How-To: Preoxygenation via SIMV Noninvasive Ventilation

Inspired by a morning report discussion from our very own Lara Vanyo on preoxygenation strategies, I thought it would helpful for a brief run-down on the button-pushing needed to perform preoxygenation by way of noninvasive ventilation. The video below is specific to the vents we have at Sinai–Weingart and Elmer have already shown us how to do the same at Elmhurst on EMCrit.

How-to Video for SIMV Noninvasive Ventilation for Preoxygenation


Picture of SIMV Home Screen on Puritan Bennett 840

Explanation of the Puritan Bennett 840 SIMV Buttons and Settings:

Introduction: The pressure control settings and pressure support settings are the two parts of the NIV settings. The pressure control part runs in the background delivering breaths when the patient is not triggering. The pressure support settings are used when the patient triggers a spontaneous breath.

Rate: Especially important in the hypercapnic patient to control the CO2. The above setting is at 18 breaths per minute, but can be whatever you want.

Pressure Control Settings: This section is for the controlled breaths. PI is the inspiratory pressure that is above PEEP. TI is the inspiratory time that determines how fast a breath is delivered for a pressure control breath. The above setting is IPAP 13 cm H20 and PEEP 3 cm H20 (the Pis above PEEP). The time for controlled breath is 0.9 seconds.

Pressure Support Settings: This section is for the spontaneous breaths (hence support) taken by the patient above the background controlled rate of pressure control. Psupp is the support given to the patient in addition to the spontaneous breath. TI SPONT is the inspiratory time for a supported breath (in contrast to TI of the aforementioned pressure control breath). It is reasonable to set this somewhere between 2.0 and 3.0 seconds depending on patient comfort.

Flow Trigger: VSENS is the flow trigger threshold required prior to breath delivery.

Why pressure control versus volume control for noninvasive ventilation for preoxygenation? After discussing with our respiratory therapist, Judah, volume control is less ideal in noninvasive compared to invasive ventilation as the potential for mask leak in noninvasive introduces potential to inadequately ventilate the patient.

Thanks to Judah, our respiratory therapist, as well as to Dr. Courtney Cassella for the assistance.

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That Vitamin C in Sepsis Newsflash

A number of really bright people are still unsure of what to make about the vitamin C, steroids and thiamine newsflash that’s taken Twitter by storm yesterday. At Sinai here we’re the curious types, so we chatted with our pharmacist who similarly didn’t know what to make of the headlines given the lack of a randomized controlled trial. What follows is some of the ground work that’s been done on animal studies and on the molecular level for vitamin C–just to catch us all up to speed while the news / evidence develops. The EMCrit and PulmCrit posts are certainly deeper dives into the purported vitamin C deficiency abnormalities of sepsis–though, normal is often a philosophical debate. Who knows what the bottom line is at this point given the limited evidence, but the following should be informative background knowledge.

 

Most of this is from the Wilson 2009 paper that predates the recent Marik sepsis media storm:

 

Endothelial health

  • Vitamin C modulates endothelial signaling.
  • Improves microvascular function, capillary blood flow and microvascular permeability barrier.
  • In vitro, vitamin C attenuates the lipopolysaccharide (LPS)-mediated increased endothelial permeability (Dimmler 1995).

 

Capillary blood flow

  • Improves the maldistribution of blood flow
    • The maldistribution initially seen in sepsis is characterized by decreased density of the perfused capillaries with a corresponding increase in the proportion of non-perfused capillaries
    • There is decreased availability of nitric oxide (NO) in endothelial cells / platelets. NO appears to keep microvessels patent.
      • There is decreased NO available inside septic endothelial cells and platelets. This may be secondary to reactive oxygen species.
      • Bolus injection of vitamin C immediately after septic insult improves the capillary blood flow in cecal ligation and puncture rat skeletal muscle.

 

 

Vit C and endogenous vasoactive compounds

  • Vit C may increase vasomotor responsiveness by increasing endogenous synthesis of norepinephrine and vasopressin.
  • Glucocorticoids and vit C may act synergistically inducing SVCT to increase vit C uptake intracellularly and restore glucocorticoid receptor function.

 

 

References

Wilson JX. Mechanism of action of vitamin C in sepsis: ascorbate modulates redox signaling in endothelium. Biofactors. 2009;35(1):5-13.

Wilson JX. Evaluation of vitamin C for adjuvant sepsis therapy. Antioxid Redox Signal 2013;19:2129.

Don’t Forget The Right Ventricle

The Right Ventricle

The right ventricle (RV) has been getting more coverage lately from the Wilcox et al review article in Annals to the continued coverage in many critical care circles where anesthesia and emergency medicine overlap.(1)  Furthermore, the increased presence of VADs and physiology-centric thinking in the resuscitation units of the ED require facility with manipulation of the RV.

Danger with Positive Pressure

The RV’s lower pressures, structural design, and interdependence with the left ventricle (LV) create unfavorable hemodynamic interactions for the RV and positive pressure ventilation.(2) Most easily appreciated when separating preload and afterload, the conceptual challenge with positive pressure is seen in the following diagram from derangedphysiology.com. Intrathoracic pressure from either non-invasive or mechanical ventilation decreases RA preload and increases RV afterload. Proceed with caution when intubating pulmonary hypertension or RV failure patients.

Structure

Anatomically, the RV is crescent-shaped in longitudinal cross-section and triangular in axial cross-section. The deep longitudinal fibers of the RV pull it from apex to base of the heart. Additionally, there is small contribution from inward motion of the RV free wall as well as left ventricular traction on the RV.

Ventricular Interdependence

Compared to the LV, the RV’s thin wall and lower resistance circuit means it contracts throughout systole; it has no isovolumic relaxation phase. Any acute rise in right sided pressures (e.g. PE, tamponade, RV infarct) push the septum to the left, impairing LV diastolic filling and contractility.

References

  1. Wilcox SR, Kabrhel C, Channick RN. Pulmonary Hypertension and Right Ventricular Failure in Emergency Medicine. Ann Emerg Med. 2015;66(6):619-28.
  2. Deranged Physiology: Effects of Positive Pressure Ventilation on Cardiovascular Physiology. Deranged Physiology. http://www.derangedphysiology.com/main/core-topics-intensive-care/mechanical-ventilation-0/Chapter%202.1.7/effects-positive-pressure-ventilation-cardiovascular-physiology. Accessed March 14, 2017.
  3. Ibrahim BS. Right Ventricular Failure. European Society of Cardiology. https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/Right-ventricular-failure. Published December 12, 2016. Accessed March 14, 2017.