Transcript RT 230
RT 230
Unit AIndication, Setup and Monitoring of CMV
INDICATIONS FOR CMV
Apnea
Acute ventilatory failure: A PCO2 of more than
50mmHg with a pH of less than 7.25
Impending acute ventilatory failure
Based on lab data and clinical findings indicating that pt is
progressing towards ventilatory failure
Quick tip:
acute hypercapnic failure ph drops 0.8 for every
10mm hg rise in co2
chronic hupercapnic ph drops 0.03 for every 10 mmhg
rise in co2
Clinical problems often resulting in impending
ventilatory failure
Pulmonary abnormalities
RDS=Respiratory Distress Syndrome
Pneumonia
Pulmonary emboli
Mechanical ability of lung to move air=muscle fatigue
Ventilatory muscle fatigue
Chest injury
Thoracic abnormalities=scoliosis, kyphoscoliosis
Neurologic disease=GB, MG
Pleural disease=pleurasy
Clinical evaluation
Vital signs: Pulse and BP increase
Ventilatory parameters
VT decreases
RR increases
Accessory muscle use increases
Paradoxical breathing (abdomen out, rib cage in)
Retractions may be noted
Development of impending acute vent failure may
demonstrate
Progressive muscle weakness in pt with Neurologic
disease
Increasing fatigue
ABGs demonstrating a trend toward failure
9am 10am
pH
PCO2
HCO3
PO2
11am
7.58
22
21
60
12pm
7.53
28
22
55
1pm
7.46
35
23
50
7.38
42
24
43
7.35
48
24
40
Non-responsive hypoxemia
PaO2 less than 50% on an FIO2
greater than 50%
PEEP is indicated
REFRACTORY HYPOXEMIA
PHYSIOLOGIC EFFECTS OF POSITIVE PRESSURE
VENTILATION
Increased mean intrathoracic pressure
Decreased venous return
Thoracic pump is eliminated***
Pressure gradient of flow to right side of heart is decreased
Right ventricular filling is impaired
Give fluid
Decreased cardiac output
Caused by decreased venous return
Give drugs and fluid
Monitor I and O. Normal urine output 1000-1500
cc/24 hours
THORACIC PUMP
The "thoracic pump" is the thoracic cavity, the
diaphragm, the lungs, and the heart.
The diaphragm moves down, pressure in the
cavity decreases and venous blood rushes
through the vena cava via the right heart into the
lungs. Pulmonary blood vessels expand
dramatically, filling with blood, air and blood
meeting across the very thin alveolar surface.
The deeper the inhalation, the more negative the
pressure, the more blood flows, and the fuller the
lungs become.
THORACIC PUMP
As the diaphragm moves up the pressure in the
thoracic cavity reverses. Pulmonary blood vessels
shrink ejecting an equal volume of blood out of
the pulmonary veins into the left heart. The left
heart raises the pressure and checks and
regulates the flow. The more complete the
exhalation, the more positive the pressure
becomes and the more blood is ejected from the
lungs.
Decrease exhalation, more pressure in cavity
decrease CO
EFFECTS OF PPV CONT.
Increased intracranial pressure
Blood pools in periphery and cranium because of decreased
venous return
Increased volume of blood in cranium increases intracranial
pressure
Decreased urinary output
PPV could cause 30-50% decrease renal output
Decreased CO results in decreased renal blood flow
Alters filtration pressures and diminishes urine
formation
Decreased venous return and decreased atrial pressure are
interpreted as a decrease in overall blood volume
ADH is increased and urine formation is decreased
ADH=VASOPRESSIN
Roughly 60% of the mass of the body is water,
and despite wide variation in the amount of
water taken in each day, body water content
remains incredibly stable. Such precise control of
body water and solute concentrations is a
function of several hormones acting on both the
kidneys and vascular system, but there is no
doubt that antidiuretic hormone is a key player
in this process.
Antidiuretic hormone, also known commonly as
arginine vasopressin
The single most important effect of antidiuretic
hormone is to conserve body water by reducing
the loss of water in urine. A diuretic is an agent
that increases the rate of urine formation.
high concentrations of antidiuretic hormone
cause widespread constriction of arterioles, which
leads to increased arterial pressure.
Retention of fluids will cause EDEMA
EFFECTS OF PPV CONT.
Decreased work of breathing
Force to ventilate is provided by the ventilator
Increased deadspace ventilation
Positive pressure distends conducting airways & inhibits
venous return
The portion of VT that is deadspace increases
Greater percentage of ventilation goes to apices
Increased intrapulmonary shunt
Ventilation to gravity dependent areas is decreased
Perfusion to gravity dependent areas increase
Shunt fraction increases from 2-5% to 10%
A pulmonary shunt is a physiological condition which results when the
alveoli of the lung are perfused with blood as normal, but ventilation (the
supply of air) fails to supply the perfused region. In other words, the
ventilation/perfusion ratio (the ratio of air reaching the alveoli to blood
perfusing them) is zero. A pulmonary shunt often occurs when the alveoli fill
with fluid, causing parts of the lung to be unventilated although they
are still perfused. Intrapulmonary shunting is the main cause of
hypoxemia (inadequate blood oxygen) in pulmonary edema and conditions
such as pneumonia in which the lungs become consolidated.
The shunt fraction is the percentage of blood put out by the heart that is
not completely oxygenated. A small degree of shunt is normal and may
be described as 'physiological shunt'. In a normal healthy person, the
physiological shunt is rarely over 4%; in pathological conditions such as
pulmonary contusion, the shunt fraction is significantly greater and even
breathing 100% oxygen does not fully oxygenate the blood.[1]
EFFECTS OF PPV CONT.
