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Hypovolaemia
CORE: TRAUMA
Hypovolaemia
Learning objectives
Laura Kettley After reading this article, you should be able to: C define hypovolaemia C define fluid responsiveness C summarize the FrankeStarling curve and heartelung interactions during mechanical ventilation C recognize the limitations of central venous pressure in assessing fluid responsiveness C understand the principles of dynamic indices of fluid responsiveness and their limitations
Aidan Marsh
Abstract The determination of intravascular volume in haemodynamically unstable patients is key to subsequent management. Administration of fluid remains the cornerstone of treatment but fluid loading in those patients not responsive to fluid is detrimental to outcome, as interstitial oedema impedes tissue oxygenation. Traditionally, static markers of cardiac preload such as central venous pressure have guided fluid therapy. Such markers have been shown to poorly predict fluid responsiveness. This has led to increased interest in dynamic variables such as the fluctuation of blood pressure and stroke volume in response to mechanical ventilation. These variables use the cyclical changes induced by positive pressure ventilation on right and left ventricular loading to measure changes in left ventricular stroke volume and arterial pressure. These dynamic indices, termed systolic pressure variation, pulse pressure variation and stroke volume variation, are superior in predicting fluid responsiveness in mechanically ventilated patients with a regular cardiac rhythm. In patients with spontaneous respiratory effort, the response of stroke volume to a passive leg raise is also an accurate indicator of fluid status.
body initially responds with arterial and venous vasoconstriction to decrease the capacitance of the circulatory system and redistribute fluid from the skin and gastrointestinal tract. These compensatory mechanisms can maintain blood pressure until 30% of circulating volume has been lost. With insufficient intravascular volume cardiac output will fall secondary to inadequate left ventricular filling and hypotension will ensue.
Fluid responsiveness Optimizing cardiac output and tissue oxygenation in haemodynamically unstable patients is of vital importance. Fluids remain the principal management of haemodynamically unstable patients, however studies have shown that only 50% of critically ill patients will be fluid responsive (i.e. respond to a fluid challenge by increasing stroke volume and cardiac output).1 The dangers of insufficient fluid resuscitation have been recognized for years, but there is increasing awareness that excessive fluid administration increases morbidity and mortality in the critically ill. Therefore accurate predictors of fluid responsiveness are key in the management of haemodynamic instability e guiding the fluid requirements for those who are fluid responsive or indicating the need for vasopressors and inotropes and avoiding the detrimental effects of excess fluid in those who are not.
Keywords Fluid responsiveness; heartelung interactions; hypovolaemia; passive leg raise; pulse pressure variation; stroke volume variation; systolic pressure variation Royal College of Anaesthetists CPD Matrix: 1A01, 2A02, 2A05
Definition Hypovolaemia is defined as inadequate filling of the circulation. In health, one-third of total body fluid is distributed in the extracellular compartment (ECF), of which one-quarter resides within the vasculature. The causes of fluid loss from the intravascular compartment are broad but can be divided for ease into absolute and relative hypovolaemia. Absolute hypovolaemia is usually caused by excessive fluid loss, such as blood loss from trauma or surgery, plasma loss from burns, or ECF loss from diarrhoea and vomiting. Relative hypovolaemia occurs in sepsis and anaphylaxis, where total body fluid content is high but the intravascular compartment is deplete.
The FrankeStarling curve and central venous pressure The FrankeStarling principle states that with increasing preload, left ventricular stroke volume will increase until an optimal preload is reached and stroke volume won’t increase despite further fluid loading (Figure 1). A patient who is fluid responsive is on the ascending limb of the FrankeStarling curve and those who are non-responsive are on the plateau. Central venous pressure (CVP) is traditionally used to guide fluid administration. As a measure of right atrial pressure, it has been assumed that CVP is a good indicator of right ventricular preload and, indirectly, left ventricular preload. However, studies have shown that CVP is a poor predictor of fluid responsiveness, with neither the initial value nor the response to fluid accurately indicating where a patient lies on the FrankeStarling curve.1
Pathophysiology Lack of adequate circulatory volume results in reduced organ blood flow, oxygenation and organ damage. To compensate, the
Laura Kettley MBChB is a Core Trainee in Emergency Medicine at Royal United Hospital, Bath, UK. Conflicts of interest: none declared.
