Disclosures. ICU Management of Advanced Lung Disease 5/9/2015. No Disclosures. All pictures from commercial sources

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1 Disclosures ICU Management of Advanced Lung Disease No Disclosures All pictures from commercial sources Lundy J. Campbell, MD UCSF Department of Anesthesia and Perioperative Care Division of Critical Care Medicine Why Are Patients with ILD Admitted to the ICU Progression of chronic disease Acute precipitating event Leading to exacerbation on top of underlying disease Acute infection Rapidly worsening symptoms (< 30 days) New bilateral opacities on imaging No other identifiable cause Fig. 3 High-resolution computed tomography of the chest of a patient with IPF who developed an acute exacerbation. HRCT sections (left) done at baseline show areas of bilateral, subpleural, intralobular septal thickening and honeycomb cysts (arrow showing... Ritesh Agarwal, Surinder K. Jindal Acute exacerbation of idiopathic pulmonary fibrosis: A systematic review European Journal of Internal Medicine, Volume 19, Issue 4, 2008,

2 Overall Treatment Goals Treat underlying causes of exacerbation Continue to support patient Treat sequelae of exacerbation Hypotension Hypoxia Hypercarbia MOSF Limited Treatment Options Broad spectrum antibiotics Steroids Cyclosporine and cyclophosphamide Pirfenidone Supportive care Lung transplantation (?) ECMO (?) Agarwal, Jindal. Eur J Int Med2008 Problems Encountered Hypoxia, Hypercarbia, Hypotension Worsening pulmonary hypertension RV Ischemia RV dysfunction RV/LV failure Date of download: 5/7/2015 Copyright American College of Chest Physicians. All rights reserved. Prevalence and Outcomes of Pulmonary Arterial Hypertension in Advanced Idiopathic Pulmonary Fibrosis * Chest. 2006;129(3): doi: /chest Figure Legend: PAH as a predictor of survival in patients with IPF. 2

3 The Right Ventricle Low-pressure Usually 20/8 mmhg Thin-walled Dependent on septal architecture for proper function/ejection Decreased CPP RV Ischemia Decreased RV Output Decreased LV Output Hypotension PH/RV Dysfunction Few options for treatment Goal: Increase RV perfusion, decrease RV afterload Without decreasing LV output Respiratory Failure Tx Avoid intubation if at all possible If able use noninvasive ventilation modes HFNC NIPPV Mechanical Ventilation 3

4 High Flow Nasal Cannula Provides high levels of inspired O2 Provides small degree of CPAP Can be used with inhaled pulm vasodilators Patient comfort NIPPV More reliable: Delivered oxygen Ventilation Delivery of inhaled pulm vasodilators Limited by: Still has issues with ppv Patient compliance Skin breakdown from tight-fitting mask Difficulty taking po Intubation/Induction of Anesthesia Very Risky Patients have little reserve Desaturate quickly Become hypercarbic V/Q changes Increased pulm resistance Decreased LV preload and afterload Decreases RV perfusion RV Failure Inability to perform adequate CPR Hypoxia and Mechanical Ventilation Lung protective ventilation Low V t (~6-8 cc/kg) Minimize P plat (< 30cm H 2 O) Many salvage therapies HFOV, prone ventilation Selective pulmonary vasodilators Different modes of mechanical ventilation 4

5 Practical Considerations Avoid dysynchrony Sedation, +/- paralysis PEEP and PCV may help Selective pulmonary vasodilators ECMO/transplant (?) Little role for: Prone ventilation HFOV Mechanical Ventilation and the Right Ventricle Liu, L. et al. Anesth Analg2010. Jardin and Vieillard-Baron. Applied Physiol in Int Care Med 2006 Mechanical Ventilation and the Right Ventricle Monitoring Goal is to monitor PAP Ultimately RV function Red-light rule: If PASP > 2/3 LVSP (or mean pressures) then RV at risk for becoming ischemic Jardin and Vieillard-Baron. Applied Physiol in Int Care Med

6 Monitors for PH Arterial line Essential to know beat to beat pressure. If RV doing poorly, BP will rapidly fall CV access May need to rapidly and reliably give inotropes and pulmonary vasodilators Change in RAP may reflect change in RV function PAC May need to guide therapy of pulmonary vasodilator Use depends on pre-op state of RV If RV suspect or impaired, then essential Treating RV Failure Pulmonary vasodilators Inhaled nitric oxide (if you have it) Milrinone (will also decrease SVR), dobutamine Inotropic support Many opinions, little data Epi, norepi, dobutamine, milrinone Don t forget vasopressin Will increase SVR but not PVR Pulmonary Vasodilators No selective IV agents Systemic vasodilation Worsen V/Q mismatch Inhaled nitric oxide is ideal Expensive Not widely available Associated with renal dysfunction Inhaled prostacyclin, iloprost Require frequent or continuous administration Inhaled Pulmonary Vasodilators Inhaled NO Direct pulmonary vasodilator Ultra-short duration of action Does not leave pulmonary circulation $$$$$ Inhaled Flolan Cheap Just as effective as ino Messy: Requires separate delivery system Hard to dose directly Dose: ng/kg-min Wouters, et al. Intensive Care Med

7 Vasopressors Maintain systemic BP to ensure myocardial perfusion Restore normal ventricular architecture α-adrenergic agents will affect PVR and SVR Vasopressin (at low doses) may be preferable Less impact on PVR vs. SVR Wouters, et al. Intensive Care Med 2008 Inotropes Decrease PAP Increase RV Systolic Function Dobutamine (Beta-1 Agonist) Short duration of action, rapid onset Good inotropy May cause systemic vasodilation Arrythmogenic Milrinone (PDE III Inhibitor) Long duration of action Excellent inotropy Less chronotropy Systemic vasodilation esp. with loading dose Epinephrine May increase RV output Low dose vasodilation Vasopressors Fluid Balance Phenylephrine Familiar to everyone Increases PVR as well as SVR Norepinephrine Very effective Increases SVR>PVR Vasopressin Increases SVR with no effect on PVR Patients frequently have decreased SVR Hypotension Low UO Require careful fluid adminstration Lung functions better dry RV volume overload worsens RV and LV function 7

8 Ventricular Interdependence in RV Failure Fluid Therapy Slow controlled fluid administration Use of vasopressors/inotropes May need diuresis Improve cardiac output May require early initiation of dialysis (CRRT) Often can not wait for renal function to return Haddad F et al. Circulation. 2008;117: Copyright American Heart Association, Inc. All rights reserved. Acidosis Worsens bi-ventricular function Combination of respiratory and metabolic causes May need to treat aggressively Careful with bicarbonate administration THAM (tris-hyroxymethyl aminomethane) 0.3 mol/l solution Initial loading dose (ml) = lean body wt (Kg) x base deficit Dialysis Needs to be a bridge to something: Transplantation / Recovery Little benefit without transplantation Allows for mobilization and rehabilitation Early referral is critical Role for ECMO 8

9 Supporting the RV: Summary Minimize elevations in PVR Optimize RV afterload Avoid hypothermia, hypoxia, hypercarbia, and acidosis Maintain SVR and normal systemic BP Optimize perfusion of the RV Coronary perfusion dependent on diastolic blood pressure Avoid excessive fluid overload Avoid hypervolemia and RV dilatation which can worsen systolic function High ventilatory pressures can increase RV work and PA pressures Questions? Fischer, et al. Anesth Analg