CardioNerds Spotlight: Positive Pressure Ventilation in the CICU

In this episode, experts discuss the basics of mechanical ventilation, including the physiology/pathophysiology of negative and positive pressure breathing, a review of ventilator modes, and a framework for outlining the goals of mechanical ventilation. They also apply these principles to patients in the CICU, focusing on those with RV predominant failure due to pulmonary hypertension and patients with LV predominant failure.

Join Drs. Eunice Dugan and Dr. Karan Desai—along with CardioNerds Co-founder Dr. Amit Goyal—as they speak Dr. Sam Brusca, who completed his NIH Critical Care and UCSF Cardiology fellowship and is currently faculty at UCSF; Dr. Burton Lee, Head of Medical Education and Global Critical Care within the National Institutes of Health Critical Care Medicine Department and master clinician educator with the ATS Scholar’s Critical Care for Non-Intensivists program; and Dr. Chris Barnett, ACC Critical Care Cardiology council member and Section Chair of Critical Care Cardiology at UCSF; as they discuss how the CICU has evolved to include patients with complex pulmonary mechanics.

Audio editing by CardioNerds Academy Intern, student doctor, Shivani Reddy.

Pearls and Quotes

● Respiratory distress, during spontaneous negative pressure breathing can lead to high transpulmonary pressures and potentially large tidal volumes. This will increase both RV afterload (by increasing pulmonary vascular resistance) and LV afterload (by increasing LV wall stress).

● An analogy for the impact of negative pleural pressure during spontaneous respiration on LV function is that of a person jumping over a hurdle. The height of the hurdle does not increase, but the ground starts to sink, so it is still harder to jump over.

● Intubation in patients with right ventricular failure is a tenuous situation, especially in patients with chronic RV failure and remodeling (increased RV thickness, perfusion predominantly during diastole, RV pressure near or higher than systemic pressure). The key tenant to safe intubation is avoiding hypotension, utilizing induction agents such as ketamine or etomidate, infusing pressors, and potentially even performing awake intubations.

● Non-invasive positive pressure ventilation in HFrEF has hemodynamic effects similar to a cocktail of IV inotropes, dilators, and diuretics. CPAP decreases pulmonary capillary wedge pressure (LV preload), decreases systemic vascular resistance (afterload), and increases cardiac output.

● Airway pressure during mechanical ventilation is based on the “equation of motion”: Pressure = Volume/Compliance + Flow*Resistance + PEEP.

● Our goals of oxygenation on mechanical ventilation include achieving acceptable PaO2/Sat with the lowest FiO2 possible (avoiding oxygen toxicity) and optimal PEEP (which increases oxygenation but can have detrimental impact on cardiac output)

● Our goals of ventilation on mechanical ventilation include achieving acceptable pH and PaCO2 while preventing ventilator induced lung injury and avoiding auto-PEEP. We prevent lung injury by reducing tidal volume (ideally <8cc/kg, plateau pressure < 30 cmH20, driving pressure < 15 cmH20) and auto-peep by reducing respiratory rate (and allowing for full expiration).

● No ventilator mode is “superior” to the others. What is most important is that providers are comfortable with the applied mode and able to appropriately respond to active changes in patient effort and mechanics.

Show Notes

1. What are the hemodynamic effects of Negative Pressure breathing in the RV and LV?

● RV
o Negative pleural pressure is transmitted to pericardium and RV
o Negative pleural pressure is also transmitted to the pulmonary vasculature
o Thus, the pressure drop is net neutral across the RV-PA circuit and does not affect afterload
o However, large negative pleural pressure swings still lead to increased transpulmonary pressure, increased lung volumes, and associated increased PVR (RV afterload).

● LV
o Negative pleural pressure is transmitted to the pericardium and LV
o Negative pleural pressure is NOT transmitted to the extra-thoracic aorta
o Transmural pressure across the LV increases and the gradient for flow from LV to distal aorta decreases (as LV pressure drops but distal aorta doesn’t)
o Overall, this increases LV afterload

2. What are the hemodynamic effects of Positive Pressure breathing on the RV and LV?

● RV
o Positive pressure is transmitted to the pericardium and the RV
o Positive pressure is transmitted to the pulmonary vasculature
o Thus, the pressure increase is net neutral across the RV-PA circuit and does not affect afterload
o However, positive pressure and increased transpulmonary pressure with instilled flow/volume increases PVR (RV afterload)
o Notably, PVR and lung volume can graphically be illustrated as a U-shaped curve. PVR initially decreases as volume is instilled toward functional residual capacity (FRC), with traction of extra-alveolar vessels. As lung volume increases above FRC, PVR increases, with intra-alveolar vessel compression
● LV
o Positive pressure is transmitted to the pericardium and the LV
o Positive pressure is NOT transmitted to the extra-thoracic aorta
o Transmural pressure across the LV decreases and the gradient for flow from LV to distal aorta increase (as LV pressure increases but distal aorta doesn’t)
o Overall, this decreases LV afterload