Heartelung interactions in the mechanically ventilated
Aidan Marsh MRCP FRCA DICM is a Consultant in Anaesthesia and Intensive Care Medicine at Frenchay Hospital, Bristol, UK. Conflicts of interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:1
Positive pressure ventilation produces cyclical variation in the loading of the right and left ventricles (Figure 2). During
5
Ó 2013 Elsevier Ltd. All rights reserved.
CORE: TRAUMA
Frank–Starling curve Preload reserve
Stroke volume
No preload reserve
→ high PPV/SVV → positive PLR/EEO tests → positive response to VE
→ low PPV/SVV → negative PLR/EEO tests → low response to VE
Family of curves
Cardiac preload
Figure 1 On the ascending part of the FrankeStarling curve the ventricle has reserve and is able to increase stroke volume in response to a fluid challenge and volume expansion (VE). On the flat part of the curve the ventricle has no preload reserve and volume expansion has little effect on stroke volume. Variation in dynamic indices of fluid responsiveness such as pulse pressure variation (PPV), stroke volume variation (SVV) and passive leg raise (PLR) are greatest on the ascending portion of the curve. (From Marik et al. Haemodynamic parameters to guide fluid replacement. Ann Intensive Care 2011; 1: 1. Reproduced with permission from SpringerOpen.)
responsive.3e5 However, systolic pressures may be more susceptible to variations in transmural and pleural pressures during mechanical ventilation and other dynamic indices such as pulse pressure variation have been shown to be superior.
inspiration, venous return to the right ventricle is reduced due to increased pleural pressure and a decrease in the venous return pressure gradient. Right ventricular afterload is increased due to an increase in trans-pulmonary pressure. This results in decreased right ventricular output. Conversely, during inspiration, the left ventricular output is transiently increased due to an increase in venous return from increased trans-pulmonary pressures, and decreased afterload. The decrease in right ventricular output seen during inspiration is echoed in a decrease in left ventricular output during expiration, the lag being accountable for by the transit time of pulmonary blood flow.2 The magnitude of variation will be greater when operating on the ascending portion of the FrankeStarling curve and will be exacerbated by hypovolaemia and diminished by fluid administration (Figure 1). The studies investigating these dynamic indices are only replicable in mechanically ventilated patients with tidal volumes of at least 8 ml/kg with a regular cardiac rhythm.
Pulse pressure variation (PPV) Pulse pressure variation is derived from the arterial waveform. It is defined as the maximum pulse pressure in a respiratory cycle minus the minimum pulse pressure divided by the mean of these two values. It has been suggested as superior to SPV as changes in pleural pressures will affect both systolic and diastolic pressures and thus PPV will reflect changes in stroke volume alone. Studies suggest variations greater than 13e15% are highly accurate in assessing fluid responsiveness.3e5 Stroke volume variation (SVV) With the advent of cardiac output monitoring technology the estimation of actual variation in stroke volume through pulse contour analysis, rather than using surrogates such as PPV or SPV, is now possible. Variation between 9 and 13% has been reliably shown to predict fluid responsiveness.5
Dynamic indices of fluid responsiveness Systolic pressure variation (SPV) SPV can be calculated from the arterial waveform based on the fact that systolic pressure is proportional to left ventricular stroke volume. A variation in systolic pressure between 8 and 10 mmHg reflects a high likelihood that the patient will be fluid
ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:1
Spontaneously breathing patients A limitation of the dynamic indices considered above is that they cannot be used in spontaneously ventilating patients. A recent
6
Ó 2013 Elsevier Ltd. All rights reserved.
CORE: TRAUMA
Heart–lung interactions during mechanical ventilation
↓ RV preload Blood pulmonary transit time
↓ RV stroke volume ↑ Pleural pressure
↓ LV preload
↓ LV stroke volume
↑ RV afterload
↓ LV afterload ↑ Transpulmonary pressure
↑ LV stroke volume ↑ LV preload
Pulse pressure MAXIMUM at the end of inspiration
Pulse pressure MINIMUM during expiratory period
Figure 2 Left ventricular stroke volume is at its maximum at the end the inspiratory period and at its minimum during the expiratory period. These cyclic changes occur as a result of changes in right ventricular loading secondary to changes in trans-pulmonary and pleural pressures. (From Michard F, Teboul JL. Using hearte lung interactions to assess fluid responsiveness during mechanical ventilation. Crit Care 2000; 4: 282e289. By kind permission of Biomed Central.)
meta-analysis6 shows that the technique of passive leg raise (PLR), which acts as reversible fluid challenge (Figure 3), is highly accurate in predicting the response to subsequent fluid challenges. However, a measure of cardiac output such as pulse contour analysis or aortic blood flow must be used. Using surrogate measurements such as PPV are not sensitive enough to detect changes with this technique.
