P Gokal Whats in the Pipeline

7/28/2019 P Gokal Whats in the Pipeline

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03 February 2012No. 04

Whats in the pipeline?

P Gokal

Commentator: K Govender Moderator: SS Ramsamy

Department of Anaesthetics


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CONTENTS

INTRODUCTION.....................................................................................................3Basic Science 32...................................................................................................4

Fundamental bases and haemodynamic principles........................................4

Hydrostatic and Hydrodynamic pressures......................................................5

Resistance...........................................................................................................6

HagenPoiseuille Equation...............................................................................6

Stroke Volume....................................................................................................6

Ventricular Preload.............................................................................................6

Wall Motion Abnormalities................................................................................8

Dynamic Indices....................................................................................................9Physiologic Explanation of Arterial Pressure Variation ................................9

Fig 3 17..............................................................................................................11

Systolic Blood Pressure Variability ( SBP)..................................................11

Pulse Pressure Variability (PP).....................................................................13

Limitations of the Dynamic Parameters.........................................................17

Diastolic, Pulse, and Systolic Blood Pressures ..............................................19Diastolic Blood Pressure.................................................................................19

Pulse Pressure..................................................................................................19

Systolic Blood Pressure..................................................................................19

.............................................................................................................................20

Conclusion...........................................................................................................21References ..........................................................................................................22

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INTRODUCTION

Fluid management and optimization involve an important part of daily decisionmaking in Anesthetics and Critical Care. The trouble is that it is difficult todetermine if hypotension is due to hypovolaemia or some other cause.

Hemodynamic management is related to the optimization of oxygen delivery to thetissues and has been shown to be able to advance postoperative outcome and todecrease the cost of surgery.1-3There are two distinctive complications when itcomes to fluid management hypovolaemia on one side and hypervolaemia, orfluid overload on the other. Both perioperative complications can result in adecrease in oxygen delivery to the tissues and can also cause an increase inpostoperative morbidity.4

Hypovolaemia can be defined as a state of reduced blood volume. This definition

is less useful in clinical medicine as there is no one diagnostic test to quantifyblood volume. Generally speaking it is a state in which a patient hashypoperfusion, which will improve with fluid therapy. In current literature,hypovolaemia is most often defined as, the shocked patient in whom strokevolume (SV) or cardiac output (CO) increases after a fluid bolus. This is alsotermed Preload, Volume or Fluid Responsiveness.

Evidence shows that organ perfusion requires adequate perfusion pressure inorder to drive blood into the capillaries of all organs and adequate cardiac outputto ensure oxygen delivery. Data also exists showing the impact of cardiac outputoptimization on postoperative outcome.5The issue is that determining organperfusion can be tricky. Cardiac output monitoring rarely is used in dailyanaesthetic practice simply because of availability and skills. Clinicians have totherefore rely on clinical judgment and blood loss estimates to determineintravascular volume.6

Clinical judgment may be guided by the more available and less invasivemonitoring. Blood Pressure is commonly used as a surrogate of Cardiac Output. Itis however a crude correlation. Blood Pressure is actually a function of Cardiac

Output and Stroke Volume. Intravascular volume is an important factor indetermining stroke volume. There are various indices that are commonly availableeveryday which provides an idea of Intravascular Volume. Arterial Pulse Contouranalysis provides three types of data on the patients hemodynamic status. Thefirst type of data comes from Analysis of BP variations induced by applyingpositive inspiratory pressure which provides specific information predictinghemodynamic effects of volume loading. The second type of data is that of theStatic Indices. Those are the Mean Arterial Pressure (MBP), Systolic BloodPressure (SBP), Diastolic Blood Pressure (DBP), and Pulse Pressure (PP). The

third type of data is a mathematical analysis of the pulse wave shape.

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The capability of the circulation to increase cardiac output in response to volumeexpansion is a well described concept.7-9

There is clear evidence that dynamic parameters of fluid responsiveness, basedon cardiopulmonary interactions in patients under general anaesthesia andmechanical ventilation, are superior to Central Venous Pressure.10 Dynamicindicators can be derived from the arterial pressure waveform. Systolic Pressure

Variations (SPV), including up and down, and Pulse Pressure Variation (PPV)are two of the concepts that will be reviewed.

