clinical

INVASIVE HAEMODYNAAAIC MONITORING:THE ROLE OF EMERGENCY NURSES IN

ELPING TO PROVIDE CRITICAL CAREEmergency nurses can increase their knowledge and develop their skills by evaluating the

haemodynamic function of critically ill patients by invasive monitoring, says HEATHER JARMAN

Heather Jarman

RCN, MSc Dist

BSc(Hons), is

consultant nurse

in emergency

care, St George's

Healthcare NHS

Trust, London

This article has been

subjected to double

blind peer review

Accurate monitoring of critically ill patients inemergency departments (EDs) is crucial to pro-

viding the information needed to optimise patientoutcome.

Advances in the use of technology and earlyintervention in patient management have led toa need for greater knowledge and skills amongnurses who care for such patients in EDs,

By evaluating critically ill patients' haemodynamicfunctions, information about their circulatorysystems and their ability to perfuse tissues andremove metabolic waste, can be discerned.Monitoring haemodynamic function also acts as aguide to a patient's response to treatment.

This article describes the faaors involved in tissueperfusion and three different invasive methods ofassessing haemodynamic function in the ED. It alsoaims to help nurses provide safe and effective carefor critically ill patients.

TISSUE PERFUSIONNurses who care for critically ill patients mustunderstand tissue perfusion and the factors involvedin this that are measured by haemodynamicmonitoring.

Adequate tissue perfusion requires adequateblood pressure, which is determined by cardiacoutput and systemic vascular resistance (SVR).

The pressure exerted as the left ventricle ejects bloodinto the aorta is termed systolic pressure. Pressure inthe aorta falls after the left ventricle contracts, and thelowest point, just before the left ventricle ejects bloodagain, is known as the diastolic pressure.

Pressure varies widely throughout the cardiaccycle, and the mean arterial pressure (MAP), ratherthan systolic and diastolic values, most directlyreflects tissue perfusion. Mean arterial pressure isdetermined by CO, SVR and centra! venous pressure(CVP)(Box 1).

But the MAP is not a true average of the systolicand diastolic pressures, and the often citedformula, MAP = diastolic + 1/3 (systolic + diastolic).

Haemodynamic equations

Mean arterial _ Cardiac output xpressure Systemic vascular resistance

Cardiac _ Stroke volume xoutput Heart rate

Blood _ Heart rate Xpressure Stroke volume x

Systemic vascular resistance

is accurate only if the diastole length is two thirds ofthat of the total cardiac cycle (Darovic 2002).

This makes the values displayed on blood pressuremonitors usually more accurate than papercalculations (Woodrow 2006).

A MAP of between 70 and lOOmmHg is usuallyregarded as normal, although the aim should beto produce adequate renal perfusion, which isindicated by a urine output of between 0.5 andIml/kg/hr (Ball 2000).

Cardiac outputCardiac output is determined by stroke volume(SV) and heart rate. Stroke volume is the quantityof blood ejected forward from the left ventriclewith each contraction. It is around 70ml at rest(Woodrow 2006).

PreloadPreload is determined by the amount of bloodreturning to the heart, which is known as thevenous return. It is the degree to which cardiacfibres stretch at the end of the diastole as the heartfills. The amount of stretch affects the strengthof the next cardiac contraction and the SV, This isknown as Starling's Law.

Preload is influenced by intravascular volume andvenous tone (Adams 2004). It can be manipulatedmost easily by administering fluid but also byadministering vasopressors-

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Normal arterial line trace

Normal

(Andrews and Nolan 2006)

'Dampened' arterial line trace

Dampened

(Andrews and Nolan 2006)

AfterloadAfterload is the resistance the aorta and thesystemic vascular system apply to the blood ejectedfrom the left ventricle (Ball 2000).

Systemic vascular resistance is determined by theresistance of the peripheral vessels to blood flow,which is decreased by vasodilatation and increasedby vasoconstnction,

Vasodilatation therefore causes a decrease inafterload and so reduces the amount of effortrequired by the left ventricle. This in turn decreasesmyocardial oxygeri consumption.

Vasoconstnction, which can be caused by aresponse to hypovolaemia or the use of positiveinotropes or vasopressors, increases SVR andtherefore afterload.

