hemodynamics advanced orientation, july 2008 - copy
TRANSCRIPT
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Advanced HemodynamicsAdvanced Hemodynamics
Kathleen Brownrigg, RN, MNKathleen Brownrigg, RN, MNPediatric Critical Care UnitPediatric Critical Care Unit
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ObjectivesObjectives
Discuss invasive monitoring linesDiscuss invasive monitoring lines
Review IndicationsReview Indications
Understand normal hemodynamicsUnderstand normal hemodynamics
Gain competency in monitoringGain competency in monitoring
Interpret hemodynamic dataInterpret hemodynamic data
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Objectives Understand hemodynamic variations of congenital cardiac Understand hemodynamic variations of congenital cardiac
diseasedisease
Review hemodynamic waveforms and intracardiac pressuresReview hemodynamic waveforms and intracardiac pressures
Describe complications of invasive linesDescribe complications of invasive lines
Correlate hemodynamic data with clinical assessmentCorrelate hemodynamic data with clinical assessment
Discuss the impact of preload, afterload, contractility and Discuss the impact of preload, afterload, contractility and ventricular complianceventricular compliance
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History
1st measurements in 1773 by Stephen Hale, an English theologian/scientist and assistant
Measuring directly 1st mean BP on an unanesthetized horse
Measurement of BP evolved slowly
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Cardiac OutputCardiac Output
Measure of performanceMeasure of performance
Volume of blood ejected in 1 minVolume of blood ejected in 1 min
C.O. = HR X SVC.O. = HR X SV
Varies with sizeVaries with size CI = CI = COCO BSABSA
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Heart RateHeart Rate
Vital for good cardiac performanceVital for good cardiac performance
Children are less able to vary stroke volume as their Children are less able to vary stroke volume as their myocardial performance is working near max under myocardial performance is working near max under basal conditionsbasal conditions
SV is less dynamic – HR influences CO to a greater SV is less dynamic – HR influences CO to a greater extent that in adultsextent that in adults
Tachycardia – shortening of diastolic component of Tachycardia – shortening of diastolic component of cardiac cycle = 30% of total cycle timecardiac cycle = 30% of total cycle time
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Indications For HemodynamicMonitoring
Shock states: Cardiogenic, hypovolemic, distributive
Surgical patients
Respiratory patients
Multiple trauma
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Invasive Monitoring
Provides objective quantitative data:Provides objective quantitative data:
Cardiac output Cardiac output PreloadPreload AfterloadAfterload Rt & Lt heart functionRt & Lt heart function Assessment of intracardiac shuntingAssessment of intracardiac shunting Assessment of pharmacologic responseAssessment of pharmacologic response
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Risk vs Benefit
Necessity vs risk assessment Necessity vs risk assessment
EmbolismEmbolism
Vessel thrombosis Vessel thrombosis
Vessel patency - palliative cavopulmonary Vessel patency - palliative cavopulmonary connection, cardiac transplantation and repeated connection, cardiac transplantation and repeated biopsybiopsy
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Goal
Increase stroke volume
Increase cardiac output
Maximize filling pressures
Decrease pulmonary congestion
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Monitoring
Tailored to the individual infant, defect & reparative surgical intervention- Line placement – ie left radial art line and repair of - Line placement – ie left radial art line and repair of
coarctation with subclavian flap is inappropriatecoarctation with subclavian flap is inappropriate
Information outweighs risks/complications – remove lines ASAP
Line should be transduced for a waveform prior to potent or corrosive drugs. i.e. cyanosed & hypotensive patient, …..color or force of ejection may not be helpful in determining ART vs venous line
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Invasive Monitoring
Oxygenated blood (ABP, UAC, Pulmonary veins - LAP)Oxygenated blood (ABP, UAC, Pulmonary veins - LAP)
Deoxygenated blood (CVL, PA Lines, UVC)Deoxygenated blood (CVL, PA Lines, UVC)
Requires a fluid filled system (catheter & tubing)
Requires a pressure transducer to transmit one energy form to another – ie physical energy to an electrical signal that is amplified
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Transducing Solutions
ART Lines: 0.9 NaCl with 100 units of Heparin/50 ml
Run at 1.5 to 2ml/hr. Cardiac neonate rate 1.0 ml/hr
All other: D5W & 0.2 NaCl with 100 units of Heparin/ 50 ml
Run at 2ml/hr (minimum rate 1.5 ml/hr). May decrease to 0.5 ml/hr if sufficient fluid infusing through line to keep vein open.
DO NOT TURN TRANSDUCING FLUID OFFDO NOT TURN TRANSDUCING FLUID OFF completely - completely - stagnation of fluid in transducerstagnation of fluid in transducer
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Proper Leveling/Rezeroing Point?
