Echocardiography provides invaluable and prompt infor- mation about systolic and diastolic function, \201 lling status and the function of the intracardiac valves and the great ves sels. This has a signi \201 cant in \202 uence on decision making and management in the I CU. fd = 2.fo.v.cos /c Where: v is the velocity of blood \202 ow; is the angle between th e ultrasound beam and blood \202 ow; c is the ultrasound velocity in that medium; fo is t he transmitting frequency. The Doppler shift can therefore be used to measure the velocity of blood \202 ow. Physics of ultrasound \200 Sound is an example of a longitudinal wave oscillating back and forth through a transmittin g medium at a \201 xed velocity, resulting in zones of compression and rarefaction. Ultra sound includes that proportion of the sound spec- trum above 20kHz. Echo machines use frequ encies of 2 \200\22310MHz. The wavelength ( ) is inversely related to the frequency (f) by the sound velocity (c) so that c = f. Sound velocity in a given material is constant but varies in different materials. Ultrasound propagates poorly in air. c in blood is 1570m/s, soft tissue 1540m/s and air 330m/s. v = fd.c/2fo.cos v is most accurately measured when is zero and the ultrasound beam is in line with the blood \202 ow. Doppler calculations cannot be made when the ultrasound beam is perpendicular to the \202 ow of blood as the cosine of 90 is zero. As long as is <20 then the measurement error is <6%. Doppler calculated velocities are displayed g raphically on the echo machine with v on the x-axis and time on the y-axis. This process re quires a formidable amount of electronic processing. Color Doppler is a real-time colorized display of blood \202 ow superimposed on a 2D image. This also requires an enormous amou nt of computation and is used to iden- tify turbulent \202 ow within the heart that may o ccur, for example, with valvular pathology. Imaging by ultrasound \200 Ultrasound waves are generated by piezoelectric crys- tals in a transducer that vibrate whe n an alternating cur- rent is applied. Imaging is achieved by emitting ultrasound pulses fr om the transducer which are reflected by a boundary between two tissue structures and recei ved by the same transducer, generating a current which is processed to generate an image. W avelength is a determinant of image quality as the spatial resolution is limited to approxi mately one . Therefore, shorter s (obtained with higher fs as c is constant) produce be tter resolution. However, higher fs give reduced tissue penetration and thus a reduced imag e depth. The pulsed ultrasound signal is described by the pulse repetition frequency (PRF). This must be set so that there is suf \201 cient time for the pulsed wave to be trans- mi tted, re \202 ected and received in order to display all objects uniquely within a typical 10cm viewing window. There must only be a single pulse present between the transducer and the re \202 ected object at any point in time in order to avoid range ambiguity. With a c in tissue of 1540m/s this means that at a depth of 10cm the PRF must be no more than 7.7kHz . The strength of re \202 ection at an interface depends on the difference in acoustic im pedance (AI) between two media. AI is the product of density and the c within the medium. T here is a large AI mismatch between tissue and air, preventing imaging within the lung. Thi s also occurs between the transducer and tissue, necessitating a layer of gel between tissu e and transducer. Indications for echocardiography in the ICU \200 Haemodynamic instability: ventricular failure, hypovolae- mia, vasodilation, acute valvular dysfunction, cardiac tamponade, pulmonary embolism Aortic dissection Infective endocarditi s Source of systemic embolus Unexplained hypoxaemia \200 \200 \200 Indications for transthoracic echo (TTE) \200 Imaging of the ascending aorta which is not visualized by transoesophageal echo (TOE) due t o interposition of the left main bronchus. Imaging of the left ventricular (LV) apex which is frequently foreshortened by TOE. Accurate measurement of the pressure gradient across th e aortic valve which is frequently underestimated with TOE where alignment of the Doppler b eam can be suboptimal. When TOE is contraindicated. Indications for TOE \200 Conditions that prevent image acquisition with TTE such as in the presence of hyperin \202 ated lungs, surgical dressings, wounds, drains, prone position or excess fat tissue. Exami nation of posterior structures which are better visualized with TOE such as thoracic aorta, pulmonary veins, left atrium, mitral valve. Pathologies where TOE is more sensitive than T TE, e.g. left atrial thrombus, interatrial septal defects, cardiac tamponade. In conditions where diagnosis and treatment require more detailed information