Presentation on theme: "Dr Caroline Daly Cardiologist, SJH"— Presentation transcript:
1Dr Caroline Daly Cardiologist, SJH Echo in the ITUDr Caroline DalyCardiologist, SJH
2Scope of uses of ECHO in ICU Following cardiac surgeryDiagnosisMonitoring
3Advantages Cheap Portable Widely available Non invasive, no toxic contrast, no radiation
4Rationale for use of Echo in ITU Point-of care echocardiography in the management of the critically ill patientProvides rapid assessment of cardiac function and physiologyComplements data available from standard invasive hemodynamic monitoringBoth a diagnostic and monitoring tool for rapid bedside assessment of cardiovascular pathophysiology in the critically ill
5Key Questions in ITU Systolic function and RWMA tamponade and pericardial effusionhypovolemia and volume responsivenessacute cor pulmonalehypoxemiacomplication of AMIchest traumaassessment of shock
6Disadvantages of TTE in ITU Poor ECHO images in:ObeseCOAD/hyperinflated chestChest wall deformityOedemaPost cardiac surgery –wounds, pain, drains
7TOE Invasive - but minimally invasive vs other Ix Overcomes the issues of poor image qualityBetter spatial resolution & better views of posterior structuresMore sensitive for detection of endocarditis - >90 % vs 68%Complications (retrospective series n= 7200 pts in cardiac surgery : Kallmeyer et al.)severe odynophagia (0.1%)dental injury (0.03%)endotracheal tube malpositioning (0.03%)upper gastrointestinal hemorrhage (0.03%)oesophageal perforation (0.01%)
8Emergency EchoFEEL: focused echocardiography evaluation in life supportFATE: focused assessed transthoracic echoGoalsacquire standard TTE views in ACLS compliant mannerrecognise major causes of arrest/ shockrecognise when referral for second opinion
9FATE - interpretation Look for obvious pathology Masses, vegetations, intra thoracic foreign bodiesAssess morphology/dimensionsAssess myocardial functionAssess valvesImage pleura on both sideRelate the information to the clinical context
10Normal FATE view Subcostal 4 chamber Apical 4 chamber Parasternal long axisParasternal LV short axisPleural scanning
11Extended FATE Normal FATE + Subcostal vena cava Apical 2 chamber Apical long axisApical 5 chamberParasternal short axis mitral planeParasternal aorta short axis
14Pathologies to be considered Pericardial effusionpost cardiac surgery, post cardiac catheterization, trauma, renal failure, infectionDilated RA + RVpulmonary embolism, RV infarction, pulmonaryhypertension, volume overloadDilated LA + LVischemic heart disease, dilated cardiomyopathy,sepsis, volume overload, aortic insufficiency
15Pathologies to be considered Ctd LV hypertrophyAortic stenosis, arterial hypertension, left ventricular outflow tract obstruction ( eg SAM or sub-aortic membrane), hypertrophic cardiomyopathy, myocardial deposition (amyloid, haemochromatosis)
16Pre-existing cardiac disease? RV dilatation = acute or chronicLV dilatation = almost always chronicBiventricular dilatation = chronic failureAtrial dilatation = chronic pressure or volume overloadRV or LV hypertrophy = chronic pressure overload
17Severe hypovolaemia End systolic LV obliteration (kissing walls) LV end diastolic area (LVEDA) < 5.5 cm/m2 BSA(or < 10 cm2)LVEDA variation with loading
20Basic Volume Status Assessment Easy in severe hypovolaemiaEasy in clear volume overloadDifficult in less severe hypovolemia/significant cardiac diseaseConsider pre-existing cardiac diseaseConsider respiratory status
21Ventricular Function assessment LV global systolic functionfractional shortening (FS)FS% = (LVEDD-LVESD)/LVEDD x 100%With RWMA is unreliable, but, simplified Teicholz method EF % = FS % x 2visual ejection fraction (eyeballing)Simpsons (planimetry of LV cavity)LV regional functionRV systolic function
22Qualitative Assessment of Function Qualitative assessment of LV functiontend to be underestimated in a dilated LVoverestimated in small cavity LVInterpret findings in the context of drugs and preload (volume status)Repeated echo assessment of LV functionInterpret findings considering inotropic/ mechanical supportMarked tachycardia/atrial fibrillation may underestimate of LV systolic function
23RV function RVEDA / LVEDA > 0.6 moderate dysfunction > 1 severe dysfunctionParadoxical septal movement
28Focused Echo -Focused echocardiography as an adjunct in the peri-arrest period is likely to become a core competency for acute medicine traineesWorld Interactive Network Focused on Critical Ultrasound = “Winfocus” basic echo“Echocardiography practice, training and accreditation in the intensive care”
29FEEL: focused echocardiography evaluation in life support To assess the function of the heart and identify treatable conditions in peri-resuscitation careDifferentiates"true" PEA from "pseudo-PEA"Identify 4 treatable causes of cardiac arrestcardiac tamponadehypovolemiapulmonary embolismsevere LV dysfunction
30FEELhigh quality CPR with minimal interruptions to reduce the no-flow intervalsFEEL < 10 sec
31RV Small and hyperkinetic RV: tamponade Dilated and hypokinetic RV: RV failureLV dysfunctionRV AMIAcute pulmonary embolism
32LV Severe LV hypokinesia LV hyperkinesia LV AMI, Sepsis related MyocarditisDCMLV hyperkinesiaAcute valvular dysfunction (AR, MR),HOCM,diastolic dysfunction
33BibliographyICU echocardiography- should we use it in a heartbeat? Chest 2002Portable echocardiography- is essential for the treatment of acutely ill patients BMJ 2006Echocardiography for the intensivists Care of the Critically Ill 2003Beside Ultrasonography in the ICU Chest 2005Echo in ICU- time for widespread use ICM 2006
34Advanced Critical Care Echo Evaluating LV systolic functionEvaluating RV functionMonitoring Cardiac OutputFluid ResponsivenessIVC and LVDiastolic functionRV functionTamponade
35Cardiac Output Cardiac output = Stroke volume x Heart Rate Calculated from (i) Pulse Wave VTI and CSA ofLVOTRVOTMitral inflow (at annulus)(ii) Simpson’s (EDV - ESV = SV).(May be overestimated if RWMAs)
36CO by TOE in liver transplantation Curr Cardiol Rev August; 7(3): 184–196.
