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RT Hmwrk Advanced 6
Create a comprehensive outline/study guide of all material covered in the last 7 weeks.
Advanced Modes of MV
Basic Review
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Elastance = change pressure/ change volume
Resistance = elasticity + frictional resistance
Static Compliance
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Used for trending (is pt getting better or worse?)
CS = Vt/plateau-PEEP
Normal = 100-200ml/cmH2O, you will see (40-60)
Decreases: Compliance
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Mainstem intubation
CHF
ARDS
Atelectasis
Consolidation
Chest wall edema
Fibrosis
Hyperinflation
Tension pneumothorax
Pleural Effusion
Abdominal distention
Thoracic deformity
Ventilation
 Goal is to release CO2 and maintain normal PaCO2
 Ve = total amount of gas exhaled/minute
 Ve = Vt x f
Increased CO2:
 Fever, sepsis, injury, diet
 Increased VD:
 Vent circuit, ETT
 Adjust; Vt and f
Oxygenation
 Goal is to maintain O2 into the blood, PaO2
 A-a gradient, measures efficiency of oxygenation
 PaO2 depends on ventilation, but more on V/Q matching
 a/A ratio, indicates O2 transport
 Adjust: FiO2 and PEEP
Breath Types
Volume Control:
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Can be used in either AC or SIMV modes,
Set Vt, flow, I-time varies
Pressure Control:
 Can be used in either AC or SIMV mode
 Set pressure, I-time, rise-time
Note:
AC – all breath are pt or vent initiated and are time-cycle and pressure limited
SIMV – only vent initiated breaths are time-cycled and pressure-limited
Spontaneous breaths are pressure supported
Volume Control
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VS
Constant volume delivery
PIP varies
Constant inspiratory flow
I-time determined by flow and Vt
Disadvantages:
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Limited flow may not meet pt demand
Can lead to fatigue
Lead to excessive airway pressure,
cause barotrauma, volutrauma,
hemodynamic effects
Pressure Control
 Vt varies
 Pressure limit constant
 Flow varies
 I-time is set
Advantages:
 Limits risk of barotrauma
 May recruit collapse alveoli
 Improved gas distribution
Disadvantages:
 Vt vary when compliance changes
 With increased I-times pt may require
sedation, asynchrony
 Potential excessive Vt with high
compliance
Waveforms and Graphs
 Flow-time – auto-PEEP
 Pressure-time – patient trigger, rise-time, flow starvation
 Pressure-Volume – Raw, overdistention, leaks
 Flow-Volume – obstructive/restrictive, leaks, bronchodilator effectiveness
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Initial Vent Settings
Volume Control
 Vt = normal 8-12ml/kg, restrictive 57ml/kg
 V(flow) = 40-60L/min
 f = 8-12 bpm
 FiO2 = 40-60%
 PEEP = 0-5
 Sensitivity 1-3
Vent Changes
 Vt = 50-100mL
 Pressure = 2-5cmH2O
 V(flow) = 5-10L
 f = 2-6 bpm
 FiO2 = 10-15%
 PEEP = 1-2
 Sensitivity = 0.5
Pressure Control
 Pressure limit = 15-25 cmH2O
 TI = 0.8-1.2 seconds
 f =8-12
 FiO2 = 40-60%
 PEEP = 0-5
 Sensitivity = 1-3
Note:
Lung Protective Strategies: high rates and low Vt
 Used with ALI & ARDS
 Plateau pressures below <30cmH2O
 Low VT (4-6 mL/kg)
 Use PEEP to restore FRC (ARDS,15 start)
 Start with a rate of 16
 “Open Lung Approach”, uses reduced VT (6mL/kg or less) to prevent high-volume injury and
overdistention and the addition of PEEP to prevent low volume lung injury from cyclic alveolar
closure and reopening
New Modes: Dual Modes (ie: AVAPS, PRVC, VSV)
 Within-breath adjustment, makes adjustments within that breath
 Automatic tube compensation (ATC)
 Average Volume-Assured Pressure Support (AVAPS)
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Between-breath adjustment, based on last breath
 Volume Support (VS)
 Pressure-Regulated Volume Control (PRVC)
Note: adapting to pt – input adjusts flow, makes changes in real time, faster weaning
Newer modes were developed to prevent VILI, asynchrony, improved oxygenation, faster
weaning, easier use, improve comfort
Common vent asynchrony – missed effort (sensitivity), double-triggering, auto-cycling
Terminology
 Control variable – a set pressure or a set volume, the mechanical breath goal