Must be leveled to an anatomically consistent point
Phlebostatic axis provides an external reference point
Reference point that approximates the anatomic level of the atria and PA
Ensures accuracy of readings
Must be zeroed to eliminate effects of hydrostatic & atmospheric pressures
Zeroing stopcock should be used
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Phlebostatic Axis
Midpoint between the anterior and posterior surfaces of the chest at the 4th intercostal space midaxillary line
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Zeroing/Calibrating
Inaccurate transducer position can result in large errors in reading!!!!!
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Zeroing
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Zeroing
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Causes of Error?
Air bubbles in the system = underestimation of systolic pressure and overestimation of diastolic pressure
Blood clots
Use of non-compliant tubing
Tighten loose fitting connections
Catheter lodged again vessel wall
Improper zero
Interpretive
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Arterial Pressures?
Moment by moment pressure
Visual display of systolic, diastolic and MAP
MAP = 2X(DAP) + SAP
3
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Dicrotic Notch
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Intrathoracic LinesIntrathoracic Lines
Directly positioned at time of surgeryDirectly positioned at time of surgery
RA, LA PA, RVRA, LA PA, RV
Fixed to the thorax by a sutureFixed to the thorax by a suture
Maintained with 1.5-2.0 ml/hrMaintained with 1.5-2.0 ml/hr
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RA LinesRA Lines Information about:Information about:
systemic venous returnsystemic venous return
vascular volumevascular volume
right heart eventsright heart events
Reported as a mean pressureReported as a mean pressure
Ideal location is within the body of RA where Ideal location is within the body of RA where venous blood return is mixedvenous blood return is mixed
RA line is a low pressure lineRA line is a low pressure line
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RA Lines
Reflects preload or right ventricular end diastolic Reflects preload or right ventricular end diastolic pressure (RVEDP)pressure (RVEDP)
Placed through RA appendage during surgeryPlaced through RA appendage during surgery
oror
Threaded into the RA by venous cannulation or Threaded into the RA by venous cannulation or umbilical venous lineumbilical venous line
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RA Line
Low RAP: hypovolemiaLow RAP: hypovolemia
waveform dampeningwaveform dampening
faulty positioning of transducerfaulty positioning of transducer
line placement in the coronary line placement in the coronary
sinus or low in IVCsinus or low in IVC
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RA Line
High RAP: RV dysfunction
Tricuspid stenosis or insufficiency
Hypervolemia
Tamponade
Constrictive pericarditis
Pericardial effusion
LV to RA shunt
Pulmonary hypertension
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LA Catheters
Provides a measurement of pulmonary venous pressure
Indicates systemic volume, LV preload, LV function
Placement: Posteriorly through the wall of LA at the junction of superior pulmonary vein and advanced across the LA
Xray display a straight line across the chamber
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LA Catheters Low pressure: hypovolemia
Increased LAP:
Deep inspiration
PEEP
Hypervolemia
Mitral valve insufficiency
Loss of AV conduction
Ventricular dysfunction
Coronary artery occlusion
Pericardial effusion/tamponade
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Cardiac Output Cardiac Output is a product of stroke volume X HR SV 60-130 ml Adult Factors affecting SV: preload, afterload contractility
Cardiac Index: adjusts CO to individual persons body size = blood flow relative to a square meter of body surface area.
1/3 cardiac cycle – consuming O2 2/3 diastolic & perfusing coronary arteries Cardiac index is highest in childhood and diminishes with age
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Principles of Hemodynamics
Blood Pressure = C.O. X SVRBlood Pressure = C.O. X SVR
C.O. & SVRC.O. & SVR have an inverse relationship: If blood pressure drops, SVR increases to compensate = equilibrium
SVR is the strongest component regulating BP
A vasoconstrictor has a greater effect than an inotrope
Cardiac medications manipulate the:
Contractility (improve/depress)Contractility (improve/depress)
Preload (increase/decrease)Preload (increase/decrease)
Afterload (increase/decrease)Afterload (increase/decrease)
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Alpha Adrenergic Receptors
Receptors in the peripheral and coronary arteries.
