A free online resource for Intensive Care Medicine.
An unofficial Fellowship Exam (CICM Part 2) preparation resource.
Deranged Physiologyis a slowly growing archive of discussions and study notes relevant (or if not relevant, then at least interesting) to the practice of intensive care medicine. The content provides an introduction to the fundamental themes in intensive care: mechanical ventilation, vasopressors, electrolyte management, hemodynamic monitoring, dialysis, and so forth. Attention is directed at equipment in intensive care, and there are attempts to revisit interesting pharmacology and physiology. The aim of this resource is to supplement the bedside teaching of senior staff, and to consolidate resources for intensive care trainees in the initial stages of their training.
Leland C. Clark never called his device "the Clark Oxygen Electrode", as such a gesture would probably have been viewed by his contemporaries as mildly disgusting. The paper he published discusses the "continuous recording of blood oxygen tensions by polarography"- it was a "polarographic" electrode, and this is also how it is referred to in some of the earlier literature. The polarogram is the graphed relationship of current and voltage which is discussed at length elsewhere.
The oxygen cathode is essentially an electrolytic cell. The potential difference across the oxygen-containing electolyte allows a reduction of the dissolved oxygen; the oxygen borrows electrons from the cathode and hydrogen ions from the water molecules of the aqueous solution. A satisfactory amount of detail about these methods is available in William L. Nastuk's 1962 textbook, "Electrophysiological Methods:Physical Techniques in Biological Research".
This equation describes the concentration of gases in the alveolus, and thus allows us to make educated guesses as to the effectiveness of gas exchange. One can use this to calculate the tension-based indices of oxygenation, such as A-a gradient or the a/A ratio (which is expressed as a percentage). The ABG machine frequently does this work for you, provided you have entered the FiO2 and have specified that your sample is "arterial". The result is usually reported aspO2(a/A).
The point of these is to estimate the magnitude of the oxygen transfer deficit, and thus assess how well the lung is functioning as an oxygenator of pulmonary blood. Essentially, one is attempting to make an estimate of intrapulmonary shunt. However, these indices perform poorly in this role. In general it is fair to say that indices based on oxygen tension are popular because of simplicity, not validity. The best index of pulmonary oxygen transfer is still the measured intrapulmonary shunt.
With worsening shunt, the oxygenation of arterial blood will decrease. PaO2 of arterial blood decreases roughly in proportion to increasing shunt, and the greater the shunt, the less effect increasing FiO2 has on improving oxygenation. with a shunt fraction of 50% or more, increasing the FiO2 will have minimal effect on the PaO2. Shunt has little effect on PaCO2 clearance; the main reason is the increase in alveolar ventilation associated with hypercapnia. In patients who are unable to increase their alveolar ventilation, PaCO2 may increase slightly (eg. by up to 15-30% with a shunt fraction of 50%).
The shunt equation, otherwise known as the Berggren equation, is used to calculate the shunt fraction. This yields Qs/Qt, the ratio of the shunt and the total cardiac output. The estimated shunt fraction (Fshunte) can be calculated if an assumed value is substituted for CvO2) in the Berggren equation "True" shunt can be identified if the subject is made to breathe 100% FiO2, which decreases the contribution from V/Q scatter (with 100% FiO2, the measured shunt fraction is the "true" intrapulmonary shunt).
Shunt is the volume of blood which enters the systemic arterial circulation without participating in gas exchange. Venous admixture is that amount of mixed venous blood which would have to be added to ideal pulmonary end-capillary blood to explain the observed difference between pulmonary end-capillary PO2 and arterial PO2. Shunt fraction is the calculated ratio of venous admixture to total cardiac output. The shunt equation, otherwise known as the Berggren equation, is used to calculate the shunt fraction. Sources of venous admixture include "true" intrapulmonary shunt, V/Q scatter, contributions from Thebesian veins and bronchial veins, and intracardiac right-to-left shunts. The normal shunt fraction in healthy adults is 4-10%.
Increasing dead space has the same effect as decreasing the tidal volume. Clearance of CO2 decreases, and therefore minute volume requirements and work of breathing are increased. Additionally, because CO2 elimination is impaired, alveolar CO2 may increase, which may decrease alveolar pO2 and produce hypoxia due to hypoventilation. The effects of increasing alveolar dead space and apparatus dead space are functionally almost the same.
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.
Dead space is the fraction of tidal volume which does not participate in gas exchange. It is composed of apparatus dead space and physiological dead space. Physiological dead space is usually measured by the Enghoff modification of Bohr's method, and consists of anatomical and alveolar dead space. Anatomical dead space is the volume of gas in the conducting airways, and alveolar dead space is the volume of gas which ventilates poorly perfused alveoli. The contribution of shunt can increase the arterial CO2 and give the appearance of increased dead space.
The FRC is the volume of gas present in the lung at end-expiration during tidal breathing. It is composed of ERV and RV. This is usually 30-35 ml/kg, or 2100-2400ml in a normal-sized person. It represents the point where elastic recoil force of the lung is in equilibrium with the elastic recoil of the chest wall, i.e. where the alveolar pressure equilibrates with atmospheric pressure. The measurement of FRC is an important starting point for the measurement of other lung volumes, and its decrease has consequences for gas exchange and lung mechanics
Acute status asthmaticus is a fragile thing which, most ICU specialists would agree, is a good reason to get out of bed and drive to the hospital. These people tend to die rather readily, typically of cardiac arrest due to dynamic hyperinflation and the resulting loss of preload. This is made worse by the fact that the excellent outpatient management of asthma has filtered out the mild and moderate patient groups, and left only the incredibly brittle severe asthmatics. Only these are the people who ever get admitted to ICU for mechanical ventilation. Thankfully, even the ICU management of these people is improving, and in spite of an overall worsening severity of their illness, their ICU mortality has been steadily improving.
For measurement of V/Q distribution, there are functional techniques and imaging techniques. Functional techniques include MIGET and the three-compartment model. Imaging techniques include radionuclide imaging (SPECT V/Q scans and PET scans), as well as MRI using IV gadolinium and 3He or 129Xe.