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Trigger variable – that which starts a breath, pressure or flow changes, or a set rate (time
between breaths)
Limit variable – max value on inspiration
Cycle variable - that which ends inspiration
Set point – vent that delivers and maintains a set goal, goal is constant
Servo – vent adjusts its output to a given pt variable – inspiratory flow follows and amplifies the
pt flow pattern
Adaptive – vent adjusts a set point to maintain a different operator set point (PRVC- inspiratory
pressure is adjusted breath to breath to achieve a target volume)
Optimal – vent use algorithm to calculate the set points to achieve a goal (ASV, the pressure,
rate, Vt are adjusted to a achieve a goal VE)
Time Constants – the time it takes the individual alveoli to open, is a product of compliance and
resistance
Mean airway pressure (MAP)- is affected by PIP, EEP(end expiratory pressure, duty cycle
(Ti/TCT)
PRVC – Pressure-Regulated Volume Control
 Used in AC and SIMV modes
 Combines volume & pressure control
 Set targeted VT
 Guarantees a min, not a max volume
 Estimated volume/pressure with each breath
 Adjusts level of pressure breath to breath
 Delivers pt or time triggered, pressure-targeted, time-cycled breaths
 Slowly Increases/decreases pressure until set Vt is delivered, adjusts pressure 1-3 cmH2O and
reassesses the Vt
 If pressure comes within 5cmH2O of pressure limit, automatically dumps volume
 First breath is test breath, 5-10cmH2O above PEEP, next 3, pressure increases 75%
 Time ends inspiration, time-cycled
 Best on pt with weak respiratory drive or apneic, those requiring variable flow, those with CL or
Raw changes
PRVC - Settings
 Pressure limit, set in alarms (30-40cmH2O)
 Target Vt
 TI
 BUR
 Rise-time
 FiO2
 PEEP
 Sensitivity
Advantages: maintains min PIP, targeted Vt and Ve, little WOB, allows pt control of f and Ve, ramp flow
pattern for improved aeration, breath by breath analysis
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Disadvantages: varying MAP, may cause auto-PEEP, poor toleration, cough may cause reduced vent
support, not good for pt with erratic breathing patterns
Note:
Auto Flow on Drager is the same as PRVC, Auto-Mode/Volume Support on PRVC – for pt that
are making intermittent inspiratory effort or spontaneously breathing, it automatically switches
vent back and from PRVC to Volume Support
Volume Support works same as PRVC, is Pressure Support that guarantees a set VT
AutoMode & Volume Support on PRVC
 For pt that have intermittent inspiratory efforts or spontaneous breathing
 AutoMode switches between PRVC and Volume support mode
 PRVC breaths with no effort and VS breath with effort
VS - Volume Support
 Use only in spontaneous mode
 Pressure limited, flow cycled
 Pt triggered (pressure/flow), pressure targeted, flow cycled breaths
 Similar to pressure support, VS sets target VT, adjusts pressure to achieve set VT
 Automatic weaning of pressure support as long as VT matches min VT
 Used to wean, pt who cannot do all the WOB but are breathing spontaneously
Advantages: targeted volume, pressure supported breath (lowest possible), decreases spontaneous
rate, decreased WOB, allows pt control I:E, breath by breath analysis, variable flow
Disadvantages: spontaneous breathing, varying MAP, auto-PEEP may affect function, targeted VT
maybe too large/small
ASV – Adaptive Support Ventilation
 Dual mode that uses both PC and PSV to maintain set min Ve
 Automatically adapts to pt demand by increase/decrease support
 Delivers pressure-controlled breaths using an optimal (adaptive), min mechanical WOB, vent
selects a Vt and rate
 Most adaptive
 Very few things set
 Changes with compliance
ASV – Settings
 Enter IBW, it then chooses a required Ve
 Percent of normal predicted Ve (usually 80%)
 FiO2
 PEEP
 Series test breaths measures CS, RAW, auto-PEEP
 No spontaneous breaths, vent determines and delivers a mandatory rate, VT and pressure limit
Disadvantages: inability to adjust changes in VD, muscular atrophy, varying MAP, COPD needs longer TE,
sudden increase in rate and demand can result in decrease in vent support
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AVAPS – Average Volume Pressure Support