Their aim is to diagnose the cause of the hypotensive type of hemodynamicinstability and attribute it to hypovolaemia. This is not an old concept and hasbeen described more than 40 years ago,11 and termed Dynamic Indices. Theseindices have undergone significant improvement of late. During the past 3 yearsnew algorithms have been developed to constantly calculate these indices. Suchalgorithms have been built into various modern devices such as the

Vigileo/FloTrac system.12

The various types of data available to the Anaesthetist in theatre provide goodinformation of a patients volume status. The Static parameters, Dynamicparameters and analysis of the arterial pulse waveform can be used in clinicalpractice as a means to guide fluid management.

BASIC SCIENCE 32

Fundamental bases and haemodynamic principles

Blood Pressure (BP)

Blood Pressure is the force per unit area exerted on the wall of a blood vessel byits contained blood. It usually refers to blood pressure in aorta there is a pressuregradient keeps blood flowing. This gradient varies through the vascular system.

Arterial Blood Pressure (ABP)

Arterial Blood Pressure varies with age, gender, weight, stress level, mood,

posture, physical activity. ABP depends on the compliance of elastic arteries andstroke volume. Systolic pressure is the maximum pressure in arteries duringventricular systole and diastolic pressure is the minimum pressure in arteriesduring ventricular diastole.

Venous Blood Pressure

Venous Pressure is a low, steady pressure. Venous return is supported by; valvesthat prevent backflow, the muscle pump, the respiratory pump, the changes inthoracic and abdominal pressures during breathing.

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Mean Arterial Pressure

BP signal fluctuates around a mean value according to a complex mechanism.Physiology responds to MAP. BP reaches Systolic Blood Pressure (SBP), andthen drops to Diastolic Blood Pressure (DBP). The difference between both valuesis the Arterial Pulse Pressure (APP)

APP = SBP DBP

The BP trace undergoes changes along its course from the proximal aorta (aorticpressure) to the peripheral arteries (peripheral blood pressure) that may bemodelled by wave reflection and pulse wave amplification phenomena. Thearterial system may be considered as a functional unit interposed between the leftventricle (LV) and the capillary exchange and is divided into two subunits

o the large arteries (characterized by their capacitive function)

o distal arterioles (characterized by high resistance)

This enables transformation of the pulsatile flow into a continuous flow. Major

haemodynamic principles are derived from the dynamics of a Newtonian fluid(water) circulating continuously in rigid tubes. Neither conditions are met inphysiology where the assumptions are that the flow is described by linearequations and that the pressure/flow relationship obeys Ohms law.

Continuous Flow

Cardiac output (CO) is continuous rather than pulsatile flow. MBP would be thepressure required to obtain an identical CO in the absence of pulsatility.

Hydrostatic and Hydrodynamic pressuresPascals first principle of fluid pressure establishes that below the fluid surfacethere is a hydrostatic pressure. Hydrostatic pressure is the physical pressureblood exerts on vascular wall. Mean Systemic Filling pressure can be observedunder no-flow conditions. Hydrodynamic pressure is the pressure created bymoving fluid which exerts additional pressure. This moving pressure is generatedby cardiac activity.

Controlling Factors

BF = P / R

When blood flows through a lumen the rate of flow is directly proportional to blood

pressure gradient (P) and inversely proportional to peripheral resistance (R).

Resistance is important in controlling local flow.

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ResistanceThis is the amount of friction blood encounters as it passes through vessels.Peripheral resistance is known as Systemic Resistance as peripheral vesselsaccounts for most resistance in system

Sources of resistance:

1. Blood viscosity directly proportional to resistance

affected by number of blood cells (e.g., polycythaemia)

2. Blood volume directly proportional

dehydration decreases volume decreases resistance

overhydration increases volume increases resistance

3. Blood vessel length directly proportional4. Blood vessel diameter main source affecting resistance

Inversely proportional to resistance

o increased diameter decreased resistance

o varies as inverse of radius to 4th power (1/r4)

Controlled mainly at small arterioles

HagenPoiseuille Equation

Stroke VolumeThere are five determinants of stroke volume, with the first three being mostimportant:1. Preload: the stretch of the myocardium just before contraction2. Afterload: tension against which muscle must contract.3. Contractility: intrinsic property of the muscle that is related to the force of

contraction4. Wall motion5. Valvular Function

Ventricular PreloadVentricular preload is defined as the degree of tension of the cardiac muscle whenit begins to contract. In practice, it is almost impossible to determine the degree oftension of the cardiac muscle when it begins to contract. Clinicians may usepressure or volume parameters for the assessment of preload. The pressure

parameters used are left and right ventricular filling pressures, and the volumeparameter used is mainly left ventricular end-diastolic volume obtained through

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left ventricular end-diastolic area. Indices of preload have been used extensivelyover the past decades to guide volume expansion.The underlying principle behind the use of these indices, to predict the effects ofvolume expansion on stroke volume and cardiac output, is related to the Frank-Starling relationship.