Respiratory rate, VT, Inspiratory time, and
flow rate can be controlled
May cause stress ulcers and bleeding in GI
tract
COMPLICATIONS OF MECHANICAL
VENTILATION
High pressures are associated with barotrauma
Pneumothorax, pneumomediastinum, pneumopericardium,
subcutaneous emphysema
Pneumothorax has decreased chest movement,
hyperresonance to percussion, on affected side
If tension pneumothorax: medical emergency
Relieved by needle insertion, then chest tube
Use 100% oxygen to speed reabsorption.
16
Complications related to pressure
Ventilator-associated lung injury (VALI)
DETERMINATION OF SETTINGS ON THE
MECHANICAL VENTILATOR
Placing patient on CMV
Establish airway
Select VT 8-12ml/kg of ideal body weight
Select mode - a/c sensitivity at minimal to not self cycle
Set pressure limit 10cmH2O above delivery pressure
Set sigh volume 1-1/2 to 2 times VT
Sigh pressure 10cmH2O above sigh delivery pressure
Rate as ordered
PEEP as ordered: exp. resist, insp. hold, etc.
Set spirometer 100 cc less than patient volume
check for function (turn on)
Modes
Control
All of WOB is taken over by ventilator
Sedation is required
Control mode is useful
During ARDS, especially if high PEEP is required or inverse
I:E ratio
Assist
Patient is able to control ventilatory rate
Should not be used for continuous mechanical ventilation
if pt is apneic
Assist/control
Pt able to control vent rate as long as spontaneous rate >
backup rate
Machine performs majority of WOB
Sedation is often required to prevent hyperventilation
Is useful during early phase of vent support where rest is
required
Useful for long term for pt not ready to wean
SIMV
In between positive press breaths pt can breathe
spontaneously
Useful for long term for pt not ready to wean
Used as weaning technique for short-term vent dependent
pt
PS
Vent functions as constant pressure generator
Positive pressure is set
Pt initiates breath, a predetermined pressure is rapidly
established
Pt ventilates spont, establishes own rate, VT, peak flow and
I:E
Can be used independently/CPAP/SIMV
Indicated to reduce work imposed by ETT, 5 to 20cm H2O
Can be used for weaning
A set IPS (12ml/kg VT) achieved by adjusting IPS level
then slowly reducing as clinical status improves
To overcome resistance of ETT, IPS should meet Raw
To determine amount of PS needed: [(PIP – Plateau
pressure) / Ventilatory inspiratory flow] x spontaneous peak
inspiratory flow
IBW
Estimated ideal body weight in (kg)
Males: IBW = 50 kg + 2.3 kg for each inch
over 5 feet.
Females: IBW = 45.5 kg + 2.3 kg for each
inch over 5 fee.
1 Kilogram = 2.20462262 Pounds
MONITORING CMV
Observation
Look at patient!
Make a good visual assessment
Start with patient, trace circuit back to ventilator
Check and drain tubing
Check connections
Check patient
Suctioning, position, etc.
BP
Spontaneous RR
Heart rate and all vital signs
Check machine settings
VT (set, exhaled, corrected)
f (assisted, set, spontaneous)
Pressure limit: 10 above delivery pressure
PEEP if applicable: Check BP!
Peak Insp. Pressure (PIP): Keep as low as possible
I:E ratio for proper flow
FiO2: Keep as low as possible to prevent Oxygen Toxicity
yet keep them adequately oxygenated
Check all apnea alarms and settings.
Check set VT to exhaled VT for any lost volumes
If difference is greater than 100 cc, check for leak.
Compliance
Measures distensibility of lung – how
much does the lung resist expansion.
Relationship between Volume and
Pressure
High compliance equals lower PIP
thus easier ventilation and less side
effects of CMV
Disease states resulting in low compliance
include the Adult Respiratory Distress Syndrome
(ARDS), pulmonary edema, pneumonectomy,
pleural effusion, pulmonary fibrosis, and
pneumonia among others.
Emphysema is a typical cause of increased lung
compliance.
YOU MUST KNOW
Dynamic =
VT (corrected or exhaled)
PIP – PEEP
Always subtract out PEEP
Consistently use exhaled or corrected VT
Used to assess volume/pressure relationships during
breathing – any changes in RR will effect it
CDYN decreases as RR increases which may cause V/Q
mismatch which may cause hypoxemia
May reflect change due to change in flow due to
turbulence instead of compliance
Normal = 30 – 40 cmH2O
VERY IMPORTANT
Static
= VT (corrected or exhaled)
Plateau – PEEP
Always subtract out PEEP
Always consistently use either VT exhaled or VT corrected
Will not change due to change in flow, more accurate
Measured pressure to keep airways open with no gas
flow.
Normal values very with pt, but usually above 80 cmh2o
will show lung overdistention
Importance
to follow trends in patient compliance
Decreased C = stiffer lung = less compliant = higher
ventilating pressures = you need a ventilator with high
internal resistance to deliver volumes using square wave.
High compliance = possible Emphysema
STATIC VS DYNAMIC COMPLIANCE
Decrease in CDYN with no change in CST indicates
worsening airway resistance
Causes
Bronchospasm
Secretions
Kinked/Occluded ETT
Inappropriate flow and/or sensitivity settings
If both CDYN and CST worsen, not likely to be an airway
problem
Causes
Pulmonary Edema
ARDS
Tension Pneumothorax
Atelectasis
Fibrosis
Pneumonia
Obesity
Patient Position
RAW = PIP – Pplat
Flow (L/sec.)
