Ashley Kuehn ICU RRT Peter Godor ICU NP Royal Alexandra Hospital, Edmonton, AB DYNAMICS 2010: Edmonton, AB September, 2010
1918 Spanish Flu decimated the world over a two year span 50-100 million died Avian subtype of H1N1 2004-2005 H1N1 present in human population Accounted for minimal percentage of total Influenza cases Spring of 2009: First wave of Pandemic Moderate impact on population Early warning signs of significant, subsequent waves Fall/Winter of 2009: Second/Most significant wave of Pandemic Largest impact on population
Late Fall of 2009 Introduction of H1N1 vaccine Historically, most wide spread and successful rollout Spring of 2010: Third wave of Pandemic Minimal impact on population Population immunity to virus (most likely) April of 2010 WHO 214 countries 18,138 deaths (Unofficial est. as high as 30,000-35,000 deaths) Summer of 2010 Negligible impact on human population Expected trajectory Endemic status at low infection rate, until major mutation of the virus
Influenza A Human, Avian, Swine, Equine, Canine, Feline Organized according to the two antigens on surface (H&N) Hemagglutinin: 16 different H antigens Neuraminidase: 9 different N antigens Influenza B Human, Seals Slow mutating Least severe Influenza C Human, Swine Very slow mutating Very rare Can be severe H1N1 Spanish Flu 1918, 2009 H2N2 Asian Flu 1950s H3N2 Hong Kong Flu 1960s H5N1 Global Mid 2000s H1N2 Global Currently
H1N1 Serotype of Influenza A virus Affected swine population only (traditionally) Not transmitted to humans (typically) If transmitted DOES NOT cause Influenza (only asymptomatic antibody production) Process of Reassortment Acquired genetic profile to infect human Caused Influenza like illness
H1N1 Influenza Virus Not unlike any other Influenza A virus (similar pathophysiology) Pathogenic capacity (virulence) contributed to serologic naivety of human population Body s immune reaction exaggerated, to detriment of host (lack of serologic exposure)
Initial Immune Response Cytokines and other inflammatory mediators released in lung parenchyma by epithelial and endothelial cells Neutrophils and T-lymphocytes migrate to inflamed parenchyma Diffuse Alveolar Damage Endothelial dysfunction in alveoli cause leaky capillaries and alveolar collapse Inflammatory exudate accumulates in the alveoli causing pulmonary edema Separation of tight junction of capillary-alveolar space impairing gas exchange
Perhaps the most researched and debated topics in the history of medicine Consensus on definition reached in 1994 at the American-European Consensus Conference on ARDS Agreed upon definitions of ALI and ARDS Research set in motion Promoted upstart of organizations (ARDSnet)
Acute onset No Hx of chronic lung Dz Bilateral infiltrates No evidence of elevated Lt atrial pressure PCWP: < 18 PaO 2 /FiO 2 ratio ALI: 200-300 ARDS: < 200
ARDSnet Clinical network established in 1994 by the National Heart, Lung and Blood Institute, and National Institutes of Health Conduct multi-centre trials for ARDS treatments Ventilation Guidelines Tidal Volume (V T ): 4-8 ml/kg PBW RR: < 35 bpm FiO 2 : 0.3 1.0 PEEP: 5-24 cm H 2 O P pl : < 30 cm H 2 O PaO 2 : 55 80 mmhg SpO 2 : 88 95% ph: 7.15 7.30 PaCO 2 : Permissive hypercapnia
Tracheal-bronchial toilet Adequate oxygenation Most physiologically beneficial combination of FiO 2 and PEEP Lung protective strategy Minimal ventilatory interventions necessary to maintain physiological values Prevention of further damage caused by ventilation
Positive End Expiratory Pressure (PEEP) Pressure maintained throughout the expiratory cycle to decrease shunting of blood through the lungs Improving oxygenation by improving gas exchange H1N1/ARDSnet PEEP guidelines Support a more aggressive approach to PEEP application
ARDSnet Protocol FiO 2 /PEEP Guidelines Lower PEEP/Higher FiO 2 FiO 2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0 PEEP 5 5 8 8 10 10 10 12 14 14 14 16 18 18-24 Higher PEEP/Lower FiO 2 FiO 2 0.3 0.3 0.3 0.3 0.4 0.4 0.5 0.5 0.5-0.8 0.8 0.9 1.0 1.0 PEEP 5 5 10 12 12 16 16 18 20 22 22 22 24
