As part of my fundamentals of Anesthesiology and Critical Care Series I have posted 3 tutorials on the Role of CO2 /HCO3 in Acid Base Balance. These are entirely new tutorials (not part of the previous acid base series – that I have not finished yet! There is some overlap and updated facts and figures) and I have put a lot of work into getting the message of why the respiratory system is so important in acid base. Tutorial 1 is the basics of acid base. Tutorial 2 discusses respiratory acidosis, acute and chronic, and respiratory alkalosis. Tutorial 3 discusses respiratory compensation for acute metabolic acidosis. Although I cover the respiratory component in great depth, I also explain what metabolic acidosis is, what causes it and briefly discuss the anion gap, expected bicarbonate, base deficit and base deficit gap. I guarantee that you will learn something.
Here are the first 9 Tutorials in the Series – the majority are useful for Anesthesiologists and Intensive Care practitioners. Every tutorial contains something that you may not have previously known: I guarantee, who ever you are, that you’ll learn something.
I published 3 tutorials on Local Anesthetics this Month. These are part of a new series of Anesthesiology Tutorials.
Tutorial 1 looks at the basic pharmacology of local anesthetics
Tutorial 2 looks at the various different drugs that we use, the volume and concentration. I discuss the maximum safe doses at the end of the tutorial.
Tutorial 3 looks at the history of, the diagnosis of and the treatment of Local Anesthetic Systemic Toxicity (LAST)
This HI-Impact tutorial looks at the common questions relating to commencement and route of nutrition in critical care. Is TPN good, bad or indifferent. Is enteral feed better than parenteral? When should we start feeding? Is it useful to add parenteral feed to enteral if the patients’ caloric goals have not been met? When should patients achieve their isocaloric goals. I guarantee you’ll learn something.
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.
This is the first in a new series of “”Bedside Tutorials in Critical Care” that reflects issues that we dynamically come across while doing rounds in the ICU.
Vasopressors are very widely used drugs in critical illness – norepinephrine (noradrenaline) is the most widely prescribed catecholamine, used in most types of shock and considered the standard of care vasopressor in septic shock. Epinephrine, these days may be added as an inotrope or used in neurogenic or anaphylactic shock. Vasopressin is used to restore vascular tone as a form of hormone replacement therapy.
Norepinephrine and Epinephrine concentration and dosing is extremely confusing. Many ICUs dose these agents in micrograms (mcg) per minute. This translates to ml/hour – often the bedside practitioner has not made the conversion. Consequently, when asked “how much norepinephrine the patient is on?” the response may be 5 or 10ml per hour. This is unsatisfactory, as, based on weight, there may be a tremendous variability in the dose received. Moreover the concentration of norepinephrine varies widely. In our hospital we have been required to use a pre-diluted formula of 4mg in 50ml (delivered by syringe driver) resulting in a concentration of 80mcg/ml. Conversely, epinephrine needs to be drawn up, using 1mg ampoules, usually 3mg in 50ml or 60mcg/ml (conveniently this works out as 1mcg/min/ml. Peripherally infused norepinephrine is constructed by placing 4mg in 250ml, leading to a concentration of 16mcg/ml.
Alternatively, norepinephrine may be diluted 16mg in 250ml to yield 64mic/ml. When a patient is transferred from another hospital or another country, it may be really difficult to translate the dilution and concentration used there to match up dosage. And that is important – escalating doses of pressors are suggestive of failure of source control, but 10ml/hour is twice to dose delivered to a 50kg person than a 100kg person. And at what dose do you start vasopressin?
Consequently, I strongly recommend that you use mcg/kg/minute as your dosing strategy for both norepinephrine and epinephrine. The starting dose is 0.01-0.03mcg/kg/min and it is titrated upwards to achieve a mean arterial pressure of 65mmHg. Once the dose has exceeded 0.25mic/kg/min, the patient should receive vaspressin 0.03 international units per minute. If 40iu is diluted in 50ml, to deliver 0.03 iu/min, the infusion should run at 2.3ml/hour.
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.
This tutorial looks at the pulse, what it is, the waveform and how that reflects systole and diastole. I then go on to look at the pulse waveform on pulse oximeters and the pulsatility index. Finally, I discuss the essential topic of Pulse Pressure Variability.
ORtoICU 