Airway Resistance
Impedance to ventilation by movement of gas
through the airways thus the smaller the
airway the more resistance which will increase
WOB (causing respiratory muscle and patient
fatigue)
Example: ETT, Ventilator Circuit,
Bronchospasm
Airway Resistance & Compliance
Decreased Compliance + Increased Airway
Resistance = High PIP, Decreased Volumes and significant
increase in WOB
Very difficult to wean a patient until problems are
resolved
PATIENT STABILITY
Vital signs
Pulse – normal, weak, thready, bounding, rate, etc.
BP – hypo/hypertensive – directly related to CO
Respirations – tachypnea, bradypnea, hyperpnea,
hypopnea, rate, etc.
Color – dusky, pale, gray, pink, cyanotic
Auscultation - bilateral, etc.
Are they bilateral, amount of air moving, rales, rhonchi or
wheezing
Are they Vesicular (normal) or Adventitious (abnormal)
Describe what you hear: fine, course, high-pitched, lowpitched, etc.
And the location where you heard it: bilateral bases,
posterior bases, right upper anterior lobe, laryngeal, upper
airway, etc.
HEMODYNAMIC MONITORING
BTFDC
Also known as
Balloon Tipped Flow Directed Catheter
Swan-Ganz Catheter
Pulmonary Artery Catheter
Done by inserting a BTFDC into R atrium, thru R ventricle,
and into pulmonary artery
SvO2 is drawn from the distal port of a BTFDC
Used to monitor tissue oxygenation and the amount of O2
consumed by the body
CATHETERS AND INSERTION SITES
PA PRESSURE WAVEFORMS
CVP
Monitors fluid levels, blood going to the right side of heart
Normal = 2 – 6 mmHg (4 – 12 cmH2O)
Increased CVP = right sided heart failure (cor pulmonale),
hypervolemia (too much fluid)
Decreased CVP = hypovolemia (too little fluid), hemorrhage,
vasodilation (as occurs with septic shock)
PAP
Pulmonary Artery Pressure = B/P lungs
Monitors blood going to lungs via Swan-Ganz catheter
(BTFDC)
Normal 25/8 (mmHg)
Increased PAP= COPD, Pulmonary Hypertension, or
Pulmonary Embolism
PCWP
Pulmonary Capillary Wedge Pressure monitors blood
moving to the L heart
Balloon is inflated to cause a wedge
Normal PCWP = 8 mmHg
Range is 4 – 12 mmHg
Increased PCWP = L heart failure, CHF
Measure backflow resistance
Cardiac Output
Expressed as QT or CO (QT= Greek alphabet, 1050 BC
scientist used qt had cardiac output expression)
Normal = 5 LPM
Range 4 – 8 LPM
Decreased CO = CHF, L heart failure, High PEEP effects
I&O
Needs to be monitored closely to prevent fluid imbalance
due to increased ADH production and decreased renal
perfusion
Fluid imbalance can develop into pulmonary edema and
hypertension
CARDIAC OUTPUT (CO)
The amount of blood pumped out of the left
ventricle in 1 minute is the CO
A product of stroke volume and heart rate
Stroke volume: amount of blood ejected from the
left ventricle with each contraction
Normal stroke volume: from 60 to 130 ml
Normal CO: from 4 to 8 L/min at rest
Fick CO: Vo2/Cao2-Cvo2
C(a-v)O2 could decrease if CO is increased due
to less oxygen needs to be extracted from each
unit of blood that passes
Fick Method
The Fick method requires that you be able to
measure the A-V oxygen content difference and
requires that you be able to measure the oxygen
consumption. An arterial blood gas from a
peripheral artery provides the blood for the
CaO2 measurement or calculation while blood
from the distal PA port of a Swan-Ganz catheter
provides the blood for the CvO2 measurement
or calculation
Dilution methods mathematically calculate
(using calculus) the cardiac output based on
how fast the flowing blood can dilute a marker
substance introduced into the circulation
normally via a pulmonary artery catheter.
(injecting a dye in prox port of Swanz. Not really
used anymore due to infections
MEASURES OF CARDIAC OUTPUT AND
PUMP FUNCTION
•CARDIAC INDEX (CI)
•Determined by dividing the
CO by body surface area
•Normal CI is 2.5 to 4.0
L/min/m2
•CI measurement allows a
standardized interpretation
of the cardiac function
•True cardiac output
compared to each persON
MEASURES OF CARDIAC OUTPUT AND
PUMP FUNCTION (CONT’D)
Cardiac
work
A measurement of the energy spent
ejecting blood from the ventricles
against aortic and pulmonary artery
pressures
It correlates well with the amount of
oxygen needed by the heart
Normally cardiac work is much higher
for the left ventricle
MEASURES OF CARDIAC OUTPUT AND
PUMP FUNCTION (CONT’D)
Ventricular stroke work
A measure of myocardial work per contraction
It is the product of stroke volume times the pressure
across the vascular bed
Ventricular volume
Estimated by measuring end-diastolic pressure
Measures of Cardiac Output and
Pump Function (cont’d)
Ejection fraction
The fraction of end-diastolic volume ejected with
each systole; normally 65% to 70%; drops with
cardiac failure
DETERMINANTS OF PUMP FUNCTION
Preload
Created by end-diastolic volume
The greater the stretch on the myocardium prior to
contraction the greater the subsequent contraction
will be
When preload is too low, SV and CO will drop
This occurs with hypovolemia
Too much stretch on the heart can also reduce SV
Determinants of Pump Function
Afterload
Two components: peripheral vascular resistance and
tension in the ventricular wall
Created by end systolic volume
Increases with ventricular wall distention and
peripheral vasoconstriction
As afterload increases, so does the oxygen demand of
the heart
Decreasing afterload with vasodilators may help
improve SV but can cause BP to drop if the blood
volume is low
Ventilation Patient Parameters
Spontaneous VT
Is it adequate for patient?