such as in suspected aorti c dissection, infective endocarditis, complex mitral valve pathology. Doppler \200 Doppler is used in echocardiography principally to look at aspects of blood \202 ow. The Doppler effect is the apparent change in f in waves that occurs when the source and observe r are in motion relative to each other, with the f increasing when the source and observer approach and decreasing when they move apart. This shift in f from the transmitted to 113 CHAPTER 7.7 Echocardiography CFM \200 Contraindications to TOE To assess the size of the regurgitant jet. For mitral regur- gitation (MR) a jet area >50% of the left atrial area is severe and for aortic regurgitation (AR) a jet width >40% of the LV out \202 ow tract. Note that this method tends to underestimate the severity of eccent ric (wall hugging) jets of MR. Absolute Relative Peforated viscus Atlantoaxial joint disease Oesophageal stricture Prior chest irradiation Oesophageal tumors Hiatus hernia Active upper GI bleeding Doppler \200 Oesophageal diverticula To assess systolic \202 ow reversal in the pulmonary veins (MR) or the descending thoraci c aorta (AR). Oesophageal scleroderma Recent upper GI surgery Systemic embolization \200 TOE is the most sensitive and speci \201 c technique for determining the source and potent ial mechanism of sys- temic embolization for patients with cerebral ischaemic events or per ipheral infarction. TOE can identify cardiac sources of embolism including atrial and ventr icular thrombi, vegetations, tumors, atrial septal defects or aneurysms, and atheromatous d isease of the aorta. In critically ill patients with AF, TOE is necessary to exclude the pr esence of thrombus before cardioversion when a long period of anticoagulation is not possib le. Indications in the ICU Pulmonary embolism (PE) \200 Echo can provide bedside diagnosis in the unstable ICU patient with massive PE when transpo rtation outside the ICU for angiography or CT may be unsafe. TOE has a sensitivity of 80 \200\22392% and a speci \201 city of almost 100%. Echocardiographic features of massive PE are; (i) Acute cor pulmonale; speci \201 cally mid-cavity hypoki- nesia with preserved fu nction at the apex in con- trast to RV dysfunction due to other causes in which wall motion is abnormal in all regions. Infective endocarditis (IE) \200 The major criteria for the diagnosis of IE are persistent bacteraemia with typical organism s with echocardio- graphic evidence of endocardial involvement. Echocardiographic features of IE are: (i) an oscillating intracardiac mass which may be on a valve and/or supporting s tructure, or in the path of a regurgitant jet or iatrogenic device (ii) Central emboli in the proximal pulmonary arteries; particularly the main and the right pulmonary artery (detection of left-sided emboli is limited by the poor propagation of ult rasound through air in the left bronchus). Valvular dysfunction Echo can be used to assess valvular lesions using 2D imag- ing, Dopple r and color \202 ow mapping (CFM). (ii) intracardiac abscess (iii) new dehiscence of a prosthetic valve (iv) new valvular regu rgitation TOE is more sensitive and speci \201 c than TTE for the detection of vegetations . The sensitivity of TOE for the detection of vegetations on native valves is 82 \200\22310 0% and on prosthetic valves is 77 \200\22394%. False-positive \201 ndings may occur from lesions that resem- ble vegetations such as: papillary \201 broma, ruptured or redundant chordae, non-speci \201 c valve thickening or calci- \201 cation, non-bacterial thrombot ic endocarditis, systemic lupus erythematosus (SLE) with cardiac involvement, thrombus, aor tic valve Lambl \200\231s excrescence or nodule of Arantius. In patients with prosthetic va lves, vegetations can be mis- taken for a sewing ring, surgically severed or retained chor- dae tendinae, \201 brin strands or periprosthetic material. Stenotic lesions Two-dimensional imaging \200 To assess valvular appearance, whether bi- or trilea \202 et, lea \202 et, calci \201 ca tion and thickening (rheumatic). To assess secondary changes such as spontaneous echo contr ast due to obstructed \202 ow ( presence of thrombus), atrial dilatation and ventricula r impairment. Planimetry can be used to trace a valve area. This is par- ticularly useful w ith aortic stenosis (AS), with severe AS being a valve area of 0.6 \200\2230.8cm2 . CFM \200 Detects turbulent \202 ow through the restricted lesion and beyond, and gives an indicati on of its direction and extent. Unexplained hypoxaemia TOE can diagnose or rule out cardiac causes of hypoxae- mia such as poor ventricular function, MR, pulmonary emboli, intracardiac shunts (patent foramen ovale or atrial septal defect (ASD)) or even to detect pleural effusions. Doppler \200 Measures the velocity(V) across a