Highlights of Unit 2 mechanical ventilation

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Highlights of Unit 2 mechanical
ventilation
Physiologic Effects of Mechanical
Ventilation:
both hazards and positive effects of
PPV & of negative pressure
ventilators
Airway pressures
• Spontaneous breathing results in a driving
pressure of 0 - -5 = 5 cmH20
• At no point during quiet spontaneous
breathing is the intrathoracic pressure positive
Airway pressures during PPV
• In the case of positive pressure ventilation
[PPV], the pressure gradient is positive at the
mouth and negative at the alveoli.
• The driving pressure is the difference between
these two pressures.
• the intrapleural pressure will rise because the
airway pressure has transmitted through the
thin walls of the lung.
Cardiovascular effects of PPV
• Positive airway pressure raises pressure in
thoracic cavity
• Prevents the RA from sucking blood back into the
heart so the venous return is decreased
• Less blood in heart- less blood out of the
ventricles so RV and LV both have decreased SV
• Compression of pulmonary capillaries
• Slows down blood return from head
• Decreases Cardiac Output CO
• Might decrease the myocardial perfusion
Who is more likely to suffer the effects
of PPV on cardiovascular system?
• The person with hypotension
• or with low blood volume
Who could benefit from the effects of
PPV on the CV system?
• patient with congestive heart failure is helpful
• need to push back the excess lung fluid
• need to decrease the amount of blood
returning to the stressed heart,
• so that the CO can actually rise with these
patients.
Effect of PPV on tissue delivery of
oxygen
• 02 delivery = 02 content (cardiac output)
– If decreases the CO ---decrease the delivery of 02
to the tissue
– If PPV causes increased VD ventilation, the 02
content can go down
Lung Compliance and CO
• If the patient’s lungs have normal compliance,
50% of pressure in the lungs is transmitted to
the thorax.
•
• If the patient has stiff, low compliant lung, the
higher alveolar pressure may not transmit to
the thorax.
reverse pulsus paradoxus
• status asthmaticus patients placed on PPV
can have such excessive driving pressures that
this dampens the systemic B/P
• decreased LV after load is so low that systemic
BP changes significantly between inspiratory
phase & expiratory phases.
Excessive VT and inappropriately
high baseline pressures
• Excessive VT and inappropriately high baseline
pressures [PEEP] will result in serious
problems with CO and with myocardial
perfusion.
Effects of PPV on hypoxemia
• alveolar recruitment, increases surface area
for gas exchange so Pa02 rises
• as the alveolar C02 drops due to increased
movement of gas into the lungs and collapsed
alveoli re-inflate the PA02 rises.
PPV and hypoxemia with CHF
• As we increase the alveolar pressure with
PEEP or CPAP, fluid is pushed back and Pa02
rises as more gas diffuses into the capillaries.
• As Pa02 rises, the Fi02 can be dropped to
avoid 02 toxicity
Treatment of hypercapnea with
PPV
VE rising decreases the PaC02.
• VT based on disease states:
• 8-10 ml/Kg IBW normal lungs
• 6-8 ml/kg IBW asthma
• 5-8 ml/ kg IBW for ARDS & for COPD
• Keep Pplateau less than 30 cmH20.
PPV can increase V/Q
• Gas distribution to Zone I instead of Zone III
• Pressure on pulmonary capillaries will
decrease Q in some areas and raise perfusion
to under-inflated areas
• Increased Ventilation without perfusion
results in increased VD—so PPV can increase
VD/VT
PPV and acid pH
• If VE is too low, respiratory acidosis will result
in increased Ventilatory demand
• Prolonged acidosis raises the serum potassium
so hyperkalemia can cause cardiac
arrhythmias
PPV and alkalosis
• If VE too high:
• Prolonged alkalosis will drop the serum
potassium so that hypokalemia results- this
can also effect the EKG
• Alters the Hb/02 affinity with shift to the left
so that tissue oxygenation can be decreased
• High pH will drop the ventilatory drive and
prolong weaning from mechanical ventilation
Time constants
• Time constant = RAW x C
• we need at least 7 time constants for both I &
E.