3. Is NIPPV useful in patients with heart failure?

● Though studies have been inconsistent, there is likely a benefit (reducing intubation +/- mortality) for implementing NIPPV in acute decompensated heart failure
● Given the hemodynamic benefits outlined above, positive pressure administered via modalities such as CPAP and Bi-PAP improve LV function
● Preload decreases (positive pressure decreases inflow into the RA), Wedge pressure decreases, SVR decreases, and Cardiac output increases
● CPAP is primarily needed for oxygenation; however, Bi-PAP can augment ventilation and of-set increased work of breathing
● Importantly, NIPPV should not unnecessarily delay intubation in patients who are failing, as this delay likely increases mortality across patient populations.

3. What are the Oxygenation Goals of Mechanical Ventilation?
● To achieve acceptable PaO2 and SaO2 (>65 mmHg, >92-94%), whilst avoiding inspired oxygen toxicity (FiO2 > 60%)
● Oxygenation is primarily impacted by FiO2 and PEEP. PEEP can be titrated to aide in reducing FiO2, though can have negative impacts on cardiac output by reducing venous return

4. What are the Ventilation Goals of Mechanical Ventilation?
● To achieve acceptable PCO2 and pH without causing harm (ventilator induced lung injury)
● We avoid ventilator induced lung injury by reducing tidal volume (ideal < 8 cc/kg), reducing mechanical power (respiratory rate), reducing plateau pressure (< 30 cmH20), reducing driving pressure (< 15 cmH20), and reducing repeated alveolar opening/closing (by having adequate lung recruitment)
● Ventilation is primarily impacted by TV and respiratory rate, which equate to minute ventilation

5. How can we calculate Airway Pressure using the Equation of Motion as related to Mechanical Ventilation?
Airway Pressure = V/C + FxR + PEEP
V/C = TV/Compliance and represents the alveolar pressure of the lung generated by a given TV at a given static lung compliance
FxR = Flow x Resistance and is akin to Ohm’s law (V=IR), representing the pressure due to dynamic/resistive forces in the larger airways
PEEP is the pressure starting point at the beginning of the inspiration

6. What considerations need to be taken when intubating a patient with RV Failure/Pulmonary Hypertension?
● – Intubation should be avoided if possible (though notably, respiratory distress and spontaneous breathing is not necessarily preferable, especially in the setting of respiratory acidosis or excessively low lung volumes)
● – Reliable vascular access and in-line pressors are key to avoiding hypotension during induction
● – Rapid sequence intubation (RSI) drugs such as etomidate and ketamine are preferred to propofol
● – Awake intubation is safest if feasible

References
1. Alviar CL, Miller PE, McAreavey D, et al. Positive Pressure Ventilation in the Cardiac Intensive Care Unit. J Am Coll Cardiol. Sep 25 2018;72(13):1532-1553. doi:10.1016/j.jacc.2018.06.074

2. Barnett CF, O’Brien C, De Marco T. Critical care management of the patient with pulmonary hypertension. Eur Heart J Acute Cardiovasc Care. Jan 12 2022;11(1):77-83. doi:10.1093/ehjacc/zuab113

3. Bradley TD, Holloway RM, McLaughlin PR, Ross BL, Walters J, Liu PP. Cardiac output response to continuous positive airway pressure in congestive heart failure. Am Rev Respir Dis. Feb 1992;145(2 Pt 1):377-82. doi:10.1164/ajrccm/145.2_Pt_1.377

4. Esteban A, Frutos-Vivar F, Ferguson ND, et al. Noninvasive positive-pressure ventilation for respiratory failure after extubation. N Engl J Med. Jun 10 2004;350(24):2452-60. doi:10.1056/NEJMoa032736

5. Girardis M, Busani S, Damiani E, et al. Effect of Conservative vs Conventional Oxygen Therapy on Mortality Among Patients in an Intensive Care Unit: The Oxygen-ICU Randomized Clinical Trial. JAMA. Oct 18 2016;316(15):1583-1589. doi:10.1001/jama.2016.11993

6. Investigators I-R, the A, New Zealand Intensive Care Society Clinical Trials G, et al. Conservative Oxygen Therapy during Mechanical Ventilation in the ICU. N Engl J Med. Mar 12 2020;382(11):989-998. doi:10.1056/NEJMoa1903297

7. Schjorring OL, Klitgaard TL, Perner A, et al. Lower or Higher Oxygenation Targets for Acute Hypoxemic Respiratory Failure. N Engl J Med. Apr 8 2021;384(14):1301-1311. doi:10.1056/NEJMoa2032510

Original Source: https://www.cardionerds.com/227-ccc-positive-pressure-ventilation-in-the-cicu-with-dr-sam-brusca-dr-chris-barnett-and-dr-burton-lee/