CASE HISTORY
A 6-year-old male underwent tissue-aortic valve replacement (AVR). Postoperative, he required high inotropic support and high antibiotic support – his heart rate (HR) was 120/min and blood pressure was 90/60 mmHg. His transesophageal echocardiography - Echo report reveals:
OBSERVATIOBS ON TEE
The patient postoperatively showed the following:
Significant mitral regurgitation (MR) due to unrecognized mitral valve pathology [Figures 1 and 2]
High ante grade trans-mitral velocity due to MR [Figure 3]
High left ventricular outflow tract (LVOT) velocity due to LVOT obstruction precipitated by inotropes [Figure 4]
Stiffened tissue aortic leaflets with high gradients [Figures 3 and 5]
High cardiac output (CO) resulting from Septicemia.
Figure 1.
Mitral regurgitation
Figure 2.
Mitral inflow pattern
Figure 3.
High gradient across tissue aortic valve (transgastric view) Vmax: 390cm/s, VTI: 54.6 cm, MaxPG: 61 mmHg; Mean PG: 35.9 mmHg
Figure 4.
Left ventricular outflow tract gradients transgastric view
Figure 5.
Transesophageal echocardiography long axis view showing transprosthetic flow
What does these parameters convey?
Hemodynamic calculations from transesophageal echocardiography parameters
Stroke volume (SV) = LVOT area × LVOT velocity time integral (VTI) =3.46 × 28 = 96.88 ml
CO = HR × SV = 120 × 96.88 = 11.6 l/min
- Systemic vascular resistance (SVR) = 80 × (MAP-5)/CO = 448.3 dyne × s/cm5
- Clues 1 - Why so high a cardiac output?
- Clues 2 - Why such a low SVR?
Dilemma in postoperative period
“What is the most likely explanation of high CO with low SVR in immediate Postoperative period?”
DISCUSSION
Patient did not have transprosthetic obstruction because of the VTI ratio - LVOT/AO = 28/54.6 = 0.51. Significant transprosthetic obstruction is likely only if this VTI ratio is <0.30
Significant mitral pathology (either regurgitation or obstructive) is unlikely; since high flow velocities are observed across both mitral and aortic valves. These finding can easily be explained by high CO state
As depicted in Figure 5 the LVOT is wide open; thus significant LVOT narrowing can be excluded
Therefore, the most logical explanation is that the patient has SEPSIS, which could be due exacerbation of preexisting and unrecognized infection or acquired intraoperatively
The classical hemodynamics of septicemia are high CO with low SVR and failure to maintain adequate arterial pressure without the use of inotropes
Therefore colistin 2 million units were added to the existing antibiotic regimen (meropenam and targocid) - to which patient responded.
Postoperative course in ICU
His blood reports later shows:
High TLC: 18,000/dl (which later increased to 25,000). N-86 L-12 E-2.
High ESR: 60 mm/h.
Blood culture – Sterile (probably due to the preoperative use of antibiotics).
Patient was discharged after 2 weeks of hospital stay with normal pressure gradients across the tissue-AVR and normal velocities across the all cardiac valves.
CONCLUSION
Thus, the intelligent interpretation of noninvasively derived hemodynamic by transesophageal echocardiography could be extremely useful in the appropriate diagnosis and management of critically ill patients.
Footnotes
Source of Support: Nil
Conflict of Interest: None declared.