Mechanical Ventilation Flashcards
Oxygen delivery equation
DO2= cardiac output x arterial O2 Content
Reasons for oxygen delivery failure
hypotension, acidosis, coagulopathy
oxygen use equation
VO2=Cardiac output x O2a-O2v
The normal oxygen extraction ratio is
about 25%
heart has very high demand
The anesthesia goal of oxygen therapy is
to maintain oxygenation and ventilation
The oxygen therapy goal is
prevention and correction of hypoxemia and tissue hypoxia
Surgical patients have an
increased risk of hypoxemia & hypoxia
Hypoxemia is
deficiency of O2 in blood
Hypoxia is
O2 delivery to tissues not sufficient to meet metabolic demand
Types of hypoxia include
hypoxic, circulatory, hemic, demand, and histotoxic
Hypoxia signs and symptoms include
vasodilation, tachycardia, tachypnea, cyanosis, confusion, and lactic acidosis
Improving oxygenation in mechanically ventilated patients includes
treatment tailored to cause
utilizing increase VE, increased cardiac output, increased O2 carrying capacity, optimize V/Q relationship, decrease O2 consumption, increase FiO2
The nasal cannula (flow rates)
flow rates 1-6 L/min
FiO2 increases about 4% per L/min
Simple face masks (FiO2)
minimum 6L flow required to prevent rebreathing
FiO2 40-60%
Face masks with reservoirs
FiO2 60-100%
Venturi masks
have more precise FiO2 of 24-50%
have to set flow rate
Based off of Bernoulli’s theory
Oxygen toxicity occurs from
high FiO2 over long periods which can be harmful to lung tissue and cause
decreased ciliary movement, alveolar epithelial damage, and interstitial fibrosis
Oxygen toxicity is dependent upon
FiO2, duration, patient susceptibility
Safe levels of oxygen to prevent oxygen toxicity is
100% O2 for up to 10-20 hours
Oxygen toxicity occurs from
50-60% O2 for more than 24-72 hours
Absorption atelectasis occurs when
nitrogen is replaced by oxygen
under-ventilated alveoli have decreased volume- due to greater uptake of oxygen
increases pulmonary shunting
Induced hypoventilation occurs due to
Chronic CO2 retainers rely on hypoxic drive
peripheral chemoreceptors are triggered by hypoxemia
Increased O2 can lead to hypoventilation
Fire hazards can occur because
O2 supports combustion
use extreme caution with head and neck cases
Retinopathy occurs
with O2 therapy in neonates; it can lead to vascular proliferation, fibrosis, retinal detachment, and blindness
Populations at risk of retinopathy include
<36 weeks gestational age
weight <1500 gm
up to 44 weeks gestational age are considered high risk
Safe O2 administration to prevent retinopathy is
PaO2 60-80 mmHg
Hypercapnia is
increased CO2 >45 mmHg
increased CO2 concentration or increased CO2 production
Hypercapnia is caused by
increased alveolar dead space- decreased alveolar perfusion, interruptions in pulmonary circulation, pulmonary disease
Decreased alveolar ventilation- can be central or peripheral defect, respiratory depression most common cause in immediate postoperative period
Clinical manifestations of hypercapnia include
directly produces vasodilation of peripheral vessels, indirectly increases HR after catecholamine release, produces effects due to an acidotic state
Non-specific signs of hypercapnia include
headache, nausea/vomiting, sweating, flushing, shivering, restlessness
Treatment for hypercapnia includes:
adjust treatment to the cause
increase minute ventilation
Considerations for hypercapnia (CNS, CV, and pulm)
CNS considerations: regulation of ventilatory drive, cerebral blood flow
cardiovascular considerations: depression of smooth muscle and cardiac muscle, increased catecholamine release, vasodilation versus vasoconstriction
Pulmonary considerations: increased respiratory rate, increased pulmonary vascular resistance
Hypocapnia is
CO2 <35 mmHg
Hypocapnia typically caused by
iatrogenic
Hypocapnia clinical manifestations include
CNS: decrease CBF
CV: decrease in CO, coronary constriction
Pulmonary: hypoxemia may result from hypoventilation
Treatment of hypocapnia includes
decreasing minute ventilation
Goals of mechanical ventilation is
to maintain homeostasis
Goals of mechanical ventilation in the OR is to
ensure adequate oxygenation and CO2 removal for safe and effective surgery
Goals of mechanical ventilation in the ICU is to
