Ventilator Modes (restrictive lung disease) Flashcards
volume cycled ventilation (VCV) is
fixed VT with inflation pressure as dependent variable
on VCV a pressure limit can be set which
when inflation pressure exceeds this value the pressure relief valve prevents durther gas flow, preventing high airway pressures
this valve warns a change in pulmonary compliance has occured
increases in peak airway pressure may reflect
worsening pulmonary edema
pneumothorax
kinked ETT
mucous plug
in VCV mode - VT is maintained despite
small changes in peak airway pressures
disadvantage of VCV is the
inability to compensate for leaks in delivery system
primary modes of VCV are
hint: youre familiar with these
Assisted/Controlled (A/C)
Synchronized Intermittent Mandatory Ventilation (SIMV)
A/C ventillation
set RR, VT
if sponatenous effort sensed - set VT will be delivered
set rate ensures the # of breaths be delivered even with no effort
SIMV allows synchornized ventilation while providining a
predefined minute ventilation
SIMV and spontanueous patient effort
the circuit provides sufficient gas flow and periodic mandatory breaths that are syncrhonous with pt inspiratory efforts
advantage of SIMV over AC
SIMV allows for continued use of respiratory muscles, lower mean airway and mean intrathroacic pressures, prevention of respiraotry alkalosis, and improved pt/ventilator coordination
pressure cycled ventilation
provides gas flow the lugns until a present airway pressure is reached. VT is the dependent variable and varies wirth changes in compliance and airway resistance
what is the most important predisoposing factor for developing nonsocimal pneumonai (VAP)
mechanically ventilated patietns with acute repsiratory failure
what is the primary cause of VAP in mechanically ventilated patients
micro-apsiration of contaminated secretions around ETT cuff
nosocomial sinusitus is related to
presence of nasotracheal tube
treatment of noscomial sinusitis includes
antibiotics, replace NT tube wtih oral tubes, decongestants, and HOB elevation to facilitate drainage
barotrauma may present as
SQ emphysema,
pneumomediastinum/peritoneum/percardium
pulmonary intersitial emphysema
arterial gas embolism
tension pneumo
barotrauma reflects
dissection or passage of air from overdistended and ruptured alveoli
infection increases the risk of
barotrauma - by weakening the pulmonary tissue
what is the common of hypoxemia with MV
atelactasis
T/F hypoxemia due to atelectasis is not responsive to incrase in FiO2
true
in actute hypo-oxygenation states check for
ETT migration
kinks
mucous plugs
other causes of sudden hypoxemia in MV patients include
tension pneumo and PE which are accompanied by hypotension
what may be necessary to remove mucous plugs
bronchoscopy
bedside lung US shows atelactasis as
presence of static air bronchograms
PaO2 reflects the adequacy of
O2 exchange across alveolar capillary membranes
the efficacy of gas exchange is measured by the difference of
calculated PAO2 (alveolar) - measured PaO2 (arterial)
of following arterial hypoxic conditions which is not responsive to supplemental O2
a. low inspired O2 concentrations (high altitude)
b. hypoventilation (drug overdose)
c. VQ mismatch (COPD, PNE)
d. right to left intrapulmonary shunt (pulm edema)
e. diffusion impairment (pulmonary fibrosis)
D. Pulmonary edema
of following arterial hypoxic conditions which has a increased PAO2- PaO2 (SATA)
a. low inspired O2 concentrations (high altitude)
b. hypoventilation (drug overdose)
c. VQ mismatch (COPD, PNE)
d. right to left intrapulmonary shunt (pulm edema)
e. diffusion impairment (pulmonary fibrosis)
C.D.E
of the following which of these arterial hypoxemic conditions have low PaO2 (SATA)
a. low inspired O2 concentrations (high altitude)
b. hypoventilation (drug overdose)
c. VQ mismatch (COPD, PNE)
d. right to left intrapulmonary shunt (pulm edema)
e. diffusion impairment (pulmonary fibrosis)
all of them!
