The kPa Rules – Part 1: Oxygen

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In the early 1970s much of the world adopted the System International (SI) approach to scientific measurement. Unfortunately, the remainder of the world ignored it. This means that, today, we have different units presented in the scientific literature depending on the location of the source of the publication.

The USA is the most notable non SI country and this presents a problem in that the majority of English language textbooks and journals in medicine as well as a lot of the international guidelines and clinical pathways are derived in the US. In critical care this is important – as blood gasses are reported in mmHg in the USA (and most of the literature) and in kPa elsewhere – notably in Europe.

In many of my tutorials I have reported clinical “rules” such as the PaO2/FiO2 ratio, the Alveolar Gas Equation and the majority of the calculations in acid base – in mmHg. This series of two tutorials serve to right the balance. However there is a twist.

In this first tutorial I am not just rehashing the approach to oxygenation by swapping out mmHg for kPa. In fact, the use of kPa to measure and monitor oxygenation provides us with a significant helping hand. Effectively, as atmospheric gas is effectively 100kPa and Oxygen exerts 21% of that – Dalton’s law – then it is clear that the partial pressure of inspired oxygen (PiO2) is 21kPa. Oxygen is poorly soluble in blood and water – the solubility co-efficient is 0.225 – meaning that the quantity of oxygen dissolved in blood is the PaO2 x 0.225 kPa. Oxygen follows Henry’s law – meaning that solubility is related to temperature (37 degrees C) and pressure – the PiO2. In the best case scenario the PaO2 – the partial pressure of oxygen in arterial blood is 13kPa. That means that the gradient between PiO2 and PaO2 is, at a minimal, 8kPa. The greater the stretch between the two the larger the lung injury or ventilation perfusion mismatch.

The oxygen content of blood is 1.34 x Hb x SaO2/100 + (PaO2 x 0.225). I explore the impact of different FiO2s and ambient pressure on the blood oxygen content. Although dissolved oxygen is very low breathing air – the use of supplemental oxygen may dramatically increase it – particularly in hyperbaric conditions.

Finally I address the issue of PaO2/FiO2 as a way of quantifying oxygenation. The PF ratio, as we call it, is a significant component of the ARDS definition. A PF ratio of 200 in mmHg is equivalent to 25 in kPa and a ratio of 100 in mmHg is equivalent to 12.5 in kPa. An easier way to look at this, though, is to divide the PiO2 by the PaO2 – the numbers look similar but you now have a proportion in kPa. That PF ratio of 25 in kPa resolves to 0.25 meaning that only 25% of inspired oxygen is reaching the pulmonary veins (PaO2). Likewise a PF ratio of 12.5 in kPa (100 in mmHg) resolves to 0.125 – which means that only 1/8th of the inspired oxygen is delivered to arterial blood. I think that this is a really good way of assessing oxygenation – and a way of clarifying hypoxemia in your brain.

Ketoacidosis

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This tutorial looks at the problem of ketoacidosis and, in particular, focuses on diabetic ketoacidosis. Ketones are produced from free fatty acids in the liver, converted to acetyl coenzyme A and oxidatively metabolized for energy production or packaged in the form of acetoacetate or beta hydroxybutyrate and exported to the tissues. This occurs continuously in the body. Control over metabolism is provided by insulin. When insulin levels are high glucose is utilized primarily for energy production and fatty acid metabolism is curtailed. When insulin levels are low fatty acids become the primary source of energy. In situations of very low carbohydrate intake ketones may be measurable in the blood and we call this ketosis. When plasma ketones exceed 3 millimoles per liter this results in a strong ion effect and ketoacidosis. This is generally only seen in states of metabolic failure such as type 1 diabetes starvation and alcoholism.

The ketones acetoacetate and beta hydroxybutyrate are strong anions and cause metabolic acidosis when they accumulate. This manifests as a fall in the bicarbonate and an increase in the base deficit. Classically there is a widened anion gap metabolic acidosis with full respiratory compensation. Nevertheless the extent of the acidosis is rarely explained by ketones alone. Lactic acidosis is frequently present as is acidosis caused by the accumulation of metabolic junk products. Iatrogenic metabolic acidosis may ensue caused by the administration of hyperchloremic (0.9% NaCl + KCl) saline solutions.

