Terlipressin versus norepinephrine to prevent milrinone-induced systemic vascular hypotension in cardiac surgery patient with pulmonary hypertension

Introduction: Milrinone at inotropic doses requires the addition of a vasoconstrictive drug. We hypothesized that terlipressin use could selectively recover the systemic vascular hypotension induced by milrinone without increasing the pulmonary vascular resistance (PVR) and mean pulmonary artery pressure (MPAP) as norepinephrine in cardiac surgery patients. Patients and Methods: Patients with pulmonary hypertension were enrolled in this study. At the start of rewarming a milrinone 25 μg/kg bolus over 10 min followed by infusion at the rate of 0.25 μg/kg/min. Just after the loading dose of milrinone, the patients were randomized to receive norepinephrine infusion at a dose of 0.1 μg/kg/min (norepinephrine group) or terlipressin infusion at a dose of 2 μg/kg/h (terlipressin group). Heart rate, mean arterial blood pressure (MAP), central venous pressure, MPAP, systemic vascular resistance (SVR), PVR, cardiac output were measured after induction of anesthesia, after loading dose of milrinone, during skin closure, and in the intensive care unit till 24 h. Results: Milrinone decreased MAP (from 79.56 ± 4.5 to 55.21 ± 2.1 and from 78.46 ± 3.3 to 54.11 ± 1.1) and decreased the MPAP (from 59.5 ± 3.5 to 25.4 ± 2.6 and from 61.3 ± 5.2 to 25.1 ± 2.3) in both groups. After norepinephrine, there was an increase in the MAP which is comparable to terlipressin group (P > 0.05). Terlipressin group shows a significant lower MPAP than norepinephrine group (24.5 ± 1.4 at skin closure vs. 43.3 ± 2.1, than 20.3 ± 2.1 at 24 h vs. 39.8 ± 3.8 postoperatively). There is a comparable increase in the SVR in both group, PVR showed a significant increase in the norepinephrine group compared to the terlipressin group (240.5 ± 23 vs. 140.6 ± 13 at skin closure than 190.3 ± 32 vs. 120.3 ± 10 at 24 h postoperatively). Conclusion: The use of terlipressin after milrinone will reverse systemic hypotension with lesser effect on the pulmonary artery pressure.

Rol del ecocardiograma en el estudio de la hipertensión arterial pulmonar / Role of echocardiography in the study of pulmonary arterial hypertension

La presencia de una presión arterial pulmonar media >25 mmHg en reposo y >30 mmHg en ejercicio, con una presión en cuña igual o menor de 15 mmHg y una resistencia vascular pulmonar >3 mmHg /L/ min (Uds. Wood) condiciona una entidad clínica heterogenea denominada hipertensión arterial pulmonar que tiene un amplio rango de causas o enfermedades que llevan a cambios estructurales de las pequeñas arterias pulmonares ocasionando un aumento progresivo de la presión arterial pulmonar y de la resistensia vascular pulmonar, produciendo finalmente una sobrecarga del ventrículo derecho, insuficiencia cardíaca y muerte. Es una entidad clínica con síntomas muy inespecíficos en sus etapas más tempranas y se necesita un buen criterio clínico para llegar a su diagnóstico más rápidamente. En este sentido es que adquiere valor el uso de la ecocardiografía, método que permitirá o solo cuantificar los valores de presión arterial pulmonar, sino también determinar la causa del problema, una adecuada evaluación anatómica y funcional del lecho pulmonar y de las cavidades derechas del corazón, predecir el pronostico de estos pacientes y vigilar el efecto terapéutico de tratamientos muy específicos al ayudar a detectar estados preclínicos de la enfermedad. Revisamos la utilidad y el papel del ecocardiograma en el estudio de la hipertensión arterial pulmonar.

The presence of Medium Arterial Pulmonary Pressure >25 mmHg at rest or >30mmHg during exercise associated with a wedge pulmonary pressure equal or less than 15mmHg, and a Pulmonary Vascular Resistance > 3 mmHg/L/min (Wood units) entails a heterogeneous clinical entity known as Pulmonary Arterial Hipertension which has a very wide spectrum of causes or diseases which produce estructural changes in the walls of the small pulmonary arteries causing a progressive increase of the arterial pulmonary pressure as well as the pulmonary vascular resistence, ultimately producing right ventricular overload, heart failure and death. It is a clinical entitywith very unspecific symptoms at the early stages. Wich makes the physician´s good clinical criteria needed to diagnose itsooner. In this way comes to great value the use of echocardiography, method that would allow not only to measure the arterial pulmonary pressure but would help to carify the cause of the disease, getting an adequate anatomical and funtional evaluation of the pulmonary bed and right heart chambers, predict the outcome in these patients by detecting pre-clinic stages of the disease. We reviewed the utility and role of the Echocardiogram in the study of Pulmonary Arterial Hypertension.

Changes of the serum myocardial enzymes in patients with acute pulmonary thromboembolism / 中华急诊医学杂志

Objective To explore the changes of the serurn cardiac enzymes in patients with acute massive pulmonary thromboembolosm(PIE),sub-massive PTE and non-massive FIE between pre-therapy and past-therapy and its relationship.Method The prospective multi-centres trial included 519 patients with confirmed PTE from 24 joint hospitals in Beijing,consisting of 54 massive FIE,195 sub-massive PTE and 270 non-massive PIE.Thrombolytic treatment was used in massive and sub-massive PTE patients with employment of urokinase and recombinant tissue plasminogen activator(rt-PA),and anti-coagulative therapy with unfractionated heparin and low molecular heparin was used in non-massive PTE.Results(1)The values of serum CPK and LDH in massive PTE patients before therapeutical intervention were obfiously higher than those in sub-massive and non-massive PTE patients(P<0.01);(2)Of 45 patients with high pulmonary pressure,24(54.4%)patients had high serum LDH(P<0.01).Of 169 patients with right ventrieular dysfunction,68(40.2%)ones has high serum LDH(P=0.049).Of 48 patients suffered from poor prognosis,15(30.8%)ones had high serum.LDH(P=0.039).Conclusions ①The vMues of serum CPK and LDH in acute PTE patients increase without elevation of CK-MB.②Serum LDH associates with pulmonary presure,right ventrieular function and prognosis.