 Reduces WOB while maintaining a Ve and a minimum Vt
 Combines an initial high flow like PC and a constant volume delivery like VC
 Allows feedback loop based on Vt
 Adjusts within single breath from PC to VC if minimum Vt is not met
AVAPS – Settings
 Pressure limit = plateau seen in VC
 Rate
 Flow
 PEEP
 FiO2
 Sensitivity
 Minimum Vt
ATC – Automatic Tube Compensation
 ET tube resistance causes highest workload with normal lung advantages
 ET tube resistances increases with smaller tubes
 Takes over the WOB induced by the ETT
ATC - Settings: size of ET tube
Advantages: pt comfort
PAV – Proportional Assist Ventilation
 Pt must have spontaneous breathing
 Vent generates pressure in proportion to the pt effort
 Provides pressure, flow assist, volume assist in proportion to pt spontaneous effort
 Greater pt effort, higher flow, volume and pressure
 Best those who have WOB problems with worsening lung conditions
 Pt that have tried to wean but have failed, will adjust support automatically
 Asynchrony pt, stable and have inspiratory effort
 Vent-dependent COPD pt
 First breath is important
PAV – Settings
 Airway type (ET, trach)
 Airway size (inside diameter)
 Percentage of work supported (5-95%) usually start at 80%
 VT limit
 Pressure limit
 Sensitivity
Advantages; pt controls variables (PIP, Ti, Te, VT, I), trends changes in vent effort,
when used with CPAP, inspiratory muscles work near normal, lowers MAP
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Disadvantages: pt must have adequate drive, variable VT and PIP, leak can cause excessive assist or auto
triggering and may cause auto-PEEP
APRV – Airway Pressure Release Ventilation
 Use in spontaneous mode
 Promotes lung recruitment with collapsed or poorly ventilated alveoli
 Sets 2 levels of PEEP, High PEEP & Low PEEP
 CPAP is released for short periods with spontaneous breathing helps eliminate CO2 and
promotes oxygenation
 Promotes alveolar ventilation, pressure release from an elevated baseline pressure facilitates
oxygenation, while the pressure release increases VE
 Promotes PEEP, release time is short to prevent the peak expiratory flow from returning to zero
 Prevents atelectasis, overdistention, derecruitment
 Promotes alveolar recruitment
 Minimizes PIP
 Used on ARDS, promotes spontaneous breathing, improvement in hemodynamics
 Permissive hypercapnia may be necessary
 Use lung protective strategies
 Also known as “Bilevel”, BiVent”, “Biphasic”
APRV – Settings
 P high (high PEEP)– (20-25 cmH2O) set a plateau pressure (adults) or mean airway pressure
(peds), neonates (10-15), maximum 30-35cmH2O, ventilation
o Pt with high plateau, set at 30cmH20
o Exceptions morbid obesity and ascites
 T high – (3-6 seconds), inspiratory time
o Progressively increased (10 to15sec)
o Target is oxygenation
 P Low (low PEEP) – (0-5 cmH2O), usually set at zero
 T low (PEEP) also known as release time – (0.2-0.8) set PEEP at 0, provides rapid drop in
pressure and max change in pressure for expiration
 FiO2 – 40-60%
 Sensitivity – 1-3
APRV – Changes
 Primary way to reduce PaCO2 is to increase gap between P High & P Low
Decrease PaCO2
 Decrease T High
 Increase P High – (2-3cmH20)
 May sacrifice oxygenation
Increase PaCO2
 Increase T High – (0.5 – 2.0 seconds)
Increase PaO2
 Increase FiO2
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Increase MAP by increasing P High (2cmH2O)
Increase T High slowly (0.5 seconds)
Weaning: “drop and stretch”, “drop pressure “P high” and stretch time “T high”
To: “15 & 15”, “15 cmH2O & 15 seconds”
Note: Release time – T PEEP: Atelectasis can develop in seconds when Paw drops below a critical value
in ARDS
Too long of a release time interferes with oxygenation and allows for alveolar collapse
Advantages: uses lower PIP to maintain ventilation and oxygenation without compromising
hemodynamics, improves V?Q mismatched, requires a lower VE which means a reduced VD/VT, may
preserve spontaneous breathing, decreases in pleural pressure, improves cardiac output, reduced
sedation
Disadvantages: pressure-targeted, volume delivery depends on compliance, resistance and spontaneous
effort, doesn’t support CO2 elimination and relies on spontaneous breathing.
