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Manajemen Perioperatif pada Pasien Hipertensi Pulmonal Akibat Kelainan Jantung Kiri yang Menjalani Operasi Bedah Jantung
Abstract
Hipertensi pulmonal akibat kelainan jantung kiri (PH-LHD) pada pasien yang menjalani bedah jantung dihubungkan dengan tingginya komplikasi, peningkatan risiko luaran buruk, dan kenaikan mortalitas perioperatif. Manajemen praoperatif pada pasien PH-LHD meliputi anamnesis, pemeriksaan fisik, pemeriksaan penunjang, serta kateterisasi jantung kanan untuk menegakkan diagnosis definitif. Optimalisasi praoperatif dilakukan dengan memastikan kondisi euvolemik, meneruskan pengobatan sebelumnya, sampai memberikan perawatan intensif pada kondisi gagal jantung dekompensasi akut. Selain pemantauan invasif standar, pemantauan transesophageal echocardiography intraoperatif digunakan untuk menganalisis PH dan mengenali kelainan jantung kiri yang menyebabkan PH. Induksi anestesi dilakukan dengan teknik anestesi balans antara opioid dan agen inhalasi dosis rendah. Pada PH-LHD yang disebabkan lesi katup, target hemodinamik disesuaikan dengan jenis kelainan katupnya. Target manajemen pascaoperatif adalah menghindari dan mengobati gagal ventrikel kanan dengan mengatasi aritmia, melakukan strategi ventilasi mekanik pelindung ventrikel kanan, memastikan keseimbangan cairan, dan memberikan dukungan obat vasoaktif jika diperlukan.
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The pulmonary artery catheter (PAC) was introduced into clinical practice in the 1970s and was initially used to monitor patients with acute myocardial infarctions. The indications for using the PAC quickly expanded to critically ill patients in the intensive care unit as well as in the perioperative setting in patients undergoing major cardiac and noncardiac surgery. The utilization of the PAC is surrounded by multiple controversies, with literature claiming its benefits in the perioperative setting, and other publications showing no benefit. The right interpretation of the hemodynamic parameters measured by the PAC and its clinical implications are of the utmost essence in order to guide a specific therapy. Even though clinical trials have not shown a reduction in mortality with the use of the PAC, it still remains a valuable tool in a wide variety of clinical settings. In general, the right selection of the patient population (high-risk patients with or without hemodynamic instability undergoing high-risk procedures) as well as the right clinical setting (centers with experience and expertise) are essential in order for the patient to benefit most from PAC use.
Pulmonary hypertension is a rare and progressive pathology defined by abnormally high pulmonary artery pressure mediated by a diverse range of aetiologies. It affects up to twenty-six individuals per one million patients currently living in the United Kingdom (UK), with a median life expectancy of 2.8 years in idiopathic pulmonary hypertension. The diagnosis of pulmonary hypertension is often delayed due to the presentation of non-specific symptoms, leading to a delay in referral to specialists services. The complexity of treatment necessitates a multidisciplinary approach, underpinned by a diverse disease aetiology from managing the underlying disease process to novel specialist treatments. This has led to the formation of dedicated specialist treatment centres within centralised UK cities. The article aimed to provide a concise overview of pulmonary hypertension’s clinical perioperative management, including key definitions, epidemiology, pathophysiology, and risk stratification.
Background
Preoperative pulmonary hypertension (PH) is associated with excess mortality among patients with severe mitral regurgitation undergoing mitral valve surgery (MVS). However, the links between PH phenotype, pulmonary vascular remodeling, and persistent postoperative PH are not well understood. We aimed to describe the associations between components of pulmonary hemodynamics as well as postoperative residual PH with longitudinal mortality in patients with severe mitral regurgitation who received MVS.
Methods and Results
Patients undergoing MVS for severe mitral regurgitation from 2011 to 2016 were retrospectively identified within our health system (n=488). Mean pulmonary artery pressure and other hemodynamic variables were determined by presurgical right‐heart catheterization. Postoperative pulmonary artery systolic pressure was assessed on echocardiogram 42 to 365 days post‐MVS. Longitudinal survival over a mean 3.9 years of follow‐up was evaluated using Cox proportional hazards modeling to compare survival after adjustment for demographics, surgical characteristics, and comorbidities. Pre‐MVS prevalence of PH was high at 85%. After adjustment, each 10‐mm Hg increase in preoperative mean pulmonary artery pressure was associated with a 1.38‐fold increase in risk of death (95% CI, 1.13–1.68). Elevated preoperative pulmonary vascular resistance, transpulmonary gradient, and right atrial pressure were similarly associated with increased mortality. Among 231 patients with postoperative echocardiogram, evidence of PH on echocardiogram (pulmonary artery systolic pressure ≥35 mm Hg) was associated with increased risk of death (hazard ratio [HR], 2.02 [95% CI, 1.17–3.47]); however, this was no longer statistically significant after adjustment (HR, 1.55 [95% CI, 0.85–2.85]).
Conclusions
In patients undergoing MVS for mitral regurgitation, preoperative PH, and postoperative PH were associated with increased mortality.
Intraoperative transesophageal echocardiography is a standard diagnostic and monitoring tool employed in the management of patients undergoing an entire spectrum of cardiac surgical procedures, ranging from “routine” surgical coronary revascularization to complex valve repair, combined procedures, and organ transplantation. Utilizing a protocol as a starting point for imaging in all procedures and all patients enables standardization of image acquisition, reduction in variability in quality of imaging and reporting, and ultimately better patient care. Clear communication of the echocardiographic findings to the surgical team, as well as understanding the impact of new findings on the surgical plan, are paramount. Equally important is the need for complete understanding of the technical steps of the surgical procedures being performed and the complications that may occur, in order to direct the postprocedure evaluation toward aspects directly related to the surgical procedure and to provide pertinent echocardiographic information.
The rationale for this document is to outline a systematic approach describing how to apply the existing guidelines to questions on cardiac structure and function specific to the intraoperative environment in open, minimally invasive, or hybrid cardiac surgery procedures.
Pulmonary hypertension (PH) is a condition associated with high morbidity and mortality. Patients with PH who require critical care usually have severe right ventricular (RV) dysfunction. Although different groups of PH have different etiologies, pulmonary vascular dysfunction is common in these groups. PH can lead to increased pulmonary artery pressure, which can ultimately cause RV failure. Clinicians should be familiar with the presentations of this disease and diagnostic tools. The contributing factors, if present (e.g., sepsis), and coexisting conditions (e.g., arrhythmias) should be identified and addressed accordingly. The preload should be optimized by fluid administration, diuretics, and dialysis, if necessary. On the other hand, the RV afterload should be reduced to improve the RV function with pulmonary vasodilators, such as prostacyclins, inhaled nitric oxide, and phosphodiesterase type 5 inhibitors, especially in group 1 PH. Inotropes are also used to improve RV contractility, and if inadequate, use of ventricular assist devices and extracorporeal life support should be considered in suitable candidates. Moreover, vasopressors should be used to maintain systemic blood pressure, albeit cautiously, as they increase the RV afterload. Measures should be also taken to ensure adequate oxygenation. However, mechanical ventilation is avoided in RV failure. In this study, we reviewed the pathophysiology, manifestations, diagnosis, monitoring, and management strategies of PH, especially in intensive care units.