Spontaneous volumes should be between 5 – 8 ml/Kg of
Ideal Body Weight (IBW)
Spontaneous VC
10 – 15 ml/Kg IBW
NIF/MIP/MIF/NIP
-20 to -25 cmH2O within 20 seconds
ABGS
PaO2 represents oxygenation – adjust with
PEEP or FiO2
PaCO2 represents ventilation – adjust with VT
or RR
pH represents Acid/Base status
pH acid: High CO2 (respiratory cause) or low HCO3
(Metabolic cause)
pH alkaline: Low CO2 (respiratory cause) or high HCO3
(Metabolic cause)
Draw ABGs
To stabilize
With any change in ventilator settings change only one vent
setting at a time
With any change in patient condition
VENTILATOR ALARMS
Appropriate for each patient
Usually 10 higher/lower than set parameter
For pressure and RR settings
VT alarms 100 ml higher/lower than set VT
Adjust all alarms for patient safety.
X-RAY WHEN INDICATED FOR
Tube placement: 2 – 4 cm above carina
Possible pneumothorax
To check for disease process reversal, or lack
of, for treatment purposes and weaning
FREQUENCY OF VENTILATOR CHECKS
Must be done as often as required by the
patients condition unstable patients
continuous to hourly
In general patients and ventilators need
evaluation Q1-Q4h
With every vent check, patient assessment
should take place
Use VT exhaled for calculations.
Corrected VT = exhaled vt-tubing lost volume
Tubing volume lost factor 1-8 cc x pressure
Exhaled vt 650= pip-peep x (3) = 60
650-60=590 corrected vt
WAVEFORM ANALYSIS
Three wave forms typically presented together
Pressure
Flow
Volume
Plotted versus time
Horizontal axis is time
Vertical axis is variable
Other common wave forms:
Pressure vs Volume
Flow vs Volume
Pressure vs Time Assessment
Patient Effort: Negative pressure deflection at beginning of
inspiration indicates patient initiated breath
Peak & Plateau Pressures
Adequacy of inspiratory flow: If pressure rises slowly, or if
curve is concave, flow is inadequate to meet patient’s
demand.
Flow vs Time Assessment
Inspiratory flow patterns
Air Trapping – a.k.a. AutoPEEP – expiratory flow fails to
reach baseline prior to delivery of next breath
Airway Resistance
Lower slope (smaller angle) indicative of high resistance
to flow
Steeper slope (greater angle) indicative of lower
resistance to flow
Also increased resistance manifests itself as decreased
peak expiratory flowrate (depth of expiratory portion of
flow pattern) with more gradual return to baseline as
expiratory flow meets with resistance
Bronchodilator = increased peak expiratory flow rate
with quicker return to baseline
Volume vs Time Assessment
VT = peak value reached during inspiration
Air Trapping = fails to reach baseline before commencement
of next breath
Identifying breath type
Larger volumes = mechanical breaths
Smaller volumes = spontaneous breaths
Pressure vs Volume Loop
Volume on vertical axis
Pressure on horizontal axis
Positive pressure on right of vertical axis
Indicates mechanical breath
Application of positive pressure to the lung
Tracing is in a “counter-clockwise” rotation
Subambient pressure to the left of the vertical axis
Indicates a spontaneous breath
Spontaneous inspiration is to the left of the vertical axis
– subatmospheric pressure at start of inspiration
(Intrapulmonary pressure = -3 cmH2O)
Spontaneous expiration is to the left of the vertical axis –
+3 cmH2O intrapulmonary pressure on expiration
Tracing is in a “clockwise” rotation
Useful in helping diagnosing
Alveolar Overdistension = looks like bird’s beak, or the
“Partridge Family” symbol
Increased RAW = looks “pregnant” or “fat”
Decreased compliance = looks “lazy” or like it’s lying
down
Flow vs Volume Loop
Helpful in assessing changes in RAW, such as after the
administration of a bronchodilator
Flow on vertical axis
Volume on horizontal axis
Inspiration is top part of loop, expiration on bottom
When RAW improved, expiratory flows are greater and the
slope of the expiratory flow is greater
To determine patient effort, use the following
curves
Pressure vs Time
Pressure vs Volume Loop
Volume vs Time
All show subambient drops in pressure/volume when
patient initiates the breath
To determine Auto-PEEP, use
Volume vs Time
Flow vs Time
Pressure vs Volume Loop
For all curves, ask “does the exhalation reach baseline
before the next breath starts
To determine the adequacy of inspiratory flow
Pressure vs Time = concave or slow rise to pressure means
inadequate flow on inspiration
Volume vs Time = Too slow flow = increased I – Time =
decreased E-Time = AutoPEEP
Volume vs Pressure = Slope is shallow, may look similar to
loop associated with increased RAW
If you detect the patient actively working
during mechanical breath, increase the flow to
help meet the patient’s demand and decrease
the WOB
To assess changes in compliance, use
Pressure vs Volume Loop
Steeper slope = increased compliance, or larger volume at
lower pressure
Shallow slope = decreased compliance, or smaller volume
at higher pressure
To assess changes in RAW, use
Pressure vs Volume Loop
Space – “hysteresis” – between inspiratory and
expiratory portions of loop
“Bowed” appearance – inspiratory portion more rounded
and distends toward the pressure axis
Flow vs Volume Loop
Observe peak flow on Flow-Volume Loop
Increased RAW = Decreased Peak Flow
UNIT B
Acute & Critical Care
PEEP/CPAP
PEEP – Positive End Expiratory Pressure
Definition
Application of pressure above atmospheric at the airway
throughout expiration
Goal
To enhance tissue oxygenation
Maintain a PaO2 above 60 mmHg with least amount of
supplemental oxygen
Recruit alveoli
Indications
Cardiogenic pulmonary edema
Left sided heart failure
Prevents transudation of fluid
Improves gas exchange
ARDS
Increases lung compliance
Decreases intrapulmonary shunting
Increases FRC
Refractory hypoxemia
PaO2 < 50 mmHg with an FIO2 >50%
Increase FRC
Opens collapsed alveoli
