Cath-Lab Hemodynamics – I : Pressure tracings in the diseased heart

1. Cath-Lab Hemodynamics – I :Pressure tracings in the diseased heart Sriram Rajagopal, Department of Cardiology, Southern Railway Headquarters Hospital, Perambur, Chennai.

2. Cath Lab Hemodynamics - I Pressure tracing interpretation – some general principles: • Pathophysiology of the underlying primary lesion and of compensatory mechanisms. • Technical aspects of pressure recording need close attention – e.g. scale on which pressures recorded, proper zero reference, presence of artifacts etc. • Information from the pressure tracing has to be interpreted in the context of other information such as clinical setting, flow data, time intervals, resistance etc.

3. Cath Lab Hemodynamics – I Pressure tracing interpretation – some general principles: • Heart is an electromechanical device – always correlate pressure information with electrical events as shown in the ECG trace. • Interpret changes in the tracing due to modifying factors such as heart rate, contractility, changes in preload or afterload, effects of drugs or maneuvers etc. • Practice , practice and practice – keep your eyes ( and mind) open and alert !

4. Cath Lab Hemodynamics - I Valvular heart disease : • Mitral valve disease • Aortic valve disease • Pulmonary and tricuspid valve disease

5. Cath Lab Hemodynamics - I Mitral stenosis : LA and LV pressure traces : How severe is the stenosis? Mild Moderate Severe 50 mmHg

6. Cath Lab Hemodynamics - I Mitral stenosis : LA and LV pressure traces : How severe is this stenosis? Mild Moderate Severe 50 mmHg

7. Cath Lab Hemodynamics - I

8. Cath Lab Hemodynamics - I Valve Stenosis – general principles : • Presence of a pressure gradient • But never interpret gradient data alone • If flow rate ( volume of flow per unit time ) doubles the gradient increases by a factor of four (for a given valve orifice size) • If valve area decreases by half (assuming constant flow) gradient increases by factor of four

9. Evaluation of Mitral Stenosis- Change in heart rate Baseline Atropine

10. Cath Lab Hemodynamics - I Mitral stenosis – effects of stenosis

11. Mitral stenosis – contd. PRE POST More than just a gradient !

12. Mitral regurgitation Cath Lab Hemodynamics - I

13. Mitral Regurgitation Acute mitral regurgitation – no time for LA to accomodate

14. Mitral regurgitation – contd. Left ventricular and pulmonary wedge pressures B A

15. Mitral regurgitation – contd. B A Severe MR with tall v waves . After nitroprusside infusion, LV systolic pressure and after-load fall, with fall in “v” wave height .(Note patient has AF).

16. Cath Lab Hemodynamics - I Aortic stenosis

17. Cath Lab Hemodynamics - I AS – peak to peak vs peak instantaneous gradient

18. Cath Lab Hemodynamics - I LV and Arterial pressure traces Comparison of LV- Asc. Ao. vs LV- FA trace

19. LV to Aorta pullback trace Left ventricular (LV) and femoral arterial (FA) traces during left heart hemodynamic study.

20. Hemodynamic Quiz Increase in femoral arterial pressure by around 20 mm Hg. Carabello’s sign - seen only in patients with critical AS ( AVA < 0.6 sq. cm.) Carabello BA. Am J Cardiol 44 :424;1979

21. Cath Lab Hemodynamics - I Technical aspects – catheter position

22. Cath Lab Hemodynamics - I Aortic regurgitation

23. Cath Lab Hemodynamics - I Chronic vs Acute aortic regurgitation – Importance of compensatory mechanisms

24. Cath Lab Hemodynamics - I Severe TR – “Ventricularization” of RA trace

25. Acute severe TR What is your interpretation of this tracing?

26. RVEDP and LVEDP elevated with almost identical pressures throughout diastole. RV systolic pressure minimally raised, so high RVEDP is not due to PAH. Restrictive physiology due to restraining effect of pericardium with acute volume overload of RV.

27. Cath Lab Hemodynamics - I Constrictive Pericarditis

28. Cath Lab Hemodynamics - I Inspiratory rise in RA pressure Note phase lag in PCWP

29. Cath Lab Hemodynamics - I Ventricular interdependence in CP Contrast with restrictive cardiomyopathy

30. Cath Lab Hemodynamics - I Hypertrophic Obstructive Cardiomyopathy

31. LV to Aorta pullback trace HOCM – LV cavity to outflow gradient. No valvar gradient “Spike and dome” pattern rules out discrete subaortic stenosis

32. HOCM HOCM showing fall in pulse pressure in the post-ectopic beat ( Brockenbrough’s sign )

33. HOCM Spontaneous change from nodal to sinus rhythm in patient with HOCM. With restoration of sinus there is an increase in LV stroke volume ( seen on LBA trace) and fall in gradient.

34. Cath Lab Hemodynamics - I HCM – provocation of gradient

35. Cath Lab Hemodynamics - I HCM – effects of drugs and relation of MR to gradient

36. Effects of Drugs IV infusion of Milrinone - Positive and negative dp/dt increased without increase in arterial pressure and with decline in preload , suggesting positive inotropic effect. LV minimum pressure lower.

37. Thank you for your kind attention !

38. Cath Lab Hemodynamics - I Inspiratory rise in RA pressure Note phase lag in PCWP