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CENTRAL VENOUS PRESSURE MONITORING- IACTACON 2018
1. Central Line
Interpretation of waveform & Clinical
application in Cardiac Surgeries and ICU
Dr. Harshil Joshi DM
Chief - Cardiac Anesthesia
Century Super speciality Hospital
Prerna Anesthesia &Critical Care Services
01/02/2018
2. What is CVP
⢠The central venous pressure (CVP) is the pressure measured in the
central veins close to the heart.
⢠It is the pressure measured at the junction of the superior vena cava
and the right atrium. And No valve in between.
⢠It indicates mean right atrial pressure and is frequently used as an
estimate of right ventricular preload.
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3. ⢠It reflects the driving force for filling of the right atrium & ventricle
⢠It indicates the relationship of blood volume to the capacity of the
venous system.
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4. Indication
⢠Major operative procedures involving large fluid shifts or blood loss
⢠Intravascular volume assessment when urine output is not reliable or unavailable
⢠Temporary Hemodialysis
⢠Surgical procedures with a high risk for air embolism, CVP catheter may be used to aspirate
intracardiac air
⢠Frequent venous blood sampling, Inadequate peripheral intravenous access
⢠Temporary pacing
⢠Venous access for vasoactive or irritating drugs & Chronic drug administration
⢠Rapid infusion of intravenous fluids (using large cannulae)
⢠Total parenteral nutrition
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5. Common Insertion Site
⢠Internal Jugular
⢠Subclavian
⢠Femoral
⢠External Jugular
⢠Basilic
⢠Axillary
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6. Right IJV is Preferred
⢠Consistent, predictable anatomy
⢠Alignment with RA
⢠Palpable landmark and high success rate
⢠No thoracic duct injury
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7. Complication
Complications of Central Venous
Access and Cannulation
⢠Arterial puncture with hematoma
⢠Arteriovenous fistula
⢠Hemothorax, Chylothorax or Pneumothorax
⢠Nerve injury
⢠Air embolus
⢠Catheter or wire shearing
⢠Right atrial or right ventricular perforation
Complications of Catheter
Presence
⢠Thrombosis, thromboembolism
⢠Infection, sepsis, endocarditis
⢠Arrhythmias
⢠Hydrothorax
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8. Factors Affecting CVP
⢠Cardiac Function
⢠Blood Volume
⢠Capacitance of vessel
⢠Intrathoracic & Intraperitoneal pressure
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9. Interpretation from Numbers
⢠CVP is recorded in centimetres of water (cm H2O) or millimetres of
mercury (mm Hg) read from manometer markings.
⢠Normal CVP ranges from 5 to 10 cm H2O or 2 to 6 mm Hg.
⢠Single value has no value. Trend is important.
⢠CVP is surrogate marker.
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10. Series Circulation
⢠Right Atrium Right Ventricle Pulmonary Circulation
TV PV
Left Ventricle Left Atrium
MV
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12. PhysiologyâŚ
⢠It would be ideal to monitor cardiac chamber volumes continuously in
critically ill patients, this goal remains elusive in clinical practice.
⢠The relationship between ventricular volume and filling pressure
depends on the portion of the pressure-volume curve over which the
patient's heart is operating and the shape or slope of the curve.
Commonly termed ventricular compliance
01/02/2018
13. Transmural Pressure
⢠The cardiac chambers are all contained within the pericardium and
thorax. Changes in pressure in the structures surrounding the heart
will influence pressures recorded within the heart.
⢠Transmural pressure is the difference between chamber pressure and
juxtacardiac or pericardial pressure.
01/02/2018
14. Measurement
⢠The phlebostatic axis is the reference point for zeroing the
hemodynamic monitoring device.
⢠4th intercostal space, mid-axillary line
⢠1 mmHg = 1.36 cm H2O.
⢠the first step in pressure transducer setup is to zero the transducer by
exposing it to atmospheric pressure
⢠Thus, a cardiac filling pressure of 10 mm Hg is 10 mm Hg higher than
ambient atmospheric pressure.
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15. Respiratory Effect
A, During spontaneous ventilation, the onset of
inspiration (arrows) causes a reduction in
intrathoracic pressure, which is transmitted to
both the CVP and pulmonary artery pressure
(PAP) waveforms. CVP should be recorded at
end-expiration.
B, During positive-pressure ventilation, the
onset of inspiration (arrows) causes an increase
in intrathoracic pressure. CVP is still recorded at
end-expiration.
