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Review of pulmonary pathology and ventilator management

Review of pulmonary pathology and ventilator management. By Elizabeth Kelley Buzbee AAS, RRT-NPS, RCP Kingwood college. Obstructive defects will have. wheezing, prolonged exhalation from airway issues increased WOB due to narrowed airways causing increased R AW

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Review of pulmonary pathology and ventilator management

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  1. Review of pulmonary pathology and ventilator management By Elizabeth Kelley Buzbee AAS, RRT-NPS, RCP Kingwood college

  2. Obstructive defects will have • wheezing, prolonged exhalation from airway issues • increased WOB due to narrowed airways causing increased RAW • s/s of air trapping on X-ray, on inspection of the chest and on ventilator graphics • compliance is usually ok • Hyper-resonance on percussion • May or may not have response to bronchodilators depending on the exact disorder • Respiratory failure will be due to acute hypercapnic respiratory failure in the case of asthma, and acute or chronic hypercapnic respiratory failure in the case of COPD • Chest film: hyper-inflation, flatten diaphragms, areas of consolidation if pneumonia is part of the picture

  3. COPD [Egan’s pp. 507] • progressive airflow obstruction with hyper-reactive airways that can be, sometimes, reversed a little. Most patients with COPD have either chronic bronchitis or emphysema. • While there are patients with asthma who also present with chronic bronchitis, persons with asthma are generally excluded from the definition of COPD. • Others with chronic obstructive diseases directly attributed to diseases such as cystic fibrosis are also excluded.

  4. Ventilator management • Volume controlled, PPV, but some patients could be managed by NIPPV as long as patient is alert and not apnic • end stage COPD: NIPPV and frank discussion of quality of life issues • Prolonged expiratory times will demand : • longer I:E ratios: Shorter Ti, faster flow rates up to 100 LPM • Ventilator f 10-12, but may need to drop to 6-8 BPM • If airways are high consider decreasing VT • will generally require full support ventilation for at least 24-48 hours but A/C could lead to air-trapping; SIMV might be safer , could be moved to partial support with or without PS after resting

  5. Ventilator management cont • Set VT for obstructive diseases • 6-8 ml/kg IBW asthma • 8-10 ml/kg IBW COPD/emphysema • PEEP can raise the FRC which is already high; minimize PEEP or use auto PEEP to determine set PEEP level that could help keep airways open • If chronic hypercapnia is an issue, the patient’s Pa02 will have to be reduced to 55-65 torr before the patient will attempt to breath on his own

  6. Ventilator management cont • Decision to intubate the COPD patient is made when the patient’s ABG reach partially compensated respiratory acidosis or when the patient is in acute respiratory acidosis. • The asthmatic patient , however, may need to be intubated before he becomes hypercapnia. If the asthmatic patient is tachypnic and has increased WOB, his PaC02 are usually lower than normal, if his PaC02 rises over 2-3 ABG, he is getting tired and we don’t wait for respiratory acidosis

  7. Ventilator management cont • Constant Flow pattern has advantage of decreasing the Ti, but disadvantage of increasing the PIP • Descending flow pattern has advantage of decreasing PIP, but increasing PAW because Ti is increased • Inspiratory pause is not helpful in COPD • Fi02 40-50% works with most patients • May use Fi02 100% to ‘sedate’ the end stage COPD patient, then wean Fi02 quickly

  8. Chronic bronchitis • Any person who suffers a productive cough 3 months a year for two years and this cough is not directly attributed to such disorders as GERD, post-nasal drip or asthma. • Risk factors for chronic bronchitis include inhalation of cigarette smoke and other noxious chemicals. • Chronic bronchitis can lead to COPD

  9. Emphysema [Egan’s pp. 470] • abnormal permanent enlargement of the air spaces beyond the terminal bronchioles which destroys the walls of the airways and alveoli without causing fibrosis. • Can be caused by exposure to chemicals include cigarettes, but 10% could be genetic alpha-1 antitrypsin • Bulbous emphysema: When a person has such significant air trapping that areas of trapped air in the apical lung fields get bulea which place patient at high risk for rupture.

