scholarly journals Perioperative Anesthesiological Management of Patients with Pulmonary Hypertension

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Jochen Gille ◽  
Hans-Jürgen Seyfarth ◽  
Stefan Gerlach ◽  
Michael Malcharek ◽  
Elke Czeslick ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Surgical Procedures ◽  
Blood Circulation ◽  
Nitrogen Monoxide ◽  
Postoperative Phase ◽  
Perioperative Morbidity ◽  
Pulmonary Vasodilation ◽  
Invasive Hemodynamic Monitoring ◽  
Intraoperative Management ◽  
Selective Pulmonary Vasodilation

Pulmonary hypertension is a major reason for elevated perioperative morbidity and mortality, even in noncardiac surgical procedures. Patients should be thoroughly prepared for the intervention and allowed plenty of time for consideration. All specialty units involved in treatment should play a role in these preparations. After selecting each of the suitable individual anesthetic and surgical procedures, intraoperative management should focus on avoiding all circumstances that could contribute to exacerbating pulmonary hypertension (hypoxemia, hypercapnia, acidosis, hypothermia, hypervolemia, and insufficientanesthesia and analgesia). Due to possible induction of hypotonic blood circulation, intravenous vasodilators (milrinone, dobutamine, prostacyclin, Na-nitroprusside, and nitroglycerine) should be administered with the greatest care. A method of treating elevations in pulmonary pressure with selective pulmonary vasodilation by inhalation should be available intraoperatively (iloprost, nitrogen monoxide, prostacyclin, and milrinone) in addition to invasive hemodynamic monitoring. During the postoperative phase, patients must be monitored continuously and receive sufficient analgesic therapy over an adequate period of time. All in all, perioperative management of patients with pulmonary hypertension presents an interdisciplinary challenge that requires the adequate involvement of anesthetists, surgeons, pulmonologists, and cardiologists alike.

Search for an animal model to investigate selective pulmonary vasodilation

2016 ◽  
Vol 51 (4) ◽  
pp. 376-387
Author(s):  
Bodil Petersen ◽  
Thilo Busch ◽  
Katharina Noreikat ◽  
Lorenz Homeister ◽  
Ralf Regenthal ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Animal Models ◽  
Vascular Tone ◽  
Acute Hypoxia ◽  
Haemodynamic Instability ◽  
Time Interval ◽  
Systemic Hypotension ◽  
Pulmonary Vasodilation ◽  
Selective Pulmonary Vasodilation

Pulmonary arterial hypertension is a life-threatening disease with a poor prognosis. Oral treatment with vasodilators is often limited by systemic hypotension. Inhalation of vasodilators offers the opportunity for selective pulmonary vasodilation. Testing selective pulmonary vasodilation by inhaled nitric oxide or alternative substances in animal models requires an increased pulmonary vascular tone. The aim of this study was to identify animal models that are suitable for investigating selective pulmonary vasodilation. To do so, a haemodynamic stable pulmonary hypertension was initiated, with a 30 min duration deemed to be a sufficient time interval before and after a possible intervention. In anaesthetized and mechanically-ventilated Sprague–Dawley rats pulmonary hypertension was induced either by acute hypoxia due to reduction of the inspired oxygen fraction from 0.21 to 0.1 ( n = 6), a fixed infusion rate of the thromboxane analogue U46619 (240 ng/min; n = 6) or a monocrotaline injection (MCT; 60 mg/kg applied 23 days before the investigation; n = 7). The animals were instrumented to measure right ventricular and systemic arterial pressures. Acute hypoxia caused a short, and only transient, increase of pulmonary artery pressure as well as profound systemic hypotension which suggested haemodynamic instability. U46619 infusion induced variable changes in the pulmonary and systemic vascular tone without sufficient stabilization within 30 min. MCT provoked sustained pulmonary hypertension with normal systemic pressure values and inhalation of nitric oxide caused selective pulmonary vasodilation. In conclusion, out of the three examined rat animal models only MCT-induced pulmonary hypertension is a solid and reliable model for investigating selective pulmonary vasodilation.

