Author: Brandon O

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We talk the nitty-gritty of assessing the right heart using echocardiography, with our friend Matt Siuba (@msiuba), intensivist at the Cleveland Clinic and master of zentensivism.

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Takeaway lessons

1. RV echo starts with evaluating three things: size, squeeze, and septal kinetics.
   • Size should be <2/3 the LV
   • Squeeze can be assessed in a variety of ways
   • The septum should not be bowing into the LV.
2. Dilation is an early and somewhat compensatory finding, and can be used as a screening test (the “D-dimer of RV dysfunction”). Septal changes are probably later and more of a sign of dysfunction (i.e. not compensatory).
3. Evaluating the RV’s ejection fraction is impractical due to its complex shape (without 3D echo or cardiac MRI or other advanced tools). So methods like TAPSE that reduce it to its longitudinal function become a more practical surrogate.
4. TAPSE is not an isolated marker of RV contractility, but a marker of the overall RV-PA unit. However, this is probably a feature, not a failure. You don’t really want to know how the RV is contracting in the abstract, but how it’s contracting in its current loading conditions. So TAPSE will vary by afterload and preload, but not artifactually—i.e. if the loading conditions change and TAPSE improves, then contractility is better in the current conditions.
5. s’ is similar to TAPSE, and similarly limited (mainly evaluating longitudinal function). It assesses velocity, not movement, which theoretically may represent something different (maybe a better marker of function?), although that difference is not very well studied; some studies do suggest that s’ may be more sensitive to changes after adding an inotrope, but who knows if that means anything. The most common cause for a big discrepancy between TAPSE and s’ is probably technical error, not a clinical distinction.
6. RVSP can be useful as a marker of afterload, but says nothing about the cause of RVSP—high left sided pressures vs high PVR—and also incorporates the RV function, so separating all this out can be difficult.
7. TAPSE/PASP (or TAPSE/RVSP) ratio might be a somewhat more accurate marker of RV/PA coupling, but not really clear if it’s clinically better than using the TAPSE alone, which is already a fair marker of RV/PA coupling. By measuring more things, it also introduces more room for technical error (usually underestimating RVSP), such as the need to estimate the TV gradient and the CVP. More tricuspid regurgitation will also tend to reduce the ratio, without necessarily indicating better RV function.
8. CVP estimates derived from the IVC are very unreliable in the critically ill. Many chronic PH patients have chronically distended IVCs regardless of their RAP. Using a transduced CVP is probably better. You can also just trend the TV gradient as a marker of its own and ignore the CVP component.
9. Shortening of the PA acceleration time (PAAT or PVAT) is a useful marker of pulmonary afterload. Notching of the waveform usually indicates a very high afterload, much more likely to be caused by pulmonary factors than high left heart pressures.
10. Fractional area change of the RV is another tool for approximating the LV “EF” which may work better in chronic dysfunction, where TAPSE may be misleadingly preserved. However, it requires a good view of the RV free wall, which is not always achievable.
11. Strain measurement has not yet penetrated point-of-care ultrasound machines reliably, but use is increasing. While still load-dependent, strain measurement is not angle dependent, which may make it helpful for right heart assessment.
12. In the less common clinical scenario of RV infarction/ischemia, most of the above still applies, yet the pulmonary afterload will not necessarily be elevated. In almost every other case, the problem driving RV failure is usually the afterload, hence reducing the afterload is usually the easiest treatment.
13. A proposed algorithm:
    1. Look for RV dilation
    2. Assess contractility using TAPSE and/or s’ (or other methods like eyeball gestalt, fractional area change, etc)
    3. Assess afterload using PA acceleration time and notching
    4. Compare contractility and afterload in context with the clinical scenario to understand the right heart’s function and conditions, with the understanding that your marker of contractility also incorporates the afterload to some extent.
14. Don’t forget that invasive monitoring, from CVP to a PA catheter, is always an option as well. CVP is “for free” and rarely wrong if you know how to interpret it, including the waveform, and in the sickest patients, a Swan can be quite helpful, particularly for monitoring; multiple advanced echo studies are not always possible or reliable, particularly with rotating shift staff.
15. If you have a Swan, wedge it. Otherwise it’s just a cardiac output monitor. Some fancy newer devices also allow measuring PA and RV pressures separately, which is an evolving science.

