Patients who spend significant time in critical care may lose a staggering amount of weight, particularly lean body mass. In early critical illness glucose is used as the principle energy source in the stress response; glycogen is rapidly exhausted and glycogenic amino acids are mobilized from muscular protein to generate glucose via gluconeogenesis, to maintain plasma glucose levels to feed, principally red blood cells. This has a major impact on muscle mass and in particular muscular strength, that may take years, perhaps a decade to restore. The most effective mechanism of preventing the development of critical illness cachexia is to curtail the duration of the stress response, by rapid source control, deresuscitation and early mobilization. In general, patients should be receiving full nutrition and be mobilized by day 8 following injury.
In November 2024 six tourists died of suspected Methanol Poisoning in Laos, and several more were hospitalized. Methanol, or methyl alcohol, is an industrial chemical used to thin paints, as a precursor for medley chemicals and for fuel cells. It is passed off as “vodka” (odorless, tasteless, clear) to unsuspecting victims.
Methanol is metaboized by the same pathways as ethanol, but to formaldehyde and formate. Although small amounts of methanol may be found in the body, due to gut bacterial fermentation, methanol poisoning is a life threatening problem. Formate causes a widened anion gap metabolic acidosis, blindness, brain damage and interferes with mitochondrial function resulting in cytotoxic hypoxia.
The treatment for methanol poisoning is fomipazole given 12 hourly intravenously, folate, intravenous fluids and, if necessary, renal replacement therapy. Fomipazole competitively antagonizes the metabolism of methanol by the enzyme alcohol dehyrogenase. If fomipazole is unavailable, ethanol can be given as an emergency measure, intravenously or orally.
Hypovolemic shock is one of the major problems we encounter in acute critical illness. This tutorial explains the mechanisms by which the body compensates for hemorrhage/hypovolemia, why the blood pressure and hemoglobin saturation are unhelpful and what tools may be useful at the bedside to assess the patient.
I also briefly discuss resuscitation of the bleeding patient and compartment syndromes.
This tutorial looks at the problems of Hypotension and Shock. I define the difference between the concepts – not all hypotensive patients are shocked and not all shocked patients are hypotensive. I then go through a system for exploring the hypotensive or shocked patients’ status to determine the underlying problem – illustrated by a series of clinical scenarios.
One of the most common physiologic and pathologic abnormalities that we get called for is dysfunctional blood pressure: hypotension and hypertension. This tutorial looks at the question – “What is Blood Pressure” the components and its regulation. I then go on to discuss arterial pressure monitoring, invasive (via arterial lines) and non invasive (using oscillometers) and the strengths and weaknesses of both.
One of the most intimidating things about entering the ICU for the first time is the “life support machine” – the mechanical ventilator. Although I have posted an extensive series of tutorials on Mechanical Ventilation, covering most of the modes, oxygen therapy and applied respiratory physiology, I have attempted, in this tutorial, to distill everything to the “least you have to know” in 40 minutes. Keep in mind that modern machines look more like iPhones, and are far easier to use than the devices I grew up with that looked to me, on day 1, like something in the cartoon below.
I start with a discussion about the difference between normal breathing, CPAP and Positive Pressure Ventilation (PPV). PEEP is, effectively, CPAP during PPV. I then go on to discuss pressure limited modes of ventilation; worldwide this are the most widely used modes in ICU. I limit my discussion to Pressure Assist Control, Volume Guaranteed Pressure Control (VG_PC) and Pressure Support Ventilation (PSV). VG-PC is a popular and flexible option as an ICU’s default mode. However, as it is a pressure controlled mode, there is significant variability in tidal volume and airway pressure from minute to minute.
Several important rules are emphasized: the tidal volume should, in general be lower than 6ml/kg of ideal body weight, the plateau pressure lower than 30cmH2O and the driving pressure lower than 15cmH2O. I introduce the Spontaneous Breathing Index (SBI = RR/TV in L). The magic number is 100. We use the SBI to determine the success of weaning on PSV.