This relationship describes the intrinsic ability of the heart to adapt to increasingvolumes of inflowing blood. In essence, the greater the heart muscle is stretchedduring filling, the greater is the force of contraction and the greater the quantity ofblood pumped into the aorta. Stated another way, within physiologic limits, theheart pumps all the blood that returns to it by the way of the veins.13

Fig. 1 17

The Frank-Starling Curve has two portions. The first portion of this relationship iscalled the steep portion, and the second portion is called the plateau. In a low

preload state the heart functions on the steep portion. Here an increase in preloadwill induce a significant increase in stroke volume. This can be achieved byvolume expansion. On the steep portion the heart is said to be preload dependentand the patient is a responder to volume expansion.

If the heart is functioning on the plateau (elevated preload), then an increase inpreload will not bring about any major increase in stroke volume. Here the heartcan be said to be preload independent, and the patient is a non-responder tovolume expansion.

It becomes apparent that knowing the preload will then help to predict fluidresponsiveness. However, the Frank-Starling relationship does not depend only

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on preload and stroke volume, but it also depends on ventricular function becausethe Frank-Starling curve is flattened when ventricular function is impaired (Fig 1).Consequently, for a given preload value or central venous pressure, it is notpossible to predict the effects of an increase in preload on stroke volume.10

Preload or its surrogates are therefore not accurate predictors of fluidresponsiveness.

Afterload

Afterload is the myocardial tension (force) required to overcome opposition toventricular ejection during systole and is related to the aortic pressure andchamber radius as well as wall thickness. It is essentially the pressure theventricle must overcome to reduce its cavity. Myocardial Tension can beexplained using Laplaces Law. Surface tension is directly proportional to thetransmural pressure and chamber radius. It is also inversely proportional to thewall thickness. Ventricular wall tension is therefore directly proportional to the

transmural pressure and the ventricular chamber radius, and indirectlyproportional to the ventricular wall thickness. The other force the ventricle mustovercome to empty its volume is that of arterial impedance to ejection determinedby arteriolar tone. Arteriolar tone is the chief determinant of Systemic VascularResistance. Cardiac output is inversely related to afterload, and the RV is moresensitive to afterload than the LV because of its thinner wall. Patients withmyocardial dysfunction become increasingly more sensitive to increase inafterload.

Contractility

Contractility is an intrinsic ability of the myocardium to pump in the absence ofchanges in the preload, afterload or heart rate. It is related to the rate ofmyocardial muscle shortening, which in turn is dependent on the intracellularcalcium. Factors which increase contractility are related to the amount ofintracellular calcium availability or degree of sensitization, ATP availability forcontinued cycling, and enhanced states of relaxation (lusitripsy).

Wall Motion AbnormalitiesWhen the ventricular cavity does not collapse symmetrically or fully, emptying

becomes impaired. Although contractility may be normal or even enhanced insome areas, abnormalities in other areas of the ventricle can impair emptying andreduce stroke volume.

Cardiac output is a function of stroke volume and heart rate. It is evident from thisphysiology review that there are many factors affecting stroke volume. Essentiallyclinicians would like to know a patients cardiac output. This is however a difficultparameter to directly measure. Blood Pressure is used as a surrogate of cardiacoutput. It is however also a function of Systemic Vascular Resistance. BP is

therefore a crude surrogate of CO. There are many variables effecting BP so thedifficulty is knowing how to treat the BP reading and when a patient is fluid

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responsive. This gives place to Dynamic and Static Parameters which has provento be useful in diagnosing hypovolaemia.

DYNAMIC INDICES

Physiologic Explanation of Arterial Pressure Variation

With volume expansion an increase in right ventricular end-diastolic volume, leftventricular end-diastolic volume, stroke volume, and cardiac output is expected.This is due to the positive relationship between them.

