Presentation on theme: "Echo in the ITU Dr Caroline Daly Cardiologist, SJH."— Presentation transcript:
Echo in the ITU Dr Caroline Daly Cardiologist, SJH
Scope of uses of ECHO in ICU Following cardiac surgery Diagnosis Monitoring
Advantages Cheap Portable Widely available Non invasive, no toxic contrast, no radiation
Rationale for use of Echo in ITU Point-of care echocardiography in the management of the critically ill patient Provides rapid assessment of cardiac function and physiology Complements data available from standard invasive hemodynamic monitoring Both a diagnostic and monitoring tool for rapid bedside assessment of cardiovascular pathophysiology in the critically ill
Key Questions in ITU Systolic function and RWMA tamponade and pericardial effusion hypovolemia and volume responsiveness acute cor pulmonale hypoxemia complication of AMI chest trauma assessment of shock
Disadvantages of TTE in ITU Poor ECHO images in: Obese COAD/hyperinflated chest Chest wall deformity Oedema Post cardiac surgery –wounds, pain, drains
TOE Invasive - but minimally invasive vs other Ix Overcomes the issues of poor image quality Better spatial resolution & better views of posterior structures More 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%)
Emergency Echo FEEL: focused echocardiography evaluation in life support FATE: focused assessed transthoracic echo Goals acquire standard TTE views in ACLS compliant manner recognise major causes of arrest/ shock recognise when referral for second opinion
FATE - interpretation Look for obvious pathology – Masses, vegetations, intra thoracic foreign bodies Assess morphology/dimensions Assess myocardial function Assess valves Image pleura on both side Relate the information to the clinical context
Normal FATE view Subcostal 4 chamber Apical 4 chamber Parasternal long axis Parasternal LV short axis Pleural scanning
Extended FATE Normal FATE + Subcostal vena cava Apical 2 chamber Apical long axis Apical 5 chamber Parasternal short axis mitral plane Parasternal aorta short axis
FATE Hypovolemia Myocardial dysfunction Pericardial effusion Pulmonary embolism Papillary muscle rupture VSD in AMI Severe valve dysfunction Pleural effusion/ pneumothorax
Pathologies to be considered Pericardial effusion post cardiac surgery, post cardiac catheterization, trauma, renal failure, infection Dilated RA + RV pulmonary embolism, RV infarction, pulmonary hypertension, volume overload Dilated LA + LV ischemic heart disease, dilated cardiomyopathy, sepsis, volume overload, aortic insufficiency
Pathologies to be considered Ctd LV hypertrophy Aortic stenosis, arterial hypertension, left ventricular outflow tract obstruction ( eg SAM or sub-aortic membrane), hypertrophic cardiomyopathy, myocardial deposition (amyloid, haemochromatosis)
Pre-existing cardiac disease? RV dilatation = acute or chronic LV dilatation = almost always chronic Biventricular dilatation = chronic failure Atrial dilatation = chronic pressure or volume overload RV or LV hypertrophy = chronic pressure overload
Severe hypovolaemia End systolic LV obliteration (kissing walls) LV end diastolic area (LVEDA) < 5.5 cm/m2 BSA (or < 10 cm2) LVEDA variation with loading
Severe Hypovolaemia IVC diameter – spontaneous respiration: EED < 9 mm – mechanical ventilation: EED < 15 mm IVC respiratory variation – spontaneous respiration: > 50% – mechanical ventilation: > 18% IVC variation with loading EED = End expiratory dimension
Basic Volume Status Assessment Easy in severe hypovolaemia Easy in clear volume overload Difficult in less severe hypovolemia/significant cardiac disease Consider pre-existing cardiac disease Consider respiratory status
Ventricular Function assessment LV global systolic function – fractional shortening (FS) – FS% = (LVEDD-LVESD)/LVEDD x 100% – With RWMA is unreliable, but, simplified Teicholz method EF % = FS % x 2 – visual ejection fraction (eyeballing) – Simpsons (planimetry of LV cavity) LV regional function RV systolic function
Qualitative Assessment of Function Qualitative assessment of LV function – tend to be underestimated in a dilated LV – overestimated in small cavity LV Interpret findings in the context of drugs and preload (volume status) Repeated echo assessment of LV function Interpret findings considering inotropic/ mechanical support Marked tachycardia/atrial fibrillation may underestimate of LV systolic function
RV function RVEDA / LVEDA > 0.6 moderate dysfunction > 1 severe dysfunction Paradoxical septal movement
Focused Echo - Focused echocardiography as an adjunct in the peri-arrest period is likely to become a core competency for acute medicine trainees World Interactive Network Focused on Critical Ultrasound = “Winfocus” basic echo “Echocardiography practice, training and accreditation in the intensive care”
FEEL: focused echocardiography evaluation in life support To assess the function of the heart and identify treatable conditions in peri-resuscitation care Differentiates"true" PEA from "pseudo-PEA" Identify 4 treatable causes of cardiac arrest – cardiac tamponade – hypovolemia – pulmonary embolism – severe LV dysfunction
FEEL high quality CPR with minimal interruptions to reduce the no-flow intervals FEEL < 10 sec
RV Small and hyperkinetic RV: tamponade Dilated and hypokinetic RV: RV failure – LV dysfunction – RV AMI – Acute pulmonary embolism
Bibliography ICU echocardiography- should we use it in a heartbeat? Chest 2002 Portable echocardiography- is essential for the treatment of acutely ill patients BMJ 2006 Echocardiography for the intensivists Care of the Critically Ill 2003 Beside Ultrasonography in the ICU Chest 2005 Echo in ICU- time for widespread use ICM 2006
Advanced Critical Care Echo Evaluating LV systolic function Evaluating RV function Monitoring Cardiac Output Fluid Responsiveness – IVC and LV Diastolic function RV function Tamponade
Cardiac Output Cardiac output = Stroke volume x Heart Rate Stroke Volume Calculated from (i) Pulse Wave VTI and CSA of – LVOT – RVOT – Mitral inflow (at annulus) (ii) Simpson’s (EDV - ESV = SV). – (May be overestimated if RWMAs)
CO by TOE in liver transplantation Curr Cardiol Rev August; 7(3): 184–196.
Continuous 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 PA Left 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 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
Haemodynamics in ITU
Fluid Responsiveness IVC IVC size correlated to CVP/RAP spontaneous breathing In 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 responders IVC collapsibility index = max diameter - minimum diameter / mean diameter x100 to get percentage
LV : 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 respiration Impractical/time consuming without appropriate software in machine.
LVOT : fluid responsiveness LVOT Vmax or VTI variation with respiration of >12% predicts fluid responsiveness (max - min / mean) x 100 VTI increase of >12% 1min after PLR predicts fluid responsiveness
Diastolic Dysfunction Important cause of cardiogenic pulmonary oedema and failure to wean even with reasonable systolic function. – IHD – Hypertension – AS – Cardiomyopathy – Sepsis (sepsis induced cardiomyopathy) – Inotropes (adrenaline). PDE inhibitors (lusitropes) preserve diastolic function better.
Diastolic 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.
Causes 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.
RV Volume Overload RV 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
RV Pressure Overload RV 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 overload Dilated 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.
Tamponade 2D 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.
Tamponade 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 ventilation Measure max and min E wave velocities for each valve. Assess outflow of RVOT and LVOT by measuring Vmax and/or VTI.
Ultrasound in cardiac arrest due to pneumothorax. Typically, cardiac chambers are small and hyperkinetic (a), inferior vena cava is dilated (b)