Summary Fluid administration remains a cornerstone of resuscitating unstable patients but it is now recognized that not all patients will benefit from fluid resuscitation and morbidity and mortality may be adversely affected. Dynamic markers such as PPV, SPV, SVV in the mechanically ventilated and PLR in those breathing spontaneously are superior to static markers such as CVP in predicting fluid responsiveness. Future studies should focus on the ability of dynamic markers to improve fluid administration strategies beyond the identification of fluid responsive patients. A
Passive leg raise
REFERENCES 1 Marik P, Monnet X, Teboul J-L. Haemodynamic parameters to guide fluid therapy. Ann Intensive Care 2011; 1: 1. 2 Michard F, Teboul J-L. Using heart lung interactions to assess fluid responsiveness during mechanical ventilation. Crit Care 2000; 4: 282e9. 3 Michard F, Teboul J-L. Predicting fluid responsiveness in ICU patients. Chest 2002; 121: 2000e8. 4 Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med 2000; 162: 134e8. 5 Michard F. Changes in arterial pressure during mechanical ventilation. Anaesthesiol 2005; 103: 419e28. 6 Callavaro F, Sandroni C, Marano C, et al. Diagnostic accuracy of passive leg raising for prediction of fluid responsiveness in adults: systematic review and meta-analysis of clinical studies. Intensive Care Med 2010; 36: 1475e83.
Transfer of blood from the legs and abdominal compartments = test for fluid responsiveness
Passive leg raising
Figure 3 Passively moving a patient from a 45 semi-recumbent position to supine with the legs raised to 45 induces a gravitational transfer of blood from the lower limbs and abdomen towards the heart. (From Marik et al. Haemodynamic parameters to guide fluid replacement. Ann Intensive Care 2011; 1: 1. Reproduced with permission from SpringerOpen.)
ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:1
7
Ó 2013 Elsevier Ltd. All rights reserved.
Hypovolaemia
Learning objectives
Laura Kettley After reading this article, you should be able to: C define hypovolaemia C define fluid responsiveness C summarize the FrankeStarling curve and heartelung interactions during mechanical ventilation C recognize the limitations of central venous pressure in assessing fluid responsiveness C understand the principles of dynamic indices of fluid responsiveness and their limitations
Aidan Marsh
Abstract The determination of intravascular volume in haemodynamically unstable patients is key to subsequent management. Administration of fluid remains the cornerstone of treatment but fluid loading in those patients not responsive to fluid is detrimental to outcome, as interstitial oedema impedes tissue oxygenation. Traditionally, static markers of cardiac preload such as central venous pressure have guided fluid therapy. Such markers have been shown to poorly predict fluid responsiveness. This has led to increased interest in dynamic variables such as the fluctuation of blood pressure and stroke volume in response to mechanical ventilation. These variables use the cyclical changes induced by positive pressure ventilation on right and left ventricular loading to measure changes in left ventricular stroke volume and arterial pressure. These dynamic indices, termed systolic pressure variation, pulse pressure variation and stroke volume variation, are superior in predicting fluid responsiveness in mechanically ventilated patients with a regular cardiac rhythm. In patients with spontaneous respiratory effort, the response of stroke volume to a passive leg raise is also an accurate indicator of fluid status.
body initially responds with arterial and venous vasoconstriction to decrease the capacitance of the circulatory system and redistribute fluid from the skin and gastrointestinal tract. These compensatory mechanisms can maintain blood pressure until 30% of circulating volume has been lost. With insufficient intravascular volume cardiac output will fall secondary to inadequate left ventricular filling and hypotension will ensue.
Fluid responsiveness Optimizing cardiac output and tissue oxygenation in haemodynamically unstable patients is of vital importance. Fluids remain the principal management of haemodynamically unstable patients, however studies have shown that only 50% of critically ill patients will be fluid responsive (i.e. respond to a fluid challenge by increasing stroke volume and cardiac output).1 The dangers of insufficient fluid resuscitation have been recognized for years, but there is increasing awareness that excessive fluid administration increases morbidity and mortality in the critically ill. Therefore accurate predictors of fluid responsiveness are key in the management of haemodynamic instability e guiding the fluid requirements for those who are fluid responsive or indicating the need for vasopressors and inotropes and avoiding the detrimental effects of excess fluid in those who are not.