AEROSOLISED PROSTACYCLIN FOR SELECTIVE PULMONARY VASODILATION IN TXA2 INDUCED PULMONARY HYPERTENSION

1998 ◽  
Vol 89 (Supplement) ◽  
pp. 410A
Author(s):  
M. Chinzei ◽  
M. Hayashida ◽  
Y. Sato ◽  
K. Komatsu ◽  
T. Chinzei ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Vasodilation ◽  
Selective Pulmonary Vasodilation

Selective Pulmonary Vasodilation Induced by Aerosolized Zaprinast 

1998 ◽  
Vol 88 (2) ◽  
pp. 410-416 ◽  
Author(s):  
Fumito Ichinose ◽  
Christophe Adrie ◽  
William E. Hurford ◽  
Kenneth D. Bloch ◽  
Warren M. Zapol
Keyword(s):  
Pulmonary Hypertension ◽  
Muscle Relaxation ◽  
Recovery Period ◽  
Phosphodiesterase Inhibitor ◽  
Smooth Muscle Relaxation ◽  
Pulmonary Vasculature ◽  
Pulmonary Vasodilation ◽  
Chronic Pulmonary Hypertension ◽  
Selective Pulmonary Vasodilation ◽  
Inhaled No

Background Zaprinast, an inhibitor of guanosine-3',5'-cyclic monophosphate (cGMP)-selective phosphodiesterase, augments smooth muscle relaxation induced by endothelium-dependent vasodilators (including inhaled nitric oxide [NO]). The present study was designed to examine the effects of inhaled nebulized zaprinast, alone, and combined with inhaled NO. Methods Eight awake lambs with U46619-induced pulmonary hypertension sequentially breathed two concentrations of NO (5 and 20 ppm), followed by inhalation of aerosols generated from solutions containing four concentrations of zaprinast (10, 20, 30, and 50 mg/ml). The delivered doses of nebulized zaprinast at each concentration (mean +/- SD) were 0.23 +/- 0.06, 0.49 +/- 0.14, 0.71 +/- 0.24, and 1.20 +/- 0.98 mg x kg(-1) x min(-1), respectively. Each lamb also breathed NO (5 and 20 ppm) and zaprinast (0.23 +/- 0.06 mg x kg[-1] x min[-1]) in combination after a 2-h recovery period. Results Inhaled NO selectively dilated the pulmonary vasculature. Inhaled zaprinast selectively dilated the pulmonary circulation and potentiated and prolonged the pulmonary vasodilating effects of inhaled NO. The net transpulmonary release of cGMP was increased by inhalation of NO, zaprinast, or both. The duration of the vasodilation induced by zaprinast inhalation was greater than that induced by NO inhalation. Conclusions Aerosolization of a cGMP-selective phosphodiesterase inhibitor alone or combined with NO may be a useful noninvasive therapeutic method to treat acute or chronic pulmonary hypertension.

Combination of nonspecific PDE inhibitors with inhaled prostacyclin in experimental pulmonary hypertension

2001 ◽  
Vol 281 (6) ◽  
pp. L1361-L1368 ◽  
Author(s):  
Ralph Theo Schermuly ◽  
Axel Roehl ◽  
Norbert Weissmann ◽  
Hossein Ardeschir Ghofrani ◽  
Hanno Leuchte ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Hemodynamics ◽  
Shunt Flow ◽  
Pulmonary Vasodilation ◽  
Pde Inhibitors ◽  
Inhaled Prostacyclin ◽  
Pulmonary Arterial ◽  
Selective Pulmonary Vasodilation