With increased Raw, difficult to eliminate CO2, may lead to increased WOB, discomfort
Lung Recruitment
 Elevated baseline pressure may produce near complete recruitment
 Maintaining a constant airway pressure facilitates alveolar recruitment
 Enhances diffusion
 Allows alveolar units with slow time constants to fill
 Prevents overdistention
 Augment collateral ventilation (pores of Kohn in septa, Lamberts canal connects terminal
bronchi and respiratory bronchioles with adjacent peribronchial alveoli and channels of Martin
interconnect bronchioles)
Spontaneous vs Paralyzed
 Provides ventilation to dependent lung regions which have best perfusion
 Reduces atrophy associated with PPV and paralytics
 PPV, anterior diaphragm is displaced towards abdomen
 PPV, atelectasis forms occur near diaphragm when muscle activity is absent
 With spontaneous breathing, formation of atelectasis is reduced by activity of the diaphragm
HFV – High Frequency Ventilation
Types:
 High frequency jet ventilation
 High frequency oscillatory ventilation
 High frequency percussive ventilation
 High frequency positive pressure ventilation
 INO with HFV – used mainly with neonates
HFV
 Delivers small Vt with high respiratory rates >150bpm
 Safer and more effective to use smaller Vt at higher PEEP (MAP)
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Goal – provide adequate ventilation/oxygenation with a severe restrictive disease to
prevent/reduce risk of VILI
Uses momentum of flow into the lung rather than airway pressure to overcome compliance
Good alveolar recruitment
Major difference is that Vt is smaller than average dead space
Considerable mixing of fresh and exhaled gas is the key to ventilating the lung at very low tidal
volumes
Amplitude (power) = height of wave, depth of breath, volume
Hertz (frequency) = how close waves are, number of breath per minute (350-1200)
1Hz = 60 breaths per minute
Have to sedate patient
Allow for Permissive Hypercapnia
Greatest benefit in diseases with low lung compliance
Used for Rescue and Prophylactic
Reduced risk of pneumothorax, subcutaneous emphysema, pneumos-pericardium
Indications:
o ARDS/ALI
o RDS, respiratory distress syndrome
o PIE, pulmonary interstial emphysema
o PPHN, primary pulmonary hypertension
o PN
o MAS, meconium aspiration syndrome
o CDH, Congenital diaphragmatic hernia
o TEF, transesophageal fistula
How does HFV Work:
 Enhances Convection (bulk flow) and diffusion of gas
 Fresh gas washes out expired gas from airways
 Changes in rate have less influence on gas exchange
 Additional Mechanisms:
o Pendalluft effect
o Turbulence
o Taylor dispersion
o Collateral ventilation
o Cardiogenic mixing
o Molecular diffusion
Oxygenation:
 Is determined by lung volume and FiO2, important to maintain lung volume to prevent
atelectasis
 Adequate MAP (PEEP) should be used for alveolar recruitment and maintain lung volume above
FRC
 Lung volume is maintained at a constant level
 V/Q improves as a result of alveolar recruitment with increased lung volumes
 The constant lung volume results in better gas distribution
 Avoids development of atelectasis in low compliance lungs
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Adjustments:
 Increasing Amplitude – reduces PaCO2
 Increasing Hertz (frequency) – increases PaCO2
 Decreasing Hertz (frequency) – decreases PaCO2
 Add 5-10 above their normal MAP – too low atelectasis
Assessment:
 Look for chest wiggle
 CXR