treat severe respiratory distress, provoke lungs with a “break” to rest and heal, decreases O2 consumption by providing rest for respiratory muscles
Peak inspiratory pressure (PiP) is
total pressure required to distend LUNGS and AIRWAYS
Pressure used to calculate DYNAMIC COMPLIANCE
Plateau pressure is
distending pressure to expand ONLY THE LUNGS
measures redistribution of air flow through lungs
plateau pressure is used to calculate STATIC COMPLIANCE
The variables we control include (control variables)
respiratory rate, tidal volume, pressure (PiP, Plat/ PAW)
I:E ratio (I:E)
Depending on the mode of ventilation selected you can control
either tidal volume or pressure delivered
In the total respiratory cycle, each breath has 4 parts:
- start of inspiration
- inspiration itself
- end of inspiration
- expiration
The trigger variable is
the start of inspiration
The limit variable is
maintenance of inspiration
The cycling variable is
transition to expiration
The baseline variable is
end expiration
The trigger variable represents
the start of inspiration
can be affected with or without patient inspiratory effort by either pressure, volume, flow, or time
Pressure as the trigger variable:
pressure decrease in circuit stimulates ventilator to deliver breath
Volume as the trigger variable:
volume change in circuit can stimulate ventilator to deliver breath
Flow as the trigger variable:
change of flow in circuit stimulates ventilator to deliver breath
Time as the trigger variable:
set time interval triggers ventilator to deliver breath
*** this occurs independent of patient effort
The limit variable
controls how an inspiratory breath is maintained, once threshold is reached variable will not exceed set limit
-this DOES NOT cause termination of inspiration
When pressure is set as the limit variable:
sets upper pressure limit that cannot be exceeded
When volume is set as limit variable:
sets upper volume limit that cannot be exceeded
When flow is set as the limit variable:
sets maximum airflow that cannot be exceeded
The cycling variable is the
transition from inspiration to expiration
based on either volume, pressure, flow, or time
With volume set as the cycling variable:
ventilator delivers flow until set volume achieved
if inspiratory pause set (typically 10-20%) this variable changes to time-based cycling variable
With pressure set as the cycling variable:
once pressure achieved flow will transition to expiration
With flow set as the cycling variable:
once inspiratory flow drops below set threshold (default at 25%) ventilator will transition to expiration
-noted in pressure support ventilation mode
With time set as the cycling variable:
ventilator terminates inspiratory breath after predetermined inspiratory time has been delivered
The baseline variable is
the pressure maintained in the circuit at end expiration (PEEP), must be individualized to patient, used to prevent atelectasis
PEEP is
the alveolar pressure above atmospheric
goal: used to improve oxygenation
Intrinsic PEEP is
secondary to incomplete expiration
–referred to as auto-PEEP
Extrinsic PEEP is:
provided by a mechanical ventilator
-referred to as applied PEEP
Auto PEEP is
incomplete expiration prior to initiation of next breath
causes progressive air trapping
Causes of PEEP include
high minute ventilation
expiratory flow limitation
expiratory resistance
Volume control ventilation:
delivers set tidal volume at set respiratory rate -TIME is the set trigger variable -VOLUME is the limit variable -TIME is cycling variable airflow will remain constant
With volume control ventilation, airway pressure will
change on a breath-by-breath basis during this mode of ventilation based on changing respiratory compliance
Reasons for choosing VCV include:
maintenance of set minute ventilation through direct manipulation of Vt and RR
- must set individualized alarms for airway pressure to protect patient
- increasing airway or lung resistance will stimulate generation of higher pressure to deliver set Vt
Pressure control ventilation:
delivers set inspiratory pressure at set respiratory rate
TIME is the trigger variable
PRESSURE is the limit variable
TIME is the cycle variable
With pressure control ventilation, airway pressures are controlled by
the user, Vt can change on a breath-by-breath basis depending on total respiratory system compliance