Inhalation of aerosolized prostacyclin (PGI2) exerts selective pulmonary vasodilation, but its effect is rapidly lost after termination of nebulization. Amplification of the vasodilatory response to inhaled PGI2 might be achieved by phosphodiesterase (PDE) inhibitors to stabilize its second messenger, cAMP. We established stable pulmonary hypertension in perfused rabbit lungs by continuous infusion of U-46619. Short-term (10-min) aerosolization maneuvers of PGI2 effected a rapid, moderate decrease in pulmonary arterial pressure, with post-PGI2 vasorelaxation being lost within 10–15 min, accompanied by a marginal reduction in shunt flow. Preceding administration of subthreshold doses of the PDE inhibitors theophylline, dipyridamole, and pentoxifylline via the intravascular or inhalational route, which per se did not influence pulmonary hemodynamics, caused more than doubling of the immediate pulmonary arterial pressure drop in response to PGI2 and marked prolongation of the post-PGI2 vasorelaxation to >60 min (all PDE inhibitors via both routes of application). This was accompanied by a reduction in shunt flow in the case of aerosolized theophylline (27.5%), pentoxifylline (30.5%), and dipyridamole (33.4%). Coaerosolization of PGI2 and PDE inhibitors may be considered as a therapeutic strategy in pulmonary hypertension.

Pulmonary vasodilation by nitric oxide gas and prodrug aerosols in acute pulmonary hypertension

1998 ◽  
Vol 84 (2) ◽  
pp. 435-441 ◽  
Author(s):  
Christophe Adrie ◽  
Fumito Ichinose ◽  
Alexandra Holzmann ◽  
Larry Keefer ◽  
William E. Hurford ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Half Life ◽  
Hemodynamic Effects ◽  
Pulmonary Vasodilation ◽  
Short Half Life ◽  
Acute Pulmonary Hypertension ◽  
Inhaled No

Adrie, Christophe, Fumito Ichinose, Alexandra Holzmann, Larry Keefer, William E. Hurford, and Warren M. Zapol. Pulmonary vasodilation by nitric oxide gas and prodrug aerosols in acute pulmonary hypertension. J. Appl. Physiol. 84(2): 435–441, 1998.—Sodium 1-( N, N-diethylamino)diazen-1-ium-1,2-diolate {DEA/NO; Et2N[N(O)NO]Na} is a compound that spontaneously generates nitric oxide (NO). Because of its short half-life (2.1 min), we hypothesized that inhaling DEA/NO aerosol would selectively dilate the pulmonary circulation without decreasing systemic arterial pressure. We compared the pulmonary selectivity of this new NO donor with two other reference drugs: inhaled NO and inhaled sodium nitroprusside (SNP). In seven awake sheep with pulmonary hypertension induced by the infusion of U-46619, we compared the hemodynamic effects of DEA/NO with those of incremental doses of inhaled NO gas. In seven additional awake sheep, we examined the hemodynamic effects of incremental doses of inhaled nitroprusside (i.e., SNP). Inhaled NO gas selectively dilated the pulmonary vasculature. Inhaled DEA/NO produced nonselective vasodilation; both systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were reduced. Inhaled SNP selectively dilated the pulmonary circulation at low concentrations (≤10−2 M), inducing a decrease of PVR of up to 42% without any significant decrease of SVR (−5%), but nonselectively dilated the systemic circulation at larger doses (>10−2 M). In conclusion, despite its short half-life, DEA/NO is not a selective pulmonary vasodilator compared with inhaled NO. Inhaled SNP appears to be selective to the pulmonary circulation at low doses but not at higher levels.

scholarly journals Cinaciguat, a soluble guanylate cyclase activator, causes potent and sustained pulmonary vasodilation in the ovine fetus

2009 ◽  
Vol 297 (2) ◽  
pp. L318-L325 ◽  
Author(s):  
Marc Chester ◽  
Pierre Tourneux ◽  
Greg Seedorf ◽  
Theresa R. Grover ◽  
Jason Gien ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Left Pulmonary Artery ◽  
Flow Transducer ◽  
Pulmonary Vasodilation