Purpose of Review
Pulmonary hypertension (PH) frequently complicates heart failure and portends a worse prognosis. This review will summarize and discuss recent updates in the classification and management of patients with PH due to left heart disease.
Recent Findings
Careful hemodynamic assessment is critical to the classification of patients with PH and heart failure. Two hemodynamic subgroups of PH in heart failure patients have been described: isolated post-capillary pulmonary hypertension and combined post- and precapillary pulmonary hypertension. The cornerstone in management of PH due to left heart disease is the treatment of the underlying left heart pathology; however, ongoing trials have been designed to test pulmonary vasodilators in this cohort.
Summary
PH-specific therapies have not demonstrated a benefit in patients with pulmonary hypertension due to left heart disease. Understanding the distinct pathobiology of each hemodynamic subgroup may lead to the development of useful biomarkers and effective targeted therapies.
Pulmonary hypertension (PH) is frequent in left heart disease (LHD), as a consequence of the underlying condition. Significant advances have occurred over the past 5 years since the 5th World Symposium on Pulmonary Hypertension in 2013, leading to a better understanding of PH-LHD, challenges and gaps in evidence. PH in heart failure with preserved ejection fraction represents the most complex situation, as it may be misdiagnosed with group 1 PH. Based on the latest evidence, we propose a new haemodynamic definition for PH due to LHD and a three-step pragmatic approach to differential diagnosis. This includes the identification of a specific "left heart" phenotype and a non-invasive probability of PH-LHD. Invasive confirmation of PH-LHD is based on the accurate measurement of pulmonary arterial wedge pressure and, in patients with high probability, provocative testing to clarify the diagnosis. Finally, recent clinical trials did not demonstrate a benefit in treating PH due to LHD with pulmonary arterial hypertension-approved therapies.
Since the 1st World Symposium on Pulmonary Hypertension (WSPH) in 1973, pulmonary hypertension (PH) has been arbitrarily defined as mean pulmonary arterial pressure (mPAP) ≥25 mmHg at rest, measured by right heart catheterisation. Recent data from normal subjects has shown that normal mPAP was 14.0±3.3 mmHg. Two standard deviations above this mean value would suggest mPAP >20 mmHg as above the upper limit of normal (above the 97.5th percentile). This definition is no longer arbitrary, but based on a scientific approach. However, this abnormal elevation of mPAP is not sufficient to define pulmonary vascular disease as it can be due to an increase in cardiac output or pulmonary arterial wedge pressure. Thus, this 6th WSPH Task Force proposes to include pulmonary vascular resistance ≥3 Wood Units in the definition of all forms of pre-capillary PH associated with mPAP >20 mmHg. Prospective trials are required to determine whether this PH population might benefit from specific management.
Regarding clinical classification, the main Task Force changes were the inclusion in group 1 of a subgroup “pulmonary arterial hypertension (PAH) long-term responders to calcium channel blockers”, due to the specific prognostic and management of these patients, and a subgroup “PAH with overt features of venous/capillaries (pulmonary veno-occlusive disease/pulmonary capillary haemangiomatosis) involvement”, due to evidence suggesting a continuum between arterial, capillary and vein involvement in PAH.
Pulmonary hypertension due to left heart disease (PH-LHD) is caused by left ventricular (LV) systolic and/or diastolic dysfunction and left heart valve disease. LV diseases lead to left ventricular filling pressure increases, pulmonary venous obstruction and pulmonary venous pressure increases, and thus to secondary PH. Exercise tolerance is lower and fatality rates are higher in patients with PH-LHD than those in subjects with normal pulmonary arterial pressure. In spite of the progress in the study of the mechanisms of PH-LHD in recent years, no specific treatment is currently available. The efficacy and safety of targeted therapies for pulmonary arterial hypertension remain to be fully established. In the present study, PH-LHD patients were treated with milrinone injection. It was concluded that milrinone significantly reduces pulmonary artery systolic pressure (PASP) in patients with PH-LHD, and significantly improves the cardiac structure, cardiac function and biochemical indexes. PASP was significantly correlated with the left atrial diameter, LV end diastolic diameter, LV ejection fraction, tricuspid annular plane systolic excursion, right ventricular fractional area change, N-terminal pro-B-type natriuretic peptide and hypersensitive C-reactive protein.
Pulmonary hypertension due to left heart disease (PH-LHD) is the most common type of pulmonary hypertension, although an accurate prevalence is challenging. PH-LHD includes PH due to systolic or diastolic left ventricular dysfunction, mitral or aortic valve disease and congenital left heart disease. In recent years a new and distinct phenotype of “combined post-capillary and pre-capillary PH,” based on diastolic pulmonary gradient and pulmonary vascular resistance, has been recognized. The roles of right ventricular dysfunction and pulmonary vascular compliance in PH-LHD have also been elucidated recently and they appear to have significant clinical implications. Echocardiography continues to play a seminal role in diagnosis of PH-LHD and heart failure with preserved LV ejection fraction, as it can identify valve disease and help to distinguish PH-LHD from pre-capillary PH. Right, and occasionally left heart catheterization, remains the gold-standard for diagnosis and phenotyping of PH-LHD, although Cardiac Magnetic Resonance Imaging is emerging as a useful alternative tool in non-invasive diagnostic and prognostic assessment of PH-LHD. In this review, the latest evidence for more recent advances will be discussed, including the role of fluid challenge and exercise during cardiac catheterization to unravel occult post-capillary and the role of vasoreactivity testing. The use of many or all of these diagnostic techniques will undoubtedly provide key information about sub-groups of patients with PH-LHD that might benefit from medical therapy previously considered to be only suitable for pulmonary arterial hypertension.
Perioperative management of pulmonary hypertension remains one of the most challenging scenarios during cardiac surgery. It is associated with high morbidity and mortality due to right ventricular failure, arrhythmias, myocardial ischemia, and intractable hypoxia. Therefore, this review article is intended toward the anesthetic considerations in the perioperative period, with particular emphasis on the selection of technique and choice of anesthesia with maintenance, anesthetic drugs, and the recent intraoperative recommendations for prevention and treatment of pulmonary hypertensive crisis.