Peripheral vasoconstriction - skin, lungs, GI tract, and kidneys
Increases sweating
Dilates pupils
Norepinephrine, Epinephrine, DopamineNorepinephrine, Epinephrine, Dopamine
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Beta 1 Adrenergic Beta 1 Adrenergic ReceptorsReceptors
B1:B1: Receptors in the heart, lungs and coronary arteries. (lesser in vessels)
Found largely in the heart
Increases: HR, contractility, conductivity
Norepinephrine, Epinephrine, Dopamine, Dobutamine, Norepinephrine, Epinephrine, Dopamine, Dobutamine, Isuprel Isuprel
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Beta 2 Adrenergic ReceptorsBeta 2 Adrenergic Receptors
Found largely in the lungs
Bronchodilation
Peripheral vasodilation: skeletal muscles, heart and lungs
Arteriolar dilation = O2 delivery to the cells
Adrenalin, Isuprel, VentolinAdrenalin, Isuprel, Ventolin
Caution: B-Blockers: Propanolol, Esmolol, Labetolol, Caution: B-Blockers: Propanolol, Esmolol, Labetolol, AtenololAtenolol
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Preload
Preload:Preload: End diastolic stretch of the muscle fibres. Vol and pressures in ventricle just prior to systole
Frank Starling principleFrank Starling principle: The greater the muscle fibres are stretched in diastole, the more they will shorten and with > force in systole
If preload increases so does C.O. to an optimum level
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Preload
The ideal preload is associated with optimal cardiac output
What is that norm for your patient??????
Influencing factors: circulating blood volume, distribution of blood volume, atrial contraction
Estimating preload: PAD
LAP
RAP
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AfterloadAfterload
ResistanceResistance to blood flow as it leaves the ventricles
Major influences – vascular compliance & outflow obstruction
A function of: Arterial pressure
Ventricular size
An increase in vascular resistance (PVR or SVR)(PVR or SVR) results in an increased contractility in order to maintain: stroke volume and C.O
Increase in SVR or PVR - more energy required for ejection - myocardial O2 demand increases myocardial O2 demand increases
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AfterloadAfterload
Systemic hypertension (functional)
Pulmonary hypertension (functional)
Aortic stenosis/Coarctation (structural)
Pulmonary stenosis (structural)
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SVRSVR
SVR (Woods units) = MAP – Mean RAP(CVP)
Cardiac output
= 10 – 15 Woods units
SVRI (dynes-sec-cm -5) = MAP – Mean RAP(CVP) X 80
Cardiac index
= 800-1600 dynes/sec/cm-5
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PVR
PVR (Woods units) = MAP – Mean RAP
Cardiac output
= 1-3 Woods units over 8 wks of age
8-10 Woods units < 8 weeks of age
PVRI (dynes-sec-cm -5) = MAP – Mean PCWP (or LA ) X 80
Cardiac index
= 80-240 80-240 dynes/sec/cm-5
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Factors Causing Increased Factors Causing Increased PVRPVR
Alveolar hypoxia and PA vasoconstriction: Alveolar hypoxia and PA vasoconstriction: hypoventilationhypoventilationETT obstruction ETT obstruction pneumothoraxpneumothorax
Obstruction to flow: Obstruction to flow: pulmonary venous obstructionpulmonary venous obstructionmitral valve stenosis, mitral valve stenosis, severe left ventricular failure severe left ventricular failure
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Potential Vasoconstrictors for Potential Vasoconstrictors for PVRPVR
Potential VasoconstrictorsPotential VasoconstrictorsAcidosisAcidosisBody temperature – hypothermiaBody temperature – hypothermiaStimulation – PainStimulation – Pain
Potential Vasodilators:Potential Vasodilators:Good oxygenationGood oxygenationAlkalosisAlkalosisMild hyperventilationMild hyperventilationSedationSedationInhaled nitric oxideInhaled nitric oxide
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Contractility Inotropic state of the muscle. The ability of the myofibrils Inotropic state of the muscle. The ability of the myofibrils to shorten in length and produce a contraction for any given to shorten in length and produce a contraction for any given preload and afterload.preload and afterload.
Preload & afterload
Drugs – concentrations of circulating catecholamines,
inotropic agents, pharmacologic depressants
Cardiac oxygenation
Physiological depressants: hypoxia, hypercapnia,
acidosis
Functional myocardium
Ionized Ca++
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Contractility
Not measured directly
Use SWI (stroke work index) to assess ventricular contractility
SVI SVI 33-47 cm/m2/beat33-47 cm/m2/beat
RVSWI RVSWI 7-12 gm/m2/beat 7-12 gm/m2/beat (6 - 7 Curley)(6 - 7 Curley)
LVSWILVSWI 35-85 gm/m2/beat35-85 gm/m2/beat (50 - 62 Curley)(50 - 62 Curley)
If high:If high: B-blockers: Propanolol
If low:If low: +ve inotropes: Dopamine, Milrinone, Epinephrine
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Normal Saturations
75%
70%
75%
95%
95%
75%
75%
35%Coronary sinus
May be falsely high or low depending on catheter placement or residual lesions
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Step UpCorrelation of RA to PA sat with residual lesions
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LA Saturations
Decreased LA O2 SAT:
- intrapulmonary shunting as a result of atelactasis, lung collapse, consolidation - R to L cardiac shunt
Can not really be assumed
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Cardiac Function
Adequate C.O. and balance between:
O2 DELIVERY O2 DELIVERY & O2 Consumption or DEMANDO2 Consumption or DEMAND
If balance is altered then anaerobic glycolysis (lactic acidosis)
Blood leaves heart 100% O2 saturated
Tissue extraction is 25%
SvO2 (mixed venous oxygen saturation) is 75% (60-80%) ….blood returning to right side of heart
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Tissue Metabolism
O2 Delivery
(DO2)
O2 Consumption
(VO2)
Systemic O2 balance is critical!Systemic O2 balance is critical!
