Perioperative Pharmacological Management of Pulmonary Hypertensive Crisis during Congenital Heart Surgery

Brunner, Nathan W.; Perez, Vinicio A. de Jesus; Richter, Alice; Haddad, François; Denault, André; Rojas, Vanessa; Yuan, Ke; Orcholski, Mark; Liao, Xiao‐Bo

doi:10.1086/674885

Cited by 34 publications

(35 citation statements)

References 135 publications

(230 reference statements)

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“…The present case is considered to be high risk because the PVR was greater than 5 Woods units m 2 , and pulmonary artery pres-1 month before the operation. Although severe pulmonary hypertension was observed in this case, pulmonary artery dilators were not used before the procedure contrary to current recommendations for surgical treatment [6]. This is because a possible increase in left-toright shunt due to a reduction in pulmonary artery resistance might increase left ventricular inflow, leading to left ventricular heart failure due to masked left ventricular restriction [7] at the time of ASD closure.…”

Section: Discussionmentioning

confidence: 67%

Successful Percutaneous Device Closure for Giant Atrial Septal Defect with Massive Pericardial Effusion and Pulmonary Hypertension in an Elderly Patient

Kikuchi¹,

Sakamoto²,

Saito³

et al. 2017

jshd

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An 82-year-old man suffering from shortness of breath, leg edema, and appetite loss visited our outpatient clinic. Although he was diagnosed with atrial septal defect (ASD) requiring surgical repair 40 years ago, he had refused an operation at that time. Echocardiography revealed a 37-mm ASD and massive pericardial effusion. Cardiac catheterization showed significant left-to-right shunt flow with Qp/Qs of 4.6 and pulmonary artery pressure of 93/35/52 mmHg. Pulmonary vascular resistance was calculated as 8.3 Wood units. Surgical treatment was no longer indicated due to his condition, and percutaneous treatment with an Amplatzer septal occluder (ASO) was planned instead. Diuretics, a PDE3 inhibitor and nasal oxygen, were administered preoperatively for 1 month. A 38-mm ASO, the maximum occluder size available in Japan, was implanted successfully. No acute decompensation occurred after ASD closure, and the patient's symptoms improved after ASO implantation. Cardiac catheterization on postoperative day 13 revealed no evidence of residual shunt, and pulmonary artery pressure decreased to 63/20/33 mmHg. As postoperative therapy, a PDE5 inhibitor, endothelin receptor blocker, and PGI 2 analog were administered for residual pulmonary hypertension. Because pericardial effusion did not disappear after pericardiocentesis, surgical pericardiostomy was performed 6 months after ASD closure, which reduced PA pressure to 34/16/24. Appropriate pre-and postoperative medical therapy, device closure with an ASO, and pericardiostomy were effective in this frail patient with a giant ASD with pulmonary hypertension and massive pericardial effusion.

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Section: Discussionmentioning

confidence: 67%

Successful Percutaneous Device Closure for Giant Atrial Septal Defect with Massive Pericardial Effusion and Pulmonary Hypertension in an Elderly Patient

Kikuchi¹,

Sakamoto²,

Saito³

et al. 2017

jshd

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“…In patients with pulmonary hypertension (PH) from congenital heart diseases, a pulmonary hypertensive crisis (PHC) is a lifethreatening situation characterised by a sudden increase in pulmonary vascular resistance, right heart failure, and systemic hypotension during the perioperative period of cardiovascular surgeries. 1 This crisis also can occur in idiopathic pulmonary arterial hypertension, sarcoidosis, pulmonary fibrosis during cardiac 2 and non-cardiac surgeries, 3,4 and lung transplantation. 5,6 Management of the crisis is challenging, because there is no treatment guideline or expert consensus specifying concrete agents as standard medication and diagnostic criteria for PHC.…”

Section: Editor's Key Pointsmentioning

confidence: 99%

“…5,6 Management of the crisis is challenging, because there is no treatment guideline or expert consensus specifying concrete agents as standard medication and diagnostic criteria for PHC. 1,7,8 In addition, no animal model of PHC has been reported to investigate PHC management to date, despite the availability of various models of PH. 9,10 Thus, there are few comparative data on the agents for PHC treatment either clinically or experimentally.…”

Section: Editor's Key Pointsmentioning

confidence: 99%

Effects of vasopressin during a pulmonary hypertensive crisis induced by acute hypoxia in a rat model of pulmonary hypertension

