The kPa Rules – Part 1: Oxygen

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.

Fluids In Hospital Medicine (Part 1)

Intravenous fluid, fluid management, the physiology of body fluids – all relentlessly controversial and complicated issues. I decided a couple of years ago to put together a course that covers the whole spectrum of fluids – from basic chemistry to basic and advanced physiology, applied physiology, fluid and electrolyte disorders and therapy and acid base chemistry. I will also cover diseases and disorders associated with fluids – either as therapies for, or iatrogenic causes of, disease.

Introduction to the Course

This is a quick introduction to the course, explaining what I am proposing to cover over four parts.

Preliminary Material

This is some really basic chemistry that will allow you to understand the content of subsequent tutorials.

Tutorial 1 Water and Concentrations

This tutorial convers the physical properties of water, what a mole and mmol is and what is g%. I use dextrose as my major example and look at the different ways that glucose concentration is measured in the USA (mg/dl) versus the rest of the world (mmol/L). The end of the tutorial covers the alcohol and calorie content of drinks and drink driving limits.

PART 1 MODULE 1

1 Supplement

I rather like caffeinated drinks and am frequently the subject of sanctimonious comments about my caffeine habit. This tutorial covers caffeine content. Subsequently I look at the issue of 1% versus 2% lidocaine and explain exactly what 1:200,000 epinephrine (adrenaline) is.

Tutorial 2 Salts

This tutorial explains how to calculate out the quantity of electrolytes released from salts as they are dissolved in intravenous fluids. I also take an early look at hypertonic saline solutions.

Tutorial 2 Supplement 1 – More Salt

This tutorial goes through a couple of conundrums where I look at intravenous fluid products and show you how to calculate out the electrolyte contents when you are only given the salts in g/L

Tutorial 2 Supplement 2

This is an early look at calcium supplement products that we typically use in critical care. What exactly is the difference between Calcium Chloride and Calcium Gluconate?

Tutorial 3 Osmosis

Fundamental to understanding how water behaves in body fluids is the concept of osmosis. It is also very important when we visit renal replacement therapies in Part 4 of the course. In this tutorial I use traumatic brain injury and mannitol as my main example.

Tutorial 4 Osmolality and Tonicity

What is the difference between osmolality and osmolarity? What are mOsm? How do you calculate Osmolarity? This tutorial looks at the concept of Osmolality and the Tonicity of intravenous fluids, and why understanding this concept is essential for practitioners of hospital medicine. The clinical scenario is of a patient with hypotonic hyponatremia. I will revisit hypertonic saline solutions and look at the concept of the Osmotic Co-efficient.

Tutorial 5 Electrolyte Distribution

This tutorial looks at the distribution of electrolytes in the body – between the intracellular and extracellular compartments. I look at the needs of a patient who is unable to take oral fluids and electrolytes. I emphasize the importance of maintenance fluids in this situation rather than resuscitation fluids. This tutorial also looks at the interstitial matrix and how it is vulnerable to hydraulic fracturing (“fracking”) caused by intravenous fluids.

This is the end of Module 1.

PART 1 MODULE 2

Tutorial 6 The Adaptive Perioperative Stress Response

Whether we are injured, assaulted or undergo surgery, our bodies respond with an inflammatory response that involves endocrine, metabolic and immune components. The “adaptive” stress response is predictable and its magnitude mirrors the degree of injury. To understand emergency and perioperative medicine and critical illness you must understand the stress response. Having explained the basic physiology, I then go on to discuss fluids and fluid balance and describe the conventional approach (that I do not necessarily subscribe to) to perioperative fluid therapy.

Tutorial 7 Critical Illness and Resuscitation

A patient presents with an “acute abdomen.” His bowel is obstructed and he is losing fluid and becoming both dehydrated and electrolyte depleted. This tutorial looks at the different types of body fluids that may be lost – how they all resemble extracellular fluid and suggests a type of fluid that can be used for resuscitation. I then progress to describing the maladaptive stress response of critical illness, and why it is associated with capillary leak syndrome. There follows a discussion of fluid overload and the need for de-resuscitation. Finally I introduce the topic of chronic critical illness and death.

Tutorial 8 The Macro Circulation

What happens to the body when there is major blood loss? This tutorial looks at the different components of the circulation and how blood flow is redistributed in shocked states. I also look at the assessment of hypovolemic shock, oxygen consumption versus delivery and the mixed venous oxygen saturation. Finally I address resuscitation strategies in acute blood loss.

This ends Part 1 Module 2.

PART 1 MODULE 3 ADVANCES

Tutorial 9 Venous Return

Since the 1970s the venous (and lymphatic) side of the circulation and the right side of the heart seem to have been ignored by doctors. At worst is the widely held belief that central venous pressure represents an appropriate measure of blood volume and resuscitation status. This tutorial looks at the concept of cardiac output versus venous return. I discuss the Guyton concept of mean systemic pressure, the stressed and unstressed blood volume and vascular compliance. I then go on to look at venous return during anesthesia, the impact of low and high dose vasopressors and the impact of fluid overload.

Tutorial 10 The Microcirculation & Capillaries

For the past 125 years or so, the vast majority of clinicians have based their understanding about transendothelial fluid flux on the work of Ernest Starling. Problem is that his hypothesis – the Starling Principle – is wrong. The presence of the capillary glycocalyx and enhanced understanding of fluid kinetics has changed our view of fluid therapy, in particular the role of colloids in treating critically ill patients. This tutorial looks at the capillary network, the traditional Starling method, the “Revised” Starling method, the glycocalyx, oncotic pressure gradients, the impact of fluid extravascation and the lymphatic system.

Tutorial 11 Albumin & Colloids

Colloids, whether they are hydroxyethyl starches, dextrans, gelatins or even albumin, were popular resuscitation fluids until the 2010s. Multiple studies failed to demonstrate the effectiveness of these agents. However, the use of hyperoncotic human albumin solution has gained popularity, based on no real evidence, in recent years. Given our knowledge of the microcirculation, is there any compelling reason to be treating a patient with human albumin solution in the 2020s?

Tutorial 12 Fluid Kinetics

In this last tutorial in Part 1 of this course, we are returning to the operating room. What happens to intravenous fluid once it is injected into the veins a) in normal volunteers, b) during anesthesia, c) during the stress response? This tutorial is all about fluid or volume kinetics and is based on the work of Robert Hahn, from Sweden. I discuss fast versus slow boluses, resuscitation with crystalloid in hypovolemic states, the urinary output during surgery and what happens during hypervolemia.

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