Increased pulmonary venous pressure secondary to left heart disease is the most common cause of pulmonary hypertension (PH). The diagnosis of PH due to left heart disease relies on a clinical probability assessment followed by the invasive measurements of a mean pulmonary artery pressure (PAP) ≥25 mm Hg and mean wedged PAP (PAWP) >15 mm Hg. A combination of mean PAP and mean PAWP defines postcapillary PH. Postcapillary PH is generally associated with a diastolic pulmonary pressure gradient (diastolic PAP minus mean PAWP) <7 mm Hg, a transpulmonary pressure gradient (mean PAP minus mean PAWP) <12 mm Hg, and pulmonary vascular resistance ≤3 Wood units (WU). This combination of criteria defines isolated postcapillary PH. Postcapillary PH with elevated vascular gradients and pulmonary vascular resistance defines combined post- and precapillary PH (Cpc-PH). Postcapillary PH is associated with a decreased survival in proportion to increased pulmonary vascular gradients, decreased pulmonary arterial compliance, and reduced right ventricular function. The Cpc-PH subcategory occurs in 12% to 13% of patients with PH due to left heart disease. Patients with Cpc-PH have severe PH, with higher diastolic pulmonary pressure gradient, transpulmonary pressure gradient, and pulmonary vascular resistance and more pronounced ventilatory responses to exercise, lower pulmonary arterial compliance, depressed right ventricular ejection fraction, and shorter life expectancy than isolated postcapillary PH. Cpc-PH bears similarities to pulmonary arterial hypertension. Whether Cpc-PH is amenable to therapies targeting the pulmonary circulation remains to be tested by properly designed randomized controlled trials.
Background:
Pulmonary hypertension (PH) is a common and morbid complication of left heart disease with 2 subtypes: isolated post-capillary pulmonary hypertension (Ipc-PH) and combined post-capillary and pre-capillary pulmonary hypertension (Cpc-PH). Little is known about the clinical or physiological characteristics that distinguish these 2 subphenotypes or if Cpc-PH shares molecular similarities to pulmonary arterial hypertension (PAH).
Objectives:
The goal of this study was to test the hypothesis that the hemodynamic and genetic profile of Cpc-PH would more closely resemble PAH than Ipc-PH.
Methods:
Vanderbilt University's electronic medical record linked to a DNA biorepository was used to extract demographic characteristics, clinical data, invasive hemodynamic data, echocardiography, and vital status for all patients referred for right heart catheterization between 1998 and 2014. Shared genetic variants between PAH and Cpc-PH compared with Ipc-PH were identified by using pre-existing single-nucleotide polymorphism data.
Results:
A total of 2,817 patients with PH (13% Cpc-PH, 52% Ipc-PH, and 20% PAH) were identified. Patients with Cpc-PH were on average 6 years younger, with more severe pulmonary vascular disease than patients with Ipc-PH, despite similar comorbidities and prevalence, severity, and chronicity of left heart disease. After adjusting for relevant covariates, the risk of death was similar between the Cpc-PH and Ipc-PH groups (hazard ratio: 1.14; 95% confidence interval: 0.96 to 1.35; p = 0.15) when defined according to diastolic pressure gradient. We identified 75 shared exonic single-nucleotide polymorphisms between Cpc-PH and PAH enriched in pathways involving cell structure, extracellular matrix, and immune function. These genes are expressed, on average, 32% higher in lungs relative to other tissues.
Conclusions:
Patients with Cpc-PH develop pulmonary vascular disease similar to patients with PAH, despite younger age and similar prevalence of obesity, diabetes mellitus, and left heart disease compared with patients with Ipc-PH. An exploratory genetic analysis in Cpc-PH identified genes and biological pathways in the lung known to contribute to PAH pathophysiology, suggesting that Cpc-PH may be a distinct and highly morbid PH subphenotype.
Guidelines summarize and evaluate all available evidence on a particular issue at the time of the writing process, with the aim of assisting health professionals in selecting the best management strategies for an individual patient with a given condition, taking into account the impact on outcome, as well as the risk–benefit ratio of particular diagnostic or therapeutic means. Guidelines and recommendations should help health professionals to make decisions in their daily practice. However, the final decisions concerning an individual patient must be made by the responsible health professional(s) in consultation with the patient and caregiver as appropriate.
2015 ESC/ERS pulmonary hypertension guidelines incorporate changes and adaptations focusing on clinical management
Pulmonary hypertension (PH) is a known risk factor for perioperative complications. Unlike in the case of cardiac surgery, PH is currently not listed as an independent risk factor for postoperative complications in guidelines for the management of noncardiac surgery. Despite the paucity of data, though, patients with PH are often counseled against having elective procedures because early and sudden postoperative deaths have been reported. Patients with PH are unable to accommodate alterations in right ventricular (RV) preload or afterload induced by fluid shifts, medications, or changes in the autonomic nervous system precipitated by hypoxia or hypercapnia. These factors become magnified in situations of added stress such as surgical intervention. Systemic hypotension and arrhythmias may precipitate RV ischemia, further worsening RV function. Patient and surgical characteristics and choice of anesthetic technique are crucial factors in perioperative management. The two main principles of perioperative management are the prevention of systemic hypotension (risk of RV ischemia) and the prevention of acute elevations in pulmonary arterial pressure (risk of RV failure). Close monitoring, optimization of systemic BP, pain control, oxygenation and ventilation, avoidance of exacerbating factors, and use of vasopressors and pulmonary vasodilators as necessary are essential elements of management. Understanding the pathophysiology, cause, and severity of PH in the individual perioperative patient allows accurate risk assessment, optimization of PH and RV function prior to surgery, and appropriate intraoperative and postoperative management.
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 insufficient anesthesia 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.
Endothelin receptor antagonism produces favorable short-term hemodynamic effects in heart failure, but the clinical effects of longer term therapy have not been evaluated.
Three hundred and seventy patients with symptoms of heart failure at rest or on minimal exertion and a left ventricular ejection fraction <35% were randomly assigned (double-blind) to placebo (n = 126) or the endothelin receptor antagonist bosentan, titrated slowly (n = 121) or rapidly (n = 123) to a target dose of 500 mg twice daily. Treatment with the study drug was to be maintained for 26 weeks, whereas background medications for heart failure were kept constant. Safety concerns led to early termination of the trial when only 174 patients had had an opportunity to complete 26 weeks of therapy. Bosentan exerted no apparent benefit when all randomized patients were analyzed (P = .709). However, in the first 174 patients who were recruited at least 26 weeks before study termination and who could therefore be followed for the planned duration of the trial, patients in the bosentan groups were more likely to be improved (26% versus 19%) and were less likely to be worse (28% versus 43%), P = .045. When compared with placebo-treated patients, bosentan-treated patients had a increased risk of heart failure during the first month of treatment but a decreased risk of heart failure during the fourth, fifth, and sixth months of therapy. The major noncardiac adverse effects of bosentan included an increase in hepatic transaminases (in 15.6% of patients) and a decrease in hemoglobin (of about 1 g/L).
Although bosentan exerted no favorable effects in the overall study, our findings suggest that the clinical responses to endothelin antagonism with bosentan in patients with severe chronic heart failure may be dependent on the duration of treatment.
