Mechanical Ventilation

Ryan J. Magnuson, DOUniversity of Rochester Medical Center

Assistant Professor of MedicineDivision of Critical Care Medicine

Ryan_Magnuson@URMC.Rochester.edu

Disclosures

None

Objectives

Understand the cardio-respiratory interaction Appreciate the influence of mechanical

ventilation on this dynamic Predict the likely cardiovascular effects of

mechanical ventilation Tailor ventilatory strategies to individual

cardiovasc-pulmonary conditions

Background

Respiration and circulation are complementary processes

Continuous interactions

Mechanical ventilation increases the complexity of these interactions

Paucity of strong-quality studies related to PPV in CICU

Background

Background Mechanical ventilation has significant

hemodynamic side-effects depending on the cardio-pulmonary status of patient

Most important clinical variables are Cardiovascular status Pulmonary status Mode of mechanical ventilation

Need to share the space (thorax) with lungs, vasculature and heart

Pulmonary MechanicsGeneral overview

Pulmonary MechanicsGeneral overview

Thoracic Anatomy and transmural pressure: Series of pumps with

pressure having direct influence on RV and LV volume and function

Duke, Crit Care and Resuscitation, 1999

Pulmonary MechanicsCardiovascular effects of spontaneous breathing

Inspiration: Facilitates RV

diastolic filling by the ‘thoracic pump’ mechanism

Pulmonary MechanicsCardiovascular effects of spontaneous breathing

Increase RVEDV increase SV and subsequent rise in pulmonary flow

Pulmonary MechanicsCardiovascular effects of spontaneous breathing

Spills into LVEDV

(preload, after delay 1-2 beats)

Pulmonary MechanicsCardiovascular effects of spontaneous breathing

Increase LV afterload thru change in transmural P

(must be overcome during systole)

Expiration Return of LV afterload to baseline, augmented

LV preload

Pulmonary MechanicsCardiovascular effects of spontaneous breathing

Pulmonary MechanicsCardiovascular effects of spontaneous breathing

Healthy subjects: Inspiratory fall in aortic blood flow and systolic

blood pressure Positive change in pleural pressure Opposite from the negative change seen in

spontaneous breathing

Pulmonary MechanicsCardiovascular effects of mechanical ventilation

Mechanisms of positive change in pleural pressure Reduced LV preload

***Predominate mechanism Reduced RV preload Increased PVR and R

impedance Ventricular interdependence

Pulmonary MechanicsCardiovascular effects of mechanical ventilation

Duke, Crit Care and Resuscitation, 1999

RVEDV transient reduction

LVEDV sustained reduction (LV afterload, preload reduced)

Spontaneous inspiratory effort

Pulmonary MechanicsCardiovascular effects of mechanical ventilation

Net effect of PEEP on CO depends on RV/LV function, preload, afterload and ventricular interdependence Atelectasis increase PVR d/t poor

compliance and hypoxia

Pulmonary MechanicsRole of PEEP

Very high PEEP causes microvascular collapse d/t alveolar overdistention and increase PVR

Pulmonary MechanicsRole of PEEP

Alviar, JACC, 2018

Decrease venous return and decrease RV preload “Best PEEP” resulting in optimum oxygen

transport without decrease in cardiac output; PEEP < 10

Pulmonary MechanicsRole of PEEP

Alviar, et al. J Am Coll Card, 2018.

Hypoxic vasoconstriction

Pulmonary MechanicsOxygenation

Harms of hyperoxia include: Direct lung toxicity (interstitial fibrosis,

tracheobronchitis) Peripheral vasoconstriction Reactive oxygen species

Pulmonary MechanicsOxygenation

Pulmonary Mechanics: Oxygenation

Rationale: To assess whether a conservative protocol for oxygen supplementation could improve outcomes in critically ill patients N=480 patients with anticipate >72h ICU stay

Primary outcome: ICU mortality Secondary outcomes: New organ failure, infection

RANDOMIZATION

Conventional(Control Group):

• Patients received an FiO2 of at least 0.4, allowing Pa02 values up to 150mmHg and an SpO2 90-100%

• If SpO2 decreased <95%, FiO2 was increased to reach target SpO2 value

Conservative (Protocol Group):

• Oxygen therapy was administered at the lowest possible Fi02 to maintain the Pa02 between 70 and 100mg Hg or SpO2 values 94-98%.

