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Mechanical ventilation & Cardiopulmonary Interactions. Deborah Franzon, MD Pediatric Critical Care Lucille Packard Children’s Hospital. Overview. Review modes of mechanical ventilation Cardiopulmonary interactions Lesion specific approaches Approach to extubation.
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Mechanical ventilation &Cardiopulmonary Interactions Deborah Franzon, MDPediatric Critical Care Lucille Packard Children’s Hospital
Overview • Review modes of mechanical ventilation • Cardiopulmonary interactions • Lesion specific approaches • Approach to extubation
Anatomy Infant vs adult airways • Anterior and cephalad • Floppy U-shaped epiglottis • Subglottic area narrowest • Increased resistance Poiseulle’s Law R = 1/r4) • Compliant chest wall • Increased VO2 (8ml/kg)
Mechanics of ventilation • Inspiration • Active contraction of diaphragm and intercostal muscles • Generate negative intrathoracic pressure • Expiration • Passive chest wall relaxation • Passive lung recoil
Respiratory failure • Compliant chest cavity limits ability to increase gas exchange • Increased WOB • Increased VO2 • V/Q mismatch ensues • Indication for assisted ventilation
Mechanical ventilation Oxygenation • Determined by inspired oxygen and sufficient mean airway pressure • FIO2 • PIP, PEEP, i-time, flow Carbon dioxide removal • Determined by (Minute ventilation - dead space ventilation)= alveolar ventilation • Rate, TV
Ventilatory support Assisted breaths determined by • Trigger: time, flow, pressure • Cycle: time cycled breaths • Limit--volume or pressure
Modes of Ventilation Volume-limited(SIMV) • Constant flow during inspiration • Square flow wave pattern • Set parameters: TV, rate, PEEP, i-time • PIP--dependent variable • Fixed minute ventilation • Paco2 and pH remain stable
SIMV Mode Mechanical breath Spontaneous breath
Modes of ventilation Pressure Limited (A/C) • Set parameter: PIP, PEEP, rate, IT • Pressure constant throughout • Tidal volume dependent variable • Decelerating flow pattern • Lung compliance and airway resistance determine gas delivery • Theoretically less barotrauma
Modes of ventilation Pressure support ventilation • Decelerating inspiratory flow • Patient triggers breath • Constant pressure delivered • Better patient-ventilator synchrony • Used with volume or pressure mode or weaning mode
SIMV + Pressure Support Mechanical breath Spontaneous breath
Pressure Regulated + Volume Control (PRVC)/APV • Pressure limited • Tidal volume targeted • Decelerating flow waveform • Achieve TV goals without barotrauma, mean airway pressure maintained
Neonates <5.0 kg IT 0.4-0.7 sec I:E ratio 1:1.5-2 PEEP 5 cmH20 PS +6-8 cmH2O TV 8-10cc/kg Rate 25-40/min PIPmax 20cmH20 Infant/Child IT 0.7-1.0 sec I:E ratio 1:2-3 PEEP 5 cmH2O PS+ 5 cmH2O TV 10 ml/kg Rate 15-40/ 8-20 PIPmax 30 cmH2O Initial ventilator settings
Interpreting pressure/volume loops • Effect of PEEP • Increased resistance • Altered compliance • Overdistension • Air leak
PEEP is ideally set at the point of lower inflection point on normal Volume-Pressure curve--shifting entire curve rightward
As resistance increases PIP increase (A to B)--Hysteresis refers to abnormal widening of PV loop
Alterations in compliance affect PIP. Pulmonary edema or ARDS represent decreased compliance states.
Overdistension results in “bird-beaking”, lungs have reached capacity and for added pressure, get no additional lung volume--need to adjust set tidal volume to minimize barotrauma.
Volume does not return to zero--representing leak in system or around endotracheal tube.