Increased preload

Fig. 2 30

Fig 2 32

With an increase in Preload, there is an increase in EDV due to an increase infilling during diastole (Fig. 2). The EDV point therefore moves to the right and thevolume ejected (Stroke Volume) is also increased.

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The expected response to volume expansion is not so simple in practice. Theresponse is actually depends on several complicated parameters.For example, the increase in end-diastolic volume induced by volume expansion

is related to the partitioning of the fluids into the different cardiovascularcompartments organized in series.

In theory volume expansion can result in an increase in cardiac output. In practicethere are many other variables which determine this. Ventricular function is one ofthese variables.

In clinical practice, anaesthetists never know how fluids are partitioned or howcontractile the ventricles are. Therefore volume expansion does not always

achieve its main objective: an increase in cardiac output. More significantly, aninappropriate volume can induce tissue oedema and oxygen delivery alteration,counteracting the original goal of increased oxygen delivery. Therefore, it is ofmajor importance for anaesthetists to be able to predict the effects of volumeexpansion before actually performing volume expansion.

Preload Dependence

Preload dependence is defined as the ability of the heart to increase strokevolume in response to an increase in preload. The main question anaesthetistshave to answer before they perform volume expansion is if the fluid will increasethe patients cardiac output increase after volume expansion or really if the patientis preload dependent or not. Preload on its own is not predictive of preloaddependence. In practice, cardiopulmonary interactions can be used to assess theeffects of fluid challenges on stroke volume.7

In patients under general anaesthesia, the changes in intrathoracic pressureduring positive-pressure ventilation induce cyclic changes in Inferior Vena Cavablood flow, pulmonary artery flow, and aortic blood flow. During inspiration there isan increase in intrathoracic pressure. This results in a decrease in vena cava

blood flow. There is a consequent decrease in venous return and therefore adecrease in End Diastolic Volume. According to the Frank-Starling relationshippulmonary artery flow decreases.7

Approximately 3 beats later this decrease in pulmonary artery flow is transmittedto the left ventricle, inducing a decrease in aortic stroke volume. During anexpiratory pause, the inverse happens and the stroke volume increases.Consequently, mechanically ventilated patients under general anaesthesiapresent with cyclic changes in left ventricular stroke volume. Some variability in

stroke volume is therefore expected in normovolaemic states but duringhypovolaemic states there is excessive variability. This variability is a morespecific surrogate marker of hypovolaemia than hypotension alone.

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When the heart is working on the steep portion of the Frank-Starling relationship,these respiratory variations are important because slight changes in rightventricular preload induced by mechanical ventilation will induce significantchanges in stroke volume; whereas when the heart is working on the plateau of

this relationship, respiratory variations are small because changes in rightventricular preload induced by mechanical ventilation have little impact on strokevolume (Fig. 3). Because arterial pressure parameters are related to strokevolume and arterial compliance, variations in arterial pressure parameters reflectrespiratory variations in left ventricular stroke volume if arterial compliance isconsidered stable during a single respiratory cycle. This is translated intoexcessive blood pressure variability during the inspiratory phase.

Fig 3 17

Systolic Blood Pressure Variability ( SBP)

SBP is the difference between maximum and minimal SBP during a respiratorycycle. SBP can be broken down into two other indices: delta up (up) and deltadown (down). The measurement of these two indices is performed withreference to the SBP measured during an end-expiratory pause (SBPref). down

is the difference between SBPref and the lowest value obtained during therespiratory cycle. down illustrates the decrease in LV preload and SV during

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expiration as an out-of-phase response to the RV decrease in SV occurring duringinsufflation. (Fig. 4

Fig 4 18

Using Systolic Pressure Variation

Loosely the variability in Stroke Volume is referred to as swing. This is owing tothe morphology of the arterial line trace. Substantial amounts of literature haveconfirmed the utility of the analysis of systolic pressure variation in theassessment of fluid status.14,15 Excessive swing of the trace can be identified asbeing either predominantly up or down. Where the swing is predominantly down,hypovolaemia may be identified and a positive result of fluid administrationexpected.

