Use of echocardiography in icu

comprehensive presentation on 2D echo use in ICu set up. helpful in finding causes of shock and also in monitoring of fluid status in critically ill patients.

1. Use of echocardiography in ICU Dr. Nisheeth M. Patel M. D (Medicine ), FCCCM Consultant Physician & Intensivist

2. Introduction: Echocardiography has evolved to become a crucial noninvasive imaging modality in the critically ill patients. Its portability, safety, and widespread availability allow for the rapid diagnosis of life-threatening cardiac problems and rapid exclusion of cardiac disease in critically ill patients. These benefits encourage the use of 2D Echo in ICU on routine day to day basis.

3. Indications for Transthoracic Echocardiography in Critical Care Hemodynamics: Left ventricular function Regional wall motion abnormalities Global dysfunction Transient dysfunction (sepsis, ischemic/catecholamine stunning) Right ventricular function Hypotension Pericardial effusion/ tamponade Assess volume status Outflow tract obstruction Valvular stenosis/insufficiency

4. Hypoxia Right ventricular function Right ventricular pressure Intracardiac / extracardiac shunting Pulmonary embolus Infections Bacterial endocarditis

5. Trauma Blunt thoracic trauma Penetrating thoracic trauma General Assess proximal ascending aorta—dissection, hematoma Source of murmur Source of embolus Procedural guidance (especially pericardiocentesis )

6. Indications for Transesophageal Echocardiography in Critical Care Inadequate or non diagnostic transthoracic echocardiographic images Evaluate suspected aortic dissection or trauma Evaluate prosthetic valves, especially mitral Investigate persistent hypoxemia Detect presence of valvular vegetations

7. Identify complications of infective endocarditis : Abscesses Leaflet perforation Pseudoaneurysm formation Fistulas Identify cardiac source of systemic embolus: Thrombus in left atrium and left atrial appendage Patent foramen ovale /atrial septal aneurysm Atheromatous debris of the aorta

8. Identify pulmonary embolus in transit Characterize intracardiac shunts: Atrial septal defect (ASD) Ventricular septal defect (VSD) Anomalous pulmonary venous connections Guide invasive procedures: Shunt closure Percutaneous balloon valvuloplasty

9. Diagnostic echocardiography Clinical findings Cardiac Cause 2D echo findings Low CO unresponsive to inotropes Valvular disease Any severe stenotic or regurgitant lesion Intrinsic cardiac disease HOCM/LVH with LVOTO Large VSD/ASD Severe LV/RV dysfunction Extrinsic cardiac disease Cardiac Tamponade Pericardial effusion Pericardial disease

10. Clinical findings Cardiac Cause 2D echo findings Oligouria Underfilling Low transmitral /tricuspid velocities Small ventricular volumes Apposition of LV papillary muscles in systole Intrinsic cardiac disease Poor LV function, severe AS Pericardial disease: Pericardial Peri cardial effusion, pericardial tamponade , pericardial constriction

11. ) Clinical findings Cardiac Cause 2D echo findings Increased filling pressures (left-sided) Impaired LV Increased E > A ratio, short IVRT MV disease Significant MS or MR Increased filling pressures (right-sided) Secondary to left-sided disease Significant AS, AR, MS, MR/LV disease Impaired RV Reduced TAPSE TR Annular dilatation or endocarditis

12. . Clinical findings Cardiac Cause 2D echo findings Sepsis/SIRS LV/RV dysfunction Ventricular dilatation, systolic/diastolic dysfunction Source of sepsis masked endocarditis Endocarditis : Native/prosthetic valve pacemaker wires extracardiac ‘ endocarditis ’ Vegetations paraprosthetic leaks aortic root abscess Pulmonary hypertension Acute PE Dilated RV, severe TR Post- pneumonectomy Displaced heart, increased pulmonary acceleration time Mitral valve disease Significant MS or MR 

13. Clinical findings Cardiac Cause 2D echo findings Failure to wean from ventilator Intrinsic cardiac disease Ischaemia severe MR HOCM LV/RV dysfunction CVA/embolic event Intracardiac thrombus LA appendage RA apical LV thrombus Endocarditis Cyanosis Intracardiac shunting Positive contrast study

14. Ventricular function Assessment Left ventricle Systolic Function: Techniques exist to assess LV function measurement of dimensions and volumes in two/three dimensions wall thickness and motion assessment of filling patterns measurement of myocardial deformation. All these measures are variably load and inotropy dependent; therefore measured values should be interpreted with caution in the critically ill.

15. LV contractility has depended upon linear measurement of changes in LV internal dimensions (fractional shortening, FS) Differences between systolic and diastolic areas/volumes in the minor axis (ejection fraction, EF) Normal values of FS/EF are unknown for the critically ill patient population Measured values should be interpreted with caution in the critically ill.

16. Regional functional abnormalities: Myocardial thinning (normal 6–12 mm) Abnormal motion ( hypokinesis / akinesis / dyskinesis ) ICU echocardiogram should be interpreted in the context of the level of inotropic support, and where abnormalities in contractility conform to known coronary artery territories, ischemia/infarction should be suspected.

