Ventilator management of acute respiratory failure in a case of

eosinophilic bronchopneumopathy

Signalment and history

‘Mr Magoo’18mth NM Great Dane

• productive cough for 7 days

• progressive dyspneaover last 12 hours

• no travel history, fully vaccinated, no previous medical problems

Physical exam findings

• poorly responsive

• sinus tachycardia @ 170bpm →ventricular bradycardia @ 40bpm

• severe tachypnea and dyspnea, minimal to no improvement with flow-by oxygen

• generalized crackles and wheezes all lung fields, cardiac auscultation difficult

• impending respiratory failure

Initial intervention•ketamine/valium induction, intubation and

manual ventilation via AMBU bag on 100% 02

Differential diagnosis•acute CHF•generalised pneumonia- bacterial, fungal,

aspiration•ARDS- but no concurrent predisposers identified•lung lobe torsion•neoplasia•small airway disease ????? atypical presentation

Arterial blood gas• Severe respiratory

acidosis- partial metabolic compensation

• Significant hypercapnia-hallmark of hypoventilation

• A-a gradient= 453mmHg (normal <150 on 100% O2)

• Hypoventilation + venous admixture

Bronchoscopy

• Mucosal hyperemia and thickening

• Diffuse airway hemorrhage, suspected secondary to increased transmural pressure and mucosal capillary rupture during acute respiratory distress

• Quantity of mucoidsecretions at carina

• Exaggerated concentric airway closure during expiration

BAL cytology

Hypoventilation- mechanisms• Alveolar ventilation = frequency X (tidal volume –

(anatomic dead space + physiologic dead space))

• Reduced by

– Reduced tidal volume• respiratory m. failure

• dynamic hyperinflation

• Increased resp frequency -esp in context of prolonged expiratory time

– Increased anatomic dead space- ET tube/Y piece

– Increased physiologic dead space- areas of high V/Q or shunt

Dynamic hyperinflation

Dynamic hyperinflation/ intrinsic PEEP predispositions

• Small airway inflammation/ secretions/ collapse

• High respiratory rate

• Short expiratory time

• Large I:E ratio

• Patient/ ventilator asynchrony and breath stacking

Effects of dynamic hyperinflation

• ↑ end expiratory volume

• ↓tidal volume, with tidal ventilation occurring near total lung capacity

• ↓venous return and compromised cardiac output→ hemodynamic collapse and arrest

• Inspiratory muscles placed at a mechanical disadvantage- inefficient force/length relationship

• Increased risk of barotrauma, non-cardiogenic edema, pneumothorax

• Increased pulmonary hypertension, increased RV load

Elevated V/Q ratioNormal V/Q=1.0

Areas of V/Q of 10-40 in acute small airway disease

Compromised RV functionNormal Dynamic hyperinflation

•Acute RV failure

•Acute tricuspid regurgitation

•Right atrial stretch-arrhythmogenesis

Ventilator strategies to minimise dynamic hyperinflation

Prolong expiratory time by• Reducing respiratory rate- sedation/ NM blockade

• Decreasing inspiratory/expiratory ratio- prolong expiratory times

• Increase inspiratory flow rate

Maximise patient/ventilator synchrony by• Applying PEEP at 50% of intrinsic PEEP value to reduce

effort of ventilator triggering if spontaneously breathing

• Aggressive NM blockade and ventilation in mandatory-only mode

Strategies to reduce airway inflammation, secretions and bronchospasm

• Parenteral steroids prednisolone sodium succinate 1mg/kg IV Q12

• Nebulisation of bronchodilators + acetylcysteine + steroids (topical effect=5X systemic)

• Maximisation of airway hydration

• Periodic mechanical insufflation- from +40 to -40cm H2O ‘milking’ effect on airways

• Patient mobilisation

Additional therapies

• Pre-emptive pleural catheter in the face of high airway pressures and risk of alveolar rupture/ tension pneumothorax

• Continuous tracheal insufflation of O2 via catheter positioned at carina- increased deadspace washout of CO2

• Sodium bicarbonate low 0.5mEq/kg dose

Positives

• Protective against increased cerebral blood flow and ICP elevations associated with hypercapnic acidosis post anoxic brain injury

• May relieve severe pulmonary hypertension exacerbated by hypercapnic acidosis mediated pulmonary vasoconstriction

• Treats decreased contractility of cardiac and vascular muscle ?

Respiratory acidosis- NaHCO3 ?

Negatives

• Effectiveness depends on ability to eliminate CO2

• May raise PaCO2 in the context of hypoventilation

• May correct arterial pH but worsen intracellular acidosis

• Removal of the acidosis-mediated protective effects of hypercapnia on the cardiovascular system

• Extracellular pH may not reflect intracellular

Effects of hypercapnic acidosis• Augmentation of pulmonary hypoxic

vasoconstriction, reducing shunt• Increased lung compliance -surfactant• Protective against pulmonary ischemia/

reperfusion injury• Facilitation of O2 unloading to tissues via Bohr

effect on Hb dissociation curve• Elevated cardiac output mediated through

endogenous catecholamine release, same effect reduces GFR and increases renal fluid retention

• Increased cerebral tissue, intestinal wall and renal PO2

• Protective vs cell death in anoxic hepatocytes

Monitoring of ventilation• PaO2/ FiO2 ratio

<200 ARDS, <300 ALI

• Oxygen Index Pmean %O2-------------------------

PaO2

normal <2.0

• Dead space fractionVD/VT=(PaCO2-PECO2)/PaCO2

• Rapid shallow indexf/VT<105 without mechanical

support via ET tube

Progression in ventilatory indices

Indices Hour 1 Hour 30 Hour 60

PaO2/FiO2 131 283 346

Oxygen index 8.3 2.8 2.3

Dead space fraction 82% 32% 7%

Overview of eosinophilicbronchopneumopathy

• Aetiology uncertain, suspected hypersensitivity to aerosolized antigens

• Increased CD4+:CD8+ T cell ratio

• ↑MMP activity → collagenolysis/proteolysis with airway destruction/remodeling

• ↑eosinophil specific chemokines

• Gender bias towards females

• Average age at presentation 4-6 years (range 3mths-13yrs)

• Cough +/- nasal discharge

• Diagnosis on BALF cytology

• R/O heartworm dx

• R/O helminth trigger vs fenbendazole trial

• Oral/inhaled glucocorticoids- avoid abrupt discontinuation/ parenteral depots

• Start @ 1mg/kg prednisone bid and taper after one to 2 weeks

Outcome for Mr Magoo

• Successfully weaned from mechanical ventilation after 60 hours of support

• 48 hrs later

– Nasal O2 support d/c

– Pneumothorax resolved and pleural catheter removed

• Left forelimb lameness

Suprascapular neuropathy

• Marked atrophy supraspinatus + infraspinatus m.

• Radial n reflex and proprioception intact

• Weak withdrawal

• Suspected critical illness polyneuropathy

Critical illness polyneuropathy- human context

• Typical onset 3-6 weeks post admission

• Striking atrophy proximal musculature

• Increased incidence post status asthmaticus

• Associated with• steroid therapy

• NM blockers??? Link now in question

• cytokine release

• eosinophilia myalgia

• Good prognosis

Questions?