. Current controversies in shock and resuscitation. Surg Clin North Am 2001; 81: 1217–62. Palazzo M. Circulating volume and clinical assessment of the circulation. Br J Anaesth 2001; 86: 742–6.
62
© 2007 Elsevier Ltd. All rights reserved.