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We discuss the practicalities of using airway pressure release ventilation (APRV) with Dr. Rory Spiegel (@EMnerd_), emergency physician and intensivist at MedStar Washington Hospital Center (and EMNerd at Emcrit).

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Takeaway lessons

1. The most immediate benefit of APRV is to help restore lungs to FRC (functional residual capacity). While this can be achieved with PEEP, most people don’t use enough PEEP. APRV proves a higher mean airway pressure while also reducing sedation requirements, and provides a physiologically automatic titration of “PEEP” based on lung compliance.
2. Phigh can usually be set to equal the previous plateau pressure on a conventional mode (assuming reasonably appropriate settings there). This helps match higher Phigh to a more poorly compliant lung and vice versa. The release volume that results should be checked to give a sense of the effects; it should be more or less in the range of normal tidal volumes, although usually lower than your previous tidal volume on a conventional mode due to the intentional air trapping. (If it’s not lower, your Tlow may be set too long, allowing too much release.)
3. Thigh can range from 1.5 seconds to infinity. Longer T-high is better for recruitment, shorter is better for ventilation. When initially flipping to APRV, shorter Thigh is usually needed; try to match the patient’s minute ventilation (from the prior mode) fairly closely, although usually you’ll need to accept a small loss of ventilation. A too-long initial T-high is a common error; patients this sick usually cannot tolerate more acidosis. Usually an initial T-high of 2 seconds is about right.
4. Tlow should be set to terminate when the expiratory flow drops to 75% of the peak expiratory flow (so if the peak was 100 L/s, terminate Tlow when it drops to 75 L/s). This was about the point in pig models where alveolar derecruitment began to occur. Peak and end expiratory flow can be checked on most modern vents, although it may not be easy to find in the screens. Usually the right T-low is around 0.3–0.6 seconds.
5. Occasional patients may need a shorter T-low than this for optimal recruitment. But few need longer; Tlow should rarely be lengthened, even as patients recruit. Although the amount of air trapping will usually increase as the lung becomes more compliant (e.g. the same T-low duration will terminate expiration at 85% instead of 75% of peak expiratory flow), this is usually fine; this is when you’ll start weaning and stretching your Thigh.
6. Plow should be set to zero in almost all cases, allowing the fastest expiration (higher Plow reduces the driving pressure and substantially reduces expiratory flow). In a few vents (older Puritan Bennett, older Servos), the machine may attempt to synchronize with patient efforts by allowing the Tlow to “kick out” and extend, creating large release volumes and loss of desired air trapping. Increasing the Plow may provide some safety margin in this case, although switching from APRV altogether is probably the best solution.
7. As the patient recruits on APRV, release volume should gradually increase despite a fixed Phigh, as the lung recruits. The expiratory flow curve will flatten and the compliance will increase. Thus, release volumes are initially small—”lung protective” in conventional thinking—and later will increase. This increase should be allowed, as it’s still associated with a normal/low driving pressure, since the “PEEP” gradually increases as trapping increases. A large release volume + low driving pressure is felt to be lung protective in APRV thinking.
8. Driving pressure on ARPV can be checked on most vents by performing an expiratory (not inspiratory) hold to determine the effective “PEEP.”