An increase in SVR increases blood pressure,provided there is no change in the other factors.

ARTERIAL BLOOD PRESSURE MONITORINGArterial blood pressure monitoring is an invasivetechnique that is becoming increasingly common inEDs as a way of evaluating haemodynamic status.

It can provide direct and continuousmeasurement of the blood pressure of critically

Time

ill patients who require frequent blood pressurerecordings. It is especially useful when cuff inflationis uncomfortable or when compromise of thecirculatory system makes conventional recordingdifficult (Sargent 2006).

Such monitoring is also more accurate thannon-invasive measurement, which is affected bythe tissues between the arteries and skin, andgives readings that are between 5 and 20mmHgmore accurate than those obtained from a cuff(Woodrow2006).

Measuring arterial blood pressure requiresa cannula and a transducer tubing system.The cannula is usually inserted in the radial arterybecause this is an accessible and visible site, butbrachial, femoral or dorsalis paedis arteries can alsobe used {Andrews and Nolan 2006).

Transducer systems differ depending on whatequipment is available locally, but they all consist ofa transducer cable and tubing connected to a bagof fluid, usually saline.

The fluid is kept under a pressure of 300mmHg toprevent backflow to the transducer tubing (Jevonand Ewens (2002), which occurs when arterialpressure is greater than the pressure exerted bythe fluid. This can cause occlusion of the tubingand lead to inaccurate arterial blood pressurereadings.

The transducer cable senses the pressure ofblood flow past the cannula tip and convertsthis information into arterial pressure waveforms(Figs. 1 and 2) and numerical data visible on themonitor.

Calibrating, or 'zeroing', transducers

There are minor variations betweendifferent monitoring systems but inprinciple:

• Turn the three-way tap off to thepatient and open to air. This registersatmospheric pressure

• Press the 'zero' button and wait for themachine to display '0'. There may be anaudible tone when this is achieved

• Turn the three-way tap off to air andopen to the patient

• Ensure that there is return of a traceand that the values shown are, in yourclinical judgement, of a reasonablevalue.

(Adapted from Jevon and Ewens 2002)

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A trace of central venous pressure

Dampened

Time

a: point of right atrial contraction

c: tricuspid valve closure

v: right atrial pressure during ventricular contraction

The transducer has a 'zero' reference point, whichshould be placed m line with the middle of thepatient's underarm. Incorrea 'zeroing' procedures,the patient's position and long transducer tubingcan all affect the accuracy of arterial blood pressuremonitoring (Box 2).

Placing the transducer below the middle ofthe underarm gives artificially high pressures;conversely, placing it too high records falsely lowblood pressures.

The general principles in the use of transducersare summarised in Box 3.

ARTERIAL PRESSURE WAVEFORMAs shown in Fig. 1, a normal arterial trace shouldhave a rapid upstroke, known as the anacroticrise, indicating the force of ventricular contraction.The trace then slopes downwards as arteriaipressure decreases. This is followed by a smallsecond upstroke, called the diacrotic notch, as theaortic valve closes,

A 'dampened' trace, an example of which isshown in Fig, 2, looks abnormal or flattened.It usually occurs because of a blocked cannula ortubing, or because the pressure bag has deflated sothat its pressure is less than 300mmHg.

A significant complication with arterial lines isdisplacement, which can lead to bleeding orartenalocclusion.

The risk of bleeding can be reduced by ensuringthat the line is secured and covered with atransparent dressing, and that the site of lineinsertion is exposed to allow for observation.

Arterial occlusion interrupts blood flow and causesblanching to the hand and possibly ischaemia. Theline should be removed immediately if occlusionoccurs.

CENTRAL VENOUS PRESSURE MONITORINGCentral venous pressure monitoring is used toassess patients' intravascular volume. It measuresthe pressure in the vena cava and right atrialfilling.

There is a wide variation in normal CVP, from6 to 20mmHg (Andrews and Nolan 2006),because it depends on venous tone, intrathoracicpressure and patient position, as well asintravascuiar volume. A value of between 0 and8mmHg is considered normal (Woodrow 2006) formonitoring purposes.

Central venous pressure does not directlymeasure blood volume so should be interpretedalongside other values such as blood pressure andurine output. For a fuller picture, it is important totake serial measurements, rather than single values,to monitor response to treatment.