when does significant desaturation occur
when PaO2 < 60 mmHg
3 main causes of arterial hypoxemia
VQ mismatch
right to left pulmonary shunting
hypoventilation
increasing inspired O2 concentration improves PaO2 in which causes of arterial hypoxemia (SATA)
VQ mismatch
right to left pulmonary shunting
hypoventilation
VQ mismatch
hypoventilation
compensatory responses when PaO2 < 60mmHg
same responses present in chronic hypoxemia (PaO2< 50)
carotid body - induces increase alveolar ventilation
HPV - divert pulmonary blood flow away from hypoxic alveoli
incrreased SNS activity to increase COP and enhance O2 delivery
chronic hypoxemia leads to
increased RBCs to improve O2 carrying capacity
PaCO2 reflects the adequacy of
alveolar ventilation to relative CO2 production
dead space: VT ratio refelcts the efficcay of
CO2 transfer across alevolar membranes
wht is normal VD:VT ratio
less than 0.3
in increased deadspace ventilation what can the VD:VT ratio increase to
greater equal to 0.6
what causes an increased VD:VT ratio
acute respiratory failure
decreased cardiac ouput
and PE
VD:VT ratio indicates
areas in the lung that recieve adequate ventilation but inadequate or no pulmonary blood flow
hypercarbia is defined as
PaCO2>45 mmHg
permissive hypercarbia can be used to
to avoid or delay the need intubation and ventilation
acute increases in PaCO2 are associated with
increased CBF and ICP
extreme istances in PaCO2 > 80 mmHg results in
CNS depression
mixed venous partial O2 is the difference between
PaO2 - PvO2 reflecting the overal adequacy of cardiac output relative to tissue oxygen extraction
a PvO2 < 30 mmHg or AV O2 content > 6 mL/dL indicates the need to
increase CO to facilitate oxygenation
what invasive montioring tool can be used to measure PvO2 and calculate CvO2
pulmonary artery catheter
in regards to pH what accompanies arterial hypoxemia
metabolic acidosis
acidemia caused by metbaolic/respiratory derangements is assocaited with
dysrhtymias and pulmonary HTN
alkalemia is assoaited with
mechanical hyperventilation and diuretic use
leading to loss of chloride and K+ ion
T/F dysrhtymias may be increased with respiratory alkalosis
true
alkalemia in patients recovering from acute respiratory failure may exhibit
compensatory hypoventilation which may delay weaning from the ventilator
what is an intrapulmonary shunt
right to left shunt
perfusing nonventialted alveoli
what is the net effect with intrapulmonary shunting
decrease in PaO2 reflecting the dilution of oxygenated blood with hypo-oxygenated blood from underventilated alveoli
a physiologic shunt accounts for
2-5% cardiac output
what does the physiologic shunt of 2-5% of cardiac output reflect
passage of arterial blood directly to the left side of the circualtion through the bronchial and thebesian veins
determing the shunt fraction in patients breathing < 100% O2 reflects contributions of
VQ mismatching as well as right to left intrapulmonary shunting
to calculate shunt fraction - the patient needs to breathe
100% O2 which eliminates the contribution of VQ mismatching
guidelines for discontinuing mechanical ventilation
VC of >15mL/kg
alveolar-arterial O2 difference <350 cmH2O while breathing 100% O2
PaO2 > 60 mmHg with an FiO2 < 50%
normal pH
RR < 20
VD:VT <0.6
what other criteria is needed to determine if patients can safely be weaned from ventialtion and tolerate extubation
pt is alert and cooperative and can tolerate a spotaneous breathing trial without excessive tachypnea, tachycardia, or respiratory distress
t/f breathing at rapid rates with low volumes signifies inability to tolerate extubation
true
but remember ur restrictive lung disease pt breathes like this baseline
3 options for ventilatory weaning
SIMV, allows progressive fewer mandatory breaths until. breathing on their own
intermittent trails of total support removal and breathing through a T piece
use of decreasing elvels of pressure support
if you notice a deteroriation in oxygenation after vent withdrawal reflecting alveolar collapse what are your’e options
a. re-intubate
b. CPAP/NIPPV
CPAP/Non-invasive Positive pressure ventilation
what can interfere with sucessful extubation
excessive workload on the respiratory muscles due to hyperinflation, copious secretions, bronchospasm, increased lung water, increased CO2 production
what can be used as a bridge between intubation and extubation
noninvasive ventilation immediately after early extubation
decreases incidence of VAP, shortens ICU syay, and reduce mortality
drawback of NIV post extubation
impairs the ability to clear secretions and may have inadequate minute ventilation
extubation should be considered when
patients tolerate 30 min of SV with CPAP 5 cmH2O without deteroration in ABG, mental status, or cardiac functions
PaO2 during vent weaning needs to be above with an FiO2 less than
PaO2 > 60 mmhg
FiO2 < 50 %
where should the PaCO2 be during vent weaning, and where should the pH be
PaCO2< 50 mmhg
pH > 7.3
additional criteria for vent weaning
PEEP < 5 cmH2O
RR < 20
VC > 15 mL/kg
patients during vent weaning should be
Alert, with active laryngeal reflexes, and the ability to generate an effective cough and clear secretions
why is O2 supplementation needed immediately after extubatiom
VQ mismatchign
O2 is weaned by decreasing the FiO2 and is guided by
PaO2 and SpO2