9. Patients can breathe spontaneously on APRV and be comfortable, but this is mostly determined by lung recruitment and how close they are to FRC. When the lungs are still tightly closed, spontaneously breathing will not be either comfortable or safe, so when initially flipped to APRV, patients should NOT be breathing; they will look uncomfortable, require very high minute ventilation, and generate high pressures. (There is also great discomfort here due to the hypercarbia usually unavoidably present.) Use a shorter Thigh and ventilate using the vent releases in this period, while using deep sedation and/or paralysis to suppress breathing.
10. As patients stabilize and recruit, the minute ventilation needed to maintain pCO2 will drop as ventilation becomes more efficient. When MV and the CO2 approach normal physiologic ranges, sedation can be lightened and patients allowed to breathe. Ultimately, severe ARDS patients on APRV require less total sedation and need for paralysis than in other modes.
11. Weaning occurs as thus: CO2 will gradually fall and release volumes naturally increase as the lungs recruit. Eventually they become hypocapnic, so Thigh must be increased to reduce the minute ventilation. As MV reaches normal, stretching the Thigh further causes hypercapnia, so patients should now be allowed to start breathing spontaneously to make up the difference in MV. Breathing should look comfortable, with a benign clinical appearance and gentle inspiratory flows (not sharp peaks); if not, recruitment may not yet be optimal and it may not be time for spontaneous breathing.
12. Rory does not drop the Phigh during the weaning period, although many teach this; he finds it often causes derecruitment. He adjusts Phigh only in response to the perceived disease state; for example, it may need to be weaned as the disease improves and the initial Phigh may start to cause overdistention. He rarely touches it until the patient is ready for breathing. Once the patient is breathing spontaneously, this provides a good feedback tool to adjust Phigh; if you drop Phigh and spontaneous breathing looks worse (like a failed SBT – lower volumes, high rates), you derecruited them and Phigh should go back up. Spontaneous effort is a more sensitive and faster method of feedback than monitoring the release volumes alone.
13. Permissive hypercarbia is okay. But severe hypercarbia before starting APRV is a marker of advanced underlying disease and lung injury which may make it difficult to tolerate APRV, and persistent hypercarbia on APRV is a marker of failure—the lung is not recruiting, and the mode is probably not totally safe as a result (persistent acidosis + persistently high driving pressures and risk of overdistention of ventilated lung).
14. Hypotension is not necessarily a contraindication to APRV. Cardiac output is best when the lungs are at FRC, neither over- or under-distended. However, it’s true that the lungs “overdistend instantly, but recruit over time,” so until the lung recruits, intrathoracic pressure may be elevated, and delicate patients (eg hypovolemic) may not tolerate this well.
15. Pneumothorax should not be a contraindication to APRV. The more recruited the lungs, the less strain on each individual lung unit given the same overall driving pressure.
16. Using APRV is a skill that requires practice. However, it also helps create a general mindset of approaching the lung physiologically with the goal of restoring FRC, as well as appreciating the value of using minute ventilation as a marker of recruitment; these tools probably benefit patients even in other modes. With this approach, APRV can often be avoided, and used mainly as a rescue modality.

