Assessment of haemodynamics a critically ill patient and its management has always been a matter if debate. Over time a lot of studies and therapeutic interventions have been carried out. This presentation is a review of such interventions and their impact on the outcome.
2. Abstract
• Clinical assessment of the intravascular
volume can be difficult in critically ill patients.
• Fluid loading is considered the first step in the
resuscitation of hemodynamically unstable
patients.
• Role of cardiac filling pressures (CVP & PAOP)
• Studies using heart–lung interactions during
IPPV to assess fluid responsiveness.
3. Studies using heart–lung interactions
• The pulse pressure variation derived from
analysis of the arterial waveform.
• The stroke volume variation derived from
pulse contour analysis.
• The variation of the amplitude of the pulse
oximeter plethysmographic waveform.
• The left ventricular end-diastolic area as
determined by TEE
4. Introduction
• The multi-organ dysfunction syndrome
– Tissue hypoxia due to inadequate oxygen delivery
– Microcirculatory injury and increased tissue
metabolic demands
– Cytopathic hypoxia due to mitochondrial
dysfunction
• Early aggressive resuscitation improves
outcome (Landmark study, Rivers et al.)
• Optimization of cardiac output before major surgery
5. Why need to know fluid status?
• Fluid therapy is considered the first step in the
resuscitation of most patients with shock.
• Uncorrected hypovolemia, leading to
inappropriate infusions of vasopressor
agents, may increase organ hypoperfusion and
ischemia.
• Overzealous fluid resuscitation has been
associated with increased complications
6. Why need to know fluid status?
• The first step in the hemodynamic
management
• Targeting 'supra-normal' hemodynamic
parameters may be harmful
• Need of an accurate assessment of
– Intravascular volume status (Cardiac preload)
– The ability to predict the hemodynamic response
following fluid challange (Volume responsiveness)
9. Central Venous Pressure
• Jugular venous pressure, CVP & Rt atrial pressure
are often used interchangeably.
• The normal CVP in the spont breathing-0–5
mmHg, while 10 mmHg is generally accepted as
the upper limit during mechanical ventilation.
• CVP as fluid management guide
– Correlation between CVP and pulmonary artery
occlusion pressures (PAOP)
– The relationship between CVP and right ventricular
end-diastolic volume (RVEDV: preload)
10. Role of CVP
• Static measures of CVP
• Dynamic changes in CVP
– (in response to volume loading or related to
respiration)
– For instance, a steep increase in CVP following
volume challenge suggests the heart is functioning
on the plateau portion of the Frank–Starling
curve.
11. Black clouds over CVP
• Systematic review
• 5 studies that compared the CVP with the
measured circulating blood volume
• 19 studies determined the relationship
between the CVP/delta-CVP and the change in
cardiac performance following a fluid
challenge.
12. Assessment of role of CVP
– The pooled correlation coefficient between the CVP and the
measured blood volume was 0.16 (95% CI 0.03–0.28).
– The pooled correlation coefficient between the baseline CVP and
change in stroke index/cardiac index was 0.18 (95% CI 0.08–0.28).
– The pooled area under the receiver operator characteristic (ROC)
curve was 0.56 (95% CI 0.51–0.61).
– The pooled correlation between the delta-CVP and the change in
stroke index/cardiac index was 0.11 (95% CI 0.015–0.21).
• The results of this systematic review clearly demonstrate that
there is
• no association between the CVP and circulating blood volume,
that the CVP is
• a poor indicator of left and right ventricular preload and that
• the CVP does not predict fluid responsiveness
13. Pulmonary Artery Catheter
• Right-heart catheterisation using a flow-directed
balloon tipped catheter was introduced by Swan
and Ganz in1970.
• Traditional indications for PAC monitoring have
been to:
– characterise haemodynamic perturbation
– differentiate cardiogenic from non-cardiogenic
pulmonary oedema
– guide use of vasoactive drugs, fluids and diuretics
14. Measured Variables (PAC)
• Measures right ventricular and pulmonary
arterial pressures directly at the bedside.
• In acute respiratory distress syndrome
(ARDS), where pulmonary hypertension and
increased right ventricular afterload are linked
to excess mortality, a PAC can assist in the
titration of afterload-reducing therapies such
as inhaled prostacyclin or nitric oxide.
17. Pulmonary artery occlusion pressure
PAOP closely approximates left atrial pressure (LAP), which
approximates left ventricular end-diastolic pressure (LVEDP).
18. Black Clouds over PAC
• In 1996 a non-randomised cohort study of PAC
use in American teaching hospitals appeared
to show that, in any of nine major disease
categories, PAC in the first 24 hours increased
30-day mortality (odds ratio 1.24, 95% (CI)
1.03–1.49), mean length of stay and mean
cost per hospital stay
19. Black Clouds over PAC
• A Cochrane database systematic review of PAC
monitoring in adult ICU patients incorporated
data from two recent multicentre trials and 10
other studies.