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The World Symposium on Pulmonary Hypertension (WSPH) was organized by the World Health Organization (WHO) in 1973 in response to an increase in pulmonary arterial hypertension (PAH) in Europe caused by Aminorex, an appetite suppressant. The mandate of this meeting was to review the latest clinical and scientific research and to formulate recommendations to improve the diagnosis and management of pulmonary hypertension (PH).¹ Since 1998, the WSPH has met every 5 years and in 2018, the 6th annual WSPH revised the hemodynamic definition of PH. This two-part series will review the updated definition, classification, pathophysiology, presentation, diagnosis, management, and perioperative management of patients with PH. In the first part of this series, the definition, classification, pathophysiology, and presentation will be reviewed.
Background
The risk of complications, including death, is substantially increased in patients with pulmonary hypertension (PH) undergoing anaesthesia for surgical procedures, especially in those with pulmonary arterial hypertension (PAH) and chronic thromboembolic PH (CTEPH). Sedation also poses a risk to patients with PH. Physiological changes including tachycardia, hypotension, fluid shifts, and an increase in pulmonary vascular resistance (PH crisis) can precipitate acute right ventricular decompensation and death.
Methods
A systematic literature review was performed of studies in patients with PH undergoing non-cardiac and non-obstetric surgery. The management of patients with PH requiring sedation for endoscopy was also reviewed. Using a framework of relevant clinical questions, we review the available evidence guiding operative risk, risk assessment, preoperative optimisation, and perioperative management, and identifying areas for future research.
Results
Reported 30 day mortality after non-cardiac and non-obstetric surgery ranges between 2% and 18% in patients with PH undergoing elective procedures, and increases to 15–50% for emergency surgery, with complications and death usually relating to acute right ventricular failure. Risk factors for mortality include procedure-specific and patient-related factors, especially markers of PH severity (e.g. pulmonary haemodynamics, poor exercise performance, and right ventricular dysfunction). Most studies highlight the importance of individualised preoperative risk assessment and optimisation and advanced perioperative planning.
Conclusions
With an increasing number of patients requiring surgery in specialist and non-specialist PH centres, a systematic, evidence-based, multidisciplinary approach is required to minimise complications. Adequate risk stratification and a tailored-individualised perioperative plan is paramount.
Objective
Pulmonary artery catheterization (PAC) provides continuous monitoring of hemodynamic parameters that may aid in perioperative management of cardiac surgery patients. However, prior data suggests that PAC has limited benefit in intensive care and surgical settings. Thus, this study sought to determine the impact of PAC insertion on short-term postoperative outcomes in a large, contemporaneous cohort of patients undergoing open cardiac surgery, as compared to standard central venous pressure (CVP) monitoring.
Methods
This was an observational study of open cardiac surgeries from 2010 and 2018. Patients with PAC insertion were identified and matched against patients without PAC insertion via 1:1 nearest neighbor propensity matching. Multivariable analysis was performed to assess the impact of PAC on operative mortality in the overall cohort, as well as recent heart failure, mitral valve disease, and tricuspid insufficiency subgroups.
Results
Of the 11,820 patients undergoing an (STS indexed) coronary or valvular surgery, 4,605 (39.0%) had PAC insertion. Propensity-score matching yielded 3,519 evenly balanced pairs. As compared to CVP monitoring, PAC use was not associated with improved operative mortality in the overall cohort, nor in the recent heart failure, mitral valve disease, or tricuspid insufficiency subgroups. ICU length of stay was longer (p<0.001) and there were more packed red blood cell transfusions in the PAC group (p<0.001); however, postoperative outcomes were otherwise similar, including stroke, sepsis, and new renal failure (P>0.05).
Conclusions
These findings suggest that PAC may have limited benefit in cardiac surgery.
The incidence of pulmonary hypertension (PH) in patients undergoing noncardiac surgery has increased steadily over the past decade. Patients with known PH have significantly higher perioperative morbidity and mortality than those without PH. Moreover, a substantial number of patients may have occult disease. It, therefore, is of paramount importance for perioperative providers to recognize high-risk patients and treat them appropriately. This review first provides an overview of PH pathophysiology, then estimates the perioperative incidence of PH and its impact on surgical outcomes, and finally outlines a perioperative management strategy.
Pulmonary hypertension (PH) due to left heart disease (LHD) is a frequent complication of heart failure (HF) and is associated with exercise intolerance, poor quality of life, increased risk of hospitalizations and reduced overall survival. Since the recent 6th World Symposium on Pulmonary Hypertension in 2018, there have been significant changes in the hemodynamic definitions and clinical classification of PH-LHD. PH-LHD can be subdivided into (1) isolated postcapillary PH (IpcPH) and (2) combined precapillary and postcapillary PH (CpcPH). This categorization of PH-LHD is important as CpcPH shares certain pathophysiologic, clinical and hemodynamic characteristics with pulmonary arterial hypertension and is associated with worse outcomes compared to IpcPH. A systematic approach utilizing clinical history and non-invasive investigations, is required in the diagnosis of PH-LHD. Right heart catheterization with and without provocative testing is performed in expert centres and is indicated in selected individuals. Although the definition of IpcPH and CpcPH is based on measurements made with right heart catheterization, distinguishing between these two entities is not always necessary. Despite strong evidence for medical therapy in patients with pulmonary arterial hypertension, these options have limited benefit in PH-LHD. Expert PH centres in Canada have been established to provide ongoing care for the more complex patient subgroups.
Pulmonary artery catheters are a useful tool for hemodynamic monitoring in high-risk patients during surgery and while in intensive care. However, there are major risks inherent to the device, and with modern day technology, their routine use has decreased. We discuss the need for routine insertion of pulmonary artery catheters in cardiac surgery. We also present a case of a left ventricular assist device implantation complicated by serious pulmonary hemorrhage due to pulmonary artery catheter insertion, highlighting the potentially life-threatening risks involved.
Pulmonary hypertension (PH) due to left heart disease (LHD) is the most common type of PH and is defined as mean pulmonary artery systolic pressure of >20 mm Hg and pulmonary capillary wedge pressure >15 mm Hg during right heart catheterization. LHD may lead to elevated left atrial pressure alone, which in the absence of intrinsic pulmonary vascular disease will result in PH without changes in pulmonary vascular resistance. Persistent elevation in left atrial pressure may, however, also be associated with subsequent pulmonary vascular remodeling, vasoconstriction, and an increase in pulmonary vascular resistance. Hence, there are 2 subgroups of PH due to LHD, isolated postcapillary PH and combined post- and precapillary PH, with these groups have differing clinical implications. Differentiation of pulmonary arterial hypertension and PH due to LHD is critical to guide management planning; however, this may be challenging. Older patients, patients with metabolic syndrome, and patients with imaging and clinical features consistent with left ventricular dysfunction are suggestive of LHD etiology rather than pulmonary arterial hypertension. Hemodynamic measures such as diastolic pressure gradient, transpulmonary gradient, and pulmonary vascular resistance may assist to differentiate pre- from postcapillary PH and offer prognostic insights. However, these are influenced by fluid status and heart failure treatment. Pulmonary arterial hypertension therapies have been trialed in the treatment with concerning results reflecting disease heterogeneity, variation in inclusion criteria, and mixed end point criteria. The aim of this review is to provide an updated definition, discuss possible pathophysiology, clinical aspects, and the available treatment options for PH due to LHD.