Pulmonary Mechanics: Oxygenation

Pulmonary Mechanics: Oxygenation

Meta-analysis of 25 randomized controlled trials including 16,037 patients with sepsis, critical illness, stroke, trauma, MI, cardiac arrest or emergency surgery

Compare conservative oxygen strategy to liberal oxygen strategy

Primary outcome: In-hospital mortality

Pulmonary Mechanics: Oxygenation

Pulmonary Mechanics: Oxygenation

Pulmonary Mechanics: Oxygenation

Multicenter, prospective cohort study of adult patients with cardiac arrest who were mechanically ventilated and received targeted temperature management after return of spontaneous circulation N=280

Primary Outcome: Neurology function at time of discharge

PaO2 measured at 1 and 6 hours after return of spontaneous circulation Hyperoxia defined as PaO2>300 mm Hg during the

initial 6 hours after return of circulation 38% of patients in the cohort had exposure to

hyperoxia Poor neurologic outcome defined as modified

Rankin Scale score >3 Occurred in 70% of patients in the entire cohort

Pulmonary Mechanics: Oxygenation

Hyperoxia was independently associated with poor neurological function (RR 1.23, 95% CI 1.11-1.35)

Pulmonary Mechanics: Oxygenation

Grey bar = no hyperoxiaBlack bar = hyperoxia

Poor neurologic function occurred in: 77% in with exposure to hyperoxia 65% in patients without hyperoxia

One hour longer duration of hyperoxiaexposure was associated with 3% increase risk in poor neurologic outcome Association with poor neurologic outcome

began at ≥300 mm Hg

Pulmonary Mechanics: Oxygenation

Acidosis: pH < 7.2 Causes contractile depression

Alkalosis: Positive inotropic effect Effect is relatively modest in comparison with

the depressive effect of acidosis

Pulmonary Mechanics: pH

Pulmonary Mechanics: pH

PO2

PO2

ACIDOSIS ALKALOSIS

NORMAL STATE

Clinical implications: Acidosis increases PVR whereas PCO2 < 60

improves PVR Hypercapnia causes venoconstriction that can

lead to cardiac overload and pulmonary edema

Malik AB, pulmonary hemodynamics of intact dogs, Can J Physiol Pharmacol 1973

Pulmonary Mechanics: pH

Pulmonary MechanicsTidal Volume

Retrospective study of the effects of tidal volume on mechanically ventilated patients with CHF or cardiac arrest in a single tertiary care CICU N=51 patients Median Vt 9.3 mL/kg

Overall mortality 29% Mortality 23.1% for patients with VT/PBW <median Mortality 36% for patients with VT/PBW >median P=0.31

OR for death was 9.0 with VT/PBW >median (p=0.03)

Shorofsky, Acute Cardiac Care, 2014

Pulmonary MechanicsTidal Volume

Retrospective analysis of the effect of tidal volume on neurologic outcomes in patients admitted after out of hospital cardiac arrest

Propensity-adjusted analysis of mean Vt in first 48 hours of admission

N=256 38% of patients received time-weighted average

Vt > 8ml/kg PBW during first 48 hours

Beitler, AJRCC, 2017

Pulmonary MechanicsTidal Volume

Outcomes: Lower Vt independently associated with more

favorable neurocognitive outcome (cerebral performance category of 1 or 2 at discharge) OR 1.61, P=0.008

Lower Vt associated with more ventilator-free days P=0.012

Lower Vt associated with more shock-free days P = 0.034

Beitler, AJRCC, 2017

Pulmonary MechanicsTidal Volume

Prospective, observational study of in-hospital cardiac arrest patients evaluating the relationship between time weighted average Vt per PBw over first 6h and 48h post-arrest and neurologic outcomes N=185

Vt over first 6h was 7.7 36.8% of patients received an average Vt >8.0ml/kg

Vt over first 48h was 7.6 38% received an average Vt >8ml/kg

Moskowitz, Resuscitation, 2018

Pulmonary MechanicsTidal Volume

No relationship between Vt/PBW over the first 6 or first 48 hours and neurologic outcomes was identified P=0.89 for 6 hours P=0.83 for 48 hours

Additional investigation is needed with respect to other potential benefits of low-Vt post IHCA.

