Echokardiografické vyšetření v intenzivní medicíně Martin Balík KARIM VFN a 1.LF UK Praha
Ultrazvukový přístroj na ICU
UZ cílená kanylace cév Vyšetření žil a dg.trombóz Periferní nervové blokády Hrudní sonografie a dých. cesty Vyšetření peritonální dutiny a retroperitonea Vyšetření u těžkých traumat Echokardiografie Hrudní sonografie Traumata Transkraniální doppler
Echokardiografie a hemodynamika
Iniciální TTE může být suficientní až u 64% na IPPV Přibližně 6-36% potřebuje TEE pro nekvalitní TTE zobrazení TEE primárně u - sepse nejasné etiol., endokarditidy - zdroj embolizací - aorta - srdeční zkrat - po kardiochirurg. výkonech - chlopenní protézy - donor orgánů Relativní kontraindikace: krvácení z úst a horního GIT, esofageální a žal. chir., varixy, spinální trauma nebo nestabilita, NJS Komplikace TEE: pod 0.1%
Echokardiografie vs invazivní postupy
systolická funkce, poruchy kontraktility diastolická funkce chlopenní vady, vegetace patologie aorty perikard septální vady pleurální výpotky, mediastinum rychlejší, méně invazivní téměř nulový spotřební materiál vs cena přístroje a servisu
kontinuální monitoring tlak v plicnici přesnější měření CO SvO2 cena PAC cca 30007500 Kc dle typu
Hemodynamické vyšetření
Preload Kontraktilita globální a segm. Diastolická funkce Afterload Chlopně Srdeční výdej Pravé srdce a plicnice Aorta Perikard Pleura
Proč by měl intenzivista umět echokardiografii Znalost hemodynamiky, RTG, laboratoře a anamnézy umožňuje okamžitou aplikaci výsledků TTE/TEE Komplexnější a bez časové prodlevy Porembka DT: Crit Care Med 2007, 35: S414-S430 Benefit okamžité, neinvazivní a kompletní diagnostiky oběhu Zavádějící informace z invazivních postupů (PAC) u polytraumat, septického šoku a post KPCR Poelaert JI, Chest 1995, 107: 774-779 Burns JP, J of Trauma 2005, 59: 36-40 Osman, Crit Care Med 2007, 35: 64-67
Importance of SV estimation
Major determinant of
CO DO2
Heart-lung interactions related to changes of SV SV in
LVOT (TTE, TEE) Desc. aorta (Oesophageal doppler)
CO = SV x HR (Harvey W 1628) SV (ml) = VTI (cm)*CSA(cm2)*cos&
(Darmon 1994; McLean, Huang 1997, Poelaert 1999)
Factors determining SV Optimizing preload is cornerstone of „low CO treatment“ !!!
SV
Normal
Failure
LVEDV
Echocardiographic doppler CO
„dynamic“ measure of systolic function – rather than „static“ LVEF Excelent correlation with PAC, mean diff. 0,200,89 l/min Limited by Ao valve disorders (AR/AS over 1st degree, LVOT access) SV in LVOT for continuity equation More accurate than classic thermodilution in 3rd degree TR (Balik M, et al: Intensive Care Med 2002) TR prevalence of 90% on IPPV
Do we need a CO assessment in shocked patient ?
and
and
Variables of SV determination – normal heart, IPPV
Hypovolaemia MUST be diagnosed/excluded as part of CO measurement SV adjustment for ventilatory cycle Volume responsiveness - VTI (SV) variation within ventilatory cycle SV and CO (DO2) as volumetric endpoints of volume resuscitation
When only preload and IPPV counts......
Capnography
Physiology
Inspirium:
RA and RVEDV increase (+20% end. insp.) LA and LV preload decrease SV, BPs and Pp decrease to -10%
Exspirium:
LA, LVEDV/LVEDP increase SV, BPs and Pp increase
Constant Vt, sinus rhythm
VTI variation: aortic VTI -18% predicts the response to fluid with sens. of 90% and spec. of 94% (Monnet X: Intensive Care Med 2005, 31: 11951201, Slama M: Am J Physiol Heart Circ Physiol 2002, 283: H1729-33) Mitral flow variation as predictor of the response to volume load (Lattik R: Anaesth Analg 2002, 94:1092-9)
VTI respiratory variations in sinus rhythm
VTI: Min. 3 measurements averaged in sinus rhythm
Variables of SV determination – real life
Preload Ventilatory cycle............plus following:
Supraventricular arrhythmias RV status LV status Pericardial reserve volume / pericard. pressure Variable tidal volume Negative inspiratory pressure (asthma)
VTI variations in atrial fibrillation
VTI: Min. 6 measurements averaged
(Dubrey SW: J Am Soc Echocardiogr 1997, 10: 67-71)
AF or/and Vt variation
PLR and LVOT VTI (TTE) + 12% predicts fluid responsiveness (Monnet X: Intensive Care Med 2008, 34: 659-63) PLR and SV + 12.5% (at least) predicts SV (TTE) + 15% after volume load with sensitivity of 77% and specificity of 100% (neither EDA changes nor mitral E/E´did, Lamia: Intensive Care Med 2007,33:1125-32)
Aggresive IPPV and/or right heart compromise
1.) Vt is major determinant of the increase of PVR (Vieillard-Baron A: J Appl Physiol 1999, Poelaert J: J Cardiothorac Vasc Anesth 1994) 2.) Leads to decrease of RVEF increase of RVEDV and RV dilatation 3.) Permanent increase of PVR leads to acute cor pulmonale: a.) RV dilatation (RVEDA/LVEDA>0.6) b.) paradoxic septal movement
Interventricular septum
Acute cor pulmonale
Chronic cor pulmonale
Normal movement of IV septum
ACP
CCP
4.) Increase of CVP decreases systemic preload 5.) altogether may produce decreased SV and CO pulsus paradoxus dDown Effect (Pp, BPs variation) 6.) Volumexpansion and decrease of collapsibility of IVC/SVC eliminates significant decrease of PAvti and SV (Viellard-Baron: Anesthesiology 2001; 95: 1083-8)
D-shape LV Normal LV
Subcostal 4C plane – IVC assessment
90°
IVC diameter (subcostal window) Otto C: Echocardiographic Evaluation of Left and Right Ventricular Systolic Function. In Otto CM (ed.) Textbook of Clinical Echocardiography, 2nd ed., Saunders 2000, p. 100-131.