  10. Asthma • is defined as a disorder of highly reactive airways that are partially or completely reversible following drug therapy. • Asthmatics will have decreased exhaled flows that can be improved 15% or more with inhalation of Beta II agonist • Only stage I Asthma can be managed with only Beta II drugs – all other need inhaled steroids

  11. Cystic Fibrosis • CF, a genetic defect in which the patient presents with abnormally thick secretions. • Overtime, the patient with CF who has strong pulmonary symptoms will present with a classic COPD X-ray and ABG. • Decisions to intubate and ventilation will follow COPD standards

  12. Restrictive defects • Will have crackles, diminished breath sounds, in bases of lung or affected lobe/segments • Can have localized areas of consolidation or atelectasis or diffuse • will have decreased FRC –atelectasis results • will have decreased lung compliance; increased WOB • Patients may become refractory to supplementary 02 • May require ventilation for acute hypercapnic respiratory failure or for hypoxemia respiratory failure • Dullness to percussion; poor chest excursion to palpation

  13. Restrictive defects • Pneumonia an infection in which the respiratory zone has become infected • Pneumonitis: inflammation due to chemical thermal or other damage; • non-cardiogenic pulmonary edema: reaction to toxic substance; may go into ARDS • Hypersensitivity pneumonitis: occupational disease which creates scar tissue in alveolar areas

  14. Pneumonia Dx • Because infection, fever, chills common • CBC to determine if bacterial or viral in origin • Chest film: consolidation/ atelectasis ; if viral hyperinflation • Get sputum for gram stain/ C & S sputum may be rusty-colored or other colors based on causative agent • PCP pnx requires bronchoscopy and washings • Blood titers for viral illness • Skin test for fungal infections or serological test of complement fixation

  15. Pneumonia Dx • If bacterial in origin, most likely to have localized areas of atelectasis or consolidation • If bacterial abscesses, effusions can complicate the case • Bacterial pneumonia can progress to sepsis • If viral in origin, most likely to have diffuse hyperinflation and patient is wheezing • If viral pnx,can become ARDS rapidly

  16. pneumonia • Fungal pnx are associated with immuno-supression due to AIDS or chemotherapy • Fungal pnx may show up on chest film with fungal balls [mass] • TB and other necrotic pnx can result in rupture of air sac and hemoptasis and/or pneumothorax. • Anaerobic bacteria may be found in abscesses; an abscess that ruptures will have foul smelling sputum

  17. Ventilator management of pneumonia • Volume controlled PPV for full support by A/C to rest the patient; may need to move to PC if excessive pressures result • Start at VT 8-10 ml/kg/IBW • Ventilator f 12-16 BPM • If Pplateau above 30 cmH20, decrease VT 6-8 with increased RR 15-35 [keep VE same] • Inspiratory hold might work if patient gets to ARDS, • PEEP is helpful because FRC is decreased, unless: • If viral pnx with wheezing : ventilate like asthmatic • If lobar pnx PEEP will result in mismatched V/Q • May start Fi02 at 100% then wean rapidly to 40-50% as Pa02 determine

  18. pneumonitis usually interstitial pneumonitis; destroys type I cells replaces with stiffer type II Can be acute reaction or could trigger chronic problems

  19. Ventilator management of pneumonitis & acute non-cardiogenic pulmonary edema if the patient is alert and the PaC02 is not elevated, we could start off with NIPPV If intubated & ventilated for acute respiratory acidosis, VT will be small at 6-8 ml/kg IBW Respiratory f will be high at 15-35 BPM Keep P plateau below 30 [reduce VT to 4-6 ml/kg IBW based on this] PEEP is helpful when the Fi02 is up and the Pa02 is down. Start 5 and increase 2-3

  20. Management of ARDS • VC A/C mode • VT to 8ml/kg then [over 4 hours] reduce to 6 & even to 4 ml/kg • Increase f to keep the VE the same [highest A/C rate 35 bpm] • I:E ratio between 1:3 and 1:1 • Use suggested Fi02 and PEEP levels • maintain P plateau between 24-30 by VT and decreasing flow rate & manipulation of PEEP • Permissive hyper capnea • Maintain these parameters • Sp02 88-95 & Pa02 between 55-80 • pH between 7.30 – 7.45--If pH drops below 7.15, give bicarb

  21. Ventilator management of viral pneumonia with air trapping • If patient with viral pneumonia presents with hyperinflation on X-ray, and wheezing, his ventilator parameters need to be set up like COPD and asthma to avoid air trapping and pneumothorax • Combined obstructive and restrictive defects are troublesome

  22. Burn patients • Thermal damage could lead to • Laryngospasm/ laryngo-edema that requires immediate intubation with a smaller than normal ET even tracheostomy • Copious thin secretions & wheezing • Destruction of surfactant and pulmonary edema- restrictive defect and diffusion problems • Anemic hypoxia due to CO inhalation • So burn patient may have restrictive and obstructive defects together

  23. Ventilator management of burn patients • If alert/ breathing mask CPAP of 5-10 cmH20 with Fi02 100%.[Wilkins & Dexter] • Fi02 100% until Hbco is under control, then wean to get Pa02 80-100 torr. • PEEP so we can wean the Fi02 [after Hbco WNL] • Lower VT and faster rates for restriction • Can go into ARDS easily • in the fact of increased RAW, monitor the BBS for prolonged exhalation because we want to avoid barotrauma from auto-PEEP

