Given that the new batch of house officers have just started, it seemed like a good time to update this blog. Today’s post is the first in a two part series about the ABCs. When called to the bedside of an unwell patient, the advice given is to “attend to the ABCs” first. Without further explanation of what the ABCs actually entail, this is only minimally helpful. Today we shall focus on the first two letters.
The best way to start is to make explicit that the lung really only has two functions. The first is to maintain an appropriate blood level of oxygen. Appropriate can be considered to be an oxygen saturation somewhere in the 90s. Now, an oxygen saturation of 92% may not be normal, but it is generally sufficient for the purposes of oxygen delivery to organs. The second is to get rid of CO2. More specifically, to maintain a CO2 of 40mmHg (around 5kpa).
These two processes proceed very differently. To get oxygen into blood one needs an open alveolus and a capillary that supplies it. The blood flow through that capillary must be appropriately matched to the amount of oxygen in the alveolus- if the blood flow is too much for the amount of oxygen in the alveolus, the blood in that capillary will be desaturated. This explains why you can have patients who are much more hypoxic than you might expect from looking at their chest xray. Collapse of alveoli occurs on a microscopic level and is not necessarily visible on chest Xray. Many patients are on vasodilatory medications (antianginal or antihypertensives) that impair their ability to match capillary blood flow with the amount of oxygen in the alveolus. It can also be easy to miss collapse of an entire lobe on xray unless you know what you are looking for. The relevance of this is that it is easy to go on a wild goose chase of other causes of hypoxia if you believe that the Xray must correlate with the patient’s clinical condition. Consider the following case.
Medical school and medical training teaches us that we do tests to confirm the presence or absence of disease. This is the wrong way to think about things. A better concept is to realise that we start with a certain pre-test probability of a disease, which is determined by the base rates of that disease in the population and the patient’s clinical history. Tests can only ever modify this pre-test probability into becoming more or less likely. At a certain point the disease may become so unlikely that testing for it causes more harm than good. This greater harm may come from radiation, reactions to things such as contrast dyes, harmful therapy that might be initiated as a result of a false positive result e.g. antibiotics for a blood culture result that is a contaminant, or simply the fact that time is wasted not pursuing the most likely diagnosis. Other times the disease remains so likely that you may have to pursue repeat testing (take for example the high false-negative rate of COVID swabs).
Consider this scenario. You are the on call house officer. You get paged to the ward to review a 35 year old patient who is having abdominal pain. He was admitted 6 hours ago with severe central chest pain that came on over a matter of seconds and lasted 2 hours. His troponins and ECG have been normal. He has now developed abdominal pain of the same severity and also reaching its peak over a matter of seconds. Concerned about the possibility of aortic dissection you look for mediastinal widening on the chest Xray, pulse defecits, or any neurological symptoms as you know these are the things to look for in a dissection. None of these things are present. Satisfied, you order further ECGs and troponins. The next day you find out he died overnight of an aortic dissection. The next day your consultant tells you “it just shows you how useless clinical exam findings are for aortic dissection- you can’t rely on them. Most dissections have a normal Xray!”
Is this correct? Are these clinical exam findings useless? Is the chest Xray normal in most dissections, as commonly quoted? Well, not quite. They are actually reasonably good tests, including the chest Xray (1,2). The problem is not taking into account the pre-test probability of an aortic dissection, which in this case is high based on the clinical history. Continue reading →
It is hard to avoid anything covid related in medicine at the moment. This pesky virus does raise an important point about pathophysiology however. There has been a collective surprise at the degree of hypoxia these patients can have despite a chest X-ray that doesn’t look that bad and at how comfortable these patients can appear despite their severe hypoxia.
Except there is nothing particularly new about this and it has long been a pitfall for the intern seeing hypoxic patients on the ward. Often one comes across a patient with post operative atelectasis (or viral pneumonia!) who has some opacities on chest X-ray (such as the one pictured above) but a degree of hypoxia seemingly unexplained by the chest X-ray. These patients are often sent for unnecessary CTPAs looking for PE.
Firstly, the sensitivity of chest X-ray for pneumonia and atelectasis is not as great as we think it is. Changes to the lung parenchyma are often more extensive than what is visualized on X-ray. Secondly the hypoxia is occurring on a microscopic level. Hypoxia occurs when there is mismatch between ventilation and perfusion i.e. blood flow to an alveolus is in excess of the lowered oxygen tension in that diseased alveolus. The larger volume of hypoxic blood that mixes with ‘good blood’, the worse it is. This is called shunting. Hypoxic pulmonary vasoconstriction is the reflex that protects against this mismatch but this reflex becomes less efficient with age, the presence of vasodilator drugs (pretty much antihypertensive or antianginal drug you care to mention), and a whole host of other physiological factors some of which may be specific to the disease itself.
Unwell septic patients with their high cardiac outputs will have a large volume of blood rushing through their pulmonary circulation which further decreases ventilation perfusion matching. The end result is that the degree of hypoxia is related much more to things occurring at microscopic level that we can’t see on an X-ray (on top of the fact that X-ray doesn’t tell us the true extent of parenchymal changes anyway). It is not uncommon to have post operative patients with a chest X-ray that looks like the one above but that are on 50-60% inspired oxygen.
These patients are tachypneic (because hypoxia contributes to the ventilatory drive) but they may not appear overly distressed because the work of breathing is more mediated by lung mechanics and the stiffness of the lung rather than the degree of hypoxia. If you’ve ever seen congenital cardiac babies with right to left cardiac shunts and resting saturations of 75% you’ll know what I mean. They can look blue but pretty happy.
So if you have a good reason for shunting (a high pre-test probability) such as being immediately postoperative or having a diagnosis of a viral pneumonia, that probability remains high despite what the chest X-ray might show you, and there is not necessarily a reason to go chasing a PE or invoking the presence of an unknown hemoglobinopathy (as many people are speculating with Covid). Of course, this doesn’t mean that looking for a PE is never indicated and clinical judgement in the individual situation is paramount. But you have to evaluate the patient in front of you, and not a computer screen, and if you understand the pathophysiology you’ll have a much better chance of doing this.
Asthma is quite an interesting condition to treat acutely, not only because it is gratifying when patients get better rapidly (which most of them do) but also because they are a group that can deteriorate quickly and hide their signs of deterioration well given their young age and relative health.
Given the nature of the disease it is not uncommon for patients to feel much better after being treated down in ED, then get worse again on the ward, perhaps as the frequency of their B agonist therapy is reduced. It is therefore imperative to avoid the common pitfalls when called to see these patients on the ward. The information below is directed at adult patients, but a lot of it will also apply to paediatrics too.
Asthmatics can die quickly
If you look at near fatal asthma cases two distinct phenotypes emerge as seen in the table above- the group that worsens over several days and whose pathology involves mainly mucus plugging, and the group who mainly develops bronchoconstriction with very rapid deterioration but faster responses to therapy. The latter are more commonly known as brittle asthmatics.
It is this group that are particularly relevant to ward calls as respiratory failure can develop in as little as 2 hours, and death is often sudden and unexpected (1). Such patients often show marked diurnal variation in peak flow, especially a large dip in the early morning, even when their previous peak flow was normal (1). Looking back at a patient’s previous discharge summaries and clinic letters should help you identify who might fit into the “sudden onset” phenotype.
In hospital death is not related to admission findings but is related to the phenotypes above