This document discusses central venous pressure (CVP), including its indications, measurement sites, determinants, and limitations. Some key points: - CVP is the pressure measured in central veins close to the heart and reflects right atrial pressure. It provides information about right ventricular preload but does not indicate blood volume. - CVP can be measured through the internal jugular, femoral, or subclavian veins. Factors like cardiac function, vascular compliance, blood volume, and intrathoracic pressure determine CVP. - While CVP provides data on circulatory equilibrium between the heart and veins, it does not predict fluid responsiveness or tissue perfusion. Dynamic variables obtained through fluid challenges or

1. CENTRAL VENOUS PRESSURE

2. • CVP is the pressure measured in central veins close to the heart.
• Pressure measured at the junction of SVC & rt atrium & there are no
valves in between…..
• It is the back pressure for the return of blood to the heart.

4. INDICATIONS
• CVP measurement
• Central venous oxygen saturation of SVC
• Major operative procedures – large fluid shifts
• Temporary hemodialysis
• Frequent venous blood sampling , inadequate peripheral venous
access
• Temporary pacing
• For vasoactive drugs, parenteral nutrition
• Aspirate intracardiac air – in surgeries with high risk for air embolism

5. INSERTION SITES
• Internal jugular – consistent,
predictable anatomy
• alignment with RA
• Palpable landmark & high
success rate

6. • FEMORAL VEIN :
• No risk of pneumo
• Ease of access – esp in pts with shock
• Higher rate of infect & venous thrombosis after prolonged catheterisation
• SUBCLAVIAN VEIN :
• Less collapsible during profound hypotension – anatomical grip on clavicle
• Complicatn higher
• CHEST X – RAY – DECREASES THE PROBABILITY OF COMPLICATIONS &
PROPER POSITIONING OF CATHETER TIP.

7. DETERMINANTS OF CVP
• Relationship between CO & CVP - 2 fold…..
• Applies to heart – frank starling law – cardiac function curve
• Applies to vascular system – Guyton – vascular law
• Intersection of cardiac & vascular function curves – state of
equilibrium – nothing but CVP – intact circulation

8. • When the heart is isolated from vascular system – CVP is nothing but
pressure on the walls of heart – especially rt heart – that sets the initial
length of sarcomeres based on compliance of the heart – frank starling law
• When venous return is isolated from heart – CVP determines the pressure
diff for the return of blood.
• So combining both – heart controls the return of blood by decreasing the rt
atrial pressure
• There is little change in upstream venous reservoir during cardiac cycle.
• So change in CVP in not just change in preload but rather equilibrium of
both functn.

9. Cardiac function curve
• Frank starlings law
• CO varies with preload ( CVP )
• Governing factors – afterload & contractility
• Functional limits – pericardium / cardiac cytoskeleton ( when
pericardium is absent )
• Importance

10. Venous return function
• Guyton – vascular function curve law
• CVP inversely proportional to CO
• Determinants – arterial & venous compliances
PVR & blood volume
• Limitations – CVP < 0 in spontaneous breathing pts ( or ) < pleural
pressure in pts on ventilator – veins become collapsed – vascular
waterfall
• importance

12. Imp of interaction
• Exercise in young male….

14. • Normal CVP – 0 to 7 mm Hg
• If CVP > 7 as in ventilated patients / rt heart failure – driving pressure
is close to zero… so no filling / preload – but CO doesn’t become zero
– due to parallel increase in venoconstrictor tone.
• If CVP < 0 may not increase the venous return – due to collapse of
vein at the level of diaphragm.
• Resistance to venous return is very less – but small changes have
major consequences in terms of flow becoz the pressure gradient is
very low

15. WHAT DOES CVP NOT
TELL US……..
• BLOOD VOLUME - Stressed
volume & unstressed
volume

17. • 2ND reason – as it is the equilibrium – a change in either of these
alters the CVP for the same stressed volume.
• Increase in CVP – so there should be more upstream pressure in veins
& venules to maintain flow.
• This higher pressure causes fluid filtration – loss of stressed vol into
interstitial spaces.
• 3RD reason – doesn’t predict volume responsiveness.

