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.
I guarantee you’ll learn something.
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.
@ccmtutorials http://www.ccmtutorials.com
Is there anything more frustrating in the ICU when you decide to start weaning a patient – they look like they’re assisting the ventilator. You switch them over to a “spontaneous” mode and then……nothing…..no breaths….eventually the backup starts.
This tutorial is about triggering of mechanical ventilation. I will revisit how patients trigger the ventilator, the different systems used and introduce I-Sync – a new method of triggering.
Finally I will discuss the problem of Auto-PEEP and explain why, in the setting of Auto-PEEP, there is no point fiddling with the flow by or negative pressure.
I guarantee you will learn something. @ccmtutorials www.ccmtutorials.org
Expiratory dysynchrony is a major unrecognized problem in critical care. Usually it takes one of two forms: a terminal upstroke on the pressure waveform, indicating pressure cycling (breath too long) or a W shaped anomaly in the expiratory flow waveform – indicative of the breath being too short or too long. I call this the “Wibbly Wobbly Waveform”.
This tutorial looks at expiratory dysynchrony – why it happens and how to make adjustments to resolve the problem. I also introduce a relatively new technology: IE Sync.
The patient is turning purple in the bed, alarms are going off, he is desaturating: he is “fighting the ventilator.” Although a widely used description I believe that it is misused to redefine the problem away from an issue of ventilator operator competency and reframe it as a patient problem. It is not. Most of the time that patient have negative interactions with the ventilator it is a problem of triggering, flow or expiratory cycling. The treatment is not deep sedation and controlled ventilation. The treatment requires skill and nuance, and does not always work. This tutorial looks at inspiration and reasons why it may go wrong.
The most frequently seen patient ventilator dysynchrony is scooping of the pressure waveform, usually associated with flow limited volume controlled ventilation. This can be resolved by increasing the peak flow or changing to pressure control.
In general the ambition to establish a patient on spontaneous assisted ventilation is laudable, but oftentimes we have no idea about what is going on underneath the pressure, flow and volume waveforms. In this tutorial I try and correct the narrative about patient-ventilator interaction when using pressure support. I suggest that volume support in some situations may be a superior approach. I point out that the tidal volume in pressure support has little to do with patient effort and more to do with lung compliance.
I finish the tutorial with a discussion about the inspiratory rise time and explain why you must be careful when using older ventilators.
@ccmtutorials http://www.ccmtutorials.org
The alarm goes off like an air raid siren – everybody starts to panic – somebody starts to do the saturation countdown. There is nothing quite as distressing for the anesthesiologist or intensivist than for the ventilator to pressure cycle and fail to deliver tidal volumes due to high airway pressure.
Generally high pressures are caused by one of three things – a problem with the equipment (kinked tubing, patient biting the tubing etc.), an airway resistance problem (e.g. bronchospasm) or a pulmonary compliance problem (e.g. consolidation or pulmonary edema) or a combination of these. The first thing that the clinician should do when there pressure alarm goes off – is to silence the alarm and increase the Pmax.
Then go looking for the problem: start at the mouth and work your way back to the machine. If you can’t find a fault, put the patient on a manual breathing circuit and commence ventilation. If the patient is easy to bag, there is a machine problem, if difficult – then there is a problem with pulmonary resistance or compliance. In this first tutorial I look at assessing airway resistance. I do this in two ways. First I discuss peak to plateau pressure gradients and then look at airway resistance: dynamic versus static and how to calculate it. I will finish the discussion in the next tutorial.
There is a feature on the display of you ICU ventilator or anesthetic machine that you likely pay little attention to – the flow volume loop. Indeed, you may ignore the flow-time waveform also. This is a pity – and you are missing out on tons of information about your patient.
This tutorial commences with a description of the flow waveform (no previous knowledge required!) and the different waveforms that you are likely to encounter – sinusoidal, constant flow, decelerating flow and “shaved-off” decelerating flow (associated with pressure support).
I then show you a series of flow volume loops and – yes you can pause the video and see if you can figure out what is going on with the patients.
If you find this and my other videos useful – do me a favor and subscribe: subscriber only content coming soon.
@ccmtutorials http://www.ccmtutorials.org
For the majority of patients admitted to ICU with hypoxic respiratory failure, a conventional ventilatory strategy using volume, pressure or dual control modes with PEEP is usually very effective. With severe lung injury it may be necessary to administer neuromuscular blockade, turn the patient prone and increase the mean airway pressure using PEEP or inverse ratio ventilation (IRV). If these interventions are unavailable, ineffective or inadequate, rescue therapies may be required.
One easily available rescue therapy is Airway Pressure Release Ventilation (APRV). APRV is an extreme version of IRV that looks analogous to using CPAP at high airway pressure levels (e.g. 28cmH2O). Intermittently that high airway pressure is released to remove CO¬ – the release time (less than 1 second) being too short to cause lung derecruitment. Using modern ventilators it is possible utilize the inspiratory capacity to oxygenate the patient (flipping the respiratory cycle from expiration as the primary time of gas exchange to inspiration) and allow the patient to breath spontaneously.
The spontaneous efforts have been shown to improve both gas exchange and cardiovascular performance – but they are not necessary when using this ventilator strategy. Gasping should be avoided. This tutorial covers the science behind APRV, how to set it up, how to use it as part of a ventilator strategy in ARDS, the strengths and limitations of this approach and how to wean it.
I guarantee you will learn something. @ccmtutorials http://www.ccmtutorials.org
ORtoICU 