Proportional Assist Ventilation [PAV+]

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+.

Metabolic Acidosis – What it is, Diagnosis and Tools

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.

I guarantee you will learn something. @ccmtutorials http://www.ccm-tutorials.com

Weaning From Mechanical Ventilation (the basics)

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)

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

Help – The Patient is Fighting the Ventilator

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