Objective:
Pulmonary hypertension (PH) is a substantial preoperative risk factor. For this study, morbidity and mortality were examined after noncardiac surgery in patients with precapillary PH.
Design:
A retrospective cohort study.
Setting:
Quaternary medical center in Rochester, MN.
Participants:
Adults with PH undergoing noncardiac surgery.
Interventions:
None.
Measurements and main results:
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 transplantation surgeries. To assess whether PH-specific diagnostic or cardiopulmonary testing parameters were predictive of perioperative complications, generalized estimating equations were used. Of 196 patients with PH, 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-risk versus low-risk procedures (odds ratio [OR] 4.17 [95% confidence interval {CI} 2.07-8.40]; p < 0.001). After adjustment for age, surgical risk, and PH type, the complication risk was greater for patients with worse functional status (OR 2.39 [95% CI 1.19-4.78]; p = 0.01 for classes III/IV v classes I/II) and elevated serum N-terminal fragment of the prohormone brain natriuretic peptide (NT-proBNP) (OR 2.28 [95% CI 1.05-4.96]; p = 0.04 for ≥300 v <300 pg/mL). After adjusting for age, surgical risk, and functional status, elevated NT-proBNP remained associated with increased risk (OR 2.23 [95% CI 1.05-4.76]; p = 0.04).
Conclusion:
PH patients undergoing noncardiac surgery have a high frequency of complications. Worse functional status, elevated serum NT-proBNP, and higher-risk surgery are predictive of worse outcome.
Pulmonary hypertension (PH) is often caused by left heart disease (LHD) such as heart failure (HF) or valvular heart disease. Historically, few randomized controlled trials have evaluated the off‐label use of medications for treating pulmonary arterial hypertension (PAH) in patients with PH‐LHD. However, multiple randomized controlled trials have been published over the last decade that investigated their use in patients with PH‐LHD. In addition, recent updates in the classification and definitions of PH have led to an improved recognition of PH‐LHD phenotypes, notably combined post‐capillary and pre‐capillary PH and isolated post‐capillary PH. In this systematic review, we show that PAH medications should not be recommended in two distinct HF populations: patients with HF without definitive PH diagnosis and patients with isolated post‐capillary PH due to HF. In addition, the use of bosentan or macitentan is not recommended in patients with combined post‐capillary and pre‐capillary PH due to HF, but sildenafil may be considered to improve pulmonary hemodynamics and exercise capacity in patients with combined post‐capillary and pre‐capillary PH due to HF. Riociguat 2 mg 3 times daily may also be considered to improve pulmonary hemodynamics in patients with combined post‐capillary and pre‐capillary PH due to heart failure with reduced ejection fraction but not heart failure with preserved ejection fraction. The postoperative use of sildenafil in the setting of PH after valvular heart disease intervention was evaluated. Limited clinical data and safety concern warrants caution with the postoperative use of sildenafil in patients with PH due to valvular heart disease. Despite recent advances in the understanding of PAH medications for patients with PH‐LHD, uncertainty remains about their utility in distinct subgroups. Nonetheless, PAH pharmacotherapy should generally be avoided for most patients with PH‐LHD. This article is protected by copyright. All rights reserved.
In the summer of 2016, delegates from the German Society of Cardiology (DGK), the German Respiratory Society (DGP), and the German Society of Pediatric Cardiology (DGPK) met in Cologne, Germany, to define consensus-based practice recommendations for the management of patients with pulmonary hypertension (PH). These recommendations were built on the 2015 European Pulmonary Hypertension guidelines, aiming at their practical implementation, considering country-specific issues, and including new evidence, where available. To this end, a number of working groups was initiated, one of which was specifically dedicated to PH associated with left heart disease. In this context, the European Guidelines point out that the drugs currently approved to treat patients with PAH (prostanoids, endothelin receptor antagonists, phosphodiesterase type 5 inhibitors, sGC stimulators) have not sufficiently been investigated in other forms of PH. However, despite the lack of respective efficacy data, an uncritical use of targeted PAH drugs in patients with PH associated with left heart disease is currently observed at an increasing rate. This development is a matter of concern. On the other hand, PH is a frequent problem that is highly relevant for morbidity and mortality in patients with left heart disease. In that sense, the distinction between isolated post-capillary pulmonary hypertension (IpcPH) and combined post- and pre-capillary pulmonary hypertension (CpcPH) and their proper definition may be of particular relevance. The detailed results and recommendations of the working group on PH associated with left heart disease, which were last updated in the spring of 2018, are summarized in this article.
Pulmonary hypertension is a fatal disease of multiple etiologies that is estimated to affect over 100 million people worldwide. The disease is defined hemodynamically as a mean pulmonary artery pressure ≥ 25 mmHg at rest. Despite important advances in our understanding of the pathobiology of this disease and improvements in patient management, outcomes are still poor and no curative treatments are currently available. The complex nature of this disease requires detailed clinical evaluation for accurate diagnosis and treatment. Recent advances in clinical recognition, classification, and understanding of the underlying pathological processes in pulmonary hypertension have led to improved diagnostic testing and therapeutic options for patients. A hallmark of pulmonary hypertension is an increased pulmonary vascular resistance which leads to progressive elevations in pulmonary artery pressure, resulting in compensatory right ventricular hypertrophy and, ultimately, heart failure. Clinically, these pulmonary vascular changes initially present as nonspecific symptoms, including unexplained dyspnea on exertion, fatigue, chest pain, and syncope. Signs of right ventricular dysfunction are also frequently present. Common pathogenic features of pulmonary hypertension include sustained pulmonary vasoconstriction, vascular remodeling of the small pulmonary arteries, in situ thrombosis, and increased vascular wall stiffness, resulting in increased pulmonary arterial pressure due to increased pulmonary vascular resistance. Despite improvements in clinical classification and understanding of the underlying pathogenic mechanisms of pulmonary hypertension, current therapies are limited to supportive care and targeting pulmonary vasoconstriction. There remains a need to identify novel therapeutic targets in this disease. This review provides a succinct overview of the clinical classification and pathophysiology of PH that can be used as a reference by physicians and physician‐scientists.
Pulmonary hypertension (PH) defined by a mean pulmonary artery pressure (MPAP) >25 mm Hg at rest is confirmed by right heart catheterization (RHC). With the rapid development of surgical methods and cardiopulmonary bypass strategies, many children and adults are undergoing surgical correction for their cardiac pathologies. Presence of PH in these patients contributes to a major morbidity and poses a great challenge for the operative team during its surgical and postoperative management. With the universal use of transesophageal echocardiography (TEE) in almost all cardiac surgeries, the etiology, severity of PH, and its effect on cardiac structures and function can be evaluated in patients suspected of having PH. Since there is no established algorithm for the intraoperative TEE evaluation of such patients, we proposed an algorithm for the evaluation of PH in patients suspected of having raised pulmonary pressure using TEE in the intraoperative period.
