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For a country not traditionally prone to gunshot homicide or bombing, it is not unreasonable to expect critical care trainees to only have vicarious experience of such trauma patterns. It is therefore surprising to find questions about this topic in the CICM Part II exams. In short, most of the mortality is due to primary blast injury (supersonic pressure wave travelling through hollow organs), and most of the morbidity is due to secondary blast injury (mainly shrapnel) and tertiary blast injury (getting thrown into structures, or having them collapse atop of you).Everything else (eg. burns) falls under the category of quaternary injury.

Respiratory compliance is defined as the change in lung volume per unit change in transmural pressure gradient. It is usually about 100ml/cm H₂O. Static compliance is defined as the change in lung volume per unit change in pressure in the absence of flow. Dynamic compliance is defined as the change in lung volume per unit change in pressure in the presence of flow. Specific compliance is lung compliance which is normalised to a lung volume or capacity, which permits comparison between lungs of different size.

Somehow, the college has focused their echocardiographic interest on aortic stenosis. Of the five past paper questions which concern TTE data interpretation, two are about AS. Question 17.1 and Question 17.2 from the second paper of 2014 are perhaps more relevant, as the discussion revolves around the identification of peri-arrest findings on TTE images.

Respiratory compliance is defined as the change in lung volume per unit change in transmural pressure gradient. It is usually about 100ml/cm H₂O. Static compliance is defined as the change in lung volume per unit change in pressure in the absence of flow. Dynamic compliance is defined as the change in lung volume per unit change in pressure in the presence of flow. Specific compliance is lung compliance which is normalised to a lung volume or capacity, which permits comparison between lungs of different size.

The mechanical ventilator continuously monitors pressure, flow, gas temperature and concentration. Volume is calculated from flow measurements. Multiple sensor technologies may be in simultaneous use. Limitations of these monitors reflect the need to mass-produce sensors, and are mainly related to accuracy and drift in calibration. Generally, one should expect a +/-5% margin of error.

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.

The normal mechanics of breathing can be described in terms of diaphragm, chest wall, pleural pressures and airflow. During inspiration, as the thoracic volume expands under the influence of respiratory muscle activity, the pleural pressure becomes more negative and generates a pressure gradient between the airway and the alveoli, which promotes inspiratory airflow. At the end of inspiration alveolar pressure equalises with atmospheric pressure, and there is no flow. During expiration, with relaxation of respiratory muscle, the thoracic volume decreases and the alveolar pressure exceeds atmospheric pressure, promoting expiratory air flow.

Drugs interact with receptors in a reversible manner to produce a change in the state of the receptor, which is then translated into a physiological effect. This molecular interaction with the receptor can be modeled mathematically and obeys the Law of Mass Action. Occupancy theory rests on the concept that the proportion of occupied receptors is related to the effect of the drug (eg. for full agonists and a linear relationship, 100% occupancy = 100% effect). This has been extended into several conceptual frameworks (eg. the Operational Model, the Two State Model, the Ternary Model etc).

The cough reflex arc is mediated by mechanoreceptors and chemoreceptors in the airway and lung tissue. These are stimulated by inflammation, foreign material, and chemical stimuli. The sensors involved communicated with the nucleus tractus solitarius via vagal afferents. The mechanism of cough involves forced exhalation against a closed glottis which terminates by abrupt glottic opening and the rapid turbulent flow of gas, with the turbulence acting as the main mechanism of loosening and removing the secretions.

In summary, increasing PaCO₂ causes an increase in minute ventilation. The relationship between PaCO₂ is fairly linear in the range of 45-80 mmHg; the rate of minute volume increases by 2-5L/min per every 1mm Hg of CO₂ increase. The CO₂/ventilation response curve is shifted to the left by metabolic acidosis and hypoxia. Sleep, sedation, anaesthesia and opiates shift the curve to the right. 

Control of ventilation is a function of the medulla, with descending voluntary control from the cerebral cortex via the pons. The medullary respiratory centres integrate input from the sensory organs such as the carotid glomus and aortic chemoreceptors, as well as central chemoreceptor regions. These inputs modulate the rhythmic activity of the central respiratory pacemaker regions. Efferent fibres travel via the vagus nerve, phrenic nerve, glossopharyngeal nerve and the upper motor neuron fibres of the spinal cord to innervate the muscles of respiration.

Respiratory rate and minute volume are affected by a multitude of factors. Most notably, PaCO₂ influences the minute volume (i.e. hypercapnia increases the respriatory rate). Hypoxia increases the respiratory rate, but hyperoxia does not suppress it. Acidaemia increases the respiratory rate by acting on the central chemoreceptors. Exercise, hypotension, pregnancy and hypoglycaemia also increase respiratory rate, by a variety of mechanisms. Interestingly, acute hypertension can slow respiration to a point where total apnoea may result.

Decreasing PaO₂ causes an increase in minute ventilation. As for PaCO₂, this is mediated by peripehral chemoreceptors over the timescale of seconds. Unlike PaCO₂, arterial oxygenation does not affect central chemoreceptors. The receptors sense oxygen tension rather than content, and the responses to arterial hypoxemia are not triggered by anaemia.  The inflexion point for this relationship is approximately a PaO₂ of 50-60 mmHg; beyond this threshold value the minute volume increases steeply. Ventilatory response to hypoxia is decreased by hypocapnia, carotid endarterectomy, CNS depression  (sleep, anaesthesia, opiates) starvation and old age.

The appearance of the endothelial glycocalyx in Question 18 from the second paper of 2014 demonstrates that this topic has high penetrance and popularity among the college examiners. For a more thorough overview, the pathologically curious reader is directed to Weinbaum et al (2007)- The Structure and Function of the Endothelial Glycocalyx Layer. Additionally, there is an entire website devoted to the activities of a glycocalyx research team, which features professional-looking diagrams and a list of recent publications. For the rest of us, a brief summary will suffice. Owing to certain cognitive defects on the part of the author, the summary offered below can hardly be described as brief. Fortunately, a brilliant LITFL CCC alternative waits to rescue the time-poor exam candidate.