Is it an O2 deliveryO2 delivery or tissue extractiontissue extraction problem?
An increase in O2 consumption(VO2) is usually seen 4 hrs post op due to a rise in central body temperature
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SvO2 Monitoring: Too High
High O2 supplyHigh O2 supply: FiO2 too high
Low O2 demandLow O2 demand: Anesthesia/sedation - little muscle activity
Hypothermia lowers metabolic demands
Sepsis impairs utilization of O2 – early high output state
L to R shunt
PAPVD or TAPVD
LV-RA shunt
Aorto pulmonary collaterals
SvO2 > 80%SvO2 > 80%
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SvO2 Monitoring: Too Low
Low O2 supplyLow O2 supply: Hypoxemia (lung disease or poor supply)Low cardiac outputCatheter position in the coronary sinus or low in IVC
High O2 demandHigh O2 demand: Consumption high (demand > supply)
Shivering, Seizures
Hyperthermia
Nursing activities
Pain, anxiety
SvO2 < 60%SvO2 < 60%
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Conditions That Increase VO2
Minor Surgery 7%
Fever – for each degree rise 10%
Agitation 16%
Increased WOB 40%
Severe infection 60%
Multiple organ failure 20-80%
Shivering 50-100%
Burns 100%
Sepsis 50-100%
Darovic
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Medications That Increase VO2
Norepinephrine (0.1-0.3 mcg/kg/min)
10-21%
Dopamine 5 mcg/kg/min 6%
Dopamine 10 mcg/kg/min 15%
Epinephrine 0.1 mcg/kg/min 23-29%
Ace inhibitors for systolic failure
Used when pump not strong enough or SVR too high
B blocker –slow hr and decrease O2 requirements.
Darovic
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Procedures/Activities Increase VO2
Dressing change 10%
Nursing assessment 12%
ECG 16%
Physical exam 20%
Bath 23%
Chest Xray 25%
ET suctioning 27%
Turn 31%
Nasal intubation 25-40%
Darovic
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Factors that Decrease VO2
Hypothermia (for each degree C)
10%
Morphine Sulphate 9-21%
Anesthesia 50%
Assist control ventilation 30%
Neuromuscular blockade Abolishes the increase in VO2 incurred by shivering
Darovic
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Cardiac Function
If you have decreased C.O tissues, will extract more O2 so the MvO2 will drop
If there is a patch leak (ASD, VSD, AVSD) then MvO2 will increase
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PA Catheters
Provides information about:
Mixed venous oxygen saturations
RV function
RVOT patency
Pulmonary vascular reactivity
Venous pressure in the lungs
Placement: via RVOT into main PA
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Elevated PAP
Hypervolemia
Increased pulmonary blood flow with L to R shunt
Lung disease
Mitral stenosis
Obstructed TAPVD
Pulmonary embolus
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Understanding Waveforms
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Waveform analysis
Scale?
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Modified StarlingCurve
Relationship between ventricular
filling pressure and stroke volume
Curve B
Normal Function
As PCWP increases – SV increases
Curve A –
Enhanced Sympathetic stimulation
Curve C & D – Depressed contractility – curve shifts to right. In response to an increased filling pressure only minimal augmentation of stroke volume and addition of appropriate pharmacology is required.
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Volume administration and augmentation of preload improves stroke volume
Ventricular compliance refers to the distensibility of the ventricle and is related to the changes in volume
If the ventricle is compliant ie distensible then a large increase in LVEDV can be accommodated with min change in VEDP
Modified Starling Curve
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LVEDP
The relationship between of ventricular filling volume and ventricular filling pressure to changes in stroke volume are not consistent between patients and are not the same over time in the same patient.