Moskowitz, Resuscitation, 2018

Pulmonary MechanicsTidal Volume

Vt/PBW compression of pulmonary vessels and increase PVR

Pulmonary MechanicsTidal Volume

Adapted from Alviar, JACC, 2018

SummaryMechanism Effect

Direct effects from PEEP

• LV afterload• LV diameter causing decreased MR• transmural pressure• Palv at the end of expiration

• LV unloading• Improved cardiac output• Improved compliance

Gas exchange effects

• Reverses hypoxic vasoconstriction• preload• Improved ventilation and perfusion

matching

• Lower RV afterload• Improved pulmonary

congestion• Improved oxygenation

Effects fromventilatorysupport

• Improved work of breathing• Improved hypercarbia and acidosis

• Improved tissue perfusion• myocardial consumption

of oxygen• Improved RV afterload

Systemic effects

• Optimized gas exchange and effects on oxygenation and tissue perfusion

• Improved metabolic demand and peripheral perfusion

Adapted from Alviar, JACC 2018

General Treatment Principles

Maintain spontaneous inspiratory effort to mitigate PPV and its adverse CV effects LTVV Pplat < 30 Optimize CVP and MAP Alternate modes of PPV

Avoid ventilator-associated adverse events HOB SAT, SBT Early mobilization

Mechanical support ECLS

General Treatment Principles

Case ConsiderationsCASE #1

62yo male – HOCM, AoR Septal myomectomy, AVR Open chest

Central VA ECMO

CASE #1

Ventilator Management: Considerations: Open chest? ECMO?

CASE #1

CASE #1 continued

Ventilator adjustments: Example #1

Therapeutic interventions: Bronchoscopy

CASE #1 continued

CASE #1 continued

CASE #1 continued

CASE #2

74yo female AVR

CASE #2

Ventilator Management: Considerations: Post-op Vent weaning

CASE #2

36yo male OHCA (Vfib) Coronary angiogram without obstruction

CASE #3

CASE #3

Ventilator Management: Considerations: Cardiac arrest Hyperoxia

CASE #3

CASE #4

58yo male AMI c/b cardiogenic shock VA ECMO (explanted), Impella Aspiration, CPE, possible reactive airway

disease

CASE #4

CASE #4

Ventilator Management: Considerations: Echo

RV failure

Flolan

32yo female NICM s/p VAD Acute CHF

CASE #5

CASE #5

CASE #5

Ventilator Management: Considerations: CPE

39yo male Advanced testicular cancer ARDS

CASE #6

CASE #6

CASE #6

Ventilator Management: Considerations: ARDS

CASE #6

23yo male Acute lymphoblastic leukemia Pancreatitis with subsequent massive PE

CASE #7

CASE #7

CASE #7 Ventilator Management: Considerations: Massive PE

45yo male, no PMH Influenza, severe CAP VV ECMO

CASE #8

CASE #8

Ventilator Management: Considerations: ECMO, ‘Lung rest’

CASE #8

Conclusion Each MV setting has both intended benefits

and potential AE. Need to assess patient’s response to MV and risk of complications by re-eval including hemodynamics, blood gas, mechanics/pressures and patient-vent interactions.

CVP > 10 for preload optimization Vasopressors and inotropes to goal MAP > 60 Pulmonary vasodilators

Conclusion

Effects of PPV on cardiopulmonary physiology so that MV can be tailored to optimize hemodynamics, oxygenation and ventilation. Critical care cardiology continues to evolve

and dedicated MV strategies need to be defined in the CICU

Questions?