17. Longitudinal axis (LAX) function has three components: Amplitude Velocity Timing Measured using M-mode (mitral annular plane systolic excursion, MAPSE) (Normal 10-12 mm) Velocities of this motion assessed using tissue Doppler imaging (TDI)

18. LV diastolic function: Derived measures of diastolic function: Isovolumic relaxation time (IVRT, normal 70–110 ms) Ratio of peak velocities (E/A, normal 0.75–1.40) E-wave deceleration time (normal 160–240 ms) Normal values are age, inotropy , and filling dependent, as well as varying with pathology, interpretation in critically ill patients is challenging.

19. Pulsed Doppler echocardiographic recording of mitral inflow velocity  Tissue Doppler imaging of the septal or medial mitral annulus velocity IVRT C

20. Colour flow pro­pagation velocity (CFPV), as determined by colour M-mode Doppler Measurement to diagnose LV diastolic dysfunction ( Vp <50 cm/s indicating diastolic disease)

21. Tissue Doppler imaging (TDI) of the myocardium at the base of the heart may assist in the diagnosis. Here early myocardial tissue velocities (E′) Providing a measure of myocardial relaxation E′ of ≥10 cm/s is normal relaxation, <10 cm/s is impaired <5 cm/s is severely impaired Normal TDI velocity

22. RV systolic function: RV is exquisitely sensitive to increases in afterload and reduction in coronary perfusion In the ICU, RV dysfunction is due to: secondary to pulmonary disease Mechanical ventilation LV dysfunction A range of techniques is used to assess RV function, including M-mode, PW Doppler and TDI.

23. Measurement of the longitudinal annular movement of the RV free wall using M-mode (tricuspid annular plane systolic excursion, TAPSE) correlates well  Normal TAPSE is 2 cm, falling after cardiac surgery to 1.5 cm Any reduction in TAPSE in the setting of pulmonary hypertension indicates significant RV dysfunction Amplitude of <1 cm implies severe impairment.

24. RV diastolic function measurement on same principles of LV diastolic dysfunction; but its often unreliable in critical care setting. Positive-pressure ventilation may abolish this pulmonary arterial diastolic wave, making the diagnosis more challenging. Confounding factors include the presence of LV restriction, elevation of pulmonary arterial diastolic pressures, tachycardia and requirement for high ventilatory pressures.

25. Pericardial Disease: Pericardial effusion, cardiac tamponade can be easily diagnose in critically ill patietns who are oligouric and having low CO even with inotropes . Additional features: swinging heart, pseudosystolic anterior motion of the MV demonstration of fixed, dilated caval veins. Cardiac Tamopnade on echo: RV early-diastolic collapse RA late-diastolic collapse LA late-diastolic collapse LV early-diastolic collapse

26. Hemodynamics on Echo in ICU It is possible to calculate blood flow at several levels in the heart and aorta using Doppler echocardiography. Measurements of flow useful in the ICU setting to derive: LV stroke volume, cardiac output, regurgitant volumes of MR and AR, flow across an ASD or VSD, valve areas (by continuity principle) Response to therapeutic measures such as intravenous administration of inotropic drugs or the effect of an intra-aortic balloon pump on systemic output.

27. Stroke volume is calculated as the product of the cross-sectional area (cm 2 ) of the LVOT and the TVI (cm) by PW Doppler. Cardiac output: Stroke Volume X Heart Rate.

28. LA pressure (LAP) estimation: Combining transmitral Doppler (blood velocities) with TDI (tissue velocities) has been shown to improve the correlation with LAP. Here, the ratio E/E′ is calculated Ratio <10 corresponding to LAP < 15 mmHg (2  kPa ) Ratio >15 corresponding to LAP > 18 mmHg (2.4  kPa ) Correlation between 11–14 is poor, additional parameters should be used, generally in combination.

29. Pulmonary Art Systolic Pressure: Peak PA systolic pressure is calculated from the peak Doppler velocity (v) of TR by CW. RV pressure = 4 × (peak TR velocity) 2 RV pressure + Estimated RA Pressure = PA systolic pressure. RA pressure Estimation: Normal variation or collapse of the IVC with breathing (>50%) implies normal RA pressure (0-5 mm Hg). Partial collapse (<50%) is generally estimated at 5 to 10 mm Hg No (or only minimal) change in IVC diameter implies an RA pressure of 15 mm Hg or more.

30. When available, RA pressure can be obtained directly from a central venous pressure tracing, which is more accurate Care is needed in severe RV dysfunction, as PASP may be significantly underestimated by this technique In the absence of TR, the pulmonary regurgitation (PR) trace can be interrogated to estimate PA diastolic pressure

31. Volume responsiveness Echocardiography allows assessment of the patient’s volume status, complementary to invasive hemodynamic measurements. Echocardiographic volume status assessment: Static values (single-measure dimensions and flows) Dynamic indices (variation in flows and dimensions after dynamic maneuvers)

32. Estimation of preload- and volume-responsiveness using static measurements is generally unreliable in ICU due to changes in hemodynamics of critically ill patients . LAP does not correlate with volume responsiveness, but demonstration of abnormally high pressures with a restrictive filling pattern should signal caution in volume resuscitation. Static parameters

33. Indicators of severe hypovolemia in the critically ill: Hyperkinetic LV (in the presence of a normal RV) with end-systolic cavity obliteration LV end-diastolic area <5.5 cm 2 /m 2  BSA Small IVC (<10 mm) with inspiratory collapse (spontaneously breathing patients) Small IVC at end-expiration with variable respiratory change (mechanically ventilated patients).

