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-77M admitted to ER
-symptoms: sore throat, dry cough, mild dyspnea, subjective fevers
-temp 37°C, HR: 80, mBP: 80mmHg, RR: 18, SpO2: 87% on RA
-SARS-CoV-2 detected in nasopharyngeal swab, otherwise healthy
-unsuccesfully treated for 24h with Venturi Mask Oxygen then referred to ICU and CPAP with helmet started
-CXR: interstitial lung infiltrates
-no information on hemodyanmic instabiltiy, assumed adequate cardiac output (awake and responsive, no changes in LOC)
-suddened worsening of gas exchange, RR increased to 20
-unsuccessful prone positioning
-tripod positioning started
-Bloodwork: PaO2/FiO2 was 172, PaCO2 34 mmHg, pH 7.34
-used in severe respiratory failure to reopen collapsed lung areas
-obtain a more even tidal volume distribution
-redistribution of pulmonary blood flow
-improves gas exchange to dependent lung regions
-CPAP primarily treat hypoxemia and gas exchange issues
-BiPAP primarily treats hypercapnic and ventilation issues
-Pt in severe acute respiratory distress is experiencing primarily hypoxemic issues
-Current pt has decreased PaCO2 of 34 mmHg
-BiPAP not needed as ventilation is increased
-Pt will benefit the most with CPAP as this pt with SARS-CoV-2 pnemonia is having gas exchange issues
-Respiratory muscle function: decreased due to older age, generalized weakness from slight dyspnea
-Lung compliance: decreased due to infiltrates in the lungs and diagnosis of SARS-CoV-2 pneumonia, also likely to have secretions
-Airway resistance: increased due to inflammation from SARS-CoV-2 pneumonia, and likely to have secretions and airway edema
-Work of breathing: increased due to decreased RMF, decreased lung compliance, and increased airway resistance = increased difficulty to brearthe hence dyspnea
-Tidal volume: likely decreased with shallow breathing
-Vital capacity: decreased due to decreased respiratory muscle function
-Functional residual capacity: increased due to CPAP keeping alveoli open at end of exhalation
-Respirate: increased from 18 to 20
*VENTILATION INCREASED OVERALL AS PACO2 IS DECREASED (PACO2=34) --> compensatory mechanisms
-improved diaphragmatic breathing and thoraco-abdominal movements
-increases tidal volume by increasing chest cavity expansion --> tripod position helps to lower diaphragm
-tidal volume went from 370mL to 420mL
-easier to inhale oxygen and exhale carbon dioxide
-improved comfort, reduced feelings of dyspnea, easier for respiratory muscles to function (decreased WOB)
-pt's RR reduced from 20 to 17 after assuming tripod position
-repositioning to tripod can mobilize secretions --> decrease airway resistance --> improve WOB
-thickness of AC membrane: increased due to infiltrates in lungs, inflammation, and presence of lung infection with SARS-CoV-2 pneumonia, also likely has secretions
-anatomical surface area: slightly increased due to CPAP keeping alveoli opened and increasing surface area available for gas exchange
-diffusion coefficient: CO2 diffuses 20x faster than O2 so O2 is more significantly affected due to issues with gas exchange from pneumonia
-driving pressure: increased due to supplemental oxygen
*OVERALL DIFFUSION DECREASED
-alveoli perfused: assumed adequate perfusion with no hemodynamic/cardiac output issues
-alveoli ventilated: shunt-like unit present due to issues with ventilation (e.g. decreased compliance, increased airway resistance)
*OVERALL V/Q MISMATCH PRESENT
-tripod position allows for better blood flow redistribution to lungs
-increases ventilation to the dependent regions of the lungs --> improves V/Q matching
-pt was shown to have stable improvement of V/Q matching
-easier to take deep breath and increase oxygen delivery to more areas of the lungs
-PaO2/FiO2 ratio increased from 136 to 196 after 3 hours in tripod position
-SaO2 went from 93 to 99
-no cardiac output or hemodynamic issues indicated in research study
-will assume no hemodynamic issues for pt at this time (no contractility, preload, or afterload issues)
-HR normal at 80
-awake, alert, and cooperative throughout study --> no signs of decreased EOP to brain (no LOC changes)
-however, tripod positioning increases intrathoracic pressure --> decreases venous return --> decreases preload (be mindful of hemodynamic stability with repositioning)
-no fever, temp = 37°C
-physiological stress from increased RR, sudden decrease in gas exchange, and current pneumonia infection
-preceived stress from hospitalization and different environment
-initial repositioning to tripod position can increase oxygen demand
BUT
-easier to expand chest cavity with lowered diaphragm --> easier to breathe --> decreased WOB --> decreased RR --> decreased oxygen demand overall
-research article found:
-suggested to put patients in tripod positioning if unable to tolerate prone positioning
https://bmcanesthesiol.biomedcentral.com/articles/10.1186/s12871-020-01221-5