These relationships are prone to changes
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Non-Compliant Stiff Ventricles
A noncompliant stiff ventricle such as a hypertrophic ventricle - even a small increase in ventricular end diastolic volume may produce significant increase in LVEDP
High filling pressures lead to pulmonary edema, increased systemic venous pressure on RV.
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Intravascular Lines & Swan Ganz Catheters
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EKG and Atrial WaveformEKG and Atrial Waveform
Record atrial pressure waveform & EKG Record atrial pressure waveform & EKG simultaneouslysimultaneously
a wave occurs at approx the same time as the QRSa wave occurs at approx the same time as the QRS
v wave occurs near the T wavev wave occurs near the T wave
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A, C & V wavesA, C & V waves
The atria do not have systolic & diastolic pressuresThe atria do not have systolic & diastolic pressures
Mean atrial pressure is the average pressure in the Mean atrial pressure is the average pressure in the atrium during the cardiac cycleatrium during the cardiac cycle
3 positive deflections during each cardiac cycle – a, 3 positive deflections during each cardiac cycle – a, c & v c & v
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A, C & V WavesA, C & V Waves
a – wavea – wave produced by atrial contractions during atrial produced by atrial contractions during atrial systolesystole
c – wavec – wave produced due to the rapid rise in ventricular produced due to the rapid rise in ventricular pressure in early systole, causing the AV valve leaflets to pressure in early systole, causing the AV valve leaflets to bulge back into the atria so that the atrial pressure bulge back into the atria so that the atrial pressure increases brieflyincreases briefly
v – wavev – wave produced by blood entering the atrium produced by blood entering the atrium during late systole. during late systole.
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CVP & LAP
A wave
C wave
V wave
C wave is a notch on the a wave or may be absent
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A & C & V waves
A waveA wave
V waveV wave
C waveC wave
Atrial Contraction Bulging of valve Atrial filling
into atria Ventricular contraction
* * *
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A & C & V Waves
Atrial fibrillation = no A -wave
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A & C & V Waves Usually atrial contraction (a-wave) produces a taller wave than ventricular filling (v-wave) in the RA and reverse in the LA
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LAP A and V waves are a little away or delayed in comparison to RAP pressure waveforms.
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Cannon A Waves
Right Side
Tricuspid AtresiaEbstein’sPulmonary StenosisPulmonary venous occlusive diseasePulmonary hypertensionVentricular hypertrophyVentricular dysfunction
Cannon waves occur when the atria contracts against a closed valve, loss of normal sinus rhythm
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Cannon A Waves
Left Side
Mitral stenosisVSDPDAAortic stenosis
Cannon waves occur when the atria contracts against a closed valve, loss of normal sinus rhythm
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Right side
Tricuspid regurgitation
ASD
Congestive heart failure
Cannon V Waves
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Left side
Mitral regurgitation
CHF
Cannon V Waves
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Mitral Valve Regurgitation
5 ½ yr old Ross Procedure
Mitral, trivial tricuspid and aortic regurgitation
LAP
VV V V VLAP
LAP
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Mitral Regurgitation
Mitral Regurgitation & Cannon v- waves
LAPLAP
LAP
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3 ½ yr Old Cardiomyopathy
RAP
ART
RAP
3 ½ yr old cardiomyopathy
Cannon A – poor ventricular function
Cannon V – tricuspid valve regurgitation
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LA Waves
3 ½ cardiomyopathy awaiting a heart transplant
Cannon v due to mitral regurgitation
Cannon a waves due to ventricular failure
3
12
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RV Line
2RV
RV
1
3
RVP 58/3 (Note subsytemic RV systolic pressures)
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RV Line
RV
Infant
RV
ART
ART
33
11
11
2233
No dicrotic knotchNo dicrotic knotch
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PAP WaveformPAP Waveform
PA waveform in the pulmonary artery – differs from PA waveform in the pulmonary artery – differs from the RVthe RV
PA diastolic pressure higher than RV – pulmonary PA diastolic pressure higher than RV – pulmonary valve closes preventing PA diastolic from becoming valve closes preventing PA diastolic from becoming lowerlower
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Swan Ganz Catheter
4-5 lumens
1) RAP (right atrial pressure)
2) PAP (pulmonary artery pressure)
3) PCWP (pulmonary capillary wedge pressure)
4) Cardiac output measurement via thermodilution
5) Lumen for drug/fluid administration
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Swan Ganz Catheters: Advantages
Allows for real time determination of systemic oxygen delivery and consumption
Invasive (right heart)
Measures pressures in the heart and in the lungs
Differentiates pulmonary disease vs left ventricular failure
Guides treatment: drugs/fluids
Multilumen balloon tipped catheter
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PA Lines
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PAP
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X-ray of PA Line
The tip of the catheter should not be visible beyond the silhouette of mediastinal structures
Commonly in the right main PA
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Swan Ganz: Complications
Pulmonary embolism
Thrombus formation
Infection
PA perforation
Dysrhythmias
Dislodged & wedged
Balloon bursts
Catheter kinked
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Waveform Changes
5-10 mmHg 20-30 mmHg 20-30 mmHg 6-12 mmHg
5-10 6-12
Mean PAP (10-20) mmHg
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PA Waveform
12 3
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Swan Ganz
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RAP
LAP slightly higher than RAP.
