Pulmonary artery wedge pressure (PAWP) and pulmonary artery pressure (PAP) before (left) and 10 min after manual compression of arteriovenous fistula (right). Mean PAWP decreased from 25 to 15 mm Hg, systolic PAP from 62 to 36 mm Hg, diastolic PAP from 20 to 14 mm Hg, and mean PAP from 37 to 23 mm Hg. It is noteworthy that the large v wave of PCWP became smaller after the compression, suggesting the elevated left atrial pressure due to volume overload dramatically decreased.

Pulmonary artery wedge pressure (PAWP) and pulmonary artery pressure (PAP) before (left) and 10 min after manual compression of arteriovenous fistula (right). Mean PAWP decreased from 25 to 15 mm Hg, systolic PAP from 62 to 36 mm Hg, diastolic PAP from 20 to 14 mm Hg, and mean PAP from 37 to 23 mm Hg. It is noteworthy that the large v wave of PCWP became smaller after the compression, suggesting the elevated left atrial pressure due to volume overload dramatically decreased.

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Highlights • Arteriovenous fistula for hemodialysis occasionally causes heart failure. • Noninvasive assessment of arteriovenous fistula hemodynamics is not established. • Refractory heart failure developed in a patient with an arteriovenous fistula. • Echocardiography can monitor hemodynamics, directing arteriovenous fistula occlusion.

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Context 1
... 67-year-old woman with a history of kidney transplantation for polycystic kidney disease for 9 years was admitted to the cardiology section for worsening heart failure. She had been diagnosed with chronic heart failure due to hypertensive heart disease and hospital- ized for worsening of symptoms three times within 1 year. Coronary artery disease had been ruled out by coronary angiography 1 year before admission. On admission, the patient's blood pressure was 134/46 mm Hg, pulse rate was 62 beats/min, and body temper- ature was 37.1 C. A clinical examination revealed jugular vein disten- sion, third heart sound, and late-inspiratory fine crackles at the lower lung field. She had a brachiobasilic arteriovenous fistula in her left lower arm, which had been created for hemodialysis 13 years prior. The patient denied any signs of limb ischemia due to a steal phenom- enon caused by the fistula. Chest radiography showed lung conges- tion with apparent cardiomegaly (Figure 1). Her estimated glomerular filtration rate was 42.6 mL/min, and her plasma brain- type natriuretic peptide level was 1,138.8 pg/mL. Transthoracic echocardiography (Figure 2, Video 1) showed a mildly enlarged but hyperkinetic left ventricle with hypertrophy, a severely enlarged left atrium, mild mitral regurgitation, restrictive left ventricular (LV) filling pattern, and severe pulmonary hypertension, suggesting elevated LV filling pressure due to a hypertrophied left ventricle. Intravenous nitro- glycerin and furosemide were started in addition to oral administra- tion of furosemide (100 mg/d), tolvaptan (15 mg/d), amlodipine (10 mg/d), olmesartan (40 mg/d), and doxazosin (2 mg/d), which had already been administered before the worsening. After admission, her symptoms were gradually relieved, and chest radiography confirmed the improvement of the lung congestion, resulting in termi- nation of intravenous furosemide and nitroglycerin on the ninth day. However, soon after their discontinuation, lung congestion recurred, and intravenous medication was resumed and continued thereafter. To determine the contribution of the shunt flow via the arteriovenous fistula to heart failure, echocardiography was performed during its manual compression, which revealed decreases in LV end-diastolic dimension from 62 to 57 mm, in cardiac output from 5.2 to 4.5 L/min, in pulmonary artery systolic pressure from 76 to 53 mm Hg, and in the ratio of transmitral early diastolic to late diastolic flow veloc- ity from 4.30 to 2.76 after 10 min of occlusion, without significant change in mitral regurgitation, suggesting reduced LV preload and decrease in the filling pressure ( Figure 3, Videos 2 and 3). To further confirm these echocardiographic findings, invasive hemodynamic monitoring was repeated during the same maneuvers. Similarly to the echocardiographic study, pulmonary artery wedge pressure with large v waves and pulmonary artery pressures were dramatically decreased ( Figure 4). Cardiac output estimated using Fick's principle decreased from 7.1 to 5.5 L/min, indicating 1.6 L/min of the shunt flow. On the basis of this dramatic improvement in hemodynamics by manual compression, surgical closure of arteriovenous fistula was performed. Immediately afterward, her symptoms diminished, and intravenous medication was discontinued without any sign of recur- rence. The patient was discharged on the 40th day. Echocardiography 6 months after discharge showed a reduction of LV size, which revealed prominent apical hypertrophy, and a slight decrease in tricuspid regurgitation within the grade of mild, along with decrease in LV filling pressure suggested by transmitral flow pattern and tricuspid regurgitation velocity ( Figure 5, Video ...

Citations

... Temporary compression in patients with pre-and/or post-capillary PH can reveal the effect of elevated CO on mPAP but cannot determine the precise impact on PCWP and PVR. 52 Finally, inotropes have also been helpful in PH challenge tests. Dobutamine infusion has been used to assess pulmonary vasodilation and RV contractility reserve, especially in patients who cannot exercise. ...
Article
The classic definition of pulmonary arterial hypertension (PAH) is a mean pulmonary artery pressure (mPAP) of 20 mmHg. The gold standard for assessing pulmonary hemodynamics is right heart catheterization (RHC), which is necessary to confirm the diagnosis of PH. In some instances, RHC evaluates the degree of hemodynamic dysfunction and performs vasoreactivity tests. Measurement of the hepatic venous pressure gradient remains the gold standard diagnostic for identifying portal hypertension. This review aims to describe the procedure of RHC and the hemodynamic measurement in patients with PAH and Portopulmonary hypertension (PoPH). The RHC remains the gold standard for diagnosing PAH and PoPH.
... Temporary compression in those with pre-and/or postcapillary PH can reveal the effect of elevated CO on mPAP but cannot determine the precise impact on PCWP and PVR. 37 Finally, inotropes have also been shown to be useful in provocative testing for PH. Dobutamine infusion has been used to assess pulmonary vasodilatory and RV contractility reserve, especially in patients who cannot exercise. ...
... Patients usually have a rapid decrease in CO and PAP, that could be followed by a more pronounced drop in mPAP over time 84 . In patients with pre and/or postcapillary PH, a temporary compression will inform on the impact an elevated CO has on the mPAP, but the precise impact on PAWP and PVR needs further investigation 85 . High vascular access flow should be monitored regularly with clinical assessments (signs of congestive heart failure), access flow measurements (with ultrasonography), and echocardiographic assessments (left and right ventricular size and function and estimated right ventricular systolic pressure) 86 . ...
Article
Full-text available
Right heart catheterization (RHC) is needed to diagnose pulmonary hypertension (PH). Traditional hemodynamic determinations may be insufficient to identify early stages of the disease and the mechanism of PH, confidently allocate patients to the pre- and/or postcapillary groups of the disease and guide certain treatment decisions (e.g. use of calcium channel blockers). In this review, we discuss the role of established (pulmonary vasodilatory, exercise and rapid fluid infusion challenges) and promising maneuvers (passive leg raising, intrathoracic pressure estimation, temporary exclusion of arteriovenous dialysis accesses and dobutamine infusion) that help interrogate the pulmonary vasculature during RHC, with a focus on describing rationale for use, indications, contraindications, protocols and implications of different responses.
Article
Full-text available
Pulmonary