Given the above equation and the need to reverse anaerobic metabolism the two common areas of monitoring to determine the endpoints of resuscitation involve the macrocirculation using haemodynamics and the microcirculation assessing markers of tissue perfusion.
14.1 Haemodynamic Monitoring
14.1.1 Pulse Rate
From ancient time the character of the pulse has guided physicians. One of the early definitions of shock was a systolic pressure <100 mmHg and a pulse rate of >100 beats per minute. The endpoint of resuscitation was to reverse these numbers. A reduction in pulse rate is uncommon for a number of reasons. Firstly, shock results in an altered level of consciousness and failure to appreciate a noxious stimulus. Restoration of cerebral perfusion results in pain and anxiety. Secondly, the normal baroreceptor response is tonic and during shock baroreceptor impulses decrease. Despite restoration of an adequate intravascular volume the baroreceptor response lags behind and a tachycardia persists. Thirdly the SIRS response is defined by a tachycardia and is an almost constant feature of trauma. For these reasons relying on a fall in pulse rate to signify an endpoint of resuscitation is not recommended.
14.1.2 Arterial Saturation (SaO2)
A minimum SaO2 of 95 % must be achieved during the initial resuscitation, above this level there is minimal improvement in DO2. Anaerobic metabolism creates air hunger and tachypnoea as a compensatory mechanism with the aim of removing CO2 to eliminate acid. Even if SaO2 can be maintained by spontaneous ventilation the work of breathing is markedly increased resulting in an increase in VO2. In the presence of a moderate to severe metabolic acidosis this compensation should default to the clinician and patients with hypotension must be intubated and mechanically ventilated thereby eliminating unnecessary wastage of DO2. Protective lung ventilation has been proposed as standard of care in the critically ill but it is crucial to understand that all data from these studies have been extracted from critically ill patients in ICU with established severe lung dysfunction. These results have no relevance whatsoever to the emergency room and acute resuscitation and the use of low tidal volumes will not allow the effective removal of CO2 nor will it recruit atelectactic lung segments, a not uncommon problem in thoracic trauma. Assuming similar effects, the misguided extrapolation of results from one phase of critical care to a markedly different scenario and location is unjustifiable and dangerous. The endpoint of ventilatory resuscitation is a SaO2 of >95 % and a CO2 which allows the arterial pH to remain above 7.2 until intravascular volume expansion has been achieved and the metabolic acidosis improving. The most effective method of reducing arterial PaCO2 is by increasing the tidal volume and not the respiratory rate. The benefit of using larger tidal volumes during acute resuscitation far outweighs the potential long term risk of ventilator induced lung injury. End tidal CO2 closely reflects arterial PaCO2 and is the most practical method of monitoring and obviates the need for frequent arterial blood gas sampling.
14.2 Mixed and Central Venous Oxygen Saturation
Mixed venous saturation (SvO2) is measured in blood sampled from the pulmonary artery and therefore requires the insertion of a pulmonary artery catheter. Central venous saturation (ScvO2) is obtained from a central venous catheter and is an acceptable substitute. The normal oxygen extraction ratio (arterial saturation – venous saturation) is 25 % and ScvO2 is therefore around 75 %. Due to mixing of venous blood from the coronary sinus which drains directly into the right atrium, SvO2 is usually 5 % lower than ScvO2 although this difference may be reversed in septic shock. In the presence of shock and a low ScvO2 the assumption is that DO2 is inadequate with excessive oxygen extraction at the cellular level. The aim therefore is to achieve a ScvO2 of >70 %. Although theoretically sound there are caveats. A high ScvO2 may be present but the acidosis fails to improve and may even worsen. This suggests an unsalvageable situation where cellular hypoxia has resulted in mitochondrial dysfunction and the inability to extract and utilise delivered oxygen. There is no current evidence to substantiate the application of ScvO2 in trauma resuscitation.
14.3 Pressure and Flow
DO2 depends on adequate blood flow to the tissues but despite attempts to quantify cardiac output this has been elusive (vide infra). As a result we use pressure as a surrogate but this has certain pitfalls. The law of haemodynamics dictates that pressure is a product of flow and peripheral vascular resistance; there is no mention of volume.
