Shock taskforce – define, diagnose, monitor, treat it right.

My notes on this modern primer on shock by 11 well-known shock experts (shoxperts?). Interesting mix of evidence-base and expert opinion/enthusiasm. Definitely some echophiles amongst them.


Life-threatening, generalized, acute circulatory failure associated with inadequate oxygen utilization by cells (dysoxia leading to hyperlactataemia).


  • Insufficient circulating volume,
  • Pump failure (muscle problem or rhythm problem),
  • Obstruction (PE, pleural/pericardial effusion),
  • Distributive shock (vasodilatation – sepsis, anaphylaxis, spinal injury),

or a combination of the above.




Clinical, haemodynamic and biochemical.

3 Clinical ‘windows’
  1. Peripheral – cold, clammy, discoloured skin
  2. Renal – <0.5ml/Kg/hr
  3. Neurological – obtundation, delirium

Hence – Serial assessment HR, BP, temperature, skin features, urine output and mental state

Hypotension and shock

Hypotension (SBP<90, MAP<65, drop of 40)

  • NOT a prerequisite for diagnosing shock.


  • >1.5 mmol/l is associated with increased mortality, >2 usually. More predictive than almost any other marker (particularly inflammatory markers). But prognostic value does depend on the type of shock.
  • Elevation not simply due to abnormal oxidative phosphorylation.
  • Potentially protective and therefore a marker of severity rather than a ‘toxin’ needing to be removed.
  • Early reduction with therapy is a good sign.
  • Seems useful in guiding therapy, ie targeting lactate clearance (20%/2hr for first 8hr) – Jones and Jansen say so.


  • Low values (potentially inadequate O2 delivery) and high values (inadequate O2 use) are prognostically bad. But normal value can be misleading.
  • Elevated venoarterial CO2 difference ((ScvCO2-PaCO2) >6mmHg or 0.8KPa) may be a better marker of insufficient blood flow.


Serial lactate measurement is crucial.

If CVC in place then measure ScvO2 and venoarterial difference.



How/when to monitor cardiac function

Use cardiac monitors to 1) Identify shock 2) Select therapy 3) Evaluate response

Often a mixture of types of shock. Early echo quickly helps in decisions re fluid ‘v’ inotrope ‘v’ pressor ‘v’ definitive intervention.


Blood pressure target

Use an arterial line and CVC if not improving with initial treatment.

Individualize the target.

  • MAP >65 is default, but:
  • ‘higher’ if known hypertensive or if more seems to help.
  • ‘lower’ in uncontrolled bleeding

No new comment about targets in brain injury – ?stays at 90 mmHg.

Improving perfusion
  • Fluid early, as described below.
  • Inotropic agent (no specific recommendation) if BOTH inadequate cardiac output AND impaired cardiac function.
  • Do not use inotropes for impaired cardiac function with sufficient cardiac output.
  • Do not supranormalize oxygen delivery.
Evaluating response
  • Fluid responsiveness markers
  • End tidal CO2 changes (in ‘steady state’ ventilation)
  • Resolution of preload dependancy markers (where they were marked)
  • Arterial pressure, change in pulse pressure (not PPV), CVP, PAOP are all flawed.
  • Cellular dysoxia markers – theoretically nice but take longer to change.


Measure cardiac output if clinically not responding well to initial therapy.

Sequential assessment is key.



Preload and Fluid Responsiveness

Knowledge of preload is not knowledge of preload responsiveness.

Dynamic variables for fluid management are best:

  • Stroke volume variation
  • Pulse pressure variation
  • IVC variation
  • Passive leg raising

All have confounders (tidal volume, abdominal pressure, dysrhythmia, cardiac and pulmonaru state, open chests etc.) and SVV,

PPV and IVC variation are only valid in the absence of spontaneous breathing.


Echo may be best way to determine type of shock. If you don’t use it you may miss-manage 25% of septic patients.

Assess volume ideally using dynamic markers.

Static preload markers should not be used alone (CVP, PAOP, change in pulse pressure (not PPV)). However, immediate fluid is recommended if very low value of static markers.

Do not target LV filling pressure.

When deciding to give fluid use a measured fluid challenge and assess response, don’t just pile it in.

FLUID RESPONSIVENESS DOES NOT MEAN THEY NEED FLUID. Assess lung water where possible (TPTD or ultrasound).


Methods of monitoring


Echo can characterize the circulatory disturbance, aid therapy selection and assess response.

In addition to obvious structural abnormalities it is used to assess:

  • Direct stroke volume measurement using Doppler (velocity-time integral across an outflow tract)
  • Ejection fraction reflects the balance of contractility and afterload, so needs to be interpreted in the context of type of shock, and inotrope/pressor use.
  • Filling pressures can be estimated using pulsed Doppler and tissue Doppler. Combining these allows a ‘load-independant’ assessment (the E wave of LV inflow adjusted by the E’ wave of the MV annulus longitudinal movement). E/E’ >15 suggests high LV filling pressure, <8 suggests low. In practice it’s rarely outside this range.
  • RV size can be assessed with 2D echo, (ideally) using end-diastolic area values. RV:LV >0.6 suggests moderate RV dilatation, in turn suggesting acute cor pulmonale when accompanied byabnormal septal motion.
PA catheter
Provides a lot of numbers (RAP, PA pressure, PAOP, ScvO2, PvO2, O2 extraction etc.)
Accurate cardiac output monitor.
Use beyond specific indications is contentious (lack of benefit, possible harm, expense).
Transpulmonary thermo/lithium dilution
Less invasive. Also lots of numbers (global end-diastolic volume, extra-vascular lung water, cardiac function index).
Intermittent calibration with continuous waveform analysis in between.
Uncalibrated pulse contour analysis
Either via an arterial line or finger pleth. Complicated maths to estimate artery characteristics. Precision, accuracy and reliability is being questioned.
Oesophageal Doppler
Velocity time waveform of the descending aorta. Normogram for arterial cross-sectional area. Derived variables. Reliability issues largely relate to positioning.
Phase shift of high frequency current put across the thorax. Yet to prove itself.
Tissue microcirculation monitoring
Tissue CO2
Near-infrared spectroscopy occlusion test
Muscle O2 saturation changes with occlusion (DeOx and ReOx).
Microvideoscopic techniques, looking at capillary density, perfusion and flow heterogenity in eg tongue epithelium.
All currently research tools only.



Sequential echo is useful if not vital.

Do not use PAC routinely.

PAC or TPTD in severe shock.

Other uncalibrated and minimally invasive devices are yet to be validated.