  24. Chest wall problems • Restrictive defect from poor chest movement • Trauma patient can have flail chest, pneumothorax. can have upper airway occlusion; can have hemothorax and decreased blood volume/ hypovolemic shock • Burn patient can have stiff, scarred chest • boney deformities rarely require ventilation, but pneumonia could complicate this patient

  25. Acute closed head injury • Can cause apnea, systemic hypotension & increased ICP. • Intubate orally to avoid infection if there is connection between brain and nasal passage • Avoid wrapping ET tube tapes around head to minimize blood flow issues • Keep PaC02 around 30 torr for a short time to decrease blood flow to head; keep Pa02 100-110 • HOB up, midline head to maximize draining • Avoid high PEEP to maintain hemodynamics

  26. Acute phase Near-drowning • Problems include: laryngospasm , pulmonary surfactant destruction , Bronchospasm, may be hemodynamically unstable • if 100% NRM is not enough, as long as he can protect his airway & is not at risk for vomiting and PaC02 WNL,N-CPAP with heated, humidified 02. • Intubate based on LOC and ability to protect the airway &ventilate based on restrictive/ and or obstructive defects present • If complicated by infection, may need to move to pnx settings

  27. Ventilator management of the long-term neurological defective patient • Tracheostomy tube within 2 weeks • will have normal RAW and compliance, so we can use: • 8-10 ml/kg • 12-16 BPM • Physiological PEEP [3-5] is ok • Fi02 to get Pa02 80-100 [usually less than 40% • Patient will get frequent pneumonias which may require restrictive settings

  28. Ventilator management of CHF • Decreasing the blood return to the RA is helpful in CHF • If alert, N-CPAP of 10 or NIPPV of 15/5 [RC vol 51 (4) pp. 407] • If intubated and ventilated • VT 8-10 ml/Kg, but if airway pressures are high, decrease the VT • PEEP at 10 cmH20 and wean the Fi02 • Once the patient’s compliance gets better, we must wean the PEEP

  29. Ventilator management of the acute MI • Normal settings, but may go into CHF in which we may need to decrease VT as airway pressures rise. • Watch electrolytes which can affect cardiac rhythm • Watch I &O for increases in blood volume due to poor perfusion of kidneys

  30. chronic neuromuscular disease • have problems with muscles but not LOC • Problems w/protect their airways • Many persons with long-term muscle weakness might have compensated respiratory acidosis with mild hypoxemia as baseline • At increased risk for positional hypotension & pulmonary emboli, & recurrent pnx • Muscular dystrophy [general slow downhill] • Guillaium-Barre[acute] • Myasthenia Gravis [episodes] • ALS[general slow downhill]

  31. 10-12 ml/Kg IBW at a rate of 12-16 BPM • BiPap 12-14/4 only if they can protect airway & are alert • Negative pressure ventilation if they can protect airway; don’t need to have good LOC • PEEP at 5 to prevent atelectasis • High flow rates for comfort

  32. Permissive hypercapnia for ARDS & severe asthma • when airway pressures are high enough that barotrauma is likely, we may not be able to get PEEP high enough to fix hypoxia & we may not be able to correct hypercapnia because the airway pressures will not allow manipulation of the VE • At this point we accept this and let the PaC02 rise slowly [10mmHg/hr] and allow the patient’s Pa02 to drift down to 55 mmHg. As long as the pH is above 7.30 patient is ok; if it gets below 7.15, give Bicarb

  33. General comments about ventilation of adults • All VT have 8 ml/kg IBW in their range except acute asthma which starts at 6 ml/kg IBW & post op or neuromuscular in which the range is 10-12 • Fi02 and PEEP changes to fix Pa02/Sp02 • VE [usually respiratory f] to fix PaC02/pH problems • high FRC [ obstructive defect] can be harmed by PEEP • low FRC [restrictive defect] do much better with PEEP • Ti need to be between .8 to 1.2 seconds [ flow rates between 40-80 LPM, but obstructive defects many need to raise flow rates to 100 LPM [descending wave] • Constant flow patterns will raise the PIP, but decrease TI • Descending flows can drop the PIP, but raise the TI which can raise the PAW • Inspiratory pauses are dangerous, and usually only used for lung mechanic measurements

  34. N-IPPV or n_CPAP • N-IPPV is helpful in CHF, and in COPD and asthma patient with intact ventilatory drives and normal LOC as long as the PaC02 is ok • n-CPAP will not work in the face of high PaCo2 and is useful for hypoxemic respiratory failure such as CHF, near-drowning or other

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