Table of Contents

This is a discussion of the metabolic requirements of normal neurological function, as well as the influences on these requirements in unusual physiological circumstances. It is interesting and educational, and furthermore elements of it appear in Oh's Manual, making it a likely target for future questions. Specific questions regading this material are more likely to appear in the primaries. The fellowship candidates are more likely to dip into this as a part of the "rationale" section in questions which ask them to critically evaluate some aspect of exotic neuromonitoring,.

This is a discussion of the normal mechanisms which maintain the driving blood pressure gradient across the cerebral circulation in the face of wildly fluctuating systemic conditions. Question 1 from the second paper of 2009 briefly touched upon the definition of cerebral perfusion, and then went on to ask more pragmatic details about the utility of using CPP as a therapeutic target. Strictly speaking, cerebral perfusion pressure is the difference between cerebral arterial and cerebral venous pressure- the driving gradient for cerebral blood flow. As we have few ways of measuring the pressure in the dural venous sinuses, we have to use the intracranial pressure as a surrogate. Thus, cerebral perfusion pressure is the ICP subtracted from the mean arterial pressure (MAP). Or the CVP, for that instance. It is not inconcievable that one's CVP might be higher than one's CSF pressure in the context of some sort of severe right heart problem.

It is possible to measure anatomical dead space and physiological dead space; alveolar dead space can then be determined by subtracting the first from the second. Physiological dead space can be measured using the Bohr-Enghoff method, using either alveolar CO₂ (Bohr version) or arterial CO₂ (Enghoff modification) to determine the ratio of exhaled CO₂ concentration to PACO₂ or PaCO₂. The anatomical dead space can be determined using the Fowler method, which involves using a single breath of 100% oxygen to displace all the nitrogen from the anatomical dead space.

Systemic vascular resistance is one of the major regulatory mechanisms which control blood pressure, and its main determinants are the length of the blood vessels, the viscosity of the blood and the radius of the vessels. Arterioles of around 200μm diameter tend to produce most of the resistance in the systemic circulation. Their radius is under control by systemic events (eg. the arterial baroreceptor reflex) as well as a host of locally acting mechanisms.

A well-matched V/Q ratio is 1.0, i.e. the lung unit receives as much ventilation as blood flow, and this should establish ideal conditions for good gas exchange. Wherever the V/Q ratio is low, there is an excess of blood flow as compared to ventilation, and therefore the effluent blood will be relatively hypoxic. Wherever there is an excess of ventilation, the global CO2 clearance will be poor in spite of vigorous airflow because the amount of blood delivered to these units is insufficient. These conditions are relatively absent in the healthy organism, but they can arise in disease states such as COPD, asthma, pulmonary oedema, and under the effects of positive pressure ventiltion.

Starling's principle can be stated simply by saying that transvascular fluid exchange depends on a balance between hydrostatic and oncotic pressure gradients in the capillary lumen and the interstitial fluid. This balance can be expressed as the Starling equation, which also incorporates the reflection and permeability coefficients of the capillary membrane.

The microcirculation is the terminal vascular network of vessels smaller than 100 μm in diameter, where the exchange of substances between the blood and the tissues occurs. It consists of arterioles, capillaries and venules. Its main characteristics are its vast surface area and the low velocity of flow, which allows enough transit time for gas exchange and solute diffusion.

This chapter has some borderline relevance to Section I1(i) of the 2017 CICM Primary Syllabus, which expects the exam candidate to "explain the ...movement of body fluids". Any mention of fluid movement must sound dangerously circulatory in character, and it is true that the bulk of these discussions takes place wherever the circulatory system is discussed. Still, the college wants what it wants, and so this chapter is left here as a brief summary of the forces that govern transvascular fluid movement. Let's call them Starling forces.

Normal PaCO₂-EtCO₂ difference is 2-5 mmHg. This is due to alveolar dead space, which is small in healthy adults. It may increase in disease states (eg. where alveolar dead space is increased, or where V/Q matching is affected) or as thew result of a measurement error.

Central and mixed venous blood gases offer us a glimpse of whole-body oxygen extraction.  
A mixed venous blood gas is a sample aspirated from the most distal port of the PA catheter, offering a mixture of inferior vena cava blood, superior vena cava blood, and the coronary sinuses. Thus, the result is an average of venous blood. But what if I don't have a PA catheter, you might ask? A central venous gas may be almost as good.

This issue has never come up in the CICM exam, perhaps because it is the least serious form of traumatic brain injury. However, it comes up in discussion. Specifically, it is important to be able to use this word correctly, knowing precisely what it means, and being able to descend smoothly into academic gibberish (commotio cerebri, etc.) if asked to elaborate. The majority of the information gathered below comes from the massively authoritative Consensus statement on Concussion in Sport (The 4th International Conference on Concussion in Sport held in Zurich, November 2012). Exploration of this document requires some genuine interest in mild head injury. If one were much less interested, one would be well served by the concise treatment offered to this topic by the LITFL Clinical Case on Minor Head Injury.

Mixed venous blood is blood sampled from the pulmonary artery which is mixed in the RV and which represents a weighted average of venous blood from all tissues and organs. It is usually said to have a haemoglobin saturation of around 70-75%, which corresponds to a PO₂ of around 40 mmHg.

Lets face it, we don't really care about venous oxygenation (or arterial, for that matter). The real issue is how much oxygen is in the cells? How are those cells using it? The intracellular environment is a place of massively heterogenous oxygen demands. Some organelles are involved in enzymatic metabolism of drugs or maintenance of electrolyte gradients - these areas require a higher oxygen tension than, for example, mitochondrial ATP synthesis.

The most important determinants of total blood oxygen content are the effective haemoglobin concentration and oxygen saturation. Solubility plays little role -only about 1-2% of the total oxygen content is dissolved (though this increases with extreme hypothermia). The remaining 98% are bound to haemoglobin.