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We discuss the field of rehabilitation psychology, and how it can help patients with persistent critical illness, with Dr. Megan Hosey (@DrMeganHoseyPhD), clinical psychologist and assistant professor at Johns Hopkins School of Medicine, where she practices in the medical ICU.

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Takeaway lessons

1. Rehabilitation psychology is a specialty of clinical psychology that generally partners with patients who have acute illness or injury, and helps them adapt to life in these new circumstances. They discuss health behaviors, values and priorities, help patients find paths back to what they love, and assess cognitive and behavioral changes that accompany new illness. In the ICU, they can assist with the psychological aspects of care, particularly in patients with a prolonged stay where psychological factors play an important role in recovery, or for treatment-refractory delirium.
2. Delirium often dominates the patient experience of the ICU. This is primarily an experience of inattention, with relatively little awareness of their circumstances, the day, the context for events, and the presence of often-vivid hallucinations and delusions.
3. ICU care is highly anxiety provoking, with common questions of “when,” “why,” and many other (often unanswerable) questions. The more certainty and structure you can provide, the better.
4. Depression is common as well in longstanding inpatients, and is often better characterized as “hospital demoralization,” a fairly appropriate response to prolonged confinement and limited access to their regular life. This can lead to sensations of helplessness and hopelessness.
5. Motivation can be improved by strategies to reduce the emotional barriers to engagement, while also strengthening their sense of meaning—i.e. what matters to them, and how will their involvement help move towards that?
6. Effective psychological care relies on communication with the patient, and medical measures like tracheostomies and endotracheal tubes can be a barrier. Good care that minimizes sedation and delirium, close involvement from respiratory therapy and speech therapy (with tools like speaking valves), and non-verbal tools like speech boards, eye gaze, yes/nos, etc. are key.
7. Patients with persistent/chronic critical illness appreciate having their schedule set out for the day, to give them a clear sense for what to expect and reduce anxiety.
8. Try to build pleasurable activities into their day, aka “behavioral activation.” Doing things that are meaningful and pleasurable creates a positive feedback loop that enables more activity. Animal therapy, “sunshine therapy” (getting outside), music therapy (or just playing preferred music) are all valuable. Merely asking patients their preferred music and playing it can reduce anxiety and sedation requirement (see Linda Chlan’s work on this)
9. Relaxation strategies can be learned, and in the ICU setting, vital sign monitoring can even be used as a form of biofeedback to appreciate changes in heart rate or respiratory rate in response to stress.
10. Motivational interviewing emphasizes taking control over the aspects of their life that can be controlled.
11. Normalize and validate the difficulty of being in the hospital. (“It is very common for people to feel frustrated, scared, or down in the hospital. This makes sense as you’re away from the people and things that you love, all while not feeling well. We can work together to find ways to help you feel like yourself.”)
12. Create a schedule for the day to establish predictability and reduce anxiety. When possible, getting patient preferences (eg, morning rehab therapies, sitting up to chair for favorite tv show, evening wash up, recreate parts of bedtime routine from home, view church service remotely on Sundays via ipad, etc)
13. Give patients choice over some activities (what time of day rehab therapies? Preferred positions for peri care? pick a length of time to do trach collar trial vs. go as long as you can?)
14. Benzodiazepines as a treatment for anxiety in the hospitalized patient tend to be a short-term solution only, and may ultimately contribute to delirium. SSRIs or similar drugs might be a useful adjunct for patients who describe depressive symptoms like helplessness, hopelessness, worthlessness, guilt, etc.
15. Gentle attempts at reorientation are appropriate for the delirious patient. In more agitated patients, emphatic and repetitive attempts at reorientation are usually not helpful. “Join the journey” (or as the improv comics say, “Yes, and…”) by redirecting benign delusions toward productive ends rather than disputing them. Floridly delirious patients generally cannot comprehend, even if they are able to parrot back information to please the interrogator.
16. Consider implementing a “Get to Know Me” board; see Ognjen Gajic’s work

Resources

1. The Conversation Project: good questions about end of life care wishes
2. Vital Talk: quick guides on effective communication at end of life 
3. American Psychological Association, Division for Rehabilitation psychology: for anyone who has interest about what a rehab psychologist is and what they do
4. PADIS Guidelines
5. ABCDEF Bundle

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We discuss the principles and application of automatic tube compensation (ATC) on modern ventilators, with its creator Ben Fabry. Dr. Fabry is a professor and chair of biophysics at University of Erlangen-Nuremberg, originally trained as an electrical engineer, who originally developed ATC as part of his PhD program.