lesion which can be used to calculate the pressure gradie nt. Severe AS is a mean ZP 40 \200\22350mm Hg, and severe mitral stenosis (MS) is a mean ZP >12mm Hg. Note that ZP is \202 ow dependent and therefore underestimates stenotic severi ty when there is poor LV function. Estimating pulmonary artery pressure \200 Systolic pulmonary artery pressures can be measured in patients with tricuspid regurgitatio n(TR). The ZP of the TR jet can be measured using Doppler and, if the CVP is known, Regurgitant lesions Two-dimensional imaging \200 To assess lea \202 et function (inclubing cordal rupture and prolapse) and annular dilatat ion. To look for evidence of endocarditis (see below). systolic RVP = CVP + TR jet ZP systolic RVP = systolic PAP (if no PV pathology) 114 P QUINTON & A CRERAR-GILBERT Aortic dissection \200 of pericardial or mediastinal haematoma, the presence, mechanism and severity of AR, the po int of entry and exit between the true and false lumen, the presence of thrombus and LV fun ction. In suspected aortic dissection when TOE \201 ndings are equivocal or negative, aor tography, CT or MRI should be performed in addition to TOE. TOE provides high resolution real-time imaging of the aorta, resulting in high sensitivity (99%) for identifying dissection. The unique advantage of bedside echo over CT or aor- togr aphy lies in its portability which is of particular value in unstable patients. TOE can als o identify complications of dissection such as extension of dissection into the coronaries, the presence This page intentionally left blank 116 P QUINTON & A CRERAR-GILBERT Clinical application of echocardiography in the ICU Assessment of LV function Systolic function/ejection fraction (EF) \200 The parasternal short axis view of the LV (TTE) and the transgastric short axis view (TOE) show areas of myo- cardium supplied by all three coronaries and as such are ideally suited for looking for ischaemic RWMAs. Other causes of altered contractility include: ventricular pacing, ventricular conduction delay, old MI, marked hypovolaemia, severe mitral stenosis and post-cardiopul- monary bypass (interventricular septum). New RWMAs associated with haem odynamic instability are highly indicative of acute myocardial ischaemia. LV systolic function can be quanti \201 ed by calculating an EF using (1) linear, (2) area and (3) volume measurements. Measurements are made in systole and diastole, and machine-in tegrated software computes diameters, areas and volumes, and provides a value for EF. (1) Fractional shortening FS = EDD \200\223 ESD x 100% (30 \200\22340%) EDD Cardiac output (CO) Two echocardiographic methods can be used: 1 Based on measuring LV volu mes (EDV and ESV) using Simpson \200\231s disc method (see above) and using the patient \200\231s heart rate (HR) in the equation: Where EDD = end-diastolic diameter and ESD = end-systolic diameter. \200 Measurements are made in the parasternal long axis view using TTE or the transgastric mid s hort axis view with TOE. Fractional shortening may be inaccurate in the presence of regiona l wall motion abnormalities and must be inter- preted taking into account 2D images of the LV. CO = (EDV \200\223 ESV) x HR 2 Based on 2D and Doppler echocardiography; SV is given by the equation: SV = VTI LVOT x CSA LVOT (2) Fractional area change VTILVOT is the velocity time integral through the left ventricular out \202 ow tract (LVOT ). CSALVOT is the cross-sectional area of the LVOT. VTI LVOT is derived from Doppler analys is of the LVOT. This is obtained from the apical \201 ve-chamber view using TTE or from t he deep transgastric view using TOE. LVOT diameter is measured from the parasternal long ax is view with TTE or the mid-oesophageal aortic valve long axis view using TOE. The CSA LVOT is then given by the equation; FAC = EDA \200\223 ESA x 100% (36 \200\22364%) \200 EDA Where EDA = end-diastolic area and ESA = end-systolic area. \200 Measurements are made by tracing the endocardial bor- der in the parasternal LV short axis view with TTE or the transgastric mid short axis view with TOE. (3) Ejection fraction (Simpson \200\231s disks method) EDV \200\223 ESV EDV x 100% (55 \200\22375%) CSA LVOT = ( \200/4) x LVOTdiameter2 The heart rate is then used with the measured SV to ca lculate cardiac output as with the Simpson \200\231s method. EF = Where EDV = end-diastolic volume and ESV = end-systo- lic volume. \200 Assessment of preload 2D imaging \200 In Simpson \200\231s disc method ventricular volumes are obtained by tracing endocardial bo rders and approxi- mating the ventricular cavity with a series of disks of uni- form thickn ess. Views used in this method are the apical LV four- or two-chamber view using TTE or the mid-oesophageal four- or two-chamber views using TOE. Simpson \200\231s EF method is more