 Auscultation – not easy
 SpO2, Hr, ABG, ECG, Bp
Hazards:
 Minimize suctioning
 Air trapping
 Fighting vent
 Tracheal damage
 Pulmonary interstial emphysema
 Intraventricular hemorrhage, periventricular leukomalacia
Nitric Oxide (NO)
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Relaxes smooth muscle to improve blood flow to alveoli (binds and activates cGMP)
Improves V/Q mismatch
Decreases pulmonary vascular resistance
Decreases pulmonary pressures
Improves oxygenation
Reduces the need for ECMO
Specific pulmonary vasodilator PVR and pulmonary artery pressure
Selective vasodilator of arterioles without systemic effect
Indications:
 Hypoxic respiratory failure
 Newborns older than 34 weeks
o PPHN
o CDH
o OI (oxygen index >25)
Application:
 Dosing 20ppm
 Weaning by decreasing .5
 Wean to 1ppm
 Increase FiO2
Contraindications:
 Congenital/acquired methemoglobinemia reductase deficiency
 Bleeding diathesis, intracranial hemorrhage
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Left ventricular failure
Hazards:
 Elevated methemoglobin
 NO toxicity
 Prolonged PT/PTT
 Increased lt ventricle filling associated with rapid changes in pulmonary pressures
 Rapid withdrawal of NO, cause hypoxemia and pulmonary hypertension
Notes: an increase in exhaled Vt may be noted
Trigger sensitivity might be compromised
Hemodynamic; Movement of blood
Measures movement in terms of pressure
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Without sufficient Bp tissues will not receive O2
High Bp strain heart and vessels
Control Bp
o Heart
o Blood
o Vasculature
Heart Anatomy
 4 chambers, 4 branches of circulation
o LV – systemic arteries
o RA – systemic veins
o RV - pulmonary veins
o LA – pulmonary veins
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Each has own Bp
Pericardium
Epicardium
Myocardium
Endocardium
Preload – stretch of ventricle muscle before contraction
Afterload – resistance to ejection of blood during systole
Catheters
 A-Line; arterial
 C-line; central venous
 PAC; pulmonary artery
Liquids, non-compressible
A-line
Uses
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Measure systemic artery pressure
Collect blood gas samples
Indocyanine CO measurement
Hemodynamic unstable
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Insertion: radial, brachial, femoral, dorsal pedis (neonates)
A-line Waveform:
 Should have a clear upstroke on the left
 With a dicrotic notch
 Down stroke on the right
MAP = systolic + 2xdiastolic/3
Increases Arterial Pressure
 Improved circulation
 Sympathetic stimulation
 Vasoconstriction
 Admin of vasopressors
Decreases Arterial Pressure
 Blood loss
 Dehydration
 Shock
 Vasodilation
 Cardiac failure
Pulse Pressure = difference between systolic and diastolic pressure
Bradycardia = rate below 60 bpm
Tachycardia = rate above 100 bpm
Decrease Pulse Pressure
 Early sign of hypovolemia
 Decreased stroke volume
 Increased vessel compliance, shock
 Tachycardia
Increase in Pulse Pressure
 Sign of volume restored
 Increased stroke volume, hypervolemia
 Decreased blood vessel compliance, arteriosclerosis
 Bradycardia
Cardiac output (CO) = HR x SV, normal 4-8Lpm; Factors
 Increase/decrease heart rate
 Change of posture
 SNS activity
 PNS activity
Stroke volume (SV); measures avg CO per beat
Factors Increase SV, SVI, CO, CI
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Positive Inotropic Drugs – increase contractility
Septic shock, hyperthermia, hypervolemia, decrease vascular resistance