SBP and down as predictors of preload-dependence was also validated in astudy by Tavernier et al. involving septic shock patients.16 In that study the clinical

relevance of these predictors is apparent. There was at least a 15% response tofluid administration when the SBP > 10 mmHg and down > 5 mmHg. Patientswith values above these cut points proved to be fluid responders as they were onthe steep part of the Frank Starling Curve.

These values we good surrogate predictors of a SV with excellent positive andnegative predictive values (>90%). Administration of fluid can therefore bepredicted from the net effect of the small variations in preload down has beenshown repeatedly to be a sensitive predictor of preload.16 The same study also

showed that down also predicted the response of cardiac output to volume loadbetter than either pulmonary capillary wedge pressure or left ventricular end-diastolic area as determined by echocardiography.16

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This has since proved to be a ground breaking finding, as these parameters havetraditionally been regarded as clinical gold standards for the assessment ofintravascular fluid status.

Figure 5 shows the Receiver Operating Characteristic (ROC) curves comparingthe ability of the Pulmonary Artery Occlusion Pressure (PAOP), the left ventricularend-diastolic area index (EDAI), and the down component of the positivepressure ventilation induced arterial systolic pressure variation to discriminatebetween positive (> 15% increase in stroke volume index) and negative (


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respiratory cycle, it has been assumed that the respiratory variability of PP shouldaccurately predict fluid responsiveness.17 Figure 6 illustrates the calculation of PP.17A study by Michard et al.17 was conducted on mechanically ventilated septic shockpatients. In the 40 patient study a high PP (PP >13%) enabled differentiationbetween responders and non-responders to volume expansion. What was found

was that the higher PP before volume expansion, the more marked the increasein cardiac index induced by volume expansion. What they looked for was anincrease in cardiac index of >15%. There was a 94% sensitivity and a 96%specificity. Numerous other studies also confirmed the reliability of this parameter9, 19. The current evidence is that down and PP correlates with the degree ofresponse to volume administration. (Fig. 7)

Fig 6 15

Fig 6 17

Other work from Michard in 1999 demonstrated the effect of positive end-expiratory pressure (PEEP) on PP analysis. It was shown that the higher PP at

the zero PEEP (ZEEP), the higher the decrease in cardiac output induced byapplication of PEEP in patients with acute respiratory distress syndrome(ARDS).20

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Fig 7 17

Fluid challenge

This diagnostic test involves administering a fluid bolus of 250 500 ml andobserve changes in blood pressure. The technique is often used during the initialphase of resuscitation, but once severe hypovolaemia has been corrected, bettermarkers of stroke volume or cardiac output are needed. This method has the

obvious drawback that the clinician has to give fluid to assess whether the patientneeds it or not. Fluid boluses may be of little use in most patients and in somecases may result in hypervolaemia or even worsen cardiogenic shock. To avoidthis risk better diagnostic investigations are required to predict fluidresponsiveness.

Passive Leg Raising

The lower limbs hold blood which may be shifted to the central blood volume. APassive Leg Raise is a reversible autotransfusion maneuver by passive leg raising

combined with the assessment of changes in stroke volume has the potential todiagnose hypovolaemia without the risk of volume overloading the patients. This

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test has been less studied than those above, but may turn out to be applicable tomore patients, at least in emergency departments and general ICUs.

Boulain et al. were the first to describe the relationship between radial artery pulsepressure changes and passive leg raising.22

The passive leg raise was validated as a dynamic test of intravascular volume bylooking at the change in aortic blood flow using Esophageal Doppler21, 22 Figure 8illustrates the passive leg raising from the semi-recumbent position (likelihoodratios can be calculated as 16 and 0.03).

Fig 8 20

Generally an increase in aortic blood flow of between 8 and 15% has beenreported to be diagnostic for hypovolaemia. The optimal technique for performingpassive leg raising is debatable. Controversies exist as to whether the passive leg

raising manoeuvre should be performed from the supine or semi-recumbentposition and whether a marker of preload should be used to ensure that asufficient shift of blood volume has occurred.