accurate than fractional shortening and fractional area change in patients with signi \201 cant wall motion abnormalities. Qualitative estimation of LV volume is often adequate, particularly at the extremes of volu mes. Systolic oblit- eration of the LV cavity is a sign of severe hypovolaemia. However, a large LV EDA may not indicate adequate preload with LV dysfunction. Quantitative measuremen ts of LV preload; LV EDA (normal range 9.5 \200\22322cm2) can be obtained by endocar- dial border tracing. LV EDV (normal range 80 \200\223130ml) can be obtained with Simpson \200 \231s method (see above). Studies have demonstrated that changes in LV EDA measured with TO E are related to changes in cardiac output. and were found to be more reliable than the pul monary artery catheter in determining the cause of hypotension. Right atrial (RA) pressure can be estimated from evalua- tion of the inferior vena cava (IVC) during respiration Norma l RA pressure (5 \200\22310mm Hg) corresponds to nor- mal IVC diameter(1.2 \200\2232.3cm) a nd >50% collapse with respiration. Increased RA pressure leads to a dilated IVC and a failu re to collapse with respiration. Other indices of LV systolic function \200 dP/dt of the mitral regurgitant velocity measured with Doppler from the mid-oesophageal ven tricular view. Mitral annular displacement in systole from the mid- oesophageal ventricular view. A descent of <0.8cm is indicative of signi \201 cant systolic dysfunction. Myocardi al movement measured with tissue Doppler imaging. Regional wall motion abnormality (RWMA) \200 In the ICU this may occur in patients on increasing ino- tropic support, while attempting w eaning from ventila- tion or with severe left ventricular hypertrophy (LVH). Wall motion ca n be graded as follows: (i) normokinesia; (ii) hypokinesia; (iii) akinesia; (iv) dyskinesia ; and (v) aneurysmal. Doppler \202 ow \200 Transmitral and pulmonary venous \202 ow patterns pro- vide additional loading informatio n. 117 CHAPTER 7.8 Clinical application of echocardiography in the ICU with IVC dilatation and loss of respiratory collapse, and TR with a jet velocity >2.5m/s). The LV and RV interact due to pericardial constraint. The sum of the diastolic ventricular dimensions has to remain constant. Any acute LV or RV dilatation is associ- ated with propo rtional reduction in LV or RV diastolic dimension. RV dilatation can be quanti \201 ed by measuring the ratio between the RV EDA and LV EDA. Moderate RV dilatation corresponds to a diastolic ventricular ratio >0.6 and severe RV dilatation to a ratio >1. Acute RV failure c an lead to distortion of LV size and geometry, and as the RV enlarges the septum is pushed towards the LV, resulting in a small, \200\230D-shaped \200\231 LV cavity with compromised LV \201 lling and function. Longitudinal RV function (RV LAX) can be measured by tricusp id annular motion. <1cm = severe RV impairment (compare with mitral annular motion above). Indicators of decreased preload: (i) Decreased early diastolic \201 lling velocity (mitra l E wave) and decreased E/A ratio (A is the velocity of late mitral LV in \202 ow due to a trial systole). (ii) Decreased mitral E wave velocity together with decreased pulmonary \202 ow during sy stole (S wave). Indicators of LA pressure: (i) Normal pulmonary \202 ow pattern with predominant S wave i s indicative of an LA pressure <8mm Hg. (ii) Dominance of the D wave (pulmonary \202 ow d uring diastole) occurs with elevated LA pressure. AV Doppler \202 ow velocity variation with respiration of >12% in mechanically ventilated patients is indicative of \202 uid responsiveness (cf. pulse pressure variation seen wit h LiDCO). Cardiac tamponade \200 Tamponade is suggested by a combination of clinical and echocardiographic features which de pend upon the rate of accumulation of pericardial \202 uid and the presence or absence of cardiac disease. Unclotted blood in the pericardium appears as a circum- ferential echoluc ent space. Pericardial effusions can be classi \201 ed into small (<0.5cm), moderate (0.5 \200\2232cm) and large (>2cm). Tamponade occurs when pressure in the pericardium exceeds th e pressure in the cardiac chambers, resulting in impaired cardiac \201 lling. Even relati vely small amount of \202 uid can produce a tamponade effect if accumulated acutely or lo culated behind the atria. Classical echocardiographic signs of tamponade include: moderate to large pericardial effusion, right atrial col- lapse (duration >1/3 systole), RV collapse , reciprocal changes in right and left ventricular volumes with respi- ration, IVC plethora (with elevated right side pressures), respiratory variation in RV and LV diastolic filling , increased RV filling on first beat after inspiration, decreased LV \201 lling on the \201 rst beat after inspiration. Post-sternotomy