Category Archives: Shock

Lactic Acidosis

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  1. Lactic acidosis is one of the best biomarkers of acute critical illness, its presence should alert the clinician to a major stress response, where medical and surgical and iatrogenic sources should be considered.
  2. The magnitude and duration of hyperlactatemia (in the acute phase) is predictive of patient prognosis in critical illness. A sustained high lactate reflects a prolonged stress response. The lactate is not the cause or the problem. It is merely a biomarker.

If I were to pick one topic over which I have sweated tear during the past 2 decades, it is lactic acidosis. The problem is that every time I try to explain lactic acidosis, many of those around me become hostile, as if I was committing some atrocity against their religion. And that is because, for the past 100 years, every high school, science, nursing and medical student has been taught that lactate is a waste product that is only made in anerobic conditions. This is 100% ABSOLUTELY completely verifiably WRONG. Lactate, or lactic acid is produced all the time, continuously, in all tissues and is likely the major endpoint of glycolysis. Once produced, it is then either used for oxidative phosphorylation, shuttled to other tissues as a partially metabolized energy source (e.g. the heart and the brain – they love lactate) or metabolized in the liver, principally (the “Cori Cylcle”) – where gluconeogenesis takes place leading to subsequent glycogen storage, fat production or oxidative phosphorylation. As such, glucose is a universal substrate and lactate is a universal fuel.

Lactic acidosis occurs when the production of lactate exceeds the capacity of the liver to clear it. As we produce at least 1250mmol of lactate per day and it is barely measurable in the blood, hepatic clearance capacity is vast. Hyperadrenergic states promote the production of lactate, increase blood glucose and reduce hepatosplanchnic blood flow. The consequence is sometimes called “stress hyperlactatemia” or “aerobic glycolysis.” This is the form of hyperlactatemic seen in sepsis, for example. As such it is an acute phase reactant biomarker – lactate concentration mirrors adrenaline/epinephrine, and should be seen in the same light as CRP, IL-6 and Procalcitonin.

Hyperlactatemia results in metabolic acidosis as a consequence of water dissociation. The strong ion difference (SID) falls. The surplus “hydrogen ions” are mopped up by bicarbonate resulting in a modest fall in pH, but a mEq/L for mEq/L fall in bicarbonate and base excess. Lacate, like Chloride and Ketones, always functions as an acid surrogate and chronic hyperlactatemia is compensated for, usually, by increasing urinary Chloride loss, manifest as hypochloremia.

The terms “Type A” and “Type B” lactic acidosis were introduced by Huckabee in 1961. I believe that these monikers are still useful today. “Type A” represents lactic acidosis associated with blood loss and hypovolemia, intense systemic and splanchnic vasoconstriction, high ejection fraction, low stroke volume and cardiac output and low mixed venous oxygen saturation. Production of lactate increases (and this is multifactorial – not just anerobic), and production falls – due to hepatic hypoperfusion. The treatment is resuscitation, preferably with blood products.

For lactic acidosis, what is not Type A must be Type B – and this represents medley causes (toxic – alcohols), metabolic (end stage liver disease), inflammatory (sepsis), drug induced (metformin and particularly intravenous or inhaled catecholamines).

The term “Clearance” has been used to describe the removal of lactate from the circulation. It is a pharmacological rather than biochemical term, and that has led to some abuse in clinical practice: the belief that “Clearance” can be hurried along with aggressive fluid resuscitation. However, like any particle that is metabolized by the liver, clearance of lactate is determined by the quantity delivered, hepatic blood flow and hepatic clearance capacity. If there is a sustained surge in lactate production, then it may take a while for the liver to clear the surplus from the system while simultaneously dealing with the continued production of lactate by the tissues. In critical illness, we like to see the plasma lactate level falling, but 10-20% is sufficient to be reassuring. A rising lactate is ominous and may indicated inadequate source control or a secondary problem, such as bowel ischemia.

Lactic acidosis may or may not be a marker of tissue perfusion. It is a poor endpoint of resuscitation – and if used as such (the “drive by saline assault”), the result is fluid overload, mutiiorgan dysfunction and prolonged ICU stay.

Sodium Lactate Solutions do not cause lactic acidosis, as they are fully balanced. Most formulations contain a racemic mixture of L-Lactate (which is what the body produces) and D-Lactate (produced by fermentation by bacteria). Blood gas machines do not measure D-Lactate.

I guarantee you’ll learn something.

Fluids In Hospital Medicine (Part 1)

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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.

If you have enjoyed this course, please subscribe on youtube and post lots of likes and positive comments. I will do my best to answer queries and comments below, time permitting.