RESPIRATORY ACID BASE DISORDERS

Posted on by
Reply

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

ACID BASE 1 – The Power of HYDROGEN

Posted on by
Reply

This is the first tutorial in a new series on acid base balance. This is not a beginners course – although I will attempt to cover everything the bedside clinician should know, particularly in the ICU. I have been teaching and writing about acid base for more than 25 years and I find it disappointing how many clinicians fail to understand even the basics of physical chemistry that underpin this topic.

This course is built on the foundation of physical and electrochemistry (all acid base reactions occur in water, all ionizing processes must be accounted for electrical neutrality must always hold.

The first tutorial is titled “The Power of Hydrogen” and it looks at the chemistry of water, the tendency for water to dissociate into moieties that display hydrogen ions and hydroxyl ions, and how temperature impacts that dissociation equilibrium. It is imperative that you understand that there are effectively no free protons (hydrogen ions) in the extracellular fluid. When we measure [H+] or its corollary, pH, we are measuring hydrogen ion ACTIVITY not hydrogen ion concentration. I explain the origin of pH and how pH varies with temperature despite the aqueous solution remaining chemically neutral. I explain the history of acid base, starting with O’Shaughnessy and then moving on to Arrhenius and Bronsted and Lowry. It is easier to understand acid base if one utilizes the Arrhenius theory, but the concepts are fully consistent with the BL approach, because water is amphiprotic (it can act as a “proton donor” or “proton acceptor.”

I explain how blood gas machines measure pH and why pH (and PCO2) should almost always be measured at 37 degrees Celsius. At the end of the tutorial I explain the terms acidosis and alkalosis, respiratory and metabolic. @ccmtutorials http://www.ccmtutorials.org

Weaning From Mechanical Ventilation (the basics)

Posted on by
Reply

This tutorial is about weaning from mechanical ventilation. This is not an easy topic because every professional in the ICU has their own weaning method and their own opinions regarding how best to wean and liberate patients. The literature is unhelpful. Some patients, for example those who have been intubated for a brief period of time, can be awoken and the tube removed after a couple of spontaneous breaths. Other patients require careful multidisciplinary activity over weeks to months to liberate. This tutorial focuses on the in-between group patient who have been intubated for a week or so, who require both clinical and mechanical assessment of their ability to wean and liberate from the ventilator.

Generally the first intervention in weaning is to change the patient over to a spontaneous breathing mode – pressure support or volume support and ensure that alveolar ventilation is adequate to maintain CO2 clearance.

Then a number of clinical and mechanical assessments can be made: is the patient awake, do they have a cough, are they triggering adequately, what is their rapid shallow breathing index (RSBI)? One can estimate muscle strength by performing an occlusion test – either a partial occlusion (P0.1) or a longer occlusion (NIF). Once the patient is assessed as being a candidate for weaning, then one can perform a spontaneous breathing trial (SBT) that is either supported (PS, VS, ATC) or unsupported (T-piece, C-circuit, Trach mask, Swedish Nose).

If the SBT is successful after 90 minutes – extubate the patient. SBTs may fail due to worsening hypoxemia, hypercarbia or hypocarbia, respiratory distress (increase RSBI or use of accessory muscles) or cardiovascular instability (hypotension, hypertension, tachycardia, bradycardia, arrhythmias) or falling levels of consciousness, agitation or acute delirium.

Why isn’t the patient breathing up? (Triggering the Ventilator)

Posted on by
Reply

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

The Wibbly Wobbly Waveform – Expiratory Dysynchrony

Posted on by
Reply

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.

Help – The Patient is Fighting the Ventilator

Posted on by
Reply

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

Help- The Patient’s Airway Pressures are STILL HIGH!

Posted on by
Reply

In the previous tutorial we looked at the problem of high airway pressures and addressed inspiratory airway resistance in two ways: peak to plateau pressure gradient and dynamic and static inspiratory resistance.

In this tutorial we will look at three more ways of assessing airflow resistance: the identification and measurement of Auto-PEEP, Flow-Volume Loops and capnography.

Subsequently I discuss high airway pressure due to low total respiratory system compliance. I explain that when “compliance” is low – this may be a problem with the lungs as well as the chest wall – including the abdomen. I finish with the introduction into this course of Abdominal Compartment Syndrome.

50 Tutorials Uploaded! Now – Help the Patient’s Airway Pressures Are High!

Posted on by
Reply

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.

Volume Pressure Loops – they are on every ventilator and anesthetic machine – look at them

Posted on by
Reply

This tutorial looks at the pressure waveform in patients undergoing anesthesia or mechanically ventilated in ICU. All modern ventilators will provide a pressure time waveform and display volume pressure (often called “pressure volume” loops).

This tutorial commences with a discussion about pressure-flow loops – to demonstrate the relationship between flow and airway pressure. I then discuss and describe normal airway pressure versus time waveforms.

Subsequently I explore normal and abnormal dynamic volume pressure loops. I briefly discuss static VP-curves and why they are important in ARDS. Finally I demonstrate how you can measure real plateau pressure and static compliance by pushing one button and performing an inspiratory hold.

@ccmtutorials http://www.ccmtutorials.org

Flow Volume Loops in Anesthesia and Critical Care

Posted on by
Reply

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