34. Dynamic parameters Passive leg raising has been proposed to predict fluid responsiveness in spontaneously breathing patients Sensitivity and specificity are relatively low Confounding factors (intra-abdominal pressure, hypovolemia, arrhythmia) probably limit its usefulness in the ICU population. Respiratory variations in VTI may be used as an index of fluid responsiveness. Respiratory variation in SVC and IVC dimensions have been proposed to predict fluid responsiveness.

35. An IVC distensibility index (maximum–minimum/minimum) >18% (12% normalised to mean value) has been suggested to predict a significant increase in SV in response to fluid challenge. In contrast, a high SVC collapsibility index (maximum–minimum/maximum) >36% predicts a positive response to volume expansion (≥15% increase in SV) with sensitivity 90% and specificity 100%. Prerequisite for interpreting dynamic volume responsiveness: Sinus rhythm fully mechanically ventilated, with no spontaneous breathing effort. Further, the effects of lung protective ventilatory strategies may lead to false-negative values false-positive results may be seen in patients with RV disease.

36. Echocardiography in specific scenarios: ICU echocardiographer must know the potential pitfalls and coexisting pathologies in order to make a relevant assessment. Myocardial ischaemia /infarction: Echocardiography is included in the universal definition of myocardial infarction (MI), and suspicion of a mechanical complication of MI is a class IA indication for echocardiography. Extent of infarction/ ischaemia should be demonstrated and complications (MR, ventricular septal rupture (VSR)/cardiac rupture/RV infarction) actively excluded.

37. Acute cor pulmonale : Sudden severe increase in RV afterload resulting in acute RV dilatation and failure. Major causes: acute pulmonary embolism and ARDS. Pulmonary embolism (PE) Echocardiography provides only indirect signs of PE: Pulmonary hypertension signs of RV systolic ( septal dyskinesia ) & diastolic overload RV free wall hypokinesia moderate–severe TR. Pre-existing pulmonary hypertension is suggested by RV hypertrophy and PASP > 60 mmHg.

38. Hypoxemia Diagnosis and management of hypoxemic patients on the ICU Establishing the differential diagnosis ( cardiogenic vs non-cardiac) Assessment of secondary effects of pulmonary pathology on cardiac performance Diagnosis of a low CO state and/or diagnosis of anatomical shunt ( intracardiac or intrapulmonary).

39. Many ICU factors increase right-sided pressures, leading to right–left intracardiac shunting across an atrial septal defect/patent foramen ovale . Intrapulmonary shunts are independent of right-sided pressure, and have been described in ARDS, pneumonia, thoracic trauma and hepatic cirrhosis. Diagnosis depends on a positive agitated saline contrast study

40. Weaning from mechanical ventilation Discontinuation of positive-pressure ventilation increases LV afterload and preload, and significantly increases the rate–pressure product. In patients with cardiac disease; mismatch of the dynamic changes leads: increased work, leading to rising LAP, pulmonary edema, and/or RV dysfunction. A baseline echocardiogram should be performed at the start of the weaning trial, and evidence of inotropy , lusitropy , chronotropy (negative/positive), preload and afterload mismatch should be actively sought. Evidence of increasing LAP, myocardial ischaemia , decrease in LV/RV global function and/or worsening atrioventricular valvular regurgitation suggests a cardiac contribution to failure to wean.

41. Sepsis syndromes Echocardiography plays a key role in the management of the septic ICU patient by guiding haemodynamic management and excluding cardiac causes for sepsis. Sepsis-related LV dysfunction is well recognised , with global and regional wall motion abnormalities RV dysfunction develops either in isolation or associated with LV dysfunction. Echocardiography may reveal a cardiac source of sepsis related to either native/prosthetic valve infection or indwelling catheters/implanted devices.

42. The diagnosis of endocarditis is made on the basis of a well-established set of diagnostic criteria, of which echocardiography is one of the major factors. Three echocardiographic findings are important Mobile echo-dense mass( es ) attached to valvular /mural endocardium /implanted material Fistulae/abscess formation, and/or new disruption/dehiscence of a prosthetic valve. TOE has a higher sensitivity and specificity, and is mandated where prosthetic valve endocarditis is suspected, to identify major complications and guide surgical planning.

43. Chest trauma: Good comprehensive study should be performed to diagnose/exclude: pericardial/pleural collections Aortic and mitral valve disruption Aortic disruption VSR Coronary artery disruption ( ischaemia and/or fistulae) myocardial contusion.

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