How to cite this article
Kumar MG, Puri GD. Transesophageal Echocardiographic Approach to a Patient with Suspected Pulmonary Hypertension in the Intraoperative Period. J Perioper Echocardiogr 2017;5(2):49-63.
Introduction
Pulmonary hypertension has many causes. While It’s conventionally thought that the most prevalent is left heart disease, little information about it’s proportion, causes and implications on outcome is available.
Methods and Results
Between 1993-2015, 12,115 of 66,949 (18%) first adult transthoracic echocardiograms were found to have tricuspid incompetence gradient≥40mmHg, a pulmonary hypertension surrogate. Left heart disease was identified in 8306 (69%) and included valve malfunction in 4115 (49%), left ventricular systolic dysfunction in 2557 (31%), and diastolic dysfunction in 1776 (21%). Patients with left heart disease, as compared those without left heart disease were of similar age, less were females (50% vs 63% p<0.0001), and had higher tricuspid incompetence gradient (median 48mmHg [IQR 43;55] vs 46mmHg [42;54] p<0.0001). In reviewing trends over 20 years, the relative proportions of systolic dysfunction decreased and diastolic dysfunction increased (p for trend<0.001), while valve malfunction remained the most prevalent cause of pulmonary hypertension with left heart disease. Independent predictors of mortality were age (HR 1.05, 95% CI 1.04-1.05 p<0.0001), tricuspid incompetence gradient (HR=1.02, 95%CI 1.01-1.02, p<0.0001 per mmHg increase), and female gender (HR=0.87, 95%CI 0.83-0.91, p<0.0001). Overall, left heart disease was not an independent risk factor for mortality (HR=1.04, 95%CI 0.99-1.09, p=0.110) but patients with left ventricular systolic dysfunction and with combined systolic dysfunction and valve malfunction had increased mortality compared to patients with pulmonary hypertension but without left heart disease (HR=1.30, 95%CI 1.20-1.42; HR=1.44, 95%CI 1.33-1.55 respectively p<0.0001 for both)
Conclusions
Pulmonary hypertension was found to be associated with left heart disease in 69% of patients. Among these patients, valve malfunction and diastolic dysfunction emerged as prominent causes. Left ventricular dysfunction carries additional risk to patients with pulmonary hypertension.
Pulmonary vascular dysfunction is associated with ARDS and leads to increased right-ventricular afterload and eventually right-ventricular failure, also called acute cor pulmonale. Interest in acute cor pulmonale and its negative impact on outcome in patients with ARDS has grown in recent years. Right-ventricular function in these patients should be closely monitored, and this is helped by the widespread use of echocardiography in intensive care units. Because mechanical ventilation may worsen right-ventricular failure, the interaction between the lungs and the right ventricle appears to be a key factor in the ventilation strategy. In this review, a rationale for a right ventricle-protective ventilation approach is provided, and such a strategy is described, including the reduction of lung stress (ie, the limitation of plateau pressure and driving pressure), the reduction of PaCO2 , and the improvement of oxygenation. Prone positioning seems to be a crucial part of this strategy by protecting both the lungs and the right ventricle, resulting in increased survival of patients with ARDS. Further studies are required to validate the positive impact on prognosis of right ventricle-protective mechanical ventilation.
Pulmonary hypertension is a complex disorder of the pulmonary vasculature that leads to increased peri-operative morbidity and mortality. Non-cardiac surgery constitutes a significant risk in patients with pulmonary hypertension. The management of right ventricular failure is inherently challenging and fraught with life-threatening consequences. A thorough understanding of the pathophysiology, the severity of the disease and its treatment modalities is required to deliver optimal peri-operative care. This review provides an evidence-based overview of the definition, classification, pathophysiology, diagnosis and treatment of pulmonary hypertension and focuses on the peri-operative management and treatment of pulmonary hypertensive crises in a non-cardiac setting.
Patients with pulmonary hypertension are at increased risk for perioperative morbidity and mortality. Elective surgery is generally discouraged in this patient population; however, there are times when surgery is deemed necessary. Currently, there are no guidelines for the preoperative risk assessment or perioperative management of subjects with pulmonary hypertension. The majority of the literature evaluating perioperative risk factors and mortality rates is observational and includes subjects with multiple etiologies of pulmonary hypertension. Subjects with pulmonary arterial hypertension, also referred to as World Health Organization group I pulmonary hypertension, and particularly those receiving pulmonary arterial hypertension-specific therapy may be at increased risk. Perioperative management of these patients requires a solid understanding and careful consideration of the hemodynamic effects of anesthetic agents, positive pressure ventilation and volume shifts associated with surgery in order to prevent acute right ventricular failure. We reviewed the most recent data regarding perioperative morbidity and mortality for subjects with pulmonary hypertension in an effort to better guide preoperative risk assessment and perioperative management by a multidisciplinary team.
ULMONARY HYPERTENSION (PH) describes a vast array of disease states in which chronically elevated pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) ultimately result in right heart failure (RHF) and death. Cardiac surgical patients presenting with pre-existing PH are at a higher risk for postoperative complications. Accurate preoperative assessment and diligent anesthetic management are crucial for the best outcome. In this review, the authors describe the pathophysiology, preoperative assessment, and perioperative care including intravenous and inhaled therapies of PH in the patient undergoing cardiac surgery. Detailed discussions of the echocardiographic assessment of right ventricular (RV) function, perioperative risk factors, and outcomes of patients with PH also are included. CLASSIFICATION OF PH
Pulmonary hypertension associated with left heart disease is the most common form of pulmonary hypertension encountered in clinical practice today. Although frequently a target of therapy, its pathophysiology remains poorly understood and its treatment remains undefined. Pulmonary hypertension in the context of left heart disease is a marker of worse prognosis and disease severity, but whether its primary treatment is beneficial or harmful is unknown. An important step to the future study of this important clinical problem will be to standardize definitions across disciplines to facilitate an evidence base that is interpretable and applicable to clinical practice. In this current statement, we provide an extensive review and interpretation of the current available literature to guide current practice and future investigation. At the request of the Pulmonary Hypertension (PH) Council of the International Society for Heart and Lung Transplantation (ISHLT), a writing group was assembled and tasked to put forth this document as described above. The review process was facilitated through the peer review process of the Journal of Heart and Lung Transplantation and ultimately endorsed by the leadership of the ISHLT PH Council.