14.4 Central Venous Pressure (CVP)
CVP has been used to reflect right heart preload, defined as the degree of ventricular stretch at end diastole. In the spontaneously breathing patient this may have some merit but in those undergoing mechanical ventilation this is erroneous. It is assumed that a high CVP indicates loss of vascular compliance and therefore an adequate intravascular volume. There are many other compliance issues which impact on CVP however, namely pulmonary pressure during mechanical ventilation, right heart volume, chest wall anatomy, and intra-abdominal pressure. As such, CVP is an unreliable indicator of right heart preload and intravascular volume and cannot be used as an indicator of fluid responsiveness.
14.5 Pulmonary Arterial Pressure
For many years the pulmonary artery catheter (PAC) was regarded as the gold standard for haemodynamic monitoring with the assumption that a pulmonary artery wedge pressure (PAWP) reflects left ventricular volume. Swan and Ganz however, stated categorically that this held true only in patients with no lung pathology. For some reason this statement was ignored and the PAC became routine practice. It is nonsensical to believe that if right atrial pressure measured by a central venous catheter placed directly adjacent to that chamber is inaccurate but that a catheter measuring a pressure across a diseased organ (the lung) another chamber (the left atrium) and a valve (the mitral valve) is correct. The pulmonary artery occlusion pressure does not reflect intravascular volume or fluid responsiveness and there is no role for the PAC in acute trauma resuscitation.
14.6 Peripheral Arterial Pressure
Although more accurate than CVP as an indicator of intravascular volume, a normal mean arterial pressure may not signify a successful endpoint of resuscitation. Peripheral vasoconstriction may maintain arterial pressure despite hypoperfusion. This is especially true in children who have the ability to maintain their blood pressure by profound vasoconstriction and their cardiac output by a significant tachycardia until sudden decompensation occurs.
A simple but reliable indicator of arterial volume is the use of systolic or pulse pressure variation using invasive arterial monitoring. During the inspiratory phase of mechanical ventilation venous return is reduced by increased intrathoracic pressure resulting in a reduction in right ventricular preload and therefore stroke volume. As the lungs expand, alveolar expansion compresses pulmonary capillaries and in patients with a reduced intravascular volume may occlude forward flow to the left side of the heart. The combined effects are to reduce systolic blood pressure during inspiration and a fall in systolic pressure of >15 mmHg during inspiration is a strong indicator of a suboptimal intravascular volume despite what would appear to be an adequate mean arterial pressure. If measuring systolic pressure variation certain criteria must be fulfilled, namely that the patient must be mechanically ventilated and take no spontaneous breaths. The patient must be pre-oxygenated and briefly hyperventilated to reduce the PaCO2 and therefore eliminate triggered spontaneous breaths. Thereafter the ventilator is placed on expiratory hold and the systolic pressure determined during apnoea. This manoeuvre eliminates the effect of inspiration while maintaining PEEP and in virtually all patients the variation in systolic pressure will disappear. Mechanical ventilation is then recommenced and the effect on systolic blood pressure ascertained. A fall in systolic blood pressure during inspiration indicates hypovolaemia whereas a rise suggests the need for inotropic support.
14.7 Cardiac Output Monitoring
With the decline of the PAC less invasive methods of cardiac output (CO) monitoring have evolved using a variety of techniques. Despite concerns about the accuracy of the PAC this is used as the comparator for these monitors. No method of non-invasive CO monitoring has less than a 20 % error rate or greater than 90 % concordance with the PAC and the percentage error rises with the use of vasopressors, the very patients in whom an accurate estimation of CO is desired. There are few data demonstrating a survival advantage using these monitors. CO monitoring simply generates a number and does not indicate whether this meets tissue oxygen demands. It should never be used in isolation but if CO is determined it must be combined with markers of peripheral perfusion.
14.8 Haemoglobin and Coagulation
More than two millennia ago the Hindu doctrines of Sushruta Samhita (circa 700BCE) dictated that the best treatment of any lost substance is replacement by an identical expander. For some inexplicable reason it has taken us two and a half thousand years to adopt his philosophy. Although stroke volume may be restored using either crystalloids or colloids these solutions do not carry oxygen and in the presence of severe haemorrhage their use should be limited. The only effective mechanism for oxygen transport is haemoglobin and a massive transfusion protocol which allows the rapid administration of blood must be in place in any health facility which treats major trauma. The end point of PRBC transfusion is a haemoglobin concentration of 10 g/dl. Based on rheology this is the optimal concentration for oxygen delivery. The initial haemoglobin concentration is artificially high and misleading and should be repeated frequently during resuscitation. On average, in the absence of major ongoing haemorrhage, one unit of PRBC will raise the haemoglobin by 1 g.
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