#ThePeoplesVentricle: Reduced TAPSE (expected post-cardiac surgery). Low RVEDV. Boarderline FAC and 3D RVEF. No septal shift.
E/e' 11. E< A. sPAP 30 mmHg. Pulmonary acceleration time 110ms. No valve dysfunction, no SAM. No pericardial fluids. SV 52 mL
Differential diagnosis for hypoperfusion (Low ScvO2, high PvaCO2): 1) Hypovolemia, 2) tampoande, 3) extracardiac constriction.
DDx 1) Hypovolemia: High PPV without RV failure. Arguments against hypovolemia: high CVP, waveform X < Y-descent, indicating relative hypervolemia and fluid intolerance.
DDx 2) Tamponade: High PPV, high CVP. Arguments against tamponade: Large Y-descent, which should not be present in tamponade. No obvious signs on echo (although focal tamponade can exist post-cardiac surgery.)
DDx 3) Extracardiac RV constriction (similar physiology to "constrictive pericarditis"): Large Y-descent, high CVP and high PPV. Possible causes: blood in mediastinum, w/o tamponade.
S. Magder: journals.sagepub.com/doi/abs/10.117…
I was not in charge of management, but how should one manage this?
PLR could confirm fluid responsiveness, but fluid intolerance and edema risk was high.
Perhaps extubation could improve venous return?
Does inotropes make sense?
I think the diagnosis in functional RV constriction/limitation. The patient was eventually extubated and had a complicated postoperative course.
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1⃣ Can MAPSE redefine "the hyperdynamic heart?
The term "hyperdynamic LV" - EF > 55% - is misleading. It has no relation to a hyperdyanmic circulation; SV/CO. Someone bleeding to death has a hyperdynamic heart, but the circulation is life-threatening hypodynamic.
2/n
MAPSE is cardiac motion, and defining the hyperDYNAMIC heart as good cardiac motion makes perfect sense. Recent geometrical analysis of cardiac pumping shows that MAPSE is the main determinant of SV. Fig from @mugander: tinyurl.com/mxbfmcyk
Why? 3/n