Increases reserve
Contraindications
Unilateral lung disease
Hypovolemia
Hypotension
Untreated pneumothorax
Increased ICP
Hazards
All of the effects of CMV are magnified
Increased intrathoracic pressure
Decreased venous return
Increased ADH
Decreased blood pressure
Decreased cardiac output
Loss of thoracic pump
Barotrauma
Physiological effects
Baseline pressure increases
Increased intrapleural pressures
Increased FRC—recruiting collapsed alveoli
Dead space—increased in non-uniform lung disease and
healthy lungs by distending alveoli
Increased alveolar volumes
Can increase compliance
Cardiovascular
Decrease venous return
Decrease cardiac output
Decrease blood pressure
Decreases intrapulmonary shunt
Increases mixed venous value (PvO2)--Drawn from
pulmonary artery via Swan-Ganz
Increased intracranial pressures
Decrease in A-a gradient (A-a DO2)
Increased PaO2
Decrease in FIO2, which causes a decrease in PAO2
INITIATION AND MONITORING OF PEEP
Start off at 5 cmH2O and increase by 3 to 5
cmH2O increments
Adjust sensitivity
With an increase in baseline pressure the sensitivity must
be increased or the patient will have to increase inspiratory
effort to initiate a breath
Monitor
Blood pressure: First thing you look at when adding PEEP
Cardiac output: Goal is least cardiac embarrassment with
the best PaO2 and least FIO2
Pulse
If the patient is hypoxemic their heart rate is probably
increased
With addition of PEEP the hypoxemia should resolve and
pulse should decrease to normal level
PaO2: Goal is best PaO2 with the lowest possible
FIO2
MAINTENANCE LEVEL OF PEEP
PEEP trial
Used to determine best level of PEEP
This is the pressure at which cardiac output and total lung
compliance is maximized,the VD/VT is minimal, and the best
PaO2 and PvO2, and the lowest P(A-a)O2 are obtained
1. Best PEEP or Optimum PEEP
Level at which physiological shunt (Qs/Qt) is lowest without
detrimental drop in cardiac output
A C(A-V)O2 of less than 3.5 vol% should reflect adequate CO
Fick’s law CO = VO2/C(a-v)O2
Cardiac output and C(a-v)O2 are inversely related
2. Optimal PEEP
Level which provides maximal O2 delivery(DO2) and lowest
VD/VT
Cardiac output can often be compromised but not concerned
with if using optimal PEEP
CPAP
Physiologically the same as PEEP
Used in spontaneously breathing patients
Maintains continuous positive airway pressure during
inspiration and expiration
Accomplished by a continuous flow of gas or a
demand valve
Used to treat OSA
System flow must be enough to meet patient’s peak
inspiratory demands
CPAP delivered via mask or nasal pillows
No machine breaths, all spontaneous
ventilation
NPPV
(BIPAP)
Similar to CPAP
Delivers two levels of pressure during the inspiratoryexpiratory cycle
Delivers higher pressure on inspiration
Delivers lower pressure on exhalation
Less resistance to exhalation
Two levels of pressure
EPAP
Constant pressure delivered during exhalation
Same as CPAP
Adjust for oxygenation
IPAP
Constant pressure delivered during inspiration
Same as IPPB
Adjust for ventilation
The difference between the two pressures is known as
pressure support
Used to treat OSA
Better tolerated than traditional CPAP
Delivered with mask or nasal pillows
Used in acute respiratory failure
Can prevent or delay intubation and CMV
Improves ventilation and oxygenation
Improves patient comfort
RULES OF PUTTING PATIENT ON PEEP
Obtain order
Set-up PEEP and make additional changes
(i.e., sensitivity)
Monitor patient for hazards, BP, CO if
available
Monitor for "optimum
PEEP"
Decrease FIO2 as possible until below 0.40-.50,
then decrease PEEP
IMV/SIMV
Definitions
IMV: Intermittent Mandatory Ventilation
Patient receives set number of mechanical breaths from the
ventilator. In between those breaths, the patient can take
their own spontaneous breaths at a rate and VT of their
choice.
SIMV: Synchronized Intermittent Mandatory
Ventilation
Same as IMV, except the mechanical breaths are
synchronized with the patient’s spontaneous respiratory
rate. Helps improve patient/ventilator synchrony and helps
prevent “breath stacking” (where the vent delivers the
machine set VT on top of the patient’s spontaneous VT)
IMV
Advantages
Prevents muscle atrophy – makes patient assume an
increasing, self-regulating role in their own respirations,
helping to rebuild respiratory muscles
Allows patient to reach baseline ABGs – baseline means the
patient’s baseline ABGs
Chronic CO2 retainer ABGs do not have a normal PaCO2
of 40
Decreases mean intrathoracic pressure – the lower the
IMV/SIMV rate, the lower the intrathoracic pressure
Avoids decreased venous return – lower intrathoracic
pressure = greater venous return
Avoids cardiac embarrassment – greater venous return =
less decrease in cardiac output and blood pressure
PEEP devices
Water column
Amount of water in a column
determines PEEP
Pressure in expiratory limb must
exceed pressure of water in
column
Exhalation occurs under a
Column of water
Spring loaded valve: Tension in spring
determines PEEP
Balloon type
Similar to “mushroom-type”
exhalation valve
Balloon is in exhalation valve
Balloon is inflated to a given
pressure
Pressure in balloon determines
PEEP
Diaphragm
Pressure against diaphragm
Disposable circuit with MA-1
May avoid positive fluid balance
Allows normalization of ADH production
Helps avoid cardiac embarrassment
Psychological encouragement
Some patients may exhibit anxiety, especially those who
have been on the vent for several days or weeks
Do not tell the patient they will never need the vent
again
Some patients become encouraged by progress, being able
to do more for themselves
Weaning gradually – re-evaluate if weaning takes several
days
May allow decreased use of pharmacological agents – e.g.,
morphine, diprivan, versed, etc.
If patient is too sedated, won’t be able to breathe
spontaneously and participate in weaning
May be the only way to correct respiratory alkalosis on
patient who is “over-breathing” the vent in A/C mode
Patient’s spontaneous VT will most likely be smaller than
that of the set VT on mechanical ventilator
Candidates for IMV/SIMV
IMV/SIMV is great for weaning patient from CMV
Allows patient to assume increased responsibility for
providing own respirations, with diminishing mechanical
support
Allows patient to re-build respiratory muscle strength
Patient must be stable. Not ideal for unstable patient.
Consider patient unstable if
Fever – causes increased O2 consumption and increased
CO2 production, thereby increasing WOB
Unstable cardiac status
Unresolved primary problem that caused them to be on
the vent in the first place
Problems of IMV
Fighting the ventilator – patient becomes out
of phase – or synch – with the ventilator
Stacking of breaths is not necessarily a
problem
Patient will normally synchronize self with ventilator rate
Patient disconnection from gas source (with
external IMV circuit)
Other problems of CMV
Benefits of SIMV – Synchronized IMV
Prevents stacking of breaths (pt can breath
spontaneously through demand valve)
May help patient to become in phase with vent
Breath stacking could be prevented just by
increase inspiratory
flow
INSPIRATORY PRESSURE SUPPORT (IPS)
Commonly referred to simply as “Pressure
Support”
During spontaneous breathing, the ventilator
functions as a constant pressure generator
Pressure develops rapidly in the ventilator system and
remains at the set level until spontaneous inspiratory flow
rates drop to 25% of the peak inspiratory flow (or specific
flow rate)
This mode may be used
Independently
With CPAP
With SIMV
With any spontaneous ventilatory mode
Not with any full support modes, such as Control
or A/C
PS is used to overcome the increased
resistance of the ET tube and vent circuit
Pouiselle’s Law: decrease the diameter of a tube by ½,
increase the resistance of flow through that tube by 16
times
If you apply/use PS, do not set less than 5 cmH2O of PS —
least amount needed to overcome resistance of ET tube and
vent circuit
If PS is set at a level higher than RAW, you will be adding
to patient volumes, rather than just helping overcome the
increased resistance from the ET tube and vent circuit
Can be used to help wean patient from vent and
help rebuild respiratory muscle strength
MANAGEMENT OF VENTILATORS BY ABGS
Pressure Control Ventilation
Can be used as CMV or SIMV
In SIMV mode, the machine breaths are
delivered at the preset pressure while the
spontaneous breaths are delivered with PS
PC-CMV (a.k.a., PCV) used to decrease shear
forces that damage alveoli whenever the peak
or plateau pressures meet or exceed 35cm H2O
Help prevent damage to alveoli from excessively high
ventilating pressures
Shear forces damage alveoli when they collapse (because
closing volumes are above FRC) and then are forced back
open again with the next breath. Damage occurs as this
cycle is repeated over time: alveoli collapses, then is
reinflated, collapses, reinflated, etc.
Also used when permissive hypercapnia is
desired (treatment of ARDS)
When the PaCO2 is allowed to rise through a planned
reduction in PPV, which allows for a reduction in the mean
intrathoracic pressure, which results in less incidence of
barotrauma and other commonly associated complications
of PPV
The gradual increase in PaCO2 is accomplished by a
reduction of the mechanical VT (by decreasing the pressure)
and usually does not affect the oxygenation
PC-IRV: Pressure Controlled Inverse Ratio
Ventilation
Pressure controlled ventilation with an I:E ratio > 1:1.
Causes mean airway pressure to rise with the I:E ratio
Usually used on patients with severe hypoxemia where high
FIO2s and PEEP have failed to improve oxygenation
Causes intrinsic PEEP (a.k.a. auto-PEEP), which is what
causes the mean airway pressure to increase, which is the
mechanism for alveolar recruitment and improved arterial
oxygenation
While an increase in oxygenation does occur at the lung, a
resultant decrease in cardiac output (due to the increased
mean intrathoracic pressures) may result in an overall
decrease in tissue oxygenation. Care must be exercised to
maintain adequate cardiac output in order to maintain
adequate tissue oxygenation
Because it’s not a natural way to breath (backwards from
the way we normally breath), most patients must be either
heavily sedated (Diprivan, Versed) or must be paralyzed
with a paralytic drug (such as Pavulon or Norcuron)
APRV: Airway Pressure Release Ventilation
Related to PC-IRV except that patient breathes
spontaneously throughout periods of raised and lowered
airway pressure.
APRV intermittently decreases or releases the airway
pressure from an upper CPAP (IPAP) level to a lower CPAP
(EPAP) level
The airway pressure release usually lasts 1.5 seconds or
shorter, allowing the gas to passively leave the lungs to
eliminate CO2
I:E ratio is usually > 1:1, but differs from PC-IRV in that it
allows spontaneous breathing
Because patient is breathing spontaneously, there is less
need for sedation
Usually has lower peak airway pressure than PC-IRV
Originally proposed as a treatment for severe hypoxemia,
but appears to be more useful in improving alveolar
ventilation rather than oxygenation.
END TIDAL CO2 MONITORING (PETCO2)
Measures CO2 level at end exhalation, when
CO2 levels are highest in exhaled breath
Two methods of collection
Sidestream – typically used for non-intubated patients
Mainstream – typically used for intubated patients and
more commonly seen and used
Probe is placed between the patient wye of vent tubing
and the patient’s ETT
Infrared light measures CO2 levels
Inspired gas should have value of zero
PETCO2 content should be within 2 – 5 mmHg of patient’s
PaCO2
Difference will be greater on a patient with larger amounts of
air trapping, e.g. Emphysema
CAPNOMETRY (CONT.)
96
End-tidal CO2 monitoring is for trending
Not absolute—can vary from breath to breath; similar to
pulse oximetry
Look at the trend. Is the patient’s PETCO2 increasing or
decreasing over a period of time? Similar activity should then
be also occurring with the PaCO2
When setup, correlate the PETCO2 readings with current
ABGs PaCO2. This will give you an idea of how much less the
PETCO2 is reading than the PaCO2, giving you a good idea of
future trends of the PETCO2 will relate to the PaCO2
CHEST TUBE DRAINAGE SYSTEMS
Chest tube placed high in thoracic cavity to
drain air
Second or third intercostal space at midclavicular line
Incision made right over the rib
Chest tube advanced towards anterior apex of lung.
Chest tube placed low in thoracic cavity to
drain fluid (e.g., pleural effusion)
Placement is in fourth intercostal space (or lower) at
midaxillary line
Patient is placed lying on side with affected side “up”
Once incision is made, tube is advanced posteriorly, toward
the base of the lung so gravity can help drain the fluid
Three chamber chest tube drainage system is
most common
Left chamber is the suction control chamber
Level of water determines how much suction is applied to
the chest cavity, regardless of how much the suction is set
on the suction regulator on the wall
Middle chamber is the water seal chamber
Usually no more than 2 cmH2O
Too much and you increase difficulty of air or fluid to
drain
Too little and you risk an air leak
Bubbles in water seal indicate that a leak in the lung is still
present
Spontaneous breathing patients with leak will have
bubbles on exhalation
Intubated, mechanically ventilated patients with leak
will have bubbles on inspiration
Continuous bubbling could be a sign of a leak in your
chest tube drainage system and must be corrected
immediately!
Clamp chest tube briefly where it exits patient’s chest. If
bubbling stops, leak is in your patient (intrathoracic).
If bubbling persists, then you must check your chest tube
drainage system for leaks
Move clamp down tubing in 10cm (approx. 4 inch) increments
(working from patient to chest tube drainage system), briefly
clamping as you go until bubbling stops
Right chamber is the drainage collection chamber
This is where the fluid drained from the patient is
collected
ALI=ACUTE LUNG INJURY OR ARDS
Definition agreed upon in 1994 at the American –
European Consensus Conference on ARDS
ALI Definition: a syndrome of acute and
persistent lung inflammation with increased
vascular permeability. Characterized by:
Bilateral radiographic infiltrates
A ratio PaO2/FIO2 between 201 and 300 mmHg, regardless
of the level of PEEP. The PaO2 is measured in mmHg and
the FIO2 is expressed as a decimal between 0.21 and 1.00
No clinical evidence of an elevated left atrial pressure. If
measured, the PCWP is 18 mmHg or less
ARDS Definition: same as ALI, except the
hypoxia is worse. Requires a PaO2/FIO2 ratio of
200 mmHg or less, regardless of the level of
PEEP. ARDS is ALI in its most extreme state
Mortality rate between 40 and 60% --
varies from source to source
Down from about 20 years ago when ARDS was almost
certain death sentence with approximately 90%
mortality rate.
Current Protective Lung Strategies
Lower VTs with ALI/ARDS patients: about 4-6
ml/Kg IBW to avoid “volutrauma” from
alveolar over distension
Sufficient PEEP to prevent alveolar collapse at
end expiration, yet not so much that cardiac
status is compromised
Permissive hypercapnia when treating
ALI/ARDS
PaO2 > 65 mmHg
PIP < 35cm H2O
If your PIP is greater than 35cm H2O, consider using PCV
Closed suctioning system to maintain PEEP
Do not “bag” ALI/ARDS patient to “recruit more
alveoli”; could lead to barotrauma or volutrauma
Monitor: Patient must be monitored closely as
condition can change relatively quickly!
Things to monitor:
I&O
Cardiac output
BP
PIP
PPLAT
Pulse Ox
FIO2
VT
VE
CST
PETCO2
Waveforms
A-a Gradient
Renal
vasoconstriction, due
to hypoxemia, reduces
urinary output.
Resolution of the
hypoxemic state
relieves the renal
vasoconstriction, thus
increasing urinary
output.
MANAGEMENT OF ABGS WITH CMV
ABG normal pH values
Normal range = 7.35 – 7.45
“Normal” = 7.40
PaCO2
High PaCO2 will cause a low pH, thus causing respiratory
acidosis
Low PaCO2 will cause a high pH, thus causing respiratory
alkalosis
pH needs to be corrected so that drugs being given to
patient will be metabolized
PaCO2 and Ventilation
ABG normal PaCO2 values
PaCO2/Ventilation = 35 – 45
“Normal” = 40
High PaCO2 represents hypoventilation or the patient is
under ventilated or retaining CO2
Low PaCO2 represents hyperventilation or the patient is
over ventilated or blowing off CO2
CO2 represents how well your patient is ventilating. You
would adjust VT, f, or remove dead space if on ventilator
PaCO2 & pH Calculations
PaCO2 and pH have a direct relationship.