Sugawara

Mizuno

Oku

et al. 2019

British Journal of Anaesthesia

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Background: A pulmonary hypertensive crisis (PHC) can be a life-threatening condition. We established a PHC model by exposing rats with monocrotaline (MCT)-induced pulmonary hypertension to acute hypoxia, and investigated the effects of vasopressin, phenylephrine, and norepinephrine on the PHC. Methods: Four weeks after MCT 60 mg kg À1 administration i.v., right ventricular systolic pressure (RVSP), systolic BP (SBP), mean BP (MBP), cardiac index (CI), and pulmonary vascular resistance index (PVRI) were measured. PHC defined as an RVSP exceeding or equal to SBP was induced by changing the fraction of inspiratory oxygen to 0.1. Rats were subsequently treated by vasopressin, phenylephrine, or norepinephrine, followed by assessment of systemic haemodynamics, isometric tension of femoral and pulmonary arteries, cardiac function, blood gas composition, and survival. Results: PHC was associated with increased RV dilatation and paradoxical septal motion. Vasopressin increased MBP [mean (standard error)] from 52.6 (3.8) to 125.0 (8.9) mm Hg and CI from 25.4 (2.3) to 40.6 (1.8) ml min À1 100 g À1 while decreasing PVRI. Vasopressin also improved RV dilatation, oxygenation, and survival in PHC. In contrast, phenylephrine increased MBP from 54.8 (2.3) to 96.8 (3.2) mm Hg without improving cardiac pump function. Norepinephrine did not alter MBP. Vasopressin contracted femoral but not pulmonary arteries, whereas phenylephrine contracted both arterial beds. Hence, improvements with vasopressin in PHC might be associated with decreased PVRI and selective systemic vasoconstriction. Conclusions: In this rat model of a PHC, vasopressin, but not phenylephrine or norepinephrine, resulted in better haemodynamic and vascular recovery.

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“…PAB occurs commonly for shunt defects such as muscular ventricular septal defects or unbalanced atrioventricular septal defects, which are not amenable to repair in early infancy. For those infants undergoing complete repair of these shunt lesions, postoperative reactive pulmonary hypertension can lead to acute RV pressure overload . Additionally, many surgeries reroute blood flow in order to establish the RV as the systemic pump in cases of left ventricular (LV) hypoplasia.…”

Section: Introductionmentioning

confidence: 99%

“…For those infants undergoing complete repair of these shunt lesions, postoperative reactive pulmonary hypertension can lead to acute RV pressure overload. 2,3 Additionally, many surgeries reroute blood flow in order to establish the RV as the systemic pump in cases of left ventricular (LV) hypoplasia. Surgical palliation often includes reconstruction of the aortic arch to assure adequate blood flow from the RV to the aorta.…”

mentioning

confidence: 99%

Metabolic Response of the Immature Right Ventricle to Acute Pressure Overloading

Kajimoto¹,

Nuri

Isern

et al. 2018

JAHA

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BackgroundSurgical palliation or repair of complex congenital heart disease in early infancy can produce right ventricular (RV) pressure overload, often leading to acute hemodynamic decompensation. The mechanisms causing this acute RV dysfunction remain unclear. We tested the hypothesis that the immature right ventricle lacks the ability to modify substrate metabolism in order to meet increased energy demands induced by acute pressure overloading.Methods and ResultsTwenty‐two infant male mixed breed Yorkshire piglets were randomized to a sham operation (Control) or pulmonary artery banding yielding >2‐fold elevation over baseline RV systolic pressure. We used carbon 13 (13C)‐labeled substrates and proton nuclear magnetic resonance to assess RV energy metabolism. [Phosphocreatine]/[ATP] was significantly lower after pulmonary artery banding. [Phosphocreatine]/[ATP] inversely correlated with energy demand indexed by maximal sustained RV systolic pressure/left ventricular systolic pressure. Fractional contributions of fatty acids to citric acid cycle were significantly lower in the pulmonary artery banding group than in the Control group (medium‐chain fatty acids; 14.5±1.6 versus 8.2±1.0%, long‐chain fatty acids; 9.3±1.5 versus 5.1±1.1%). 13C‐flux analysis showed that flux via pyruvate decarboxylation did not increase during RV pressure overloading.ConclusionsAcute RV pressure overload yielded a decrease in [phosphocreatine]/[ATP] ratio, implying that ATP production did not balance the increasing ATP requirement. Relative fatty acids oxidation decreased without a reciprocal increase in pyruvate decarboxylation. The data imply that RV inability to adjust substrate oxidation contributes to energy imbalance, and potentially to contractile failure. The data suggest that interventions directed at increasing RV pyruvate decarboxylation flux could ameliorate contractile dysfunction associated with acute pressure overloading.

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Perioperative Pharmacological Management of Pulmonary Hypertensive Crisis during Congenital Heart Surgery

Cited by 34 publications

References 135 publications

Successful Percutaneous Device Closure for Giant Atrial Septal Defect with Massive Pericardial Effusion and Pulmonary Hypertension in an Elderly Patient

Successful Percutaneous Device Closure for Giant Atrial Septal Defect with Massive Pericardial Effusion and Pulmonary Hypertension in an Elderly Patient

Effects of vasopressin during a pulmonary hypertensive crisis induced by acute hypoxia in a rat model of pulmonary hypertension

Metabolic Response of the Immature Right Ventricle to Acute Pressure Overloading

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