tamponade requires TOE as blood is frequen tly clotted and loculated posteriorly, and may not be visible with TTE. Further reading American Society of Echocardiography www.asecho.org con- tains comprehensiv e information regarding guidelines and stand- ards of echopractice. British Society of Echocardiography www.bseecho.org provides information about the accredit ation process, learning and courses. Cheitlin MD, Armstrong WF, Aurigemma GP, et al. American College of Cardiology; American He art Association; American Society of Echocardiography. ACC/AHA/ASE 2003 guidline update for the clinical application of echocardiography: summary article: a report of the American Co llege of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/A SE Committee to Update the 1997 Guidelines for the Clinical appli- cation of Echocardiograp hy). Circulation 2003;108: 1146 \200\22362. Assessment of RV function \200 RV dysfunction is frequently seen in critical care. RV function is altered by factors incre asing RV afterload, such as high levels of peak expiratory pressure and increased pulmonary vascular resistance (from vascular, metabolic and respiratory causes). The most common cau ses of acute cor pulmonale are massive PE and ARDS. Other causes of RV dysfunction include RV infarct, acute sickle cell crisis, air, fat embolism and myocardial contusion. RV assess ment may alter treatment (fluid loading, vasopressors, thrombolytics) and is of prognostic value. Echocardiographicaly, the RV cavity is \202 at in the four- chamber view or cresce nt shaped in the short axis view. RV walls are thinner than those of the LV, and the inter- ventricular septum acts as part of the LV, moving towards it in systole. In RV failure its cavity enlarges, resulting in apical dilata- tion (in the four-chamber view) and round sha pe (in the short axis view). RV enlargement is usually associated 118 P ANDERSON & M HAMILTON Doppler Introduction The Doppler effect was \201 rst described in 1842 by Christian Doppler, and describes the change in frequency as sound or light waves are re \202 ected off a moving o bject. This rela- tionship is described by the equation shown in Figure 7.9.1. The Doppler effect can be utilized clinically to measure the velocity of blood \202 ow. An ultrasound beam of known fre- quency is directed at an angle to intersect the path of the blood \202 ow and re \202 ected back by the red blood cells to an ultrasound detector. The chang e in the frequency of the re \202 ected ultrasound waves is directly proportional to the v elocity of the blood towards or away from the Doppler probe. Measurement of blood \202 ow using the Doppler effect has a variety of clinical applications including the measurement of \202 ow across heart valves and in the assess- ment of peripheral vascular disease. On e of the most com- mon applications of the Doppler effect in the intensive care setting is in the measurement of cardiac output. The Doppler equation is given as. The Doppler probe is most commonly introduced orally in sedated or anesthetized patients, b ut may also be intro- duced nasally in awake patients with mild sedation and topical anesth esia. The probe should be well lubricated prior to insertion to prevent air between the pro be and the oesophageal wall from attenuating the signal. When the probe is at the appropria te depth, it is rotated slowly so that the tip of the probe is facing posteriorly (towards the aorta). Once in position, the probe is manipulated to achieve the optimal Doppler wavef orm; this will be the clearest signal with the highest peak velocity. The charac- teristic waveform should be a dark/hollow center sur- rounded by red and then white in the trailing edge of the waveform. The waveform should be discrete and well con- trasted with respect to the background (Fig. 7.9.2). The gain control alters the contrast between the Doppler wave form and background noise and should be adjusted to give a black background and sharply con trasted Doppler waveform. fd = 2.fo.v.cos /c Where: v is the velocity of blood \202 ow; is the angle between th e ultrasound beam and blood \202 ow; c is the ultrasound velocity in that medium; fo is t he transmitting frequency. cm seconds \210\2221 PEAK VELOCITY Y T C O L E V I Doppler measurement of cardiac output The cardiac output can be calculated by measuring the velocity of blood through the descending aorta with a Doppler probe placed in the esophagu s, or the velocity of blood in the ascending aorta with a probe in the supraster- nal notch . The dif \201 culties inherent in maintaining the posi- tion of the probe in the supraste rnal notch have led to the dominance of oesophageal placement. Two commercially available o esophageal Doppler systems are the CardioQ \204 from Deltex Medical and the Hemosonic \204 