Factors Decrease SV, SVI, CO, CI
 Negative Inotropic Drugs – decrease contractility
 Septic shock, CHF, hypovolemia, PE, increased vascular resistance, MI
 Hyperinflation lungs – PEEP, CPAP, CMV
A-line Transducer;
 Transducer, catheter and measurement site should all be at the same level
Complications
 Hemorrhage
 Infection
 ischemia
C-Line
Measures central venous pressure CVP
 Vena cava
 Rt atrium
 Rt ventricle
 Measures rt heart function and fluid levels
 Normal;
2-6 mmHg by transducer;
 4-12 cmH2O
Uses;
 Measure CVP
 Admin fluid, blood, meds
 Blood samples
 Insertion; subclavian, jugular
Decrease CVP volume
 Blood loss
 Dehydration
 Shock
 Vasodilation
 Decreased intrathoracic pressure;
o Spontaneous breath
 Increased rt heart to move blood
Increase CVP
 Increased venous return
 Hypervolemia
 Volume overload
 Fluids
 Increased intrathoracic pressure
o Positive pressure ventilation
o Pneumothorax
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Decreased ability of right heart to move blood – Right heart failure
MI, Cardiomegaly
An increase in CVP leads to a decrease in blood return to the right heart
Left Heart Failure****
Increased pulmonary vascular resistance
o Pulmonary hypertension
o Pulmonary embolism
 Compression around heart
o Constrictive pericarditis
o Cardiac tamponade
Complications:
 Infection
 Bleeding
 Pneumothorax
Pulmonary Artery Catheter (PAC) – Swan Ganz
Indications:
 Hemodynamically unstable pts: shock
 Acute heart disease
 Multisystem traumas, large burns
 Severe, acute pulmonary disease
 Major systems dysfunction
PAC
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Measures CVP, PAP PCWP
Inject meds
Collect mixed blood samples
Monitor mixed venous O2 saturation
Measure CO
Provide cardiac pacing
Insertion: subclavian, jugular, superior vena cava,
Right atrium Normal pressure: 0-6 mmHg
Normal Pressure Readings
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Right Ventricle:
o Normal pressure: 20-30/0-5mmHg
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Pulmonary Artery:
o Normal pressure: 20-30/6-15mmHg
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Wedge pressure (PCWP)
o Normal pressure: 4-12mmHg
Complications:
 Infection
 Bleeding
 Pneumothorax
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PCWP
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Pulmonary artery hemorrhage
Pulmonary infarction
Air embolism
Cardiac arrhythmias
Monitors blood moving into left heart
Normal 8mmHg
Represents pulmonary venous drainage to left heart
Left atrial pressure
Left side preload
Left ventricular end-diastolic pressure
Left ventricular filling pressure
Increase Pulmonary Capillary Wedge Pressure – PCWP
 Left heart failure
 Mitral valve stenosis
 CHF/pulmonary edema
 High PEEP effects
 Hypervolemia
Decrease PCWP
 Right heart failure
 Cor pulmonale
 Pulmonary embolism
 Pulmonary hypertension
 Air embolism
 Hypovolemia
Clinical
Right heart failure
 CVP – increased
 PAP – N or decreased
 PCWP – N or decreased
Lung Disorders – PE, PHTN
 CVP – increased
 PAP – increased
 PCWP N or decreased
Left Heart Failure
 CVP – N or increase, late sign
 PAP – increased
 PCWP – increased
 CO – decreased
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Hypovolemia
 Everything decreases
 CVP
 PAP
 PCWP
 CO
Values to Know
Pulse pressure – 40mmHg
Stroke volume – 60-130ml/beat
EF – 65-75%
SVR - <20mmHg/L/min
PVR - <2.5 mmHg/L/min