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16. ⢠Kussmaul sign is a paradoxical rise in jugular venous pressure (JVP) on
inspiration, or a failure in the appropriate fall of the JVP with
inspiration. It can be seen in some forms of heart disease and is
usually indicative of limited right ventricular filling due to right heart
dysfunction.
⢠Hepatojugular Reflex: A positive result is variously defined as either a
sustained rise in the JVP of at least 3 cm or more or a fall of 4 cm or
more after the examiner releases pressure.
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18. ⢠Fluid Responsiveness: inspiratory fall of CVP > 1 mmHg is high
predictive of fluid responders
⢠Keeping CVP > 5 mmHg in renal transplant surgery is associated with
good graft function In first 3 post op days
⢠Post cardiac surgery CVP > 15 mmHg is associated with poor outcome
01/02/2018
19. ⢠Decrease in CVP is relatively late sign of depletion of intravascular
volume
⢠CVP is better measurement of volume status in anesthetised patient
whose autonomic reflexes are abolished
⢠Goal directed fluid therapy has not shown good results in critically ill
patients.
⢠Increasing availability of non-invasive and apparently better
measurement of preload and circulatory filling will decrease
dependence on CVP.
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22. ⢠Role of CVP monitoring for stabilizing critically ill patient in ICU will be
secondary⌠because we put central line not to monitor cvp but for
other reasons.
⢠So monitoring CVP become risk free.
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23. Interpretation from Waveform
The CVP waveform consists of five phasic events,
three peaks (a, c, v) and two descents (x, y)
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24. Mechanical Events
Waveform Component Phase of Cardiac Cycle Mechanical Events
âaâ wave End Diastole Atrial Contraction(after P wave)
âcâ wave Early Systole Isovolumic right ventricle
contraction, TV bow in RA(after
QRS)
âxâ descent Mid Systole Atrial Relaxation, Descent of RV
base(TV annulus)
âvâ wave Late Systole Filing of RA with venous blood(just
after T wave)
âyâ descent Early Diastole Early ventricular filling, opening of
TV
âhâ wave Mid to Late Diastole Diastole plateau
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25. âaâ wave
⢠Atrial Contraction(after P wave)
⢠End Diastole
⢠Prominent a wave: resistance in RV filling- RVH, TS, Temponade,
PS, Pulmonary hypertension
⢠Absent a wave: Atrial fibrillation or
⢠flutter
Cannon A waves occur as the RA
contracts against a closed TV: junctional
rhythm, CHB,ventricular arrhythmias
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26. âcâ wave
⢠Isovolumic right ventricle contraction, TV bow in RA(after QRS)
⢠Early Systole
⢠TR: Tall Systolic c-v wave
⢠It is call holosystolic cannon v waves
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27. âxâ descent
⢠Atrial Relaxation, Descent of RV base(TV annulus)
⢠Mid Systole
⢠Dominant x descent âgood RV function and vice versa
⢠Cardiac Tamponade-
⢠X descent is steep & Y descent is diminished
⢠Early diastolic runoff is impaired by the pericardial fluid collection.
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28. âvâ wave
⢠Filing of RA with venous blood(just after T wave)
⢠Late Systole
⢠Prominent v wave with increase venous return. ASD, PAPVC or TAPVC,
A-V malformation
⢠Large V waves may also appear later in systole if the ventricle becomes
noncompliant because of ischemia or RV failure.
⢠Decrease in RA emptying. TS
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29. âyâ descent
⢠Early ventricular filling, opening of TV
⢠Early Diastole
⢠Attentuation of y descent: TS, Tachycardia, RVF, Tamponade,PS
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30. Constrictive Pericarditis
⢠This causes prominent A and V waves and steep X and Y descents
(creating an M configuration) like decreased RV compliance.
⢠Blood from the RA to the right ventricle is initially rapid during
early diastolic filling of the right ventricle (creating a steep Y
descent) but is short-lived and abruptly halted by the restrictive,
noncompliant right ventricle.
⢠The right atrial pressure then increases rapidly and reaches a
plateau until the end of the A wave, at the end of diastole.
⢠This portion of the waveform is analogous to the ventricular
diastolic dip-and-plateau sign.
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31. Heart Block
⢠two-to-one heart block is recognized by A waves, that occur with
twice the frequency of the artery pulse.
⢠PR interval prolongation is recognized by an increase in the interval
between the jugular A wave and the arterial pulse
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32. LVH(AS,Coarctation,LVOTO)
⢠Directing attention to the amplitude of the jugular venous A wave in
subjects with isolated obstruction to left ventricular outflow is
seemingly paradoxical.