IVC<1.5 cm, kolabuje v inspiriu RAP 0-5 mmHg IVC1.5-2.5cm,insp. kolaps>50% RAP 5-10 mmHg IVC1.5-2.5cm, insp.kolaps<50% RAP 10-15 mmHg IVC>2.5 cm, insp.kolaps <50%
RAP 15-20 mmHg
IVC dilatována, insp.konst.
RAP>20 mmHg
IVC change of -13% in inspirium predicts the PAvti response to volumexpansion with 94% specificity (Barbier C: Intensive Care Med 2004; 30: 1740-1746)
TEE - SVC
(approx 25-30% of venous return) Collapses in inspirium, index (CI) as a predictor of volume responsivness (Vieillard-Baron, Anesthesiology 2001, Intensive Care Med 2004 – false positive PPV due to RV dysfunction)
TVI of tricuspid ring
Mahjoub Y, Slama M: Crit Care Med 2009 PPV >12%, Sta cutoff 15 cm/s discriminated nonresponders (sens 91%, spec 83%)
Recruitment manoeuvers
Increase of EI (D2/D1)= RV pressure overload, risk of ACP Decrease of SVRV and LV preload may reduce SV and CO of more than 50% and MAP of 20% (Nielsen J: Intensive Care Med 2005)
Avoid lung overinflation (Vt !) in patient with RV dysfunction and decreased preload ECHO
IPPV in compromised left ventricle
1.) Increase of RVEDV decreases LV compliance (Pinsky MR: Intensive Care Med 1997) 2.) In left heart failure (decreased EFLV): decrease of LVEDV (preload) decrease of transmural ΔP (Pinsky MR: J Appl Physiol 1993) reduces LVESV (ESA, afterload) increases SV (Naughton MT: Circulation 1995) reversed pulsus paradoxus dUp effect (Pp, BPs variation)
Septic shock, NIDDM, BW 128 kg
CO calculations
CO= CSA x VTI x HR CO= CO= 3.14 x 1.152 x (16+20+22)/3 x 80 CO= 6480 ml CI 2.5-2.6 l/min.m2
Interpretation of VTI variation up to 22%: - dUp Effect in dCMP (sepsis related ?) most likely - mildly compromised RV (TAD 18 mm) - PSV, Vt 500-600 ml
Loss of pericardial reserve volume: Echo in tamponade
RV dimension and RH flows increase in inspirium RA filling limited to systole LV dimension and LH flows decrease in inspirium Distension of IVC/SVC during respiratory and cardiac cycle
Transmitral flow variation>25%
Tricuspid flow variation>25-40%
may be present on IPPV with NO pericardial effusion infusing fluid leads to reduction in respiratory variation
Pulse variation within ventilatory cycle – open chest, pericardium
PEEP reduces CO, SV, RVEDV and increases SVLV and SVRV variations in open and closed chest – experim. pigs (Kubitz JC: Eur J Cardiothorac Surg. 2006, 30:90-5) SVI correlates with PPV only in closed chest. SV and PPV variation correlate with LV and RV preload only under closed chest and pericardium (Rex S: Acta Anaesthesiol Scand 2007,51:1258-67) Sternotomy without effects on PPV. Cyclic changes of Vt not PEEP or Paw influences PPV in open chest (De Blasi: Acta Anaesthesiol Scand 2007,51:441-6)
Likely to have little effect unless chest or pericardial tamponade
Impact of ventilator setting
1.) No spontaneous ventilation - VC-IPPV, PC-IPPV, deep sedation (GA), paralysis for the study purposes 2.) Recruitment manoeuvers – similar to 1.), extreme Paw, Ppl X spontaneous breathing activity - VC/PC-SIMV, BIPAP, APRV, PSV, CPAP......most of ICU patients
Methodology of papers on HL interactions
Sedation, paralysis, spontanneous breathing activity Modes of IPPV
Echocardiographic parameters of preload • 2D parameters • LVEDA • Interatrial septum • IVC
• Doppler parameters • Transmitral PW Doppler • Tissue PW Doppler of mitral ring (lateral)
• Pulmonary vein PW Doppler • CW Doppler estimate of LAP / LVEDP in MR, AR, ASD • SV variation 41
Interpretation of VTI (SV) variation
LV status – dUp effect – false positive for „hypovolemia“ in LV failure (Reuter 2003, Pinsky M 2008) RV status – cor pulmonale – dDown effect - false positive for „hypovolemia“ (Vieillard-Baron A 2003, Slama 2009) Pericardium – tamponade, constriction – false positive for „hypovolemia“ Impact of Vt, variation or constant ?, false negative for „euvolemia“ in Vt<6 ml/kg, false positive for „hypovolaemia“ in Vt>/=10ml/kg (De Backer D 2005, Huang CC 2008) Number of resp. cycles – ideally 5 or more (Pinsky 2008) Dynamic changes required (PLR) in spontaneous ventilation and /or in AF/SV arrhythmias (Monnet X 2007-8)