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Limitations of the Dynamic Parameters

Although Dynamic indices may seem to be the silver bullet in diagnosing

intravascular fluid status there are many provisos as to their use. Studies havebeen validated in Mechanically Ventilated patients under general anaesthesia.23 Inpatients who are spontaneously breathing, the specificity of PP is low.17 In theinstance where patients are spontaneously breathing another study suggests theelevation of PP by more than 5 mmHg at the end of a 15-s end-expiratory pausecould be useful to predict a beneficial effect of fluid infusion.24

The reliability of dynamic parameters also depends on the tidal volume. Moststudies in which these indices have been validated use tidal volumes greater than8 mL/kg and a PEEP of between 0 and 5 cmH2O.25,27 This is a major weakness inthe current literature. Studies in which dynamic variables validated fail to controlfor intrathoracic pressure.

It can therefore be said that any patient can appear fluid responsive at excessivelevels of intrathoracic pressure. In patients with lung pathology, lung compliance -the intrathoracic pressure from a given tidal volume - is variable and changing.This occurs in theatre where position or other factors such as laparoscopy cansignificantly influence effective lung compliance. Studies are limited by the factthat they typically use volume ventilation, and intrathoracic pressure is not

reported.

The use of low tidal volumes during ARDS diminishes their sensitivity. As a resultof decreased pulmonary compliance, marked cyclic variations in alveolar pressureare likely to occur during ARDS, generating marked cyclic variations intranspulmonary pressure and Intrathoracic pressure, even in the case of low tidalvolume. 27 To this end Huang et al. suggests that PP remains a valid parameterof fluid responsiveness in ARDS patients ventilated with low tidal volumes andhigh positive expiratory pressures.28

Static Indices

For 30 years, we used central venous pressure (CVP) and pulmonary arteryocclusion pressure (PAOP) to diagnose hypovolaemia. These markers of preloadhave been an integral part of patient monitoring, which is perhaps why we werelate to assess them as diagnostic tests in clinical trials. When trialled, fillingpressures were shown to have no predictive power for hypovolaemia in themajority of patients.A Review from Marik et al. included evidence from Shippy etal.10

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The study determined that there was a poor correlation between CVP and bloodvolume. 1500 simultaneous measurements of intravascular volume and CVPdemonstrated no association between these two variables (r= 0.27). (Fig. 9) Thiswas done in a heterogenous cohort of 188 ICU patients. The correlation between

CVP and change in intravascular volume was only 0.1 (r2

= 0.01). This studyessentially demonstrated that patients with a low CVP may actually have fluidoverload and similarly patients with a high CVP may yet be volume depleted.

Fig 98

Fig 9 10

Advances in technology allowed clinicians to measure heart volumes and areas,including those of the right and left ventricles at end-diastole. These static indicesof preload were also shown to have low predictive power for hypovolaemia. It islikely that extreme values of filling pressures or heart volumes/areas havepredictive power for hypovolaemia, but the cut-off points for what is a low or whatis a high value have not yet been established. Within the last ten years, clinicalresearchers have challenged the static markers of preload in studies of dynamictests for the diagnosis of hypovolaemia.10

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DIASTOLIC, PULSE, AND SYSTOLIC BLOOD PRESSURES

Diastolic Blood Pressure

DBP remains nearly constant from the aorta to the peripheral arteries. The maindeterminant of DBP is vascular tone. Low vascular tone (due to sepsis orvasodilators) is responsible for a drop in DBP. The DBP also depends on theduration of the diastole and BP decay time constant.

Therefore a short diastole (tachycardia) is associated with high DBP whereas aprolonged diastole (bradycardia) is associated with low DBP. We may assumethat BP decreases monoexponentially during diastole. It has a time constant (Tau)which is equal to the product of SVR multiplied by compliance. Tau shortening isassociated with a decrease in DBP which is related to either decreased

resistances (vasomotor tone decrease), or decreased arterial compliance. Insummary, low DBP is observed in cases of vasodilatation, bradycardia, ordecreased arterial compliance.

Pulse Pressure

PP is determined by SV and compliance of large arteries.PP = SV/C

A decrease in SV is therefore associated with decreased PP, whereas a decrease

in compliance is associated with increased PP. The decrease in vascularcompliance with age causes a decrease in DBP along with an increase in PP andSBP. Thus, detecting a lowered PP in the elderly is indicative of a decrease instroke volume. In a non pathological patient Pulse Pressure is a fair reflection ofstroke volume.24

Systolic Blood Pressure

SBP is determined by SV, arterial compliance, and SVR. SBP is physiologically anessential determinant of LV afterload. In some cases, the combined analysis ofvarious BP indices (MBP, PP, SBP, and DBP) and patient characteristics (ageand cardiovascular disease) may allow for a precise assessment ofhaemodynamic status.