Volume Controlled Ventilation is the predominant mode use in the Operating Rooms (Theatres), and Volume Assist Control is a popular mode in North America. In ICU you must set a peak inspiratory flow and be aware that this may be insufficient during assisted breaths and lead to dys-synchrony. Volume Control is often used in ARDS to “lock in” the Tidal Volume (TV) but the operator must be aware that the TV that matters is not what is dialed up on the ventilator, but what the patient exhales.
I go on to discuss how to assess the patient on invasive mechanical ventilation, by looking at whether they are breathing spontaneously, in which case we determine whether they are suitable for a Pressure Support wean or not, or whether or not there is a problem with oxygenation (increase FiO2, PEEP, Mean Airway Pressure and seriously consider Prone Positioning) or Ventilation (increase Respiratory Rate, Tidal Volume or both, reduce PEEP).
The final part of the tutorial looks at Non Invasive Ventilation (NIV), and I explain how, in general we only use 2 modes on standalone devices – CPAP and Spontaneous Timed (S/T). The latter is similar to PSV with a backup rate, but I point out that instead of PEEP+PS the breath is EPAP + IPAP and IPAP is not built upon IPAP, as is the case with PSV. If one is delivering NIV on an ICU ventilator, then “leak” adjustment or “leak sync” should be used.
I am now going to move on, in the Introduction to Critical Care course, to a systems based assessment of the patient where you are expected to compile measurements and observations from the clinical information system, radiologic system and monitors to construct an overview of the patient’s status. This is the crux of intensive care medicine and it is not easy. I am going to visit each system sequentially, and some systems will have multiple tutorials. By the end of this process, you will have compiled all of the data, assessed and processed it, and be ready for the big presentation.
The first tutorial in this part is an overview of patient assessment. It is relatively short but essential.
The Second tutorial in this sequence is on at neurological assessment in the ICU. It contains a discussion about the Glasgow Coma Scale, The Richmond Agitation Sedation Scale and CAM-ICU. I also cover the assessment of suffering (PAID) in critical care.
You will need to assess the patients neurologic status, whether or not they appear to be suffering and what interventions, both environmental and pharmacological, that you are administering to help them.
This tutorial looks at the twin problems of Alcohol related and Starvation Ketoacidosis. These diagnoses are frequently missed by clinicians because 1. they attribute the metabolic acidosis to another cause e.g. lactate or acute kidney injury or 2. they do not routinely measure blood ketones. It is my view that, in any patient presenting with a plasma bicarbonate below 20mmol or mEq/L or a base deficit of -5 or greater, it is mandatory to measure blood ketones (beta-hydroxybutyrate).
I present two cases, the first is a patient who is admitted with abdominal pain and a likely upper GI bleed, with a history of an eating disorder, who has metabolic acidosis. The second patient is an alcoholicwho recently stopped both eating and consuming alcohol. She also has a metabolic acidosis. I discuss the biochemistry of alcohol metabolism and explain why alcoholics are at risk for ketoacidosis. I also explain why this is part of a paradigm of metabolic failure that, without significant attention to detail, may result in therapy that precipitates a variety of withdrawal syndromes: these include acute Wernicke’s Encephalopathy, Alcohol Withdrawal Syndrome, and acute aquaresis and Osmotic Demyelination. Alcoholic ketoacidosis almost always follows cessation of alcohol intake – and one is unlikely to make this diagnosis in a patient who, for example, presents drunk to the ED (this results in a host of other metabolic anomalies, for example hypoglycemia despite high plasma lactate).
Starvation ketoacidosis is seen in patients who are chronically malnourished or fasted for prolonged periods for surgery, in whom the pancreatic Islet cells have either atrophied or are hibernating. Careful attention must be applied to feeding and refeeding: it is imperative that the patient does not lose further lean body mass. On the other hand refeeding syndrome may result in rhabdomyolysis and death. I guarantee you’ll learn something.
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.
ORtoICU 