A continuous infusion of furosemide was started, and in an attempt to reduce RV afterload, epoprostenol (60 µg) and milrinone (4 mg) were administered via an ultrasonic nebulizer attached to the inspiratory limb of the ventilator as previously described.2
In the next hour, hemodynamic support was quickly tapered down (Figure 2). Focused TTE performed 45 minutes after the end of nebulization revealed normalization of PV flow which was now nonpulsatile throughout the cardiac cycle (Supplemental Digital Content 2, Video 2, http://links.lww.com/AACR/A110), although the IVC was still dilated and without respiratory variation and the RV still dilated and diffusely hypokinetic. As compared to before nebulization, PAP was now lower at 30/14 mm Hg and cardiac index was unchanged at 1.83 L/min/m2 despite a significant reduction in epinephrine and norepinephrine infusion rate. Urine output began to rise. Administration of nebulized epoprostenol and milrinone was repeated 2 hours later. At 6 hours postoperatively, the patient was awakened and his trachea was extubated, further reducing right heart afterload by restoring spontaneous breathing and negative intrathoracic pressure.
Vasopressor support was rapidly weaned off and stopped 12 hours after ICU admission, and the intra-aortic balloon pump was removed. At that time, PAP was 20/10 mm Hg and the MAP/mean PAP ratio had risen to 4.6. Urine output was adequate without furosemide infusion, and creatinine levels were only mildly elevated as compared to preoperative values (83 vs 108 µmol/L) and did not rise further. Twenty-four hours after admission, repeat focused TTE revealed mildly phasic PV and normal IVC (Figure 1B and Supplemental Digital Content 3, Video 3, http://links.lww.com/AACR/A111). The patient was discharged from the ICU 36 hours after admission with a total net fluid balance of −2.4 L, and he was discharged home uneventfully on postoperative day 6.
A 49-year-old man had an unwitnessed out-of-hospital cardiac arrest. Initial rhythm was pulseless ventricular tachycardia. Emergency medical services provided prolonged resuscitation including cardioversion, which eventually resulted in return of spontaneous circulation after 43 minutes of resuscitation. On admission at a peripheral hospital, the electrocardiogram showed inferior ST-segment elevation myocardial infarction, for which thrombolytic therapy was given. Overt cardiogenic shock developed, and the patient received more than 6 L of crystalloids during the initial resuscitation efforts. The patient was found to be unresponsive to painful stimuli. Anoxic brain death was diagnosed the next day and confirmed on arrival at our hospital to which the patient was transferred for stabilization before potential organ donation.
On arrival at our center, 48 hours after the initial cardiac arrest, the patient needed significant hemodynamic support (dobutamine 15 µg/kg/min, vasopressin 2.4 U/h, and epinephrine 1.2 µg/kg/min) and was severely hypoxemic (Sao2 91% at an Fio2 of 1.0 during controlled ventilation with positive end-expiratory pressure 10 cm H2O) and anuric. Cardiac ultrasonography showed severe RV dilation and hypokinesis with a normal LV and a highly pulsatile portal venous flow (Figure 3). Liver enzymes and creatinine were elevated and still rising 48 hours after the initial cardiac arrest (alanine aminotransferase [ALT] 711 U/L, bilirubin 31 µmol/L, creatinine serum concentration 406 µmol/L).
Epoprostenol (60 µg) and milrinone (4 mg) were simultaneously administered by nebulization through the inspiratory limb of the ventilator. One hour later, central venous pressure had decreased from 17 to 9 cm H2O, and flow in the PV showed reduced pulsatility (Figure 3B).
Continuous venovenous hemofiltration was instituted, with a resultant net fluid balance of −2.8 L in 12 hours. After these interventions, ultrasonography showed a moderate improvement in RV contractility and reduced RV dilation. The flow in the PV was now phasic without significant pulsatility (Figure 3C). Hemodynamic support was tapered down (dobutamine 2.5 µg/kg/min, vasopressin 2.4 U/h, and norepinephrine 0.05 µg/min). The liver enzyme levels declined the next day (ALT 170 U/L and bilirubin 17.2 µmol/L). Approximately 48 hours after transfer to our institution, liver harvesting and subsequent transplantation were successfully performed.