Diabetic ketoacidosis is characterized by loss of control of blood glucose, loss of control of blood lipids and hypercatabolism of proteins. Failure to suppress gluconeogenesis within the liver depletes the tricarboxylic acid cycle reserves and results in uncontrolled ketone production. Patients become hyperglycemic glycosuric, keto acidotic, initially hyponatremic, later hypernatremic, and hyperkalemic. The treatment is to fluid resuscitate the patient, administer insulin by intravenous infusion, replenish glycogen stores and provide glucose for intracellular substrate and prevent further ketone production. Extra care must be taken to avoid hypoglycemia and hypokalemia. @ccmtutorials

Proportional Assist Ventilation [PAV+]

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Proportional assist ventilation has been around in various shapes and forms since the late 1990s. The most advanced current iteration – PAV+ – is unique to Puritan Bennett ventilators. It is a closed loop mode of ventilation. That means that the ventilator dynamically changes the level of assistance that the patient receives in response to patient effort.
PAV+ is neither volume controlled nor pressure controlled but is patient (and operator) controlled. The operator adjusts the percentage support that the ventilator delivers to the patient. The patient breathes – triggering the ventilator – and the ventilator amplifies the patient’s breath. Consequently the more work that the patient does to generate muscular effort the more work the ventilator performs to match the patient’s workload.

It has been known for some time that the diaphragm becomes both atrophic and dysfunctional in acute critical illness, in particular due to disuse during control of mechanical ventilation. In most assisted modes, all the patient needs to do is trigger the ventilator. Patient workload may be inversely proportional to ventilator workload. Frequently the patient’s diaphragm and ventilator are out of synchrony.

PAV+ is patient triggered and flow cycled so it should be seen as a form of pressure support ventilation. PAV+ contrasts with standard pressure support in that the degree of support changes from breath to breath and indeed within breath depending on patient effort. Pressure support delivers a fixed airway pressure for every single breath irrespective of patient effort. Consequently if we map patient effort to ventilator workload there is only one point where the two will intersect. Conversely in proportional assist ventilation the workload of the ventilator and the workload of the patient increase and decrease linearly.

PAV+ works by utilizing very high quality flow and pressure sensors. The ventilator determines when the patient initiates the breath and when the breath is completed. Having instructed the ventilator what proportion of work of breathing that the ventilator should perform, one observes, using a work of breathing bar, if the patient is doing satisfactory work or whether they need to increase or decrease their workload. The work of breathing (WOB) is determined by the ventilator by measuring compliance, resistance and intrinsic peep dynamically every 9 to 12 breaths. As such a Green Zone between 0.3 and 0.7 joules per litre is indicative of ideal work of breathing for the patient; I call this the “sweet spot.” As long as the patient’s WOB resides within the sweet spot of the toolbar the bedside clinician can be satisfied that the patient is both comfortable and safe.

As the tidal volume relates to the patient’s neural activity that results in diaphragmatic power one should not be unduly concerned about high or low tidal volumes in this mode.

If one wishes to put a patient on proportional assist ventilation it is imperative that one determines if the patient is breathing spontaneously and taking an adequate minute ventilation prior to using this mode. The reason for this is that there is no backup rate in PAV+. Usually one starts with 70% support: that means 70% of the work of breathing is performed by the ventilator on 30% by the patient. After a couple of minutes, once one has observed the work of breathing bar, one can make adjustments either to increase the workload of the ventilator or to reduce it by keeping the patient within that Green Zone sweet spot. Generally failure of the patient to settle on this mode is manifest by a respiratory rate of more than 35. Once the patient has been on 20% support for an hour or more and is awake, obeying commands, protecting their airway, and not being suctioned frequently then the patient can be extubated.

Studies that have looked at PAV+ versus pressure support have indicated that weaning is more rapid with PAV+.

Hypernatremia

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This tutorial looks at hypernatremia and hyperosmolar syndrome. Hypernatremia is usually caused by three things: 1) Profound dehydration, 2) Too much sodium intake – most of the time this is due to over-resuscitation with isotonic fluids, 3) Central or Nephrogenic Diabetes Insipidis. I explain how to calculate water deficit and water replacement and how to evaluate and treat patients with diabetes insipidus. @ccmtutorials

Osmotic Demyelination Syndrome / Central Pontine Myelinolysis – final thoughts

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I often wonder if the obsession amongst physicians regarding the prevention of Osmotic Demyelination Syndrome (ODS or Central Pontine Myelinolysis – CPM) results in adverse patient outcomes – for example a greater incidence of iatrogenic complications, prolonged length of stay etc.

In this discussion, I look at the history of ODS/CPM, how it became identified with rapid correction of hyponatremia and what patients are at particular risk of this disorder. In the second part of the discussion I address the re-ignited controversy about Sodium/Osmolality correction subsequent to the publication of a major study in NEJM Evidence in 2023.

Ultimately each clinician must make up their own minds on the evidence that is available. It appears to me that there is little or no risk of ODS/CPM in patients with acute hyponatremia, symptomatic or not, and those with a plasma sodium of greater than 120mmol/L. Patients with Sodium levels below 105mmol/L, alcoholics or cirrhotics and malnourished patient appear to be at very high risk. Finally attention should be paid not only to the speed of correction, but where the plasma sodium levels ends up. In many studies – ODS/CMP is a late diagnosis and patients, at the time of diagnosis are hypernatremic (greater than 145mmol/l) – although the rise in Sodium/Osmolality may appear slow over days or weeks.

