Cardiac
output is the product of heart rate (HR) and stroke volume (SV). The content of
oxygen in arterial blood is the sum of the oxygen carried by hemoglobin (1.34 x
Hgb x SaO2) and the amount of oxygen dissolved in plasma (0.003 x
PaO2), producing an equation that describes the variables of the
shock state:

Multiple
factors affect all elements of the shock equation. Two main factors affecting
HR, for example, are SA node firing rate (chronotropy) and speed of an impulse through
the conduction system (dromotropy). Three contributing factors to stroke volume
are preload (end diastolic volume), afterload (wall stress), and
contractility (inotropy). The content of oxygen is primarily determined by the
saturation of hemoglobin, which is dictated by the PaO2 and the Hb O2 dissociation curve (see below). The PaO2
is governed by the effectiveness of gas exchange in the lungs (PAO2
and the A-a gradient) and how much blood that bypasses the lungs (shunt). The
final component of oxygen delivery is how much oxygen is off-loaded at the
tissue level, which is predicted by the hemoglobin dissociation curve:
Deficiency
in specific nutrients or components of DO2 produce shock states with
specific names:
Glycopenic
shock: Insufficient glucose substrate
Anemic
shock: Insufficient hemoglobin
Hypoxic
shock: Insufficient oxygen saturation
Ischemic
shock: Insufficient blood flow
Types of Shock
Specific
shock states have specific physical exam findings. For example, in neurogenic
shock there is no increase in HR, making compensated shock very difficult to
diagnose. However, there may be obvious signs of trauma to the sympathetic
chain that regulates HR (T1-T5). In cardiogenic shock, there may be signs of
congestive heart failure, such as peripheral edema, jugular venous distention,
descended and firm liver edge, pulmonary crackles or presence of a sternotomy
scar.
There
are no readily available monitors to assess oxygen delivery or consumption. Many of the components of DO2 are
easily measured, such as HR, Hgb, SaO2 and PaO2, while
the pulmonary arterial catheter (Swan-Gantz catheter) is the only way to
measure stroke volume. Use of the Fick Equation (VO2 = CO x (CaO2
– CmvO2) remains the gold standard for measurement of oxygen
consumption

Note
that BP is not a component of the shock equation. Pulse contour analysis, PiCO,
LiDCO or echocardiographic measurements may estimate
stroke volume or cardiac output but must be calibrate against traditional
thermo- or dye-dilution measurements. Only with data gathered by a PA catheter
can all the parameters of the shock equation be definitively determined.
However, these devices require expertise to place and interpret, and age
specific normal values for many parameters are unknown. A partial list of the
indices is provided:

Lactate
and mixed-venous oxygen saturation are rapid tests that provide information
about the VO2/DO2 balance. Lactate is readily available
and established marker of shock, although it becomes elevated only after cells
enter anaerobic metabolism. The mixed venous oxygen saturation (SmvO2)
provides earlier recognition of DO2/VO2 imbalance. SmvO2
is most strictly measured in the heart one valve distal to the site of complete
mixing (usually in the pulmonary artery). However, SVC or right atrial
saturations may provide good enough approximations, and useful to trend. If the
arterial and mixed venous saturations are known, the oxygen extraction ratio
(OER) may be calculated:
The
oxygen extraction ratio provides a real-time assessment of the VO2/DO2
balance and will be abnormal before lactate is produced:
Treatment
The
treatment of shock has three objectives:
1.
Increase
DO2
2.
Decrease
VO2
3.
Treat
the underlying cause
Rapid
assessment with concurrent treatment are essential for the swift reversal of
shock. There are treatment considerations for all the elements of the shock
equation: