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RT 230. Unit A- Indication, Setup and Monitoring of CMV. Indications for CMV. Apnea Acute ventilatory failure: A PCO 2 of more than 50mmHg with a pH of less than 7.25 Impending acute ventilatory failure - PowerPoint PPT Presentation
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RT 230Unit A-Indication, Setup and Monitoring of CMV
INDICATIONS FOR CMV
ApneaAcute 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 10am11am12pm1pm pH 7.58 7.53 7.46 7.38 7.35 PCO2 22 28 35 42 48 HCO3 21 22 23 24 24 PO2 60 55 50 43 40
Non-responsive hypoxemia
PaO2 less than 50% on an FIO2 greater than 50%
PEEP is indicatedREFRACTORY HYPOXEMIA
PHYSIOLOGIC EFFECTS OF POSITIVE PRESSURE VENTILATION
Increased mean intrathoracic pressureDecreased venous return
Thoracic pump is eliminated*** Pressure gradient of flow to right side of heart is
decreased Right ventricular filling is impaired
Give fluidDecreased 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 outputPPV 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 controlledMay cause stress ulcers and bleeding in GI
tract
16COMPLICATIONS OF MECHANICAL VENTILATIONComplications related to pressure Ventilator-associated lung injury (VALI)
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.
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
IBWEstimated 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,
low-pitched, 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 EmbolismPCWP
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 MethodThe 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 workA 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
Ejection fraction The fraction of end-diastolic volume ejected
with each systole; normally 65% to 70%; drops with cardiac failure
Measures of Cardiac Output and Pump Function (cont’d)
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
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
Determinants of Pump Function
Ventilation Patient ParametersSpontaneous 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 IBWNIF/MIP/MIF/NIP
-20 to -25 cmH2O within 20 seconds
ABGSPaO2 represents oxygenation – adjust with
PEEP or FiO2PaCO2 represents ventilation – adjust with
VT or RRpH 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 patientUsually 10 higher/lower than set
parameterFor pressure and RR settingsVT alarms 100 ml higher/lower than set VTAdjust all alarms for patient safety.
X‑RAY WHEN INDICATED FOR
Tube placement: 2 – 4 cm above carinaPossible pneumothoraxTo 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 startsTo 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 BAcute & Critical Care
PEEP/CPAP
PEEP – Positive End Expiratory PressureDefinition
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 PEEPStart off at 5 cmH2O and increase by 3 to 5
cmH2O incrementsAdjust 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 expirationAccomplished by a continuous flow of gas
or a demand valve System flow must be enough to meet patient’s peak
inspiratory demandsUsed to treat OSA
CPAP delivered via mask or nasal pillowsNo machine breaths, all spontaneous
ventilation
NPPV (BIPAP)Similar to CPAP
Delivers two levels of pressure during the inspiratory-expiratory 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 PEEPObtain order Set‑up PEEP and make additional changes
(i.e., sensitivity)Monitor patient for hazards, BP, CO if
availableMonitor 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 devicesWater column
Amount of water in a column determines PEEPPressure in expiratory limb must exceed pressure of water in columnExhalation occurs under a Column of water
Spring loaded valve: Tension in spring determines PEEPBalloon type
Similar to “mushroom-type” exhalation valveBalloon is in exhalation valveBalloon is inflated to a given pressurePressure in balloon determines PEEP
DiaphragmPressure against diaphragmDisposable 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
ventBreath 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 VentilationCan 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
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CAPNOMETRY (CONT.)
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 stateMortality 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 StrategiesLower 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 mmHgPIP < 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&OCardiac outputBPPIPPPLATPulse OxFIO2VTVECSTPETCO2WaveformsA-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 metabolizedPaCO2 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
hypoxemiaFor 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 OXYGENATIONa/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 FIO2Decrease 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
failTo 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!