from Arrow International Inc. Measurement of the velocity of blood (cm/s) in the descendi ng aorta allows the \202 ow of blood (ml/s) to be calculated provided that the cross-sect ional area of the aorta is known. The CardioQ \204 calculates the aortic cross- sectional area from a nomogram based upon the patient \200\231s age, height and weight. The Hemosonic \204 directly meas- ures the diameter of the aorta by incorporating M-mode ultrasound cap ability into the Doppler probe. Calculation of the cardiac output using the oesophageal Dop pler method is dependent on \201 ve assumptions: 1 The distribution of blood caudally to the descending aorta and rostrally to the great vessels and coronary arteries maintains is a constant ratio of 70% to 30% 0 seconds CYCLE TIME FLOW TIME TIME Fig. 7.9.1 Typical Doppler waveform The positioning technique and waveform recognition require a degree of operator training; h owever, it has been shown that an acceptable degree of competence can be achieved after the insertion of only 12 probes. Once inserted, Doppler probes have been used in unconscious p atients for up to 14 days without complication. The use of an oesophageal Doppler probe is safe in most patients; however, contraindications include the presence of clotting abnormal ities, oesophageal varices and recent oesophageal surgery. Readings obtained from an oesoph ageal Doppler probe may be inaccurate in the following circumstances: \200 \200 Coarctation of the aorta Thoracic aortic aneurysm (especially if aortic cross- section is c alculated from nomogram) Presence of a working epidural/intrathecal anesthetic with subsequ ent vasodilatation 2 That a \202 at velocity pro \201 le exists within the aorta 3 The estimated cross-sect ional area is close to the mean systolic diameter 4 There is negligible diastolic blood \202 ow 5 The velocity of blood \202 ow in the ao rta is measured In these circumstances, whilst the absolute \201 gures from the Doppler probe may be inac curate, trends in the readings can still be used to guide therapy. accurately Practical considerations The descending aorta runs parallel and immediately adja- cent to t he esophagus at a depth of 35 \200\22340cm from the teeth. This allows uninterrupted passa ge of ultrasound waves between the probe and the aortic blood stream. 119 CHAPTER 7.9 Doppler Interpretation of waveform and variables Transoesophageal Doppler probes are capable of mea sur- ing a number of haemodynamic variables, the interpreta- tion of which can then be used to guide treatment. Afterload Afterload Peak velocity The peak velocity of blood in the aorta gives a good esti- mate of the contra ctility of the myocardium. Normal peak velocity varies with age; at the age of 20 normal pe ak veloc- ity is 90 \200\223120cm/s, falling to 50 \200\22380cm/s by the age of 70. Normovolaemia Stroke volume/cardiac output Stroke distance is the area under the velocity \200\223time wa ve- form; when multiplied by the aortic diameter this gives a good estimate of the stroke v olume. Due to slight beat- to-beat variability in stroke volume, the reading is usually ave raged over several beats. The number of beats used for this calculation is the cycle length . A cycle length of \201 ve beats is usual, but can be increased to improve the accu- rac y of stroke volume estimation when there is marked beat-to-beat variability, e.g. atrial \201 brillation. The cardiac output is calculated from the stroke volume multiplied by the heart rate. Hypovolaemia Ventricular failure Fig. 7.9.2 Characteristic waveforms. The use of oesophageal Doppler to measure cardiac out- put in critically ill patients compa res favorably with the use of the thermodilution method using a pulmonary artery catheter. There is an increasing body of evidence that intraoperative \202 uid therapy guided by oe sophageal Doppler monitoring can result in a lower rate of perioperative complications and a shorter length of hospital stay. A systematic review and meta-analysis of studies using o esophageal Doppler perioperatively found a reduction in hospital stay of nearly 3 days in t he Doppler groups. The ease of use and the data provided by oesophageal Doppler lends itsel f to use in protocol-driven \202 uid resusci- tation. McKendry et al. reported the succes sful use of a nurse-led, Doppler-guided protocol for \202 uid optimization post-cardiac s urgery. The advent of more \202 exible probes for nasal insertion in awake patients has a llowed for the development of nurse-led early \202 uid optimization in the setting of cri tical care outreach teams. Corrected \202 ow time (FTc) The \202 ow time is the duration of forward \202 ow of b lood in the aorta, i.e. the width of the base of the velocity \200\223time waveform. The \202 ow time varies with heart rate and can be corrected