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International consensus

2006

Haemodynamic monitoring

 

 The important points are summarized as follows:

Definition

Shock is defined as a life threatening condition with generalized maldistribution of blood flow causing failure of delivering and/or utilization of adequate amount of oxygen resulting in tissue dysoxia.

Hypotension (Systolic blood pressure less than 90 mmHg, drop in systolic pressure of more than 40 mmHg from baseline or mean arterial pressure less than 65 mmHg) are commonly present in shock. However, it is not required to define shock.

Signs of inadequate tissue perfusion on physical examination are required to define shock.

Targets for blood pressure

Most conditions with shock

  • Mean arterial blood pressure of more than 65 mmHg

Trauma patient with penetrating injury

  • Aggressive fluid resuscitation should be avoided and hypotension should be tolerated.

  • Mean arterial pressure of 40 mmHg until bleeding is controlled surgically

Trauma patient with blunt injury

  • No specific guideline for blunt injury

Traumatic brain injury without systemic haemorrhage

  • Mean arterial pressure of 90 mmHg

Cardiogenic shock

  • Systolic blood pressure more than 100 mmHg if there is ST elevation

Measurement of blood pressure and physical examination in shock

Frequent measurement of blood pressure is recommended in shock. Invasive blood pressure measurement is recommended if shock is present despite fluid challenge.

Clinical examination includes findings of signs of hypoperfusion, urine output and mental state. Temperature gradient between the toe and the ambient temperature correlates with cardiac index, stroke index and oxygen transport in cardiogenic shock. The absence of clinical findings of pulmonary congestion is too insensitive to rule out the diagnosis of cardiogenic shock. In general, because of the low cost and low risk nature of clinical examination, it is essential in all patients suspected to have shock. However, because of the low sensitivity and specificity, the findings should not be interpreted in isolation

Preload and fluid responsiveness

Preload measurement alone (central venous pressure, pulmonary artery occlusion pressure, end-diastolic ventricular volumes) should not be used to predict fluid responsiveness

In a state of shock, in the presence of low values of static measures of preload (central venous pressure, pulmonary artery occlusion pressure or end-diastolic ventricular volumes) should be immediately resuscitated with fluid with careful monitoring.

Fluid challenge is recommended to assess fluid responsiveness. Fluid challenge can be given by rapid infusion of 250 ml crystalloid or colloid equivalent. It can also be given by straight leg raising maneuver (45 degree elevation of leg for 4 minutes with trunk maintained at supine position) with aim of a rise in CVP of at least 2 mmHg.

Although dynamic measures of fluid responsiveness are better predictors of fluid responsiveness than static parameters, they are not recommended routinely. They may be useful in selected group of patients (heavily sedated mechanically ventilated patients without spontaneous respiratory efforts, in sinus rhythm). These measures include pulse pressure variation, systolic pressure variation, collapse of vena cava and aortic flow changes. D down of more than 5 mmHg indicates that stroke volume index will increase to fluid challenge with positive and negative predictive values of more than 90%.

Measurement of cardiac output

Routine measurement of cardiac output in patients with shock is not recommended. In most patients, shock can be treated with simple monitoring (physical signs, blood pressure measurement and urine output.

Transthoracic echocardiography or measurement of cardiac output may be considered if there is clinical evidence of ventricular failure and persistent shock despite adequate fluid. Transthoracic echocardiography can provide non-invasive assessment of ventricular filling, contractility, valve function and pericardial disease.  There is no gold standard for measurement of cardiac output. Insufficient data exists to allow recommendation of one method over the other. These include pulmonary thermodilution, transpulmonary thermodilution, arterial pulse pressure waveform analysis and esophageal Doppler measurement.

Measurement of regional perfusion and microcirculatory defects

Despite the existence of microcirculatory defects in shock and presence of various techniques in measurement, it is not known whether correction of these defects can improve patient outcome. Serial measurement of blood lactate and base deficit are recommended. They are predictors of outcome. Increased blood lactate and failure of normalization of blood lactate level are associated with increased morbidity and mortality. Routine measurement of gastric tonometry, sublingual capnography, near-infrared spectroscopy and orthogonal polarization are not recommended.

Measurement of biomarkers

If there is clinical evidence of shock, in the absence of hypotension, markers of inadequate tissue perfusion shock be measured such as decreased ScvO2, SvO2, increased blood lactate and increased base deficit.

Measurement of other biomarkers like procalcitonin level, IL-6, TNF is not recommended for routine management of shock.

Use of pulmonary artery catheters

Routine use of pulmonary artery catheters in shock is not recommended. Based on meta-analysis, use of pulmonary artery catheter is not associated with increase in overall mortality and hospital stay. But there is no additional benefit.

Early goal directed therapy

Early goal directed therapy with monitoring of ScvO2, CVP and MAP and aggressive resuscitation have been shown to reduce mortality of patients presenting with septic shock. This approach is recommended to patients especially when ScvO2 < 70%.

Supranormal oxygen delivery

Resuscitation with aim of supranormal cardiac index and oxygen delivery in patients with shock is not recommended

Reference

Antonelli M. et al. Hemodynamic monitoring in shock and implications for management. International Consensus Conference, Paris, France 27-28 April 2006. Intensive Care Medicine 2007 online publication

 


©Charles Gomersall, October, 2009 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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