• The pooled mortality odds ratio for studies of
general ICU patients was 1.05 (95% CI 0.87–1.26)
and for studies of high-risk surgery patients was
0.99 (95% CI 0.73–1.24).
• PAC monitoring had no impact on ICU or hospital
length of stay.
20. Black Clouds over PAC
• A recent multicentre trial incorporating
protocolized hemodynamic management of
patients with acute lung injury compared PACguided with CVC-guided therapy.
• There were no significant differences in 60-day
mortality or organ function between groups.
– Overall, these data suggest that PAC monitoring in
critically ill patients is not associated with
increased mortality or with survival benefit.
21. Bolus Thermodilution Cardiac Output
• A bolus injection into the right atrium of cold
injectate (usually 5% dextrose) transiently decreases
blood temperature in the PA (monitored by a
thermistor proximal to the balloon).
• Stewart–Hamilton equation
23. Left Ventricular End-diastolic Area
• The left ventricular end-diastolic area (LVEDA)
has been shown to correlate well with the
intrathoracic blood volume (ITBV) and global
end-diastolic volume (GEDV) as well as with
LVEDV as measured by scintography.
• An end-diastolic diameter of < 25 mm and a
LVEDA of < 55 cm2 have been used to
diagnose hypovolemia
24. Drawbacks
• A small LVEDA does not always reflect
decreased intravascular volume.
• Snapshot of ventricular function at a single
period in time
• Recently, a disposable transesophageal echocardiography
probe that allows continuous monitoring of LV function has
been developed (ClariTEE, ImaCor, Uniondale, NY, USA).
• Such technology allows monitoring of LV volumes and function
over time, allowing the clinician to determine the response to
various therapeutic interventions.
25. Inferior Vena Caval Diameter
• The diameter of the IVC can be measured by subcostal
echocardiography.
• A collapsed IVC vs distended IVC
• The mean end-diastolic IVC dimension correlates with
mean right atrial pressure
• Barbier and colleagues and Feissel and coworkers-the
distensibility index of the IVC
• Vieillard-Baron and colleagues -collapsibility index of the
SVC
• Drawbacks or Limitations
– Obesity & Post laparotomy cases
– Cases with increased Intra-abd pressure
– SVC is seen by TEE & it could not be continuous
26. Dynamic Indices of Intravascular Volume
• Studies have been reported that have used heart–lung
interactions during mechanical ventilation to assess fluid
responsiveness.
– The pulse pressure variation (PPV) derived from analysis of
the arterial waveform
– The stroke volume variation (SVV) derived from pulse
contour analysis
– The variation of the amplitude of the pulse oximeter
plethysmographic waveform
have shown to be highly predictive of fluid responsiveness.
27. Plethysmography variability index (PVI)
• New predictors have been obtained from
plethysmographic waveforms displayed on pulse
oxymeters.
• A new parameter called the
plethysmography variability index (PVI)
proposed by a pulse oxymetry manufacturer to
be used for the purpose of fluid responsiveness.
• Its advantage is that it can be automatically
calculated and displayed on the screen of the
pulse oxymetry monitor
28. PVI Calculation
• Automated measurement
– Changes in plethysmographic waveform amplitude over
the respiratory cycle
• PVI is a percentage from 1 to 100%:
– 1 - no pleth variability
– 100 - maximum pleth variability
29. PVI to Help Clinicians
Optimize Preload / Cardiac Output
Stroke
Volume
10 %
Lower PVI = Less likely to
respond to fluid therapy
Higher PVI = More likely to
24 %
0
0
respond to fluid therapy
Preload
45. Determining the accuracy of PPV & SVV
• 29 studies included in this meta analysis
• Demonstrated that the PPV and SVV measured
during volume controlled mechanical ventilation
predicted with a high degree of accuracy for
respond to a fluid challenge
– The sensitivity, specificity and diagnostic odds ratio
were 0.89, 0.88 and 59.86 for the PPV and 0.82, 0.86
and 27.34 for the SVV, respectively.
• The predictive value was maintained in patients
with poor LV function.
46.
47. PPV & PVI vs CVP & PCWP
Adapted from Cannesson M. et. al. Br J Anesth
2008;101(2):200-206
50. Conclusion
By virtue of its
• simplicity
• accuracy and
• availability as a continuous monitoring
tool
• would appear to be the ideal methods
for the titration of fluid resuscitation
in critically ill patients undergoing
mechanical ventilation..
•PPV
•SVV
•PVI
Echo : ventricular function and size complement the
information obtained by these indices of fluid
responsiveness
characterisehaemodynamic perturbation (e.g. distributive, cardiogenic, obstructive and hypovolaemic shock or combinations)differentiate cardiogenic from non-cardiogenic pulmonary oedemaguide use of vasoactive drugs, fluids and diuretics, especially when haemodynamic disturbances are coupled with increased lung water, right ventricular or left ventricular dysfunction, pulmonary hypertension and organ dysfunction