PCV should be chosen to
set pressure limit to avoid barotrauma from delivery of excessive pressure
- decelerating flow pattern allows for homogenous distribution of inspired gas throughout lungs- theoretically improves ventilation pattern and decreases work of breathing
- must set patient appropriate high and low Vt alarms as change in respiratory compliance can affect Vt delivered
Pressure control volume guarantee is
when respiratory cycle variables mirror PCV, however ventilator adjust pressure delivered if current volume is not at set volume
- adjustments take 3-5 breaths to complete
- can allow for atelectasis development if compliance decreases and ventilator is delayed in providing adequate pressure to distend lungs
Synchronized intermittent mandatory ventilation (SIMV)
delivers set Vt at a set respiratory rate in conjunction with patient initiated breaths
TIME or PATIENT stimulate the trigger variable
FLOW is the limit variable
VOLUME is the cycle variable
-patient initiated breaths are not supported (unless in SIMV-PSV)
Reasons for choosing SIMV
useful when weaning from controlled mechanical ventilation to spontaneous respiration- less desynchrony with patient initiated breaths
With SIMV, hypoventilation can occur
if set Vt and RR are too low and the patient’s spontaneous respiration effort is inadequate
With SIMV, hyperventilation can occur if
using SIMV-PSV and pressure support level too high
Pressure support ventilation is
supported mode of ventilation for spontaneously breathing patient Pressure support level set by user: PATIENT is the trigger variable PRESSURE is the limit variable FLOW is the cycle variable
With pressure support ventilation, patient controls most aspects of venilation
but the anesthetics can adjust certain variables to augment or limit support given to prepare patient for extubation
Reasons to choose pressure support ventilation:
great for end of case in preparation for extubation- patient must be breathing spontaneously or ventilator will switch to backup mode
Just like PCV pressure is controlled, changes in respiratory system compliance will alter Vt delivered
Physiologic respiration occurs through
negative pressure
Negative intrapleural pressure provides
a positive trans-pulmonary pressure to minimize atelectasis at baseline
Ptp= Palv-Ppl
Anesthetic and surgical factors alter
chest wall muscle tone which alters the intrapleural pressure gradient
Maintaining a positive transpulmonary pressure during surgery is dependent on
maintaining alveolar pressure
Anesthesia and surgical effects on lungs include
loss of muscle tone & elevated intraabdominal pressure
Elevated intraabdominal pressure can occur from
increased BMI, Pneumoperitoneum, trendelenburg position
Loss of muscle tone can occur from
upper airway muscle obstruction
chest wall and diaphragm- abdominal contents cephalad displacement or alveolar compression
Induction of anesthesia causes a
reduction in FRC
Transition from upright to supine position
decreases FRC by 0.8-1L
Induction agents further reduce FRC by
0.4-0.5 L
Total reduction is
1.2-1.5L, bringing lung volume close to residual volume
Non-recruitable lung tissue can result from
ARDS- cellular debris, edema
Recruitable lung tissue can result from
general anesthesia- loss of FRC, atelectasis
Factors that contribute to alveolar collapse include
position, induction, FiO2, maintenance, and emergence
Emergence can cause alveolar collapse because
high FiO2 promotes postoperative atelectasis
absence of CPAP–> continued lung collapse
Maintenance can cause alveolar collapse because
progressive airway closure with decreasing compliance
FiO2 can cause alveolar collapse because
resorption behind closed airways–> atelectasis
increased FiO2–> faster resorption
Induction can cause alveolar collapse because
loss of muscle tone–> decreased FRC
Position can cause alveolar collapse because
increased closing pressure–>decreased FRC
Ventilator induced lung injury can occur from
mechanical ventilation
ventilation induced lung injury
ventilation associated lung injury
Mechanical ventilation can induce lung injury
leading to potentially irreversible structural and functional damage
Ventilation induce lung injury is when
ventilator does not cause injury but the settings of the ventilator do
