Hemodynamic Parameters&

fluid therapy

Muhammad Asim RanaBSc, MBBS, MRCP, FCCP, EDIC, SF-CCMDepartment of Critical Care Medicine

King Saud Medical City

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.

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

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

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

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)

Preload & Frank–Starling principle

Indices of cardiac preload & fluid responsiveness

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)

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.

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.

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

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

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.

Measured Variables from PAC

Measured & Derived Variables

Pulmonary artery occlusion pressure

PAOP closely approximates left atrial pressure (LAP), which approximates left ventricular end-diastolic pressure (LVEDP).

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

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.

Black Clouds over PAC

• A recent multicentre trial incorporating protocolized hemodynamic management of patients with acute lung injury compared PAC-guided 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.

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

Transpulmonary Indicator Dilution

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

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.

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

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.

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

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

PVI to Help Clinicians Optimize Preload / Cardiac Output

Preload

Stroke Volume

00

Higher PVI = More likely to

respond to fluid therapy24 %

10 %Lower PVI = Less likely to respond to fluid therapy

BP variation -spontaneous Respiration

Reversed Pulsus Paradoxus

PPV with Mechanical Ventilation

Calculation of SVV

Heart-Lung Interaction

Ventilation

Circulation

Preload

Afterload

Contractility

Intra Thoracic Pressure

Lung Volume

SVV and PPV

Heart-Lung Interaction

Cardiac Output

Pressure

Cardiac Output

Cardiac Output

Effect of Rise of Intrathoracic Pressure on Cardiac Output & Venous R eturnCurves

CardiacOutput

Pressure

Hypovolemic Patient Normovolemic Patient

Heart-Lung Interaction

Pressure

CardiacOutput

CardiacOutput

Normovolemic Patient

Effect of Drop of Intra thoracic pressure on Cardiac output & Venous return Curves

CardiacOutput

CardiacOutput

Pressure

Hypovolemic Patient

Bed Side Utilization

MV Insp

Bed Side Utilization

Prediction of Fluid responsiveness in hypovolemic patients

Expiration

Mechanical InspExpiration

Bed Side Utilization

Prediction of Fluid responsiveness in normovolemic patient

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.

PPV & PVI vs CVP & PCWP

Adapted from Cannesson M. et. al. Br J Anesth 2008;101(2):200-206

Zimmermann M, et al. Eur J Anaesthesiol. 2010;27(66):555-561.

CO

PPV

PVI

Loupec T et al. Crit Care Med 2011 Vol. 39, No. 2

ConclusionBy 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

Questions?

Thank you