Keywords Fluid responsiveness; heartelung interactions; hypovolaemia; passive leg raise; pulse pressure variation; stroke volume variation; systolic pressure variation Royal College of Anaesthetists CPD Matrix: 1A01, 2A02, 2A05
Definition Hypovolaemia is defined as inadequate filling of the circulation. In health, one-third of total body fluid is distributed in the extracellular compartment (ECF), of which one-quarter resides within the vasculature. The causes of fluid loss from the intravascular compartment are broad but can be divided for ease into absolute and relative hypovolaemia. Absolute hypovolaemia is usually caused by excessive fluid loss, such as blood loss from trauma or surgery, plasma loss from burns, or ECF loss from diarrhoea and vomiting. Relative hypovolaemia occurs in sepsis and anaphylaxis, where total body fluid content is high but the intravascular compartment is deplete.
The FrankeStarling curve and central venous pressure The FrankeStarling principle states that with increasing preload, left ventricular stroke volume will increase until an optimal preload is reached and stroke volume won’t increase despite further fluid loading (Figure 1). A patient who is fluid responsive is on the ascending limb of the FrankeStarling curve and those who are non-responsive are on the plateau. Central venous pressure (CVP) is traditionally used to guide fluid administration. As a measure of right atrial pressure, it has been assumed that CVP is a good indicator of right ventricular preload and, indirectly, left ventricular preload. However, studies have shown that CVP is a poor predictor of fluid responsiveness, with neither the initial value nor the response to fluid accurately indicating where a patient lies on the FrankeStarling curve.1
Pathophysiology Lack of adequate circulatory volume results in reduced organ blood flow, oxygenation and organ damage. To compensate, the
Laura Kettley MBChB is a Core Trainee in Emergency Medicine at Royal United Hospital, Bath, UK. Conflicts of interest: none declared.
Heartelung interactions in the mechanically ventilated
Aidan Marsh MRCP FRCA DICM is a Consultant in Anaesthesia and Intensive Care Medicine at Frenchay Hospital, Bristol, UK. Conflicts of interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:1
Positive pressure ventilation produces cyclical variation in the loading of the right and left ventricles (Figure 2). During
5
Ó 2013 Elsevier Ltd. All rights reserved.
CORE: TRAUMA
Frank–Starling curve Preload reserve
Stroke volume
No preload reserve
→ high PPV/SVV → positive PLR/EEO tests → positive response to VE
→ low PPV/SVV → negative PLR/EEO tests → low response to VE
Family of curves
Cardiac preload
Figure 1 On the ascending part of the FrankeStarling curve the ventricle has reserve and is able to increase stroke volume in response to a fluid challenge and volume expansion (VE). On the flat part of the curve the ventricle has no preload reserve and volume expansion has little effect on stroke volume. Variation in dynamic indices of fluid responsiveness such as pulse pressure variation (PPV), stroke volume variation (SVV) and passive leg raise (PLR) are greatest on the ascending portion of the curve. (From Marik et al. Haemodynamic parameters to guide fluid replacement. Ann Intensive Care 2011; 1: 1. Reproduced with permission from SpringerOpen.)
responsive.3e5 However, systolic pressures may be more susceptible to variations in transmural and pleural pressures during mechanical ventilation and other dynamic indices such as pulse pressure variation have been shown to be superior.
inspiration, venous return to the right ventricle is reduced due to increased pleural pressure and a decrease in the venous return pressure gradient. Right ventricular afterload is increased due to an increase in trans-pulmonary pressure. This results in decreased right ventricular output. Conversely, during inspiration, the left ventricular output is transiently increased due to an increase in venous return from increased trans-pulmonary pressures, and decreased afterload. The decrease in right ventricular output seen during inspiration is echoed in a decrease in left ventricular output during expiration, the lag being accountable for by the transit time of pulmonary blood flow.2 The magnitude of variation will be greater when operating on the ascending portion of the FrankeStarling curve and will be exacerbated by hypovolaemia and diminished by fluid administration (Figure 1). The studies investigating these dynamic indices are only replicable in mechanically ventilated patients with tidal volumes of at least 8 ml/kg with a regular cardiac rhythm.