These cases highlight how point-of-care ultrasonography can be used to detect changes in PV pulsatility as a surrogate of venous congestion due to severe RV failure and, in conjunction with other echocardiographic and clinical parameters, help identify patients who might benefit from aggressive diuresis and RV afterload reduction. We also describe the combined administration of inhaled epoprostenol and milrinone in patients with severe RV failure and are the first to report their effect on PV pulsatility, which interestingly illustrates this finding’s significance as a marker of RV function and load adaptability.
RV failure results in a decrease in cardiac output and systemic perfusion. Concomitantly, the increase in right heart filling pressure induces venous congestion and globally increases outflow pressures of vital organs such as the brain, kidney, and liver, thus further reducing tissue perfusion.1,3 In such situations, administration of intravenous fluids will only exacerbate the phenomenon. This mechanism could partly explain why excessive fluid balance and elevated right atrial pressure have been associated with increased mortality in critically ill patients.4
Flow in the PV is normally hepatopetal (directed toward the liver) and exhibits small amplitude phasicity (typically less than 30%), reflecting partial transmission of hepatic venous waves through hepatic sinusoids.5 During RV failure, higher right heart filling pressures are transmitted back to the hepatic veins and sinusoids, which reduce the compliance of these vessels, thus further facilitating retrograde transmission of pulsatile pressure waves from the right atrium to the PV. The presence of PV pulsatility is defined as a pulsatility index above 50%, where the pulsatility index is the difference between peak flow velocity and through flow velocity divided by peak flow velocity (V1 − V2)/V1 (Figure 3). This finding has been clearly associated with elevated right atrial pressure, tricuspid regurgitation, and RV failure5 and has also been described in cirrhotic and normal thin (body mass index <20 kg/m2) patients, probably reflecting low abdominal and hepatic acoustical damping.6 Eventually, when RV failure progresses and right atrial pressure exceeds portal venous pressure, partial or complete reversal of flow (hepatofugal) can occur,5 as outlined in case 1. This finding reflects a severe venous congestion state that can be detrimental not only in the PV tributaries but also in other important organs such as the brain, gut,7 or kidney.3,8
Conceptually, in the right clinical context, PV pulsatility therefore represents the indirect consequence of RV failure (whether systolic or diastolic), rather than direct signs of systolic dysfunction. In a recent series of 14 cardiac surgical patients with fluid overload and PV pulsatility, only 4 patients had direct echocardiographic signs of RV failure (hypokinesis and/or dilation).9 Importantly, adequate bedside visualization of the portal flow is possible in virtually all patients (even in those with poor quality echocardiographic views) because of the location of the PV in the echogenic liver parenchyma.9 This can prove the significant value when assessing the hemodynamic status of the unstable surgical patient, for instance, as an adjunct to other clinical and echocardiographic parameters (Figure 4).
In both patients, as PV pulsatility was associated with other signs of RV failure, it prompted us to induce pulmonary vasodilation using a combination of inhaled epoprostenol and inhaled milrinone. Because these 2 inhaled agents act on pulmonary vascular tone by 2 different mechanisms, combined administration offers additive effects and was associated with significant improvement in hemodynamic parameters and reduction in vasoactive support during cardiac surgery.2,11
In summary, these 2 cases describe the assessment of PV flow with point-of-care ultrasound to detect signs of elevated RV filling pressures and to monitor response to therapy. It also outlines the use and effect of combined inhaled epoprostenol and milrinone, which resulted in rapid reduction of fluid overload and splanchnic congestion with resolution of PV pulsatility. Further research is warranted to further explore the role of this therapy as well as the role of PV pulsatility in the evaluation of the patient with suspected RV failure.
Name: Jan-Alexis Tremblay, MD.
Contribution: This author helped collect the data and write the manuscript.
Name: William Beaubien-Souligny, MD.
Contribution: This author helped revise the manuscript.
Name: Mahsa Elmi-Sarabi, MSc.
Contribution: This author helped revise the manuscript.
Name: Georges Desjardins, MD.
Contribution: This author helped revise the manuscript.
Name: André Y. Denault, MD, PhD.
Contribution: This author helped instigate the report and revise the manuscript.
This manuscript was handled by: Hans-Joachim Priebe, MD, FRCA, FCAI.
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