Ventilation associated lung injury is
specific to the OR setting
Ventilation associated lung injury can be caused by
volutrauma, barotrauma, atelectrauma, or biotrauma
Biotrauma is
damage from release of inflammatory mediators
Atelectrauma is
damage from repeated collapse and re-inflation
Barotrauma is
damage from positive pressure effects
Volutrauma is
damaged endothelium, decreased surfactant, and increased capillary leak
Conventional lung ventilation is
strategy that promotes VALI, not individualized Vt: 10-15 mL/kg TBW PEEP: 0-5 cmH2O I:E: no greater than 1:2 FiO2: provider preference
Lung protective ventilation is
a strategy that protects against VALI
individualized to patient and surgery
adjust settings based on patient monitors and ventilator data
Lung protective ventilation initial maintenance settings include:
low Vt: 6-8 mL/kg IBW Minimize FiO2: <30% Individualized PEEP: 30% of BMI Alveolar recruitment maneuvers Inspiratory: expiratory (I:E) ratio: 1:1.5
Lung protective ventilation emergence settings include
FiO2 <80%
elevate head of bed
positive pressure ventilation- maintenance of lung volume, must be greater than closing pressure
The goal of induction strategies include
attenuate anesthesia related changes
Induction strategies include
initial FiO2: 100%
elevated HOB >30%; reverse trendelenburg> back up
tightly sealed face mask- apply CPAP- use APL valve or CPAP mode on ventilator
OPA or NPA as needed
Goals of lung protective ventilation include
restore lung volume- alveolar recruitment maneuver (ARM)
maintain lung volume and minimize atelectasis formation- individualize PEEP
maximize lung compliance- use lowest possible driving pressure, compliance= Vt/delta P
Tidal volume purpose:
maintain physiologic tidal volume
initial setting: 6-8 mL/kg IBW
Maintenance of FiO2 is
initial setting: 30%
Maintain SpO2 >94%
Purpose is to reduce resorption atelectasis & use SpO2:FiO2 curve as monitor to assess if we are maintaining “open lung” ventilation
Maintenance fiO2 should be
low FiO2 can be used as a surrogate monitor to assess ventilation
at 21% if saturation less than 97%, we know greater than 10% intrapulmonary shunting is occurring
The purpose of alveolar recruitment maneuvers is to
create open-lung state
Post-intubation alveolar recruitment maneuvers include
sufficient CPAP to exceed critical opening pressure
initial performance
Alveolar recruitment maneuvers include
bag squeezing technique- ARM through ventilator is ideal
vital capacity maneuver
The initial PEEP setting is
BMI x 0.3
The purpose of the PEEP setting is to
maintain end expiratory lung volume, reduce atelectasis formation
BMI specific levels of PEEP must be proceeded by ARM or barotrauma may occur
Minimum recruitment pressure required for a BMI <30
is 40 cmH20
Minimum recruitment pressure required for a BMI of 30-40
40-50 cmH2O
Minimum recruitment pressure required for a BMI of 40-50
50-55 cmH2O
Minimum recruitment pressure required for a BMI of >50
50-60 cmH2O
The initial I:E ratio setting for BMI <45 is
1:1.5
The initial I:E ratio setting for BMI >45
1:1
The purpose of the I:E ratio is to
reduce airway pressures and increase homogenous ventilation
The goals of emergence include
maintain open-lung throughout emergence
minimize anesthesia induced changes during postoperative period
The emergence FiO2 is:
maintain FiO2 <80% throughout
purpose: reduce atelectasis formation
Positive pressure ventilation is used to
maintain CPAP and PEEP throughout
purpose: prevent atelectasis formation, maintain open-lung state
During emergence, the head of bed should be
> 30 degrees in order to decrease chest wall compression and increase lung compliance
Concerns with using excessive O2 include
activation of reactive oxygen species, peripheral/coronary vasoconstriction, decreased cardiac output, absorption atelectasis
Monitoring trends includes:
lung compliance, pressure volume loops, and flow volume loops
The pressure volume loop is an
assessment of driving pressure- pressure required to deliver set volume
want to maximize volume delivered at lowest pressure
The flow volume loop is a
representation of expiratory flow
acute angle represents expiratory flow limitation
lung compliance trending is
the trend of compliance throughout the case