Low CVP values indicate reduced preload, usuallybecause of inadequate circulating volume; highCVP values can be a sign of overfilling, right heartfailure or a rise in intrathoracic pressure caused bypulmonary embolus or mechanical ventilation.

It is important to note that high CVP valuesrelated to disease states do not necessarilyindicate volume overload and patients may still beunderfilled (Elgart 2004).

Causes of an elevated CVP include increasedintrathoracic pressure, for example in cases of non-invasive ventilation, cardiac failure or an occludedlumen (Woodrow 2006)

Central venous pressure measurements can betaken using a manometer or, as is increasinglypopular, a monitor connected to a transducersystem similar to that used for invasive bloodpressure recording.

Transducer recording of CVP produces a tracethat mirrors right atrial pressure changes during thecardiac cycle (Fig. 3).

General principles in the use of transducers

• Ensure that the transducer is level withthe 'zero' reference point, usually themiddle of the underarm

• Reduce and limit the use of extensionsets and three-way taps

• If there is a flat trace, check the patient'scondition for loss of output, check forbreaks in the transducer circuit, andcheck that the pressure bag is inflated

• Maintain a pressure bag pressure of300mmHg

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CENTRAL VENOUS OXYGEN SATURATIONMONITORINGCentral venous oxygen saturation ^monitoring is increasingly used in EDs duringearly goal directed therapy to manage sepsis(Rivers ef a/2001).

Blood sampling from pulmonary artery catheters(PACs) enables evaluation in critical care areas ofthe oxygen saturation of mixed venous blood (SvO )from the inferior and superior vena cava.

The degree of saturation gives an indication ofthe balance between oxygen supply and demandon the tissues. Consumption of oxygen fromoxygenated haemoglobin is normally 25 per cent,which leaves an SvO level of 75 per cent; an SvOof less than this indicates inadequate oxygendelivery or excessive oxygen demand.

This is an important part of haemodynamicmonitoring in critically ill patients because lowSvO, values are associated with cardiac failure andpoorer patient outcome in sepsis (Andrews andNolan 2006).

Inserting a PAC is not appropriate in EDs, but it ispossible to measure ScvO, levels by taking a sampleusing a central venous catheter and analysing itwith a gas machine.

There is close correlation between pulmonaryartery blood oxygen saturation and ScvO, valuesin critically ill patients (Andrews and Nolan 2006).

It IS possible to transduce an ScvO, with anappropriate monitoring device placed in the port ofcentral line, but these are rarely used in EDs becausethey are expensive and can be used only in patientsbeing transferred to intensive care units,

CONCLUSIONInvasive blood pressure, CVP and ScvO^ monitoringare crucial components of assessing critically illpatients in emergency departments.

The dependency and complexity of this patientgroup mean it is necessary for emergency nursingstaff to know about haemodynamic monitoringto ensure safe, effective care and to influence andimprove patient outcomes.

References

Adams KL (2004) Hemodynamic assessment:Ihe physiologic basis for turning data into clinicalinformation AACN Clinical Issues. 15, 4. 534-546.

Andrews F, Nolan J (2006) Cnlical care in theemergency department monitoring the critically (IIpatient. Emergency MedicalJournal 23, 7, 561-564

Ball C120001 Optimizing oxygen deliveryhaemodynamic workshop. Part2. IntensiveandCritical Care Nursing 16, 1, 33-44

Darovic GO (2002) Hemodynamic Monitoring:Invasive and non-invasive clinical application.Third edition. WB Saunders, Philadelphia PA

Elgart H (2004) Assessment of fluids andelectrolytes. Advanced Practice in Acute andCritical Care Clinicallssues 15, 4, 607-621

Jevon R Ewens B (20021 Mon/tonng theCritically III Patient. Slackwell Science,Oxford,

Rivera E, Nguyen B, Havstad S et al (2001)Early goal-directed therapy in the treatment ofsevere sepsis New England Journal of Medicine345. 19, 1368-1377.

Sargent A (2006) Arterial blood pressuremonitoring. Bhtisf] Journal of Cardiac Nursing.1,2,69-72,

Woodrow P t2Q06} Intensive Care Nursing.Second edition Routledge, New York NY.

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