By Elizabeth Kelley Buzbee AAS, RRT-NPS, RCPKingwood college

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

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.

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

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

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

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

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

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.

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

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

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

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

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

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

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

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

usually interstitial pneumonitis; destroys type I cells replaces with stiffer type IICan be acute reaction or could trigger chronic problems

if the patient is alert and the PaC02 is not elevated, we could start off with NIPPVIf intubated & ventilated for acute respiratory acidosis, VT will be small at 6-8 ml/kg IBWRespiratory f will be high at 15-35 BPMKeep 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

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

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

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

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

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

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

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

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

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

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

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]

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

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

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

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