to a heart rate of 60bpm by dividi ng the \202 ow time by the square root of the cardiac cycle time (analo- gous to correcti ng the Q-T interval in ECG interpretation); this value is the corrected \202 ow time (FTc ). The normal FTc is 330 \200\223360ms. Anything that impedes \201 lling or emptying of t he LV will cause a reduction in FTc. Most commonly this is seen in hypovolaemia, but may al so be seen with mitral stenosis, PE and excessive use of vasopressors. A pro- longed FTc is seen in the vasodilated circulation, e.g. in sepsis. A prolonged FTc of up to 400ms may be regarded as normal in an anesthetized patient, especially in the pres- ence of a working e pidural In addition to the variables described, the appearance of the velocity \200\223time waveform itself may be diagnostic. as described in Figure 7.9.3. Further reading Dark PM, Singer M. The validity of trans-esophageal Doppler ultra- sonograp hy as a measure of cardiac output in critically ill adults. Intensive Care Med 2004; 30: 20 60 \200\2236. McKendry M, McGloin H, Saberi D, et al. Randomized controlled trial assessing the impact of a nurse delivered, \202 ow monitored protocol for optimization of circulatory status aft er cardiac sur- gery. BMJ 2004; 329: 258 \200\22362. Clinical application To date there has been no reported mortality associated with the use o f oesophageal Doppler. Morbidity rates are also low; there are case reports of inadvertent insertion into the lower respiratory tract and of epistaxis after nasal insertion. Single r eadings may be diagnostic, but observation of dynamic changes with therapy are often more u seful. \200 Walker D, Usher S, Hartin J, et al. Early experiences with the new awake oesophageal Dopple r probe. Br J Anaesth 2004; 93 : 471. Low stroke volume. Fluid is best given as boluses, e.g. 200ml, to construct a Starling curv e for that patient. If there is less than a 5 \200\22310% increase in stroke volume with ea ch bolus it suggests that the plateau point has been reached. Low FTc. Most commonly repres ents hypovolaemia. Fluid challenge as above to achieve an FTc of 330 \200\223360ms. Other c auses, e.g. PE, will not improve with \202 uids. Low peak velocity. Consider positive ino tropes. Low peak velocity and low FTc. Consider moves to reduce afterload, e.g. peripheral warming, reduction of vaso- pressors, glyceryl trinitrate (GTN). \200 120 M CECCONI & G DELLA-ROCCA Pulse pressure algorithms this is not the case as the pressure wave is transmitted 20 times faster than the \202 o w wave. Moreover, even if it is true that in the proximal aorta the \202 ow is almost pul satile, blood \202 ows peripherally in both systole and diastole. A pulse pressure algori thm needs to take into considera- tion all these forces when transforming a pressure to a v olume in order to track stroke volume. Summarizing, an ideal algorithm should: \200 Cardiac output can be monitored continuously by different devices that analyze the arterial waveform to track changes in stroke volume and cardiac output. The analysis of the arteria l pressure wave to determine cardiac output is clas- si \201 ed as pulse contour analysis or pulse pressure analysis. Starting from a similar principle three main devices are now av ailable on the market, with different algorithms and features: \200 \200 \200 PiCCO system (Pulsion, Munich, Germany) LiDCO \204 plus system (LidCO, Cambridge, UK) Flotr ac technology and Vigileo Monitor (Edwards Lifesciences, Irvine, CA, USA) Work independently of the arterial site from where pressure is monitored despite changes in waveform shape and pressure through the arterial tree from the center to the periphery. Co rrect for non-linear compliance and take account of individual variations in aortic charact eristics, thus giving an absolute cardiac output. Not be affected by changes in vascular re sistance causing changes in re \202 ected wave augmentation of the arterial pressure. Not rely on identifying details of wave morphology. Be only minimally affected by the damping o ften seen in arterial lines. Physiological background Compliance Compliance describes the relationship between pressure and volume in the arterial vessels. Knowing the compli- ance is essential to estimate the c hanges in volume (stroke volume) from changes \200 C = ZV/ZP. Where C = compliance, ZV = changes in volume, ZP = changes in pressure. Without knowing the compliance of the arterial tree, more precisely the compliance of the proximal aorta, it i s not possible to understand the change in volume that corre- sponds to a change in pressur e. Compliance in the arterial tree is not a linear relationship, and so the same change in pressure does not always re \202 ect the same change in vol- ume. As a general rule, compl iance is higher for lower pres- sures and lower for higher pressures. Another peculiarity o f compliance is that it is not constant. The same arterial tree can behave differently in d ifferent situations and be characterized by different compliance. For example, vaso- constr iction during vasopressor therapy decreases compli- ance, vise versa vasodilation during va sodilator therapy or sepsis increases compliance. The aorta is the main arterial vessel of interest, as it is the part of the arterial tree that directly receives the stroke volume. There are three forces that contribute to how the proximal aorta is \201 lled with blood during every heart beat: \200 History The first algorithm used in clinical practice was the Wesseling algorithm in 1983. This algorithm is based on the hypothesis that the contour of the arterial pressure wavefor m is dependent on stroke volume, and that this can be estimated from the integral of the ch ange in pressure over time, considering the interval between the end of diastole to tyhe en d of systole (Asys). This is the \201 rst algorithm of pulse contour analysis used to det ermine car- diac output. From this point, new algorithms have been developed. Devices PiCCO system In clinical practice the \201 rst pulse contour method using a Wesse ling-based algorithm was the PiCCO system (Pulsion Munich, Germany). PiCCO is a cardiac mon itor that meas- ures cardiac output and several volumes (intrathoracic blood volume (ITBV), global end-diastolic volume (GEDV), extravascular lung water (EVLW)) via transpulmonary th ermodilution. This thermodilution is used to calibrate the pulse pressure algorithm. The pu lse pressure algorithm analyzes both the systolic and the diastolic part of the arte- rial pressure to study and determine the non-linear com- pliance, and the relationship \202 ow /pressure. This part of the process is called calibration and should be repeated every time there is a signi \201 cant haemodynamic change. In order to perform a thermodilutionm a c entral venous catheter needs to be in place. 15ml of cold saline is injected through a sens or that detects the temperature and time of the injection. A specialized arterial catheter (usually a femoral artery) detects the changes in blood temperature, produc- ing a thermodi lution curve. The same arterial catheter is used to monitor blood pressure, and the arteria l waveform is analyzed by the pulse pressure algorithm. PiCCO continuous cardiac output had been studied and validated against the pulmonary artery catheter in several conditions and has proven to be a reliable device, requiring calibration more often only in cases of majo r haemody- namic changes. The force of injection of the blood by the pumping of the heart The opposing force dependen t on the pulsatile in \202 ow (impedance) The opposing force dependent on the change in vo lume that we described as compliance When blood leaves the aorta there is also another force that opposes the blood \202 owing peripherally. This is the peripheral resistance. Re \202 ected waves A further problem that has to be overcome is the accurate measurement of pressure in the periphery. The arterial pressure recorded is not only dependent on the a ortic arterial pressure, but is also the result of the re \202 ection of waves generated p eripherally and returning back up the arterial system. Non-pulsatile \202 ow Although the \202 ow wave and the pressure wave in the prox- imal aorta occur almost simultaneously, more peripherally 121 CHAPTER 7.10 Pulse pressure algorithms The algorithm also provides the user with the analysis of the variation in either stroke vo lume (SVV) or pulse pres- sure (PPV). SVV and PPV represent the variation of stroke volume and of the pulse pressure during the respiratory cycle. In sedated ventilated patients, the se indexes have proven to predict the response to a \202 uid challenge. A large variation (>10 \200\22312%) identifies responders and non- responders with good sensitivity and spec i \201 city. monitor. The most interesting characteristic of this device is that it does not need to be calibrated and it needs just an arterial line to work. Compliance and resistance are derive d from the analysis of the arterial waveform. The hypothesis is that in order to calculate the effects of com- pliance and peripheral resistance on \202 ow, all the necessary infor mation can be obtained by the analysis of the arterial pressure waveform. Age, weight and s ex of the patient are the only variables that the clinician needs to input into the Vigileo monitor. The transducer (Flotrac) can be connected to any functioning arterial access. The algorithm recalcu- lates the compliance continuously, thus bypassing the need for calibrat ion. The Vigileo algorithm also allows the analy- sis SVV and PPV to be performed. This alg orithm is now under validation.