High Frequency Oscillatory Ventilation • Pistons generate frequencies of 60-3600 cpm • Tidal volumes 1-3ml/kg • Tidal volumes are less than dead space • Gas exchange via diffusion, convection, penduluft and cardiogenic oscillations • Sinusoidal waveform • Generally decreases oxygenation index
HFOV • Settings: • FIO2 • Frequency (Hz)-- affected by patient size and ventilatory goals • Mean airway pressure--2-5mmHg higher than on conventional ventilation • Amplitude (∆P)--necessary to provide sufficient “jiggle”
Effects of mechanical ventilation • Alteration of lung volume • Changes in ITP (intrathoracic pressure) • Altered acid-base balance • Altered PaO2 • Changes in neurohormonal activity All can affect cardiac function
Intrathoracic pressure changes • Venous return affects RV preload • Pressure gradient between CVP and PRA • Respiratory induced changes in ITP directly effect PRA
Venous return and RV preload Spontaneous inspiration • PRA falls, CVP constant, intra-abdominal pressure increases • Increased pressure gradient increases VR • As PRA approaches zero venous return maximized
Venous return and RV preload Positive pressure ventilation • Inhibits venous return to RA • ITP (+), decreases gradient between PRA and mean CVP, RV filling falls • More pronounced in low output state
Effects of ITP on cardiac function ITP ITP Venous return L/min 3 2 1 Mean filling pressure 5 -5 0 RA pressure
Effect of PEEP on RV preload • Increases intrathoracic pressure • Increases intrathoracic volume • Diaphragm descends • Increases both CVP and PRA • Venour return shifts to right • RV preload decreased
LV Preload Spontaneous Inspiration • RV volume increases • Intraventricular septum shifts leftward • LV compliance and filling fall • “Ventricular interdependence”
LV Preload Positive pressure ventilation • Decreased VR--decreased LV filling • Decreased RV volume--increased LV compliance • Increased lung volume--restricted LV filling
LV afterload • Function of LV transmural pressure(SBP-Ppl) • Spontaneous inspiration • Intrathoracic pressure falls and SBP unchanged and afterload increases • Positive pressure inspiration • intrathoracic pressure increases and afterload decreases
Effect of ventilation on LV Afterload Mechanical Spontaneous SBP =90 SBP =90 Ptm Ptm Ppl -10 Ppl +25 Ptm = 100mmHg Ptm = 65 mmHg
RV Afterload • Determined by Pulmonary vascular resistance (PVR) • PVR affected by lung volume via • Passive compression of pulmonary vessels • Hypoxic vasoconstriction
Pulmonary vascular resistance & functional residual capacity • PVR lowest at FRC • Below FRC (atelectasis) = PVR • Extra-alveolar vessels collapse • Terminal airways close--alveoli collapse--hypoxia-- • Above FRC (hyperinflation) =PVR • Intralveolar vessels compressed
Lung volume and PVR Intra-alveolar vessel resistance Total PVR Pressure FRC Extra-alveolar vessel resistantce Volume
Decrease PVR Hyperventilate Alkalosis PEEP FIO2 Increase PVR Acidosis Hypoventilation Hyperinflation/overdistension Mechanical ventilation PVR
Left-to-right shunts • Increasd PBF • Compression of large airways can occur due to enlarged LA and Pas • TOF/PA/MAPCAS--compression of intrapulmonary bronchi by abnormal vessels • Atelectasis, wheezing, poor gas exchange
Left-to-right shunts • Bronchiolar narrowing from high flows and venous pressure • Causes pulmonary edema • Increased PBF associated with decreased FEV25-75% • Prominent smooth muscle narrowing seen
Single ventricle lesions: s/p Stage I Norwood • Goal of balancing Qp:Qs • Maneuvers to increase/decrease PVR • Optimize Pulmonary Blood Flow? • Hyperventilation • Alkalosis • Increased Fio2 • Inhaled nitric oxide • Optimize cardiac output? • Mild respiratory acidosis • Hypoventilation • Lower Fio2
Bidirectional Glenn--Stage II • Hypoventilation improves oxygenation after bidirectional superior cavopulmonary connection. • Bradley SM, Simsic JM, Mulvihill DM.J Thorac Cardiovasc Surg. 2003 Oct;126(4):1033-9. • The effects of carbon dioxide on oxygenation and systemic, cerebral, and pulmonary vascular hemodynamics after the bidirectional superior cavopulmonary anastomosis. • Hoskote A, Li J, Hickey C, Erickson S, Van Arsdell G, Stephens D, Holtby H, Bohn D, AdatiaJAm Coll Cardiol. 2004 Oct 6;44(7):1501-9. I.
Bidirectional Glenn • Increased PCO2 (45-55 mmHg range) • Permissive hypercarbia improves systemic oxygenation • Improves Qs • Little effect on PVR
Single ventricle: Fontan • Venous return = PBF is “passive” • Minimize positive pressure ventilation and PEEP • Spontaneous ventilation ideal • Early extubation • Adequately volume load pt • Slow rate, adequate tidal volume