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Takeaway lessons

1. ATC, originally called “electronic extubation,” is meant to normalize or eliminate the resistance to flow created by the endotracheal tube. Since this resistance is always present, yet is dynamic and varies by flow (and tube size), it creates a continuous confounding variable, making the displayed pressure on the ventilator a measurement not of tracheal pressure, but of another, largely meaningless pressure (the pressure outside the patient).
2. ATC works by increasing airway pressure during spontaneous inspiration to eliminate the pressure gradient created by the tube at the current flow, and reducing it during expiration to reverse the effect.
3. While ATC can be used in any mode, it is mostly meant for pressure support or other spontaneous modes. It has no real role in volume control. In pressure control, it has little meaningful impact during inspiration, although it will reduce the airway pressure below the set PEEP during expiration, which may help facilitate expiration.
4. The original ATC test ventilator could drop pressure below atmospheric pressure during expiration, but this feature is not possible on modern ventilators, so the lowest possible pressure during ATC is zero (probably not quite even, that due to expiratory valve resistance). Some modern vents will not drop pressure during expiration at all.
5. In principal, actual tracheal pressure could be measured by a separate monitoring lumen. In practice, this is dangerous, as the lumen could be occluded by mucus, so the resistance constant is instead applied mathematically. The modifiers were derived empirically by testing a variety of tubes at different flow rates.
6. ATC will generally ask for the tube size. Length has some effect but a fairly trivial one, as resistance is mostly influenced by turbulence, which is mainly a product of diameter. Resistance is not a constant, but increases with (roughly) the square of the flow of gas.
7. A swivel connector on the ETT outlet adds about 1 cm H2O of resistance. An HME adds about 3 cm H2O.
8. Changes in gas composition at different FiO2 changes resistance trivially, although a mix like Heliox would change it significantly, and would make the internal calculations incorrect.
9. No fixed single pressure support value can accurately match tube resistance, due to its dynamic nature during and between breaths, even if you were willing to set the sort of pressure needed—which might be 50+ cm H2O in a strongly breathing patient.
10. The main downside of ATC is that modern ventilators don’t do it very well—they can only vary flow so quickly, so when there are brisk changes in pressure, they fail to match it. They usually can match only about 50% of tube resistance, with the worst at the start of a breath as they lag behind the initial drop in pressure. (You can appreciate this by seeing the airway pressure drop below the set PEEP.) Response is even less in some of the current generation of vents with radial blowers and slower valves
11. Quality check your ATC by watching the tracheal pressure—the vent will display this as a second pressure tracing. It should remain positive above the set PEEP for the whole breath. (The airway pressure should also remain positive, but the tracheal pressure will be a more sensitive marker.) If it becomes negative or drops to the PEEP at any point during inspiration, it implies a failure to fully support the patient. This problem can occur during vigorous spontaneous breathing in any mode, since it’s driven mostly by slow ventilator response; it is just compounded by ATC, because not only does flow have to vary to meet a set pressure, but the set pressure is varying during the breath too. The best way to solve this problem is probably better machines, with faster valves, and maybe situating them closer to the patient (shorter circuits) to speed up responsiveness.
12. When ATC fails to fully support, you can try adding PSV with a very fast rise time, but this is a bludgeon; the best mode is probably flow-proportional assist ventilation with ATC. PAV allows controlling not just tracheal pressure to a constant value, but alveolar pressure; it will further boost the pressure to try and maintain constant alveolar pressure during inspiration. Increase proportional assist until the tracheal pressure no longer drops below the PEEP. (You could achieve a similar effect by “lying” to your ATC and setting a smaller tube size, which will also increase the initial amount of support; but this is less precise and maybe less safe.) PAV plus ATC may be the ideal mode for patients spontaneously breathing without severe lung disease.
13. PAV could be used, by the way, in a patient with bronchospasm (or similar increase in airway resistance from physiologic factors), as it allows you to compensate for any amount of airway resistance you wish. However, it will only do this during inspiration, and will not drop pressure below the PEEP during expiration (i.e. to reduce autoPEEP and aid exhalation). This probably wouldn’t help them exhale anyway, since the resistance is in the lungs, not in the vent.
14. PSV in a weaker patient tends to mask some of their true spontaneous breathing patterns. ATC may unmask these, showing some odd patterns, such as very shallow or rapid breaths. This is not dyssynchrony; it is the true physiologic pattern that was merely being hidden in a less supportive mode. It is also not tiring, at least if the ATC is working correctly and you’re offering adequate support, because they are not experiencing resistance to breathing.
15. If present, a Cheyne Stokes pattern of breathing may also become amplified by the “signal boosting” properties of ATC, rather than being damped by inadequate support. If this results in phenomena like very long apneic pauses, it may (perhaps) be a problem.