Starting at a PaCO2 of 40
If PaCO2 increases by 20 mmHg, pH decreases by 0.10
If PaCO2 decreases by 10 mmHg, pH increases by 0.10
To increase PaCO2 decrease VA
The PaCO2 is inversely proportional to VA providing that
CO2 production remains constant
VA = (VT – VD)f
To decrease VA (increase PaCO2)
Decrease VT (keep in normal range)
Decrease f (will not blow off as much CO2)
Increase VD (only in control mode – 50cc per link of large
bore tubing)
To decrease PaCO2 increase VA
VA = (VT – VD)f
To increase VA (decrease PaCO2)
Increase VT (keep in normal range)
Increase f (will blow off more CO2)
Decrease VD
Dead Space = Ventilation without perfusion
Anatomical dead space averages about 1 ml per pound
Alveolar dead space is alveoli that are ventilated but not
perfused
Physiological dead space is the sum of the above
Normally, this is approximately 1/3 of the VT, or between
20 and 40% for spontaneously breathing, non-intubated
patient
Normal for patient on ventilator is 40 – 60%
Formulas for VD/VT, Desired VT, & Desired f
VD/VT = PaCO2 – PetCO2
PaCO2
Gives the portion/percentage of VT not taking place in gas
exchange.
STRATEGIES TO ALTER VENTILATION
Always adjust VT first, but remember to
keep it in the normal range (8 – 12 ml/kg
of ideal body weight)
If PaCO2 is high, patient is on SIMV, and the patient is
taking spontaneous breaths and the volumes are low,
initiate Pressure Support to increase spontaneous volumes.
If you cannot adjust VT up or down because it would place
the VT out of normal range, then change f (rate)
Change Mechanical Rate
Doing this alters Alveolar Ventilation
If your rate exceeds 20 bpm, auto-PEEP may develop
(patients with very stiff lungs. e.g., ARDS—may require
higher f)
Increase f = decreased PaCO2 (hyperventilate)
Decrease f = increased PaCO2 (hypoventilate)
Add or remove VDMech only in control mode
Add VDMech to increase PaCO2
Decrease VDMech to decrease PaCO2
Cut ETT to proper length to decrease dead
space
Use low compliance vent circuit to decrease
dead space
Large VT and slow f are preferred to small VT
and rapid f because
Alveolar Ventilation is increased
Distribution of inspired gas is improved
Ventilation/Oxygenation is improved
Mean intrathoracic pressure is reduced
PAO2 & OXYGENATION
PaO2/Oxygenation norm = 80 – 100
If PaO2 is below 60, the patient has hypoxemia
For patients that are hypoxic and on a
ventilator, adjust the FIO2 to > 50% then start
adding PEEP
When the patient improves, decrease FIO2 to
40 – 50%, then start removing PEEP to
prevent O2 toxicity
To increase PaO2 (in any mode)
Increase FIO2 if hypoxemia is caused by low
V/Q ratio to > 50, then add PEEP to prevent
oxygen toxicity.
When hypoxemia is present due to lung injury
or physiological shunting (as in disease states
like ARDS), go up to 100 and then add PEEP
or CPAP
TWO INDICES OF OXYGENATION
a/A Ratio
PaO2/PAO2
O2 from alveoli to blood
Divide PaO2 by PAO2
Normal = > 60%
A-a Gradient
P(A-a)O2
Difference between alveolar and arterial PO2
Subtract PaO2 from PAO2
Normal: - On 21%: 10 – 15 - On 100%: 65
On 100%, every 50 mmHg difference equals approx. 2%
shunt
If under 300, you have V/Q mismatch so increase FiO2
If over 300, you have a shunt, so add PEEP or CPAP
First calculate PAO2
Unless told otherwise
PBAR = 760
PH2O = 47
RQ = 0.8
(Pb-PH2O)fio2-(Paco2x1.25)
If FiO2 is greater than 60%, omit RQ from PAO2 formula
PaO2 is obtained from an ABG
To decrease PaO2 (in any mode)
Decrease FIO2
Decrease PEEP gradually
If FIO2 > 50% with PEEP, decrease FIO2 to 40 – 50% first
(to reduce O2 toxicity)
If patient remains stable and has an adequate PaO2, start
to reduce PEEP slowly
Monitor patient at all times for signs of
hypoxemia
MANIPULATION OF ABGS IN CONTROL
MODE
To increase PaCO2
Decrease VT
Decrease f
Increase VD
To decrease PaCO2
Increase VT
Increase f
Decrease VD
MANIPULATION OF ABGS IN A/C
To increase PaCO2
Decrease VT: May be ineffective as pt. may increase f
Decrease f: Patient can increase assisting to override
Never add VD in any mode but control
To decrease PaCO2
Increase VT
Increase f above assist rate
If ineffective, change to control or IMV modes
MANIPULATION OF ABGS IN SIMV/IMV
To increase PaCO2
Decrease VT – only to ranges for patient
Not best choice
Decrease f
Best choice towards weaning
Never add VD in this mode
Will increase patient’s WOB and they will eventually fail
To decrease PaCO2
Increase VT - stay within normal range
Increase f (blow off CO2)
Increase minute ventilation
May need to add PS to augment spontaneous volumes
Do not look at just the numbers and values
Always assess your patient with every ventilator change.
You are treating a patient, not a machine!