⢠However, left ventricular hypertrophy serves to decrease right
ventricular distensibility, so the right atrium contracts with greater
force and the amplitude of the jugular venous A wave increases in the
absence of pulmonary hypertension
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33. Pulmonary Stenosis
⢠The jugular venous A wave is distinctive and increases progressively as
the stenosis increases, culminating in a giant A wave.
⢠Attenuates y descent
⢠Powerful right atrial contraction generates a giant A wave via the
superior vena cava and a presystolic liver pulse via the inferior cava.
⢠With the advent of right ventricular failure and tricuspid regurgitation,
the large A wave is accompanied by an increase in the V wave.
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34. Ebsteinâs Anomaly
⢠Prominent C wave that coincides with mobility of the anterior tricuspid leaflet.
⢠The interval between the jugular A wave and the carotid pulse is often prolonged,
reflecting prolongation of the PR interval.
⢠Prominent A waves are seldom seen in the jugular pulse.
⢠A stenotic or imperforate tricuspid orifice is accompanied by A waves that may be giant.
⢠An attenuated X descent and a systolic venous V wave of tricuspid regurgitation seldom
appear in the jugular pulse despite severe regurgitant flow because of the damping effect
of the commodious right atrium and the thin-walled toneless atrialized right ventricle and
because tricuspid regurgitation is low-pressure and hypokinetic.
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35. ASD
⢠Most important is left atrialization of the jugular venous wave form.
⢠The crests of the A and V waves tend to be equal as they are in the left
atrium because the two atria are in common communication through
a nonrestrictive atrial septal defect.
⢠The A wave amplitude varies with heart rate and compliance of
ventricle as in healthy subjects.
⢠Pulmonary vascular disease results in an increased force of right atrial
contraction and a dominant, if not giant, A wave
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36. Lutembacherâs syndrome
⢠The right and left atrium function as a common chamber when the
atrial septal defect is nonrestrictive, so the height and contour of the
left atrial pressure pulse are transmitted into the right atrium and into
the internal jugular vein.
⢠Elevated mean jugular venous pressure in the absence of right
ventricular failure and for an elevated jugular venous A wave in the
absence of pulmonary hypertension.
⢠Post ASD closure-- Donât Target CVP
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37. AVCD
⢠The V wave is dominant in the jugular venous pulse because the right
atrium receives left ventricular systolic flow across an incompetent left
AV valve directly through the atrioventricular septal defect or indirectly
through an ostium primum atrial septal
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38. VSD
⢠Moderately restrictive and nonrestrictive ventricular septal defects
with congestive heart failure are accompanied by an elevated mean
jugular venous pressure and an increase in A and V waves.
⢠However, the jugular venous pulse in Eisenmengerâs syndrome(PDA,
AP window) is normal or nearly so, with a small dominant A wave
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39. TOF
⢠Normal- RV will offload in to LV
⢠Restrictive VSD - RV pressure will increase more then systemic: large a
wave in CVP
⢠Absent PV: initially large a wave, and after development of TR large v
wave
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40. Univentricular physiology
⢠The right atrial A wave, V wave, and mean pressure are elevated
⢠Post BDG: IJV attached to PA and IVC attached to RA which is affected
by common ventricle pressure.
⢠Post Fontan: no longer CVP, only PA pressure.
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41. Case Scenario 1
⢠Post OP CABG, extubated
⢠Breathlessness, hypotension, tachycardia
⢠BP responding to fluid bolus
⢠Drain- 400 ml
⢠Lungs â clear
⢠Swing in arterial trace
⢠Prominent x descent
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42. Case Scenario 2
⢠Post MVR, Female patient
⢠Breathlessness, hypotension, tachycardia
⢠Bilateral crepitation
⢠A wave disappear
⢠C wave more prominent
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43. Case Scenario 3
⢠Young male patient with weakness, jaundice, fatigue and dependant
odema
⢠Systolic thrill and murmur in neck
⢠Tender hepatomegaly
⢠Prominet c & v wave
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44. Summary
⢠Individual CVP waveforms provide unique diagnostic clues about the
circulation.
⢠Trends in CVP over time may also be useful in estimating fluid or
blood loss and guiding replacement therapy.
⢠It is important to remember that there is a significant range of normal
values and that a small change in CVP may reflect a significant
alteration in circulating blood volume and right ventricular preload.
⢠Additional useful information may be derived from examining how a
fluid bolus simultaneously alters CVP and other variables of clinical
interest, such as blood pressure, urine output, and so forth.
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