RAP can be used to assess volume and function in the healthy person as they correlate well….. but not one with cardiopulmonary dysfunction
Acidosis, hypoxemia, positive pressure ventilation at high pressures and CHD alter the relationship
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RVP
Elevated in
Pulmonary hypertension
Pulmonic stenosis
VSD
RV diastolic pressure elevated due to RV dysfunction
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RV Catheters
RV line
PA catheter that slips back? Vs purposeful placement
Documentation of pressures and waveforms
Watch for ventricular arrhythmias
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PAP
Elevated in pulmonary emboli
COPD
VSD
Increased PBF – L to R shunt
PA hypertension
Severe heart failure
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PCWP
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What Are Your Pressures?
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PA Wedge (PWCP)PA Wedge (PWCP)
Left heart pressureLeft heart pressure Measured by the SWANMeasured by the SWAN Measures LVEDPMeasures LVEDP Read when inflated balloon lodges in a smaller branch Read when inflated balloon lodges in a smaller branch of the PA – occlusion of the branchof the PA – occlusion of the branch Pressure of the distal catheter will be the same as the Pressure of the distal catheter will be the same as the LALA In the absence of lung disease Wedge should be 1- 5 In the absence of lung disease Wedge should be 1- 5 mmHg < than PAD mmHg < than PAD
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PAP to Wedge
End diastole
Dicrotic notch
Intentional or Not? Spontaneous wedging in the PA = pulmonary infarction!
11
33
22
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PAD not equal PCWP Pulmonary diastolic pressure do not equal LVEDP
PCWP is a static reading during diastole and systole
When wedge higher consider ARDS in the face of high ventilator settings
> 4mm difference between PAD and wedge then likely not accurately measuring LVED but more likely the lung disease
Measure over again and compare to BP, and U/O
Identify which wedge get the best C.O/pt
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Anatomy
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PAD & PCWP Analysis
When PCWP is > true LVEDPWhen PCWP is > true LVEDP
Mitral stenosis
Myxoma
Mitral valve regurgitation
Pulmonary embolism0
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Computation Constant
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Thermodilution
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Thermodilution
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Errors
Quantity of injectate
Injection time
Rewarming of injectate
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Calculating Equations
C.O.C.O. = HR X SV = 4-6 L/min
C.I.C.I. = C.O. = 3-5 L/min/m2
BSA
SVRSVR = MAP - RAP X 80 dynes/sec/cm -5
C.O.
PVR PVR = mPAP - PCWP X 80 dynes/sec/cm -5
C.O.
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Cardiac Volumes
C.O.C.O. = 4-8 L/min
C.I.C.I. = 3-5 L/min Adult – 2.5-4 L/min
Stroke volumeStroke volume = 60 - 100 ml/beat
Stroke volume in childrenStroke volume in children 1.5 ml/kg/beat
Ejection fractionEjection fraction = > 60 %
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Pressures
CVPCVP 5-10 mmHg LAPLAP 6-12 mmHg
RAPRAP 5-10 mmHg PCWPPCWP 6-12 mmHg
RVPRVP 15 - 25 mmHg MAPMAP (age related)
5-10
PAPPAP 15 - 30 mmHg
8-12
mPAPmPAP (10-20) mmHg or < 1/2 to 1/3 systemic
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Making Sense of Pressures
Increased RAP:Increased RAP: Right ventricular failure
(>10 mm Hg)(>10 mm Hg) Hypervolemia
Tricupid stenosis/regurgitation
Pulmonary stenosis/regurgitation
Cardiac tamponade
Decreased RAPDecreased RAP Hypovolemia
(< 5 mm Hg)(< 5 mm Hg) Vasodilation
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Making Sense of Pressures
PCWP reflects LVEDP onlyonly when there is no obstruction (pulmonary disease or mitral valve disease)
Increased PCWP:Increased PCWP: Left ventricular failure
(>12 mm Hg)(>12 mm Hg) Hypervolemia
Mitral stenosis/regurgitation
Aortic stenosis/regurgitation
Cardiac tamponde
Decreased PCWPDecreased PCWP Hypovolemia
(< 6mmHg)(< 6mmHg) Vasodilation
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Making Sense of Pressures
ElevationElevation & Equalization of pressures: RAP = PCWP
Filling problemsFilling problems - tamponade/constriction
- restrictive cardiomyopathy
BEWARE!!BEWARE!!