The last two decades have seen major advances in the treatment of chronic heart failure, primarily as a result of therapeutic manipulation of activated neurohormonal systems. Despite this progress, many patients still suffer significant morbidity and premature death. Antagonism of the biological effects of endothelin, a potent vasoconstrictor, represents a further potential target. To date, positive results from animal models of heart failure have not been translated into clinical practice, perhaps as a consequence of the high doses of drug used. The ENABLE (Endothelin Antagonist Bosentan for Lowering Cardiac Events in Heart Failure) study evaluated the effects of low dose bosentan, a non-selective endothelin receptor antagonist, in patients with severe heart failure (left ventricular ejection fraction <35%, New York Heart Association class IIIb–IV). A total of 1613 patients were randomized to receive either bosentan (125 mg twice a day) or placebo. The preliminary results were presented at the 51st Annual Scientific Session of the American College of Cardiology (17–20 March 2002, Atlanta, GA, USA). The primary endpoint of all-cause mortality or hospitalization for heart failure was reached in 321/808 patients on placebo and 312/805 receiving bosentan. Treatment with bosentan appeared to confer an early risk of worsening heart failure necessitating hospitalization, as a consequence of fluid retention. It has been suggested that further studies using even lower doses of bosentan or more aggressive concomitant diuretic therapy may avoid this adverse effect. The results from the ENABLE study have, however, thrown further doubt on the potential benefits of non-specific endothelin receptor blockade in heart failure.
Healthy human lungs are normally the sites of fluid and solute filtration across the pulmonary capillary endothelium. Unlike other organs, the filtrate in the lungs is confined anatomically within adjacent interstitial spaces, through which it moves by a built-in pressure gradient from its site of formation to its site of removal through pulmonary lymphatic channels. The quantity of fluid filtered and its protein content depend on the transvascular hydrostatic and protein osmotic (colloid) pressure differences, and the leakiness of the endothelial barrier to water and protein. Lymphatic drainage can increase several-fold, which means that pulmonary edema-defined as an increase in extravascular water content of the lungs-cannot occur until the rate of fluid filtration exceeds the rate of lymphatic removal. Two main types of pulmonary edema are recognized: first, cardiogenic (or hydrostatic) pulmonary edema from, as the name implies, an elevated pulmonary capillary pressure from left-sided heart failure; second, noncardiogenic (increased permeability) pulmonary edema from injury to the endothelial and (usually) epithelial barriers. Owing to their fundamental differences, each occurs in distinct clinical conditions, requires separate therapy, and has a different prognosis.
This study sought to define the prevalence, severity, and significance of pulmonary hypertension (PH) in heart failure with preserved ejection fraction (HFpEF) in the general community.
Although HFpEF is known to cause PH, its development is highly variable. Community-based data are lacking, and the relative contribution of pulmonary venous versus pulmonary arterial hypertension (HTN) to PH in HFpEF is unknown. We hypothesized that PH would be a marker of symptomatic pulmonary congestion, distinguishing HFpEF from pre-clinical hypertensive heart disease.
This community-based study of 244 HFpEF patients (age 76 +/- 13 years; 45% male) was followed up using Doppler echocardiography over 3 years. Control subjects were 719 adults with HTN without HF (age 66 +/- 10 years; 44% male). Pulmonary artery systolic pressure (PASP) was derived from the tricuspid regurgitation velocity and PH defined as PASP >35 mm Hg. Pulmonary capillary wedge pressure (PCWP) was estimated from the ratio of early transmitral flow velocity to early mitral annular diastolic velocity.
In HFpEF, PH was present in 83% and the median (25th, 75th percentile) PASP was 48 (37, 56) mm Hg. PASP increased with PCWP (r = 0.21; p < 0.007). Adjusting for PCWP, PASP was higher in HFpEF than HTN (p < 0.001). The PASP distinguished HFpEF from HTN with an area under the receiver-operating characteristic curve of 0.91 (p < 0.001) and strongly predicted mortality in HFpEF (hazard ratio: 1.3 per 10 mm Hg; p < 0.001).
PH is highly prevalent and often severe in HFpEF. Although pulmonary venous HTN contributes to PH, it does not fully account for the severity of PH in HFpEF, suggesting that a component of pulmonary arterial HTN also contributes. The potent effect of PASP on mortality lends support for therapies aimed at pulmonary arterial HTN in HFpEF.
This trial evaluated the effects of epoprostenol on patients with severe left ventricular failure. Patients with class IIIB/IV congestive heart failure and decreased left ventricular ejection fraction were eligible for enrollment if angiography documented severely compromised hemodynamics while the patient was receiving a regimen of digoxin, diuretics, and an angiotensin-converting enzyme inhibitor. We randomly assigned 471 patients to epoprostenol infusion or standard care. The primary end point was survival; secondary end points were clinical events, congestive heart failure symptoms, distance walked in 6 minutes, and quality-of-life measures. The median dose of epoprostenol was 4.0 ng/kg/min, resulting in a significant increase in cardiac index (1.81 to 2.61 L/min/m2), a decrease in pulmonary capillary wedge pressure (24.5 to 20.0 mm Hg), and a decrease in systemic vascular resistance (20.76 to 12.33 units). The trial was terminated early because of a strong trend toward decreased survival in the patients treated with epoprostenol. Chronic intravenous epoprostenol therapy is not associated with improvement in distance walked, quality of life, or morbid events and is associated with an increased risk of death.
Phosphodiesterase inhibitors including milrinone produce positive inotropic effects by slowing the hydrolysis of cyclic adenosine monophosphate in the myocardium. With a loading dose of 50 microg/kg followed by an infusion of 0.5 microg x kg(-1) x min(-1), milrinone increases stroke volume index and left ventricular velocity of circumferential fiber shortening after weaning from cardiopulmonary bypass. Milrinone has potential for the treatment and prevention of internal mammary artery spasm because of its vasodilative effect, which is similar to that of papaverine, and is a potent pulmonary vasodilator for patients with right ventricular dysfunction and pulmonary vasoconstriction. Low-dose milrinone may have antiinflammatory properties and potentially can improve splanchnic perfusion.
The last two decades have seen major advances in the treatment of chronic heart failure, primarily as a result of therapeutic manipulation of activated neurohormonal systems. Despite this progress, many patients still suffer significant morbidity and premature death. Antagonism of the biological effects of endothelin, a potent vasoconstrictor, represents a further potential target. To date, positive results from animal models of heart failure have not been translated into clinical practice, perhaps as a consequence of the high doses of drug used. The ENABLE (Endothelin Antagonist Bosentan for Lowering Cardiac Events in Heart Failure) study evaluated the effects of low dose bosentan, a non-selective endothelin receptor antagonist, in patients with severe heart failure (left ventricular ejection fraction <35%, New York Heart Association class IIIb-IV). A total of 1,613 patients were randomized to receive either bosentan (125 mg twice a day) or placebo. The preliminary results were presented at the 51st Annual Scientific Session of the American College of Cardiology (17-20 March 2002, Atlanta, GA, USA). The primary endpoint of all-cause mortality or hospitalization for heart failure was reached in 321/808 patients on placebo and 312/805 receiving bosentan. Treatment with bosentan appeared to confer an early risk of worsening heart failure necessitating hospitalization, as a consequence of fluid retention. It has been suggested that further studies using even lower doses of bosentan or more aggressive concomitant diuretic therapy may avoid this adverse effect. The results from the ENABLE study have, however, thrown further doubt on the potential benefits of non-specific endothelin receptor blockade in heart failure.