18. HYPOVOLEMIA
• Absolute & relative hypovolemia
• Absolute – total circulating vol – decrease venous return , preload, CO
• Relative – inadequate distribution b/w stressed & unstressed volumes

19. PRINCIPLES
• Reference value & physiologic variations
• Reference value – phlebhotaxic axis
• The implementation of a ZERO reference is required before each
measurement.
• Interaction between CVP & ventilation through transmural pressure is
the cause of variations in CVP curves.
• In mechanically ventilated pts, ZERO reference point is equal to atm
pressure.
• No solutions hav ebeen proposed for the reliable & reproducible
measurement of CVP values under unphysiological conditions.

20. MEASURMENT OF CVP

21. MEASUREMENT OF CVP

22. PROPER
MEASURMENT
• 5 cm below the sternal angle – approx. 5 cm
above the midpoint of rt atrium
• Mid-thoracic / mid-axillary point – easier to
identify but approx. 3 mm Hg higher than
sternal angle based measurement.
• Measured at the end-expiration becoz
pleural pressure is closest to atm pressure –
which doesn’t change during expiration &
neither CVP.

25. COMPLICATIONS
• Infection ( silver – sulfadiazine & chlorhexidine )
• Thrombosis
• Pneumothorax , hemothorax, chylothorax
• Air embolism – never ports are opened to atm while insertion

26. HOW TO USE
To measure the rt atrial
pressure – surrogate to
estimate the rt ventricular
preload – an indicator of
interaction between venoes
return & rt ventricular functn.
In spontaneously breathing
pts – decrease in CVP > 2 mm
Hg with inspiration indicates
fluid responsiveness.
Higher values of CVP also
predict the occurrence of of rt
heart failure such as in
pulmonary embolism – so
considered warning sign

28. FUNCTIONAL HEMODYNAMIC MONITORING
• Hemodynamic monitoring is the act of assessing the cardiovascular
values, such as blood pressure, heart rate, and cardiac output, and their
patterns. Its clinical utility rests in defining variations from normal ranges
and the constellation of abnormal patterns that define specific pathological
cardiovascular states, such as hypovolemia, heart failure, and sepsis.
• Functional hemodynamic monitoring, on the other hand, is the assessment
of the dynamic interactions of hemodynamic variables in response to a
defined perturbation.
• Such dynamic responses result in emergent parameters of these
commonly reported variables that greatly increase the ability of these
measures to define cardiovascular state and predict response to therapy.

29. DIFERENT TYPES OF CIRCULATORY SHOCK
• Hypovolemic
• Cardiogenic
• Obstructive
• Distributive / septic

30. • Using functional hemodynamic monitoring we can answer four
imp & interrelated que of the patient
A) Are they volume responsive?
B) Are they in compensated shock?
C) Is their arterial tone increased, normal or decreased?
D) Is their heart able to sustain flow without high filling
pressures?

31. STATIC HEMODYNAMIC VARIABLES

32. DYNAMIC VARIABLES
3 groups
• 1 st group – cyclic variations in stroke volume / related
hemodynamic parameters
• 2nd group – cyclic variations of non stroke volume related
hemodynamic parameters
• 3rd group – indices based on preload redistribution maneuvers

36. HEMODYNAMIC VARIABLES

37. FLUID CHALLENGE
• 500 ml of fluid over 30 min – increase in CO > 15 %
• Arbitrary values
• Marginal pts – fluid overload

38. a. Pulse pressure variation
b. Stroke volume variation
c. IVC distensibility index
Other variables:
• systolic pressure variation ( SPV)
• Aortic blood flow velocity ( esophageal doppler )
• Pressure wave variation by pulse oximetry ( plethysmographic wave
via pulse oximetry Pplet )
• Aortic flow velocity time
• Brachial flow variation time

39. Effect of
mechanical
ventilation on
left & right
ventricular
stroke volume
• 3) direct compression of heart by lungs
• 4) ventricular interdependence

40. PULSE PRESSURE VARIATION ( PPV )
• Defined as PPmax- PPmin / PPmean
• Ave 3 breaths
• > 13 – 15 % - predictive of volume responsive
• Tidal volume > 8 ml/kg
• Grey zone 9 – 13 %
• PPV > 12 % - TV 6 ml/kg- still responsive
• Invasive arterial monitoring & dedicated monitor