Mean Airway Pressure (MAP) Average pressure exposed to lungs during respiratory cycle Increasing MAP, improved oxygenation (generally) Controlled by manipulation of PEEP (most often) Increases chance of barotrauma (conventional ventilation) Direct relationship between MAP Peak Inspiratory Pressure (PIP) PEEP Inspiratory Time (Ti) Peak Inspiratory Flow Rate
Assist Control (AC) Full support mode Each inspiratory effort delivers set tidal volume Ventilator delivers volumes at minimum rate, if not triggered Pressure Control (PC) Full support mode Each inspiratory effort delivers set inspiratory pressure for a set inspiratory time Ventilator delivers breaths at minimum rate, if not triggered Pressure Support (PS) Weaning mode Each inspiratory effort delivers set pressure with patient determined inspiratory time No minimum respiratory rate set
Airway Pressure Release Ventilation (APRV) High set level of PEEP which intermittently releases to a lower set level of PEEP for brief periods of time Inverse I:E ratio ventilation ( MAP with less barotrauma) Spontaneous breaths allowed throughout cycles CO 2 elimination occurs during pressure releases and during spontaneous efforts Differing Names (Dependent of Manufacturer) APRV Evitas Bivent Servos Bilevel Puritan Bennett 840
High Frequency Oscillation (HFO) Delivery of small volumes (1-3 ml/kg) at extremely fast rates (200-360 bpm) Measured in Hertz (cycles/sec) Delivery of high mean airway pressures while decreasing chance of barotrauma Minimal evidence to support utilization in H1N1/ARDS Promising studies currently being conducted
Extracorporeal Membrane Oxygenation (ECMO) Cannulation Veno-Veno or Arterial-Veno Utilization Neonatal (most evidenced) Trauma ARDS H1N1 2009 season Longest ECMO Run 117 days in 2008 (alive today) Keys to success Early recognition of need Prompt consultation
Premise of prone position ventilation Recruitment of collapsed alveolar units Reduction in V/Q heterogeneity with improved ventilation and reduction of shunting Mobilization of secretions Improves functional residual capacity (FRC) Improves oxygenation Extensively researched in ARDS Local success with H1N1 precipitated ARDS
American Journal of Roentgenology High incidences of PEs and other thromboembolic diseases associated with H1N1 infection Royal Alexandra Hospital Experience Consistent with research Several incidences of PEs, DVTs, and a fatal ischemic CVA (unforeseen) Recommendations Diligent use of thromboembolic prophylaxis ie: LMWH
Allowing de-recruitment Allowing coughing Initiating PEEP too low Weaning PEEP too soon Lacking prompt escalation to unconventional ventilation modes Allowing positive fluid balance Dosing of sub-therapeutic Heparin Discounting H1N1 Tx as per negative PCR
ID 35 year old female HPI Previous night: Mild chills and fever Morning of Admission: Mild cough Mid-Day of Admission: Respiratory distress EMS arrival SpO 2 70% on RA Bilateral decreased AE Intubated in ER Type I Respiratory Failure PMHx Obese: BMI 35 (165 cm, 95 kg) Healthy Meds BCP Allergies NDKA
Rapid deterioration of ventilatory status Within 6 hrs of admission to ICU Unconventional ventilatory mode (APRV) FiO 2 : 0.90, PaO 2 : 50 ECMO consultation at U of A 24 hrs Unavailable at time of presentation Marginal improvement in oxygenation 48 hrs FiO 2 : 0.50, PaO 2 : 70 Switched to conventional ventilatory mode Subsequently, unable to wean Day 10 No progress made thus Tracheostomy
Eventually, weaned off mechanical ventilation Following week Alternating tracheostomy cradle with SSV Week 6 Discharged to ward with tracheostomy 4 weeks later Tracheostomy removed 3 months after admission Discharged home with oxygen 6 months later Off oxygen Functional status not at baseline
Prevent de-recruitment Prevent coughing Start PEEP high Wean PEEP cautiously Escalate ventilation modes aggressively Consult ECMO promptly Keep patient dry Continue thromboembolic prophylaxis LISTEN TO YOUR RT; THEY ARE THE EXPERTS
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