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Assessment of TamponadeAssessment of Tamponade
Increasing tachycardiaIncreasing tachycardia
AgitationAgitation
HypotensionHypotension
Elevated intracardiac pressuresElevated intracardiac pressures
Abrupt cessation of chest tube drainageAbrupt cessation of chest tube drainage
Cardiac arrestCardiac arrest
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Systolic/Diastolic PAP
PA systolic pressure equals RV systolic pressure unless RVOT obstruction is present
PA diastolic pressure corresponds to LA pressure if no gradient exists across the mitral valve
Oxygen Saturation: Reflects total mixed venous sample
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ShuntingShunting
Determination of L to R shunt by calculating Qp:Qs Determination of L to R shunt by calculating Qp:Qs (pulmonary to systemic blood flow ratio)(pulmonary to systemic blood flow ratio)
Uses saturation data from the intracardiac linesUses saturation data from the intracardiac lines
Qp:Qs = Qp:Qs = Art Sat – RA SatArt Sat – RA Sat
Pulm ven sat – PA satPulm ven sat – PA sat
Qp:Qs = Qp:Qs = 100 – 75100 – 75 = = 2525 Normal = 1:1Normal = 1:1
100 – 75100 – 75 25 25
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Complications of Thoracic Complications of Thoracic LinesLines
InfectionInfection
HemorrhageHemorrhage
MalpositionMalposition
EntrapmentEntrapment
FragmentationFragmentation
EmbolusEmbolus
DeathDeath
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Guidelines for Intrathoracic Line Removal
Volume available
Determine clotting factors
Stop Heparin infusion in preparation for removal
Assess patency of chest tubes
CVS removes
OBSERVE FOR CARDIAC TAMPONADE
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PAP
PVR drops by 80 % after birthPVR drops by 80 % after birth
PVR progressively falls & reaches adult levels within a PVR progressively falls & reaches adult levels within a few weeksfew weeks
Pulmonary arteries are very reactive in neonatal period Pulmonary arteries are very reactive in neonatal period
Vasoconstriction due to alveolar hypoxia, acidosis, Vasoconstriction due to alveolar hypoxia, acidosis, over-distension of the alveoli, or hypothermiaover-distension of the alveoli, or hypothermia
Vasodilation is promoted by alveolar oxygenation, an Vasodilation is promoted by alveolar oxygenation, an alkalotic pHalkalotic pH
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Wedged PA catheter• Occluded segment – looks through the non-active segment
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PA Wedge
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PA Wedge
If wedge waveform were to be on an incline = over wedging Balloon will be overdilated – build up of pressure within the flush system.
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PA Line Wedged
312
PAP
PAP Wedged
PAP
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PCWP
PCWP is used to assess: PCWP is used to assess:
Intravascular volume (preload)Intravascular volume (preload)
Function of the left ventricleFunction of the left ventricle
Is a measurement of the pressure in the left atrium
Is NOTNOT a measurement of left ventricular preload but is a reflection of LVEDP
Can reflect the pressure in the surrounding alveoli
Is NOTNOT a measure of capillary hydrostatic pressure
Is NOTNOT a transmural pressure
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PAD & PCWP Analysis
When PAD is < LVEDPWhen PAD is < LVEDP
Left ventricular failure
Aortic valve regurgitation
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PAD & PCWP analysis
When PAD = PCWPWhen PAD = PCWP
Increased PVR
Mitral valve disease
Pulmonary hypertension
Pulmonary venous disease
High Peep >10mmHg
Cor pulmonale
Pulmonary embolism
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Cardiac Output
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Case 1
2 yr old post op cardiac surgical repair of VSD
HR HR 166/min
C.OC.O 3.0 SVRSVR 1712
CICI 1.8 PVRPVR 350
BPBP 60/35 PAPPAP 46/22
CVP CVP 16 RVSWIRVSWI 4
PCWPPCWP 22 LVSWILVSWI 21
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Case 2
12 yr old patient who underwent a Ross Konno procedure for LVOT and aortic valve reconstruction
HR HR 136
C.OC.O 3.4 SVRSVR 1905
CICI 2.2 PVRPVR 150
BPBP 65/38 PAPPAP 13/5
CVP CVP 1 RVSWIRVSWI 5
PCWPPCWP 4 LVSWILVSWI 29
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Case 3
16 yr old post op cardiac surgical repair of mitral valve
HRHR 166/min
C.OC.O 3.3 SVRSVR 1689
CICI 2.1 PVRPVR 175
BPBP 70/48
CVP CVP 19 RVSWIRVSWI 5
PCWPPCWP 19 LVSWILVSWI 18
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Case 4
2 yr old previous AVSD repair at 4 weeks of age admitted with SOB post RSV.