Urinary Osmolality, Elderly Patients, Alcoholics and Hyponatremia

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This discussion came about following a discussion with my colleague, Dr Bairbre McNicholas. It focuses principally on the problem of hyponatremia in elderly patients and undernourished alcoholics. I explain why the lack of dietary salt and protein intake massively inhibits water excretion resulting in hypotonic hyponatremia, often with fluid overload. The traditional approach to managing hyponatremia – fluid restriction – frequently fails because it is a problem of solute “underload” rather than water overload. Commencing iv fluids may precipitate a rapid and potentially dangerous diuresis – hence the most effective therapy for these patients is the FEED them.

I guarantee you’ll learn something.

Careful Sodium Correction and Osmotic Demylination Syndrome

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Patients who present with symptomatic hyponatremia (usually the Na+ is lower than 120mmol/L) should be treated with hypertonic saline (HTS) and then fluid restricted. The goal of HTS therapy is to reverse the symptoms and raise the plasma Na+ by 5mmol per liter. What then? It depends on the circumstance – acute or chronic, high risk or low risk. This tutorial addresses the issue of rate of correction of plasma sodium, explains why you need to modify that rate in high risk patients (very low sodium, alcoholics, the malnourished, those with liver disease and profound hypokalemia). The reason why you need to be careful is because of concerns regarding the development of Central Pontine Myelinolysis – usually known now as Osmotic Demyelination Syndrome.

I wish to acknowledge the help of my colleagues Dr Bairbre McNicholas, Dr Peter Moran, Prof. John Bates, Dr Leo Kevin and Ms Aoife Boyle for clarifying my thoughts on this topic.

Click on this link for the 2014 European Guidelines (and a good review of the topic).

The Syndrome of Antidiuresis (SIADH)

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This tutorial is about the Syndrome of Inappropriate Diuresis. SIAD also known as SIADH is a form of hypotonic hyponatremia associated with iso- or hypervolemia, high urinary osmolality and high urinary sodium. Traditionally this is associated with high levels of circulating vasopressin (antidiuretic hormone – ADH), that may be associated with sepsis, acute critical illness, pneumonia or mechanical ventilation. However, SIAD is also associated with a variety of brain injuries, drugs (SSRIs and anticonvulsants) and a variety of cancers.

Treatment of symptomatic SIAD is with hypertonic saline (150ml of 3% over 20 minutes). Chronic or asymptomatic SIAD is treated with fluid restriction (determined by the Furst equation uNa + uK/pNa – if the result is less than1 the patient is suitable for fluid restriction).

Alternative inexpensive therapies include Urea (30 to 60mg per day), salt tablets plus frusemide or demeclocycline.

Vaptan agents, the block the V2 receptors, appear to be effective for long term therapy. Tolvaptan is available commercially but quite expensive for the majority of patients.

Cerebral salt wasting is associated with subarachnoid hemorrhage. It shares the same blood and urinary profile as SIAD(H) but is associated with hypovolemia. The disorder is self limiting and is treated with isotonic fluids.

Hyponatremia 2: Working the Problem

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This is the second tutorial in the series on Hyponatremia. I initially discuss why it is important to evaluate volume status in the setting of a low plasma sodium – patients may be isovolemic, hypovolemic or hypovolemic. The overall treatment is different in each case. Regardless, if a patient presents with symptomatic hyponatremia, then the treatment is 3% hypertonic saline solution – targeted at raising the plasma sodium or osmolality level or both and relieving symptoms. During the remainder of the tutorial I explore several clinical scenarios where patients present with acute symptomatic hyponatremia and work the problem of each seeking the definitive diagnosis.

Hyponatremia – 1. Understanding and Working the Problem

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This is the first tutorial in a short series on hyponatremia. About 15% of our critical care patients has a problem with dysnatremia — high or low sodium levels in plasma. Hyponatremia, with symptoms, is a medical emergency as it can result in cerebral edema and irreversible brain injury.

In this tutorial I first present two case of hyponatremia – one that needs to be treated emergently and one that does not, despite both having the same plasma sodium levels. I then proceed to discuss the physiology of sodium and why it is a key component of body osmolality. The main part of the tutorial is developing a decision tree for working the hyponatremic problem. The key question is whether this is hypotonic or non hypotonic hyponatremia. If it is non hypotonic you need to look for other sources of unmeasured osmoles (usually alcohols). Hypotonic hyponatremia may be associated with myriad problems – but your main concern is whether or not this is being caused by kidney injury or blockade or normal renal pathways (e.g. diuretics). Ultimately I provide an algorithm for how to make a firm diagnosis of the cause of hyponatremia.  @ccmtutorials