Heart failure (HF) is one of the few cardiac conditions that is increasing. Despite a better understanding of how hormones and other signaling systems underlie the pathophysiology, and despite improved outcomes from pharmacologic therapy, many HF patients receive no effective treatment. Patients with HF commonly require medical diagnosis and management in operating rooms and critical care units; thus anesthesiologists are obliged to remain up-to-date both with advances in outpatient (chronic) medical management and with inpatient treatments for acute exacerbations of HF. Accordingly, we reviewed angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta-adrenergic receptor blockers, and aldosterone antagonists because these drugs prolong life and are included in current clinical practice guidelines for treating patients with chronic HF. We also reviewed the implications of chronic HF for patients undergoing surgery and anesthesia and discuss how best to provide intensive treatment for acute exacerbations of symptoms, such as might be caused by excessive intravascular volume, inappropriate drug "holidays," or worsening of the underlying cardiac disease.
The phosphodiesterase inhibitor milrinone is usually preferred in patients with pulmonary hypertension and myocardial dysfunction after cardiopulmonary bypass. We investigated the effects of low-dose milrinone on pulmonary hypertension in the immediate pre- and postoperative period. Forty-seven patients were randomized to the control and milrinone groups. All patients had mean pulmonary artery pressure greater than 30 mmHg and pulmonary capillary wedge pressure greater than 20 mmHg and were candidates for mitral valve replacement for rheumatic mitral stenosis. Twenty-four patients received a loading dose of milrinone 25 microg/kg(-1) during weaning from cardiopulmonary bypass, followed by a maintenance dose of 0.25 microg/kg(-1)/min(-1) to the end of the surgery. Cardiac output and other hemodynamic variables were noted at induction, weaning from bypass, and postoperative 1 h. Pulmonary artery pressure, capillary wedge pressure, and central venous pressure were significantly lower in the milrinone group during weaning after cardiopulmonary bypass, while other variables were roughly similar. However, patients in the control group required higher doses of vasodilators, inotropes, and antiarrhythmic agents. Mean arterial pressure in the milrinone group was significantly lower at 1 h postoperatively than in the control group; however, the patients did not need many more vasopressors. Fluid restriction and diuretic agent use were more significant in the control group. Systemic arterial hypotension and vasopressor requirements with milrinone use at inotropic doses were not observed at the doses used for the study. A total of 21.7% of the patients in the control group required vasopressors in the perioperative period. Both groups demonstrated similar hematologic variables except that the hemoglobin level in the control group was significantly lower during postoperative days 1 and 7. Low-dose milrinone for a short-term during weaning from cardiopulmonary bypass may be used in patients with mitral stenosis and pulmonary hypertension for its effects on pulmonary artery pressures, less inotropic and vasopressor requirements, and fluid balance.
Patients with systolic heart failure (HF) who develop secondary pulmonary hypertension (PH) have reduced exercise capacity and increased mortality compared with HF patients without PH. We tested the hypothesis that sildenafil, an effective therapy for pulmonary arterial hypertension, would lower pulmonary vascular resistance and improve exercise capacity in patients with HF complicated by PH.
Thirty-four patients with symptomatic HF and PH were randomized to 12 weeks of treatment with sildenafil (25 to 75 mg orally 3 times daily) or placebo. Patients underwent cardiopulmonary exercise testing before and after treatment. The change in peak VO2 from baseline, the primary end point, was greater in the sildenafil group (1.8+/-0.7 mL x kg(-1) x min(-1)) than in the placebo group (-0.27 mL x kg(-1) x min(-1); P=0.02). Sildenafil reduced pulmonary vascular resistance and increased cardiac output with exercise (P<0.05 versus placebo for both) without altering pulmonary capillary wedge or mean arterial pressure, heart rate, or systemic vascular resistance. The ability of sildenafil treatment to augment peak VO2 correlated directly with baseline resting pulmonary vascular resistance (r=0.74, P=0.002) and indirectly with baseline resting right ventricular ejection fraction (r=-0.64, P=0.01). Sildenafil treatment also was associated with improvement in 6-minute walk distance (29 m versus placebo; P=0.047) and Minnesota Living With Heart Failure score (-14 versus placebo; P=0.01). Subjects in the sildenafil group experienced fewer hospitalizations for HF and a higher incidence of headache than those in the placebo group without incurring excess serious adverse events.
Phosphodiesterase 5 inhibition with sildenafil improves exercise capacity and quality of life in patients with systolic HF with secondary PH.
This study sought to test the functional exercise capacity and endothelial function in a cohort of chronic heart failure (CHF) patients treated with chronic type 5 phosphodiesterase (PDE5) inhibitor.
In CHF, endothelial dysfunction is involved in muscle underperfusion, ergoreflex oversignaling, and exercise ventilation inefficiency. Inhibition of PDE5 by improving endothelial dysfunction might be beneficial.
Stable CHF patients were randomly assigned to placebo (23 patients) or sildenafil at the dose of 50 mg twice per day (23 patients) in addition to their current drug treatment for 6 months, with assessments (at 3 and 6 months) of endothelial function by brachial artery flow-mediated dilatation (FMD), cardiopulmonary exercise testing, and ergoreflex response.
In the sildenafil group only, at 3 and 6 months we observed reduction of systolic pulmonary artery pressure (from 33.7 to 25.2 mm Hg and 23.9 mm Hg), ergoreflex effect on ventilation (from 6.9 to 2.3 l x min(-1) and 1.9 l x min(-1)), ventilation to CO2 production slope (V(E)/VCO2, from 35.5 to 32.1 and 29.8), and breathlessness (score) (from 23.6 to 16.6 and 17.2), and an increase of FMD (from 8.5% to 13.4% and 14.2%), peak VO2 (from 14.8 to 18.5 ml x min(-1) x kg(-1) and 18.7 ml x min(-1) x kg(-1)), and ratio of VO2 to work rate changes (from 7.7 to 9.3 and 10.1). All changes were significant at p < 0.01. In the sildenafil group, a significant correlation was found at 3 and 6 months between changes in FMD and those in ergoreflex. Changes in ergoreflex correlated with those in peak VO2 and V(E)/VCO2 slope. No adverse effects were noted except for flushing in 3 patients.
In CHF, improvement in exercise ventilation and aerobic efficiency with sildenafil is sustained and is significantly related with an endothelium-mediated attenuation of exercising muscle oversignaling. Chronic sildenafil seems to be a remedy based on CHF pathophysiology and devoid of remarkable adverse effects.
Pulmonary Hypertension in Heart Failure With Preserved Ejection Fraction
- Csp Lam
- V L Roger
- R J Rodeheffer
- B A Borlaug
- F T Enders
- M M Redfield
Lam CSP, Roger VL, Rodeheffer
RJ, Borlaug BA, Enders FT,
Redfield
MM.
Pulmonary
Hypertension in Heart Failure With
Preserved Ejection Fraction. J Am
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doi:10.1016/j.jacc.2008.11.051