Review of pulmonary pathology and ventilator management

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By Elizabeth Kelley Buzbee AAS, RRT-NPS, RCP
Kingwood college
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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
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progressive airflow obstruction with hyperreactive airways that can be, sometimes,
reversed a little. Most patients with COPD have
either chronic bronchitis or emphysema.
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While there are patients with asthma who also
present with chronic bronchitis, persons with
asthma are generally excluded from the
definition of COPD.
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Others with chronic obstructive diseases
directly attributed to diseases such as cystic
fibrosis are also excluded.
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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
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Set VT for obstructive diseases
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6-8 ml/kg IBW asthma
8-10 ml/kg IBW COPD/emphysema
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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
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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
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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
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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
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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
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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
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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
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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
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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
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Fungal pnx are associated with immunosupression 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
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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
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May start Fi02 at 100% then wean rapidly to 40-50%
as Pa02 determine
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usually interstitial pneumonitis;
destroys type I cells replaces with stiffer
type II
Can be acute reaction or could trigger
chronic problems
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
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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
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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
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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
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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
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Restrictive defect from poor chest movement
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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
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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 100110
HOB up, midline head to maximize draining
Avoid high PEEP to maintain hemodynamics
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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:
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› 8-10 ml/kg
› 12-16 BPM
› Physiological PEEP [3-5] is ok
› Fi02 to get Pa02 80-100 [usually less than 40%
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Patient will get frequent pneumonias which
may require restrictive settings
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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
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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
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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
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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, neardrowning or other
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