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A Simplified Stepwise Approach to Echo Guidance during Percutaneous Mitral Valve Repair
Published on: October 16, 2021
Right Ventricular Response to Hypercapnia After Mitral Valve Repair: A Hemodynamic Assessment
Markus L J Tujunen1,2, Juha Lahti2,3, Heikki Kiiski1,2
1Department of Intensive Care, Tampere University Hospital, Tampere, Finland.
Background:
Right ventricular (RV) failure is a serious complication after cardiac surgery. Postoperative hypercapnic acidosis can increase pulmonary arterial pressure (PAP) that can lead to RV dysfunction. We aimed to investigate whether hypoventilation-induced hypercapnic acidosis leads to increased PAP levels and detectable changes in RV dimensions and function in postoperative cardiac surgery patients.
Methods:
A prospective open single-center interventional cohort study was conducted on postoperative elective mitral valve prolapse repair surgery patients. Hemodynamically stable patients were studied during mechanical ventilation in the recovery room. We performed pulmonary arterial catheter (PAC) measurements and comprehensive transesophageal echocardiographic (TEE) assessment of the RV. Measurements were made in normocapnia (target PaCO2 5 kPa) and in hypoventilation induced hypercapnia (target PaCO2 7.5 kPa). A paired t-test was used to compare the measured differences in the values under normo- and hypercapnia.
Results:
Altogether, 20 patients were included in the study. We achieved a significant (p < 0.05) difference both in PaCO2 levels; mean 5.0 kPa (0.3) SD versus 7.8 kPa (0.4) and in pH values; mean 7.40 (0.03) versus 7.24 (0.03). PAP-values measured from the PAC significantly increased (p < 0.05) in hypercapnia. Systolic pulmonary pressure rose from mean 30.2 mmHg (8.4) to 44.2 mmHg (9.3). Pulmonary vascular resistance was unchanged. In hypercapnic acidosis, we noticed a hyperdynamic state with significantly (p < 0.05) elevated cardiac output (mean 4.1 L/min [0.9] vs. 5.5 L/min [1.3]) and decreased systemic vascular resistance (mean 1402.2 dynes/s/cm-5 [364.8] vs. 927.7 dynes/s/cm-5 [260.3]). In the TEE study of the RV, increased PAP-levels didn't cause detectable structural or functional changes indicating RV dysfunction or failure. Pulmonary arterial velocity time integral rose significantly (p < 0.05) from mean 13.0 cm (2.7) to 15.1 cm (3.4) associated with the hyperdynamic state.
Conclusions:
In postoperative mitral valve repair surgery patients, hypercapnic acidosis caused increased PAP values measured from the PAC. The TEE study did not detect significant structural or functional changes in the RV despite the increase in PAP. From our findings, we can speculate that it would be possible to detect increased PAP with PAC earlier than by waiting for apparent TEE changes in RV function.
Trial Registration:
Clinical trial number: NCT02757573, Principal investigator: Kati Järvelä, Date of registration: April 20, 2016. https://clinicaltrials.gov/study/NCT02757573.
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