Effect of pulmonary hypertension on hemodynamic monitoring

1. Effect of pulmonary hypertension on hemodynamic monitoring Richard Siebert Physician / critical care fellow Dept. Critical Care : Steve Biko Academic Hospital/lcm hospital

3. Why hemodynamic monitoring in ICU? • We are interested in maintaining and optimising organ perfusion. • When hemodynamics are abnormally high or low our goal of organ perfusion may be compromised. • We need to monitor trends and asses response to treatment

4. Hemodynamic monitoring is essential in patients with pulmonary hypertension but... • “ Traditionally “ used monitoring methods like CVP , Pulmonary artery catheters , thermo-dilution methods , arterial contour derived monitoring , bioimpendance and have many limitations we need too consider before interpreting the data and changing our management strategy. • Positive pressure mechanical ventilation causes increase RV afterload and decreased preload in inspiration – the effect is exacerbated with RV dysfunction found in PH leading to an increase in PPV.

5. Clinical scenario • 55 year old 70kg patient initially admitted to ICU after multi-trauma suddenly becomes hypotensive with MAP of 55mmHg and heart rate 120/min –has been mechanical ventilation - day 5 in ICU. His Hb is unchanged and his PaO2/Fi ratio deteriorates ? Our reflex action is to give fluids ? • On hemodynamic monitoring his PPV is 20% and CI 2.5 , despite 500ml RL bolus of crystalloid/colloid his PVV / CI and hemodynamics do not improve ? ????

6. Effects of pulmonary hypertension on commonly measured haemodynamic parameters and interventions • CVP => Elevation large CV waves • Elevated pulmonary artery pressures ( > 25mmHg) , • Normal or elevated PAOP : necessary to differentiate between PH and PAH elevated RV pressures ,decreased CO with thermo-dilution if severe TR • Elevated PPV and SVV in mechanically ventilated patients with RV dysfunction– elevation in PH do not necessarily imply fluid responsiveness. • Modalities using thermo-dilution may be affected by severe TR leading to decreased CO.

7. Pulmonary hypertension diagnosis : • Pulmonary artery catheter has been the traditional invasive method for diagnosing PH • Point of care cardiac echocardiography is the current non-invasive way to determine pulmonary pressures and RV function and identify patients that may be have false positive pre-load sensitive results from PPV and SVV as well as underlying cardiac causes for hemodynamic compromise.

8. PAH Effect on CVP • Variable effect depending to a large extent on the degree of tricuspid regurgitation Large CV wave. • Although CVP may exceed PAOP in PH it is not a predictor of fluid responsiveness ? • Do you still measure it ?????

9. Effect of pulmonary hypertension on PAC • Severe tricuspid regurgitation on PH makes placement of pulmonary artery catheter is more difficult. • Thermodilution methods of determining CO can be affected by severe tricuspid regurgitation.

10. Passive leg raising • Passive leg raising as dynamic modality to evaluate fluid responsiveness has limited value when RV is at the flat part of the frank starling curve although if the right ventricle is at the early portion of the curve there may be an increase in the SV/RV function and at least if the patient deteriorates it may be reversible when using PLR

11. Effect of PAH on echocardiographic monitoring • RV dilatation , function and derived pressures are easily measured and other cardiac pathology ie LV dysfunction , valvular lesions or pericardial effusions can be seen.

12. PH effects on cardiac echo parameters • RV distension and intraventricular septum deviation and LV shape change • RV function : progressive deterioration in function can be measured by TAPSE ( tricuspid annular planar systolic excursion )and the tissue dopplerinterger • Progressive tricuspid regurgitation occurs as PH progresses and improves with successful treatment • Pulmonary artery pressures van be derived with Doppler

13. TAPSE

14. Systolic velocity of tricuspid annular motion to predict PH with elevated PPV who are non-responder to fluid challenge

15. Monitoring fluid therapy • Fluid overload or volume depletion can lead to rapid deterioration in RV function and cardiac output in patient with PH • PPV and SVV values suggesting fluid responsiveness are often false positive in patients with RV dysfunction – this can lead to an inappropriate fluid challenge . • Poor response to fluid challenge in patients with elevated PPV or SVV suggests pulmonary hypertension and should prompt further assessment by echocardiography for evidence of PH

16. Monitoring the effect of treatment • Combination of invasive (PAC) and non-invasive monitoring (Echo) are often needed to follow the effect of intervention when fluid administration , diuretics , vasopressors, inotropes or pulmonary vasodilators are used. • Current commonly used hemodynamic parameter like SVV and PVV van be elevated in PH and failure or deterioration following fluid bolus treatment should prompt echocardiographic search for PH and underlying cause for it. • Hemodynamic monitoring with serial echo can reveal improvement or deterioration after specific measure have been instituted.

17. In Summary • Pulmonary hypertension reveals the limits of most certain currently used hemodynamic monitoring . • Point of care cardiac echocardiography is essential for diagnosis , monitoring and treatment. • Critical care focused cardiac (lung) echocardiography skills are essential for hands-on Intensivists. • PAC still has a role in PH diagnosis and monitoring in the ICU , the risk of complications may not as high as commonly believed ( 1.1%). • When –IF fluid boluses are given in patients with PH “micro boluses “ may be safer and the effect needs to be monitoredclosely.