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Pulse Pressure as a Measure of Stroke Volume

Fig 10 30

Pulse pressure is essentially the pressure rise from a baseline diastolic pressure.The pressure rise during ventricular ejection is predominantly a function of:1. The amount of blood ejected with each beat (stroke volume)

2. Central aortic stiffness or compliance3. Peripheral run-off of the ejected blood or peripheral vascular resistance.

Intraoperatively the compliance can be said to be relatively constant. Under theseconditions stroke volume is the main determinant of pulse pressure.29 The diagramshows the arterial pressure traces recorded from a patient during volumeresuscitation. Here a rapid infusion of a colloid (Voluven) is administered. Thereis a resultant increase in stroke volume. The increase in associated plasmavolume expansion is reflected as a corresponding increase in pulse pressure. The

progressive changes in pulse pressure during such a fluid challenge can even beplotted against time as shown in Figure 10a.

This can be compared to the Frank-Starling curve which can be informative inassessing volume responsiveness. Due to this direct relationship between strokevolume and pulse pressure30, hypovolaemia may be characterized by a reductionin pulse pressure. Hypovolaemia is usually associated with a reduced systolicpressure as there is a reduction in stroke volume. There may also be a rise indiastolic pressure. Vasoconstriction is a physiologic response to hypovolaemiaand may reflect in an elevation in diastolic pressure.

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Analysis of Pulse Pressure Waveform

Ventricular contraction creates a pulse wave. This is the pressure pulse that is feltwhen determining a patients heart rate by palpation. The pressure is transducedfrom an intra-arterial catheter into an electronic waveform. The normal arterialpressure waveform is shown in Figure 11.

Fig 1129

The systolic upstroke or Anacrotic limb (Gradient a) mainly reflects the pressurepulse produced by left ventricular contraction. The pressure pulse is followedslightly later by the flow wave caused by the actual displacement of blood volume.The Anacrotic shoulder is the rounded part at the top of the waveform. Of manythings this represents a volume displacement. The dicrotic limb is evident by thedicrotic notch. This notch occurs on the cardiac cycle as the aortic valve closes

secondary to subsequent retrograde flow. The location of the dicrotic notch variesaccording to the timing of aortic closure of the cardiac cycle. Aortic closure may bedelayed in patients with hypovolaemia. As a result the dicrotic notch occurs fartherdown on the dicrotic limb in hypovolaemic patients.31 Gradient (b) is the area underthe trace which reflects the stroke volume. 31 Gradient (c) or the run off wavereflects the afterload. 31 The position of the dicrotic notch can therefore be used asanother marker of hypovolaemia. The evidence for this relationship is weak asthere are many other variables which impact on the location of the dicrotic notch.It can however be used as another factor pointing towards hypovolaemia. 31

CONCLUSION

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Over a period of almost twenty years numerous authors have progressively andsystematically researched and reviewed the utility of filling pressures and theirsurrogates as tools for fluid assessment and optimization of cardiac output.Recent publications on the validity of central venous and pulmonary capillarywedge pressures only bear out concerns expressed almost seventy years ago

and first hinted at over a century ago.

The overwhelming consensus is that Central Venous Pressure and PulmonaryCapillary Wedge Pressure measurement and interpretation are of little value in themanagement of fluid status. Newer dynamic means, such as systolic pressurevariation, stroke volume variation and pulse pressure variation, all seem to holdmuch in store for clinical practice. Already these new derivatives appear set todisplace our old stalwarts from the clinical arena.

Monitoring systolic pressure variation enables real time prediction and monitoringof the left ventricular response to preload enhancement. It also aids in guidingfluid therapy. Even the haemodynamic response to Passive Leg Raising wouldappear to be a promising index of fluid responsiveness. Likewise, Static Indices,although less specific, can tell us so much about the patients fluid state. Fromsimple insight into the physiology of Blood Pressure one can deduce more thanjust taking it as yet another number. With the hype around fluids and theendothelium, judging a patients intravascular fluid status will come under closescrutiny. What is important to remember is that what exactly is in the pipeline (orhow much), can be guided by clinical judgment and simple indices that are

commonly available in patients with basic monitoring.

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