Pulse pressure variation (PPV) Pulse pressure variation is derived from the arterial waveform. It is defined as the maximum pulse pressure in a respiratory cycle minus the minimum pulse pressure divided by the mean of these two values. It has been suggested as superior to SPV as changes in pleural pressures will affect both systolic and diastolic pressures and thus PPV will reflect changes in stroke volume alone. Studies suggest variations greater than 13e15% are highly accurate in assessing fluid responsiveness.3e5 Stroke volume variation (SVV) With the advent of cardiac output monitoring technology the estimation of actual variation in stroke volume through pulse contour analysis, rather than using surrogates such as PPV or SPV, is now possible. Variation between 9 and 13% has been reliably shown to predict fluid responsiveness.5
Dynamic indices of fluid responsiveness Systolic pressure variation (SPV) SPV can be calculated from the arterial waveform based on the fact that systolic pressure is proportional to left ventricular stroke volume. A variation in systolic pressure between 8 and 10 mmHg reflects a high likelihood that the patient will be fluid
ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:1
Spontaneously breathing patients A limitation of the dynamic indices considered above is that they cannot be used in spontaneously ventilating patients. A recent
6
Ó 2013 Elsevier Ltd. All rights reserved.
CORE: TRAUMA
Heart–lung interactions during mechanical ventilation
↓ RV preload Blood pulmonary transit time
↓ RV stroke volume ↑ Pleural pressure
↓ LV preload
↓ LV stroke volume
↑ RV afterload
↓ LV afterload ↑ Transpulmonary pressure
↑ LV stroke volume ↑ LV preload
Pulse pressure MAXIMUM at the end of inspiration
Pulse pressure MINIMUM during expiratory period
Figure 2 Left ventricular stroke volume is at its maximum at the end the inspiratory period and at its minimum during the expiratory period. These cyclic changes occur as a result of changes in right ventricular loading secondary to changes in trans-pulmonary and pleural pressures. (From Michard F, Teboul JL. Using hearte lung interactions to assess fluid responsiveness during mechanical ventilation. Crit Care 2000; 4: 282e289. By kind permission of Biomed Central.)
meta-analysis6 shows that the technique of passive leg raise (PLR), which acts as reversible fluid challenge (Figure 3), is highly accurate in predicting the response to subsequent fluid challenges. However, a measure of cardiac output such as pulse contour analysis or aortic blood flow must be used. Using surrogate measurements such as PPV are not sensitive enough to detect changes with this technique.
Summary Fluid administration remains a cornerstone of resuscitating unstable patients but it is now recognized that not all patients will benefit from fluid resuscitation and morbidity and mortality may be adversely affected. Dynamic markers such as PPV, SPV, SVV in the mechanically ventilated and PLR in those breathing spontaneously are superior to static markers such as CVP in predicting fluid responsiveness. Future studies should focus on the ability of dynamic markers to improve fluid administration strategies beyond the identification of fluid responsive patients. A
Passive leg raise
REFERENCES 1 Marik P, Monnet X, Teboul J-L. Haemodynamic parameters to guide fluid therapy. Ann Intensive Care 2011; 1: 1. 2 Michard F, Teboul J-L. Using heart lung interactions to assess fluid responsiveness during mechanical ventilation. Crit Care 2000; 4: 282e9. 3 Michard F, Teboul J-L. Predicting fluid responsiveness in ICU patients. Chest 2002; 121: 2000e8. 4 Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med 2000; 162: 134e8. 5 Michard F. Changes in arterial pressure during mechanical ventilation. Anaesthesiol 2005; 103: 419e28. 6 Callavaro F, Sandroni C, Marano C, et al. Diagnostic accuracy of passive leg raising for prediction of fluid responsiveness in adults: systematic review and meta-analysis of clinical studies. Intensive Care Med 2010; 36: 1475e83.
Transfer of blood from the legs and abdominal compartments = test for fluid responsiveness
Passive leg raising
Figure 3 Passively moving a patient from a 45 semi-recumbent position to supine with the legs raised to 45 induces a gravitational transfer of blood from the lower limbs and abdomen towards the heart. (From Marik et al. Haemodynamic parameters to guide fluid replacement. Ann Intensive Care 2011; 1: 1. Reproduced with permission from SpringerOpen.)
ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:1
7
Ó 2013 Elsevier Ltd. All rights reserved.