Shock

Contributing Author: Richard Pierce, MD (Yale University)

Definitions

The shock state occurs when nutrient delivery is not sufficient to meet cellular demands. Although the delivery of all nutrients (and removal of waste products) are important, failure of cell energy levels occurs most rapidly when oxygen delivery (DO2) does not meet cellular demands (VO2).  Cells are then unable in engage in the aerobic metabolism of glucose, which produces approximately 32 molecules of ATP, relying instead on the two ATPs produced through anaerobic metabolism.


Pediatric Critical Care Medicine, 2006

The shock state exists when VO2 is greater than DO2, which is graphically represented by:




The “critical DO2” is the point at which individual cells will begin to produce lactate.  DO2 is a product of cardiac output (CO) and the content of oxygen in arterial blood (CaO2).  During a state of shock:

 

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


Also see: Septic Shock

Stages 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.

Monitoring

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:

 



 The most common intervention for the shock state is intravascular volume expansion with isotonic fluid. This intervention affects one component of stroke volume:

Intravascular volume expansion increases stroke volume by increasing tension on the myocardial fibers, as described by the Frank-Starling Curve:


A patient in hypovolemic shock with decreased filling pressures is indicated by the dark blue lines. Volume resuscitation (described in the septic shock section) increase filling pressures and stroke volume as indicated by the green lines:


Volume resuscitation should continue as long as increases in filling pressure result in meaningful increases in stroke volume. This is clinically manifest as a beneficial decease in heart rate and capillary refill time and increase in blood pressure.  At some point, increases in the filling pressures result in negligible increases in the stroke volume, such as the difference between red and black filling pressures:


This clinically manifests as no response in HR, BP or CPT in response to boluses along with decreased liver edge and pulmonary crackles. Among other complications, this may impair gas exchange at both levels.

 

Once volume resuscitation is no longer effective, the treatment of shock shifts to augmenting contractility and HR with catecholamine infusions:


Although these medications are used to increase cardiac output (flow) we titrate doses to the blood pressure. Blood pressure is related to cardiac output and systemic vascular resistance via Ohm’s law:


 

Selection of the specific agent is tailored to the specific clinical situation. Generally, different agents activate different receptors that produce varying clinical effects:

 

Positive pressure ventilation (PPV) is beneficial in the shock state for two reasons. First, PPV may relieve work of breathing, which may constitute 30% of VO2 in infants. Second, PPV reduces cardiac afterload (tension on the individual cardiac myocytes, T) via reduction in the ventricular transmural pressure (PTM) as described by the Law of Laplace (r is ventricular radius and Th is thickness of the ventricular wall):



Other etiologies of shock must be recognized and addressed. Suspicion of septic shock warrants immediate treatment with broad spectrum antibiotics. Shock in a neonate should raise concern for a ductal dependent cardiac lesion and treated with prostaglandin infusion until structural heart disease can be ruled out.

Dr. Kevin Kuo's Presentation on Shock

Subpages (2): Anaphylaxis Septic Shock
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