HRHR 168
C.OC.O 5.0 SVRSVR 1200
CICI 3.0 PVRPVR 385
BPBP 98/67 PAPPAP 46/22
CVP CVP 14 RVSWI RVSWI 5
PCWPPCWP 6 LVSWILVSWI 42
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Case 5A 10 yr old cardiomyopathic patient in critical care awaiting heart transplant. This is her hemodynamic data. She has a CVL, PA line, LA line. You have just returned from the cardiac catheterization lab and the following data is available for you to interpret.
HR HR 126
C.OC.O 10 SVRSVR 356
CICI 5.7 PVRPVR 302
BPBP 91/39 PAPPAP 46/22
CVP CVP 13 RVSWIRVSWI 8
PCWPPCWP 15 LVSWILVSWI 24
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Sepsis Patient
7 yr old sepsis patientGram negative septic shockMulti-organ failure: respiratory, renal, liverSvO2 = 75%Lactate of 2.2Vasopressin 0.0002 units/kg/hrEpinephrine .03 mcg/kg/min Dopamine 7.5 mcg/kg/min
Started on Milrinone .66 mcg/kg/min Nipride of 1.0 mcg/kg/min
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Sepsis Patient
PAP = 37.8 deg. Temp
Esophageal = 37.2 deg. Temp
Wt 25 kg
Ht 126 cm
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Sepsis 21:00 01:03 04.22 11:00
CO 3.87 6.29 6.27 2.07
CI 4.07 6.62 6.60 2.18
SI 30.97 48.3 47 15.7
SVRI 1060 918 787 2385
PVRI 314 85 194 550
HR 132 137 140 139
BP 110/59 148/76 123/63 116/74
PAP
(mean)
43/34 (37) 44/36 (31) 46/37 (32) 46/36 (31)
PCWP 21 29 21 21
RAP 19 17 16 21
SvO2 72 69 70 50
SVR 2511
PVR 579
SV 14.9
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Intramural MI
14 yr old sudden loss of consciousness while playing sports
SOB + O2. On oxygen. O2 sat 99% Marked ST segment depression on EKG 59.0 kg Ht 177 cm Computation constant - .547 Swan Ganz inserted. Nitroglycerine infusion started wwwemedicine.com/med/topic2956.c?htm
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coronary 1320 Insert 1325 13:29 13:38 1435
CO ST depressed 4.84 HOB 45
CI 2.86
SI
SVRI
PVRI 279
HR 90 92 92
BP 92/69 (78) 94/70 94/57
PAP
(mean)
38/10 RV
(21)
39/18 PAP
(27)
37/21 42/28
(27) (33)
30/20
(24)
PCWP 20 17 22 18
RAP 9 4 6
SvO2
SVR 1041
PVR 165
LVSWI 35.8 21.2
RVSWI 16.46 9.74
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Intramural MI ST segment depression in the night BP okay Wedge increased from 14 mm Hg -19 mm Hg Awoke – suddenly SOB – sat bolt upright O2 sats in the 80’s on 100% O2 Nitroglycerine increased to 3 mcg/kg/min Morphine 12 lead done 5:20 am Esmolol 400 mcg/kg/min Tachycardia PAP 55/22 reflecting Marked LV failure
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Intramural MI LOC decreased Emergent intubation Systole of 40 mm Hg Epi - .02 mcg/kg/min Vasopressin .0004 units/kg/hr Nitroglycerine 6 mcg/kg/min Bicarb Ca++ Volume 2 units PRBC Troponin and CPK increased Esmolol off V tachycardia
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Intramural MI Reimplantation of intramural LCAReimplantation of intramural LCA Good functionGood function LCA origin in middle of L coronary sinusLCA origin in middle of L coronary sinus Abherrent LMCA from tight sinus of aortaAbherrent LMCA from tight sinus of aorta Unroof the LMCA off the ostiumUnroof the LMCA off the ostium Bipass 91 minBipass 91 min XClamp 41 minXClamp 41 min Nitroglygerine 0.5 mcg/kg/minNitroglygerine 0.5 mcg/kg/min MilrinoneMilrinone Tylenol and KetorolacTylenol and Ketorolac EsmololEsmolol Day 2 – Post op ST depression and diastolic dysfunctionDay 2 – Post op ST depression and diastolic dysfunction