Tutorials 2 and 3 in the Introduction the Critical Care Series.
The first is titled “What is Critical Illness” and it covers the concept of Physiologic Reserve.
The third tutorial looks at the problem that many healthcare providers encounter: how do I identify the critically ill patient. In this tutorial I discuss the type of scenarios in which you might be called to the patients bedside. I principally discuss Early Warning Scores (EWS) and why I think they are helpful. I also mention the SOFA score.
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.
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+.
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
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.
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.
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.
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
This is Tutorial 4 in the Acid Base Series – on the topic of Metabolic Acidosis. The tutorial is based on a single blood gas – a random sample that was handed to me in the ICU recently. Blood Gas Used in This Tutorial: pH 7.19 PaCO2 32mmHg (4.1kPa) HCO3- 13.1 BE – 16.5 AG 20 Na+ 126 K+ 3.1 Cl- 96 Lactate- 7.2 Ketones- 0.6mmol/L Albumin 21g/L Creatinine 3.3mg/dl (293mmol/l)
Metabolic Acidosis is characterized by an increase in the relative ratio of strong anions to strong cations in the plasma. The PaCO2 and the Bicarbonate fall in a predictable manner. It is possible to compute the effectiveness of respiratory compensation for metabolic acidosis by using the Winters equation.
To understand the mechanism of metabolic acidosis – caused by accumulation of mineral (Chloride) and organic (Lactate, Ketones, Metabolic Junk Products) anions – one needs to apply the law of Electrical Neutrality. All of the positive charges must equal all of the negative charges. As Bicarbonate is consumed in the process of buffering metabolic acidosis, the change in the Bicarbonate level (downwards) can be used to quantify the degree of acidosis. This is important because the pH may be within the normal range due to respiratory compensation. Be aware that the HCO3- quantum that is displayed on a blood gas is derived from the pH and PCO2 by the Henderson Hasselbalch equation.
Unfortunately, because respiratory abnormalities may complicate the diagnosis of metabolic acidosis, and pH and PCO2 are altered by changes in temperature, the precision of a single reading of PCO2 and HCO3- may be poor. Consequently, the Standard Base Excess was developed to excise the respiratory component from the change in bicarbonate. Again it is a derived variable and may be imprecise. Nevertheless, BE (or 1-BE the Base Deficit BD) is a terrific scanning tool to identify the presence of a metabolic acidosis (BD) or alkalosis (BE). It is defined as the amount of strong cation (BD) or strong anion (BE) required to bring the pH back to 7.4 when the temperature is 37 degrees Celcius and the the PaCO2 is 40mmHg or 5.3kPa.
The Base Deficit does not indicate the source of the acidosis, but it can be recalculated to remove the impact of the [Na+], the [Cl-], the body water and the serum Albumin (and the Lactate) to determine the Base Deficit Gap – indicative of the quantity of Unmeasured Anions (UMA, Ketones, if not measured, and Renal Acids (metabolic junk products – MJP).
Traditionally clinicians use the Anion Gap to determine whether a patient has a Hyperchloremic Acidosis (no gap) from a UMA acidosis. I find this quite a dated concept. If the [Cl-] exceeds 105 and the plasma Sodium is normal, the patient has a Hypercloremic acidosis. We can easily measure Ketones and Lactate. The AG is imprecise and should be adjusted for the Albumin level, which tends to hover around 25g per liter in critically ill patients (narrowing the Gap and alkalinizing the patient). I do think if you are calculating the AG that you must include the K+ on the Cation side, the Lactate on the Anion side and adjust the Albumin.
The Strong Ion Gap is a more advanced, more precise and more cumbersome version of the AG. Regardless of the approach, one eventually ends up with a quantify of unidentifiable anions (SIG) that may be of medley origin (metabolism, poisoning etc). It is my opinion that it is useful to tease out all of the different acidifying and alkalinizing processes (the Fencl approach) to determine what is going on with the patient. All of these calculations can be done in seconds with smartphone apps and spreadsheets.
This is Tutorial 2 in the Series on Acid Base: The FIzz of CO2.
Carbon Dioxide is a gas that is produced by the mitochodria and passes through the cell membrane into the extracellular fluid and blood. There it dissolves, attaches to hemoglobin or, under the influence of carbonic anhydrase, hydrates with water to generate carbonic acid – which rapidly dissociates to release hydrogen (bound to hemoglobin) and bicarbonate. Carbon Dioxide obeys Dalton’s law and Henry’s law. The latter determines that the PCO2 is directly proportionate to the CO2 content. Carbon Dioxide becomes more soluble in the blood as temperature falls. Hence measuring gaseous CO2 requires the blood gas machine to be set at 37 degrees.
The body produces, at rest, 200ml per minute of CO2. The body excretes 200ml per minute of CO2. As metabolism increases, respiratory excretion of CO2 increases. This results in a PaCO2 of 40mmHg or 5.1kPa. There is a 3-4mmHg or 0.5kPa difference between the PaCO2 and the etCO2. Because the body exists, usually, is steady state, the etCO2 can be used to estimate the PaCO2 (most of the time). In apnea, the PaCO2 rises rapidly – it doubles in 8 minutes.
When PaCO2 rises, [HCO3-] rises also – and in a very predictable way. So, when a patient develops acute respiratory failure, or underventilates (for example under anesthesia), pH falls, predictably, the PaCO2 rises, predictably and the Bicarbonate rises, predictably. This is acute respiratory acidosis – and in this tutorial I will explain how and why this occurs.
It is imperative to understand that CO2 and [HCO3-] are different versions of the same thing in the body and the rise in bicarbonate in respiratory disorders is not some form of “compensation” it is physiology. Indeed in chronic respiratory failure, the increase in respiratory acids (Chronic respiratory acidosis) is counterbalanced by a fall in the plasma Chloride levels. Acute respiratory alkalosis is associated with pain, anxiety, agitation or over ventilation and is associated with a modest fall in Bicarbonate.
ORtoICU 