42. STROKE VOLUME VARIATION
• Defined as SVmax – SVmin / Svmean
• SVV > 10 % - fluid responsive
• PiCCO , LiDCO

43. LIMITATIONS
• Only in ventilated patients
• In most studies TV – 8ml/kg
• Req constant R – R interval
• False positive rate in rt heart failure
• Intraabdominal pressures – invalidated – remains responsive even if
their PPV < 15 % & SVV < 10 %
• SVV has no predictive value in septic shock patients in PSV
ventilation
• Falsely elevated parameters in massive & rapid blood loss –
Berkenstadt et al – animal model
• Norad infusion – increase SVV & PPV independently from volemic
state & fluid responsiveness.

44. GROUP B INDICES
• Oscillations in great diameters vessels
• SVC collapses during mechanical inspiration – collapsibilty
index
• IVC distends during mechanical inspiration – distensibilty
index
• Some studies 100 % sensitivity & specificity
• Less invasive – M mode - transthoracic echo / abdominal U/S –
approx. 2cm inferior to junction with the RA
• IVC distensibilty index > 18 %

47. LIMITATIONS
Sinus rhythm
Controlled ventilation
U/S expertise

48. FOR SPONTANEOUS BREATHING PATIENTS
• PASSIVE LEG RAISE TEST :
• Angle 45 degrees – atleast one min
• Equivalent – 300 ml in a 70 kg pt
• CO increased by 10 % - volume responsive
• Autotransfusion
• Reversible fluid challenge
• Also aortic blood flow, carotid flow are measured
• Safer in arrythmic pts & spontaneous pts
• Also in ventilated pts
• Reduce sensitivity in pts with intraabdominal HTN

50. • Dynamic changes in CVP :
decrease in CVP > 1 mm Hg during inspiration – fluid
responsive
Use of Valsalva maneuver to assess volume responsiveness

51. LIMITATIONS TO PREDICTING VOLUME RESPONSIVENESS
• Positive test doesn’t mean there is need for fluid resuscitation –
every pt under GA is virtually fluid responsive – but stable
hemodynamics – no need for fluid resuscitation
• When the test is positive – decision to give fluid depends on clinical
status & effective need to hemodynamic conditions
• No guarantee that fluid given to increase cardiac output reverse
tissue hypoperfusion
• No RCT on patient outcomes – only on evaluation of predictive value
• More efficient to use end points of fluid therapy based on
disappearance of preload responsiveness

52. EARLY IDENTIFICATION OF COMPENSATED SHOCK
• Why we need to identify early ?
• Sites for assessment of microcirculation – muscles and skin
blood flow – reason
• Tissue cardiovascular reserve – sensitive early warning measure
of impending CVS collapse
• Parameters – tissue oxygen saturation ( StO2 ) & vascular
occlusion test ( VOT ).

53. • StO2 – non invasive – NIRS – accurate & valid method
• Minimal risk
• Continuous in their measures
• Trending of states
• Assessing the severity of circulatory shock
• Absolute values – limited use – StO2 remain normal until tissue
hypoperfusion is quiet advanced
• So dynamic ischemic challenge – VOT

55. • Parameters from StO2 graph
• Down slope / deoxygenation rate DxO2 – local metabolic rate &
effective local blood flow distribution
• StO2 recovery / reoxygenation rate RxO2 – local cardiovascular
reserve & microcirculatory flow
• Validated in septic & trauma pts
• Impairment of slopes – correlates to longer ICU stay in septic pts –
Mesquida et al
• Able to predict the need of interventions earlier - resuscitaion

56. ASSESSING ARTERIAL TONE ( Ea )
• Dynamic central arterial elastance – PPV / SVV
• Surrogate marker of vasomotor tone
• Assessment of effect of of volume loading on arterial pressure in
hypotensive shock pts – whose PPV fluid responsive
• Response to fluid challenge – CO increased but pts with normal
/ increased Ea increased arterial pressure
• Ea differentiates responders from non - responders
• Ea < 0.9 – severely vasodilated state