Impaired nitric oxide-cGMP signaling contributes to severe pulmonary hypertension after birth, which may in part be due to decreased soluble guanylate cyclase (sGC) activity. Cinaciguat (BAY 58-2667) is a novel sGC activator that causes vasodilation, even in the presence of oxidized heme or heme-free sGC, but its hemodynamic effects have not been studied in the perinatal lung. We performed surgery on eight fetal (126 ± 2 days gestation) lambs (full term = 147 days) and placed catheters in the main pulmonary artery, aorta, and left atrium to measure pressures. An ultrasonic flow transducer was placed on the left pulmonary artery to measure blood flow, and a catheter was placed in the left pulmonary artery for drug infusion. Cinaciguat (0.1–100 μg over 10 min) caused dose-related increases in pulmonary blood flow greater than fourfold above baseline and reduced pulmonary vascular resistance by 80%. Treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an sGC-oxidizing inhibitor, enhanced cinaciguat-induced pulmonary vasodilation by >120%. The pulmonary vasodilator effect of cinaciguat was prolonged, decreasing pulmonary vascular resistance for >1.5 h after brief infusion. In vitro stimulation of ovine fetal pulmonary artery smooth muscle cells with cinaciguat after ODQ treatment resulted in a 14-fold increase in cGMP compared with non-ODQ-treated cells. We conclude that cinaciguat causes potent and sustained fetal pulmonary vasodilation that is augmented in the presence of oxidized sGC and speculate that cinaciguat may have therapeutic potential for severe neonatal pulmonary hypertension.

scholarly journals Perioperative Morbidity and Mortality of Patients With COVID-19 Who Undergo Urgent and Emergent Surgical Procedures

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Anne Knisely ◽  
Zhen Ni Zhou ◽  
Jenny Wu ◽  
Yongmei Huang ◽  
Kevin Holcomb ◽  
...  
Keyword(s):  
Surgical Procedures ◽  
Morbidity And Mortality ◽  
Perioperative Morbidity

Outcomes After Noncardiac Surgery For Patients With Pulmonary Hypertension: A Historical Cohort Study

2019 ◽  
Author(s):  
Juraj Sprung ◽  
Atousa Deljou ◽  
Moldovan Sabov ◽  
Garvan C Kane ◽  
Robert P. Frantz ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cohort Study ◽  
Functional Status ◽  
Perioperative Complications ◽  
Elevated Serum ◽  
Noncardiac Surgery ◽  
Historical Cohort ◽  
Surgical Risk ◽  
Perioperative Morbidity ◽  
Increased Risk

Abstract Abstract Background: Pulmonary hypertension (PH) is a significant preoperative risk factor. We aimed to determine predictors of perioperative morbidity and mortality after noncardiac surgery for patients with precapillary PH. Methods: We conducted a retrospective cohort study of adults with pulmonary hypertension having surgery at a single large medical referral center. The PH and surgical databases were reviewed from 2010 to 2017. Patients were excluded if PH was attributable to left-sided heart disease or they had undergone cardiac or transplant operations. To assess whether PH-specific diagnostic or cardiopulmonary testing parameters were predictive of perioperative complications, analyses were performed using generalized estimating equations. Results: Of 196 patients with PH undergoing noncardiac operations, 53 (27%) experienced 1 or more complications, including 5 deaths (3%) within 30 days. After adjustment for age and PH type, there were more complications in those undergoing moderate-to-high vs low-risk procedures (odds ratio [OR], 4.17 [95% CI, 2.07 to 8.40]; P<0.001). After adjustment for age, surgical risk, and PH type, the risk for complications was higher for patients with worse functional status (OR, 2.39 [95% CI, 1.19 to 4.78]; P=0.01 for class 3/4 vs class 1/2) and elevated serum N-terminal fragment of the prohormone brain natriuretic peptide (NT-proBNP) (OR, 2.28 [95% CI, 1.05 to 4.96]; P=0.04 for ≥300 vs. <300 pg/mL). From an analysis that included covariates for age, surgical risk, and functional status, elevated serum NT-proBNP levels remained associated with increased risk (OR, 2.23 [95% CI, 1.05 to 4.76]; P=0.04). Conclusions: Patients with PH undergoing noncardiac surgery with general anesthesia have a high frequency of perioperative complications. Specific clinical (functional status), diagnostic (serum NT-proBNP), and intraoperative factors (higher-risk surgery) are predictive of worse outcomes.

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