PPV and excessive airway pressures
• PIP above 50 is associated with lung tissue
trauma
• If increased RAW, check BBS for suctioning or
need for bronchodilator
• Pplateau above 30-35 will cause sheer damage.
Keep below 30, by decreasing the VT [usually
too high for disease]
Mean airway pressures
• Increasing the PEEP will raise the mPAW
• Increasing the Ti will also raise the mPAW
• Increased airway pressures raise the FRC
which can increase lung C and increase Pa02
but excessive FRC will only add to air trapping
Effects of PEEP
• PEEP can drop the Cardiac Output particularly
in persons with good compliance
• PEEP can raise the FRC which may or may not
have good effects
– Low FRC associated with atelectasis –good
– High FRC associated with asthma or COPD- bad
• Auto-PEEP created by prolonged Ti can result
in air trapping and barotrauma
volutrauma.
• Excessive VT -- in the face of problems with
gas distribution
Effect of PPV on VT
• If the patient’s parameters are based on
pressure, the delivered VT will vary based on
the patient’s compliance and RAW.
• If ventilation is based on a volume, the airway
pressures will vary based due to changes in
the patient’s compliance and RAW
Effect of PPV on WOB
• If WOB is not decreased, settings are wrong
– WOB decreased because driving pressure is
increased by ventilator
– Increased VE drops the PaC02 so ventilatory drive
drops
– VD/VT decreased because VT is increased
– Pa02 rises
– If sensitivity set appropriately, there is little WOB
Inappropriate settings result in
increased WOB
•
•
•
•
•
inspiratory flow rate too low,
sensitivity not responsive to patient effort
failure to correct hypoxemia
failure to correct hypercapnia or acidosis.
if the level of auto-PEEP is interfering with
triggering a breath
Effect on ventilator muscles
• muscle atrophy within 72 hours in adults.
• muscle mass and muscle fibers affected
• resting muscle length increases [due to
increased FRC] results in decreased muscle
strength,
• while alterations in the blood flow to the
ventilatory muscles secondary to PPV just
adds to the problem.
Ventilatory-associated pneumonia [VAP]
• VAP more an issue of artificial airways rather
than ventilation
– cuff pressures to prevent aspiration
– oral care Q2 hours,
– oral intubation
– keeping the HOB
Effects on the kidneys
• When CO drops, the body shunts blood away
from kidney so renal perfusion decreases
• Decreased perfusion decreased urine out put
– less than 400 ml/day or 160ml/8 hours shift
serious
– increases in BUN, creatinine , Potassium and
decreases in Na.
– drug clearance may be affected
Serum inappropriate Anti-diuretic
hormone [SIADH]
• baroreceptors located in the walls of the
Aortic Arch and in the carotid arteries respond
to decreases of LV pressures by sending a
message that results in secretion of ADH so
urine output decreases
Effects of negative pressure
ventilation on the body
Major differences
• Negative airway pressures more nature, but
also negative pressure on the outside of the
thorax and on the abdominal cavity
• Immobility inside the device– always supine
• Not effective ventilation in the face of
excessive secretions or other causes of
increased RAW
• None-invasive so unable to protect airway
Negative pressure ventilation
• Pooling of venous blood in the abdomen can
result in decreased CO
• If patient has paralysis, this can result in
positional hypotension
• If person with Guilliam Barre or myotonic
dystrophy may have increased cardiovascular
instability– hard to get to patient for CPR
• Must decrease VE during nursing procedures
Problems with negative pressure
ventilation
• Chest wall can-- over decades-- become
deformed
• chest cuirass cover only the chest and not the
abdomen so that there is less pooling of
venous blood—but maybe less ventilation
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