37Continuous monitoring of CO (TOE) Meta-analysis of comparison of 2 available ultrasonographic devices- CO evaluation from pulsed-wave Doppler of the descending aorta. (CardioQ and HemoSonic 100) v thermodilution via PALeft ventricular stroke volume estimated by mean systolic velocity measurement using a nomogram in the CardioQ, and an M-mode echocardiography estimate of aortic diameter using HemoSonic 100.21 studies, 314 patients, 2400 paired measurements.Reasonable correlation was found between both methods, with a mean difference of to 2.00 l/min.Is good to track changes
40Fluid Responsiveness IVC IVC size correlated to CVP/RAP spontaneous breathingIn controlled ventilation IVC will expand in inspiration (as venous return is reduced) and reduce in expiration (opposite of spont).Absence of respiratory variation : 90% chance will not be fluid responsive. >11% variation identifies respondersIVC collapsibility index= max diameter - minimum diameter / mean diameter x100 to get percentage
41LV : fluid responsiveness LV Variation in LV stroke area with respiration shown to predict fluid responsiveness (change >16%).ie area of LV in PSAX papillary level in systole and diastole and subtract systole from diastole - see how this changes with respirationImpractical/time consuming without appropriate software in machine.
42LVOT : fluid responsiveness LVOT Vmax or VTI variation with respiration of >12% predicts fluid responsiveness(max - min / mean) x 100VTI increase of >12% 1min after PLR predicts fluid responsiveness
43Diastolic Dysfunction Important cause of cardiogenic pulmonary oedema and failure to wean even with reasonable systolic function.IHDHypertensionASCardiomyopathySepsis (sepsis induced cardiomyopathy)Inotropes (adrenaline). PDE inhibitors (lusitropes) preserve diastolic function better.
44Diastolic dysfunction LV compliance reduced so LVED Pressure Volume relationship shifted up and left so:LV can be under-filled despite high filling pressures.Optimum filling range narrow (under or over filled easily)Therefore a hypovolaemic LV with diastolic dysfunction will have elevated filling pressures, may respond well to fluid, but will easily be overloaded with pulmonary oedema resulting.
45Causes of RV dysfunction RV volume overload.RV pressure overload (ARDS, PE).Myocardial contusion (most anterior cardiac chamber).Myocardial ischaemia.RCA air embolus post cardiac surgery.All forms of RV overload compromise LV diastolic function.
46RV Volume OverloadRV very compliant so volume can increase with little change in pressure.If severe volume increase will move over top of Starling curve and start to fail.TR will also develop.Acute from IV fluid or renal failure.Chronic from ASD, VSD, severe TR or PR.Chronic volume overload can cause RV hypertrophy and pressure overload.In pure volume overload the RV will not be hypertrophied
47RV Pressure OverloadRV very sensitive to increase in afterload and will quickly result in dilatation and failure if acute (eg PE or ARDS).If chronic RV will be hypertrophied, will tolerate increased afterload better.Features of pressure overloadDilated RV. Hypertrophied if chronic.Acute pressure overload (PE or ARDS) will look the same as volume overload with septal flattening in diastole.If chronic from PHT(recurrent PE, L sided regurg, L heart failure, COPD) RV will be hypertrophied and able to generate very high pressures (>50mmHg). The septum is D shaped in systole (paradoxical motion) going back to normal in diastole.
48Tamponade2D and M-mode. Look for chamber collapse in diastole. RA then RVOT then whole RV then LA then LV. RAP will be high so IVC dilated with little or no respiratory variation.
49Tamponade Pulse Wave Doppler Assess RV and LV inflow in A4C. Inspiration increases flow of blood into R heart (sucks it in) and reduced flow into L heart (pulm vessels expand).This is exaggerated in tamponade (pulsus paradoxus).This is the opposite if positive pressure ventilationMeasure max and min E wave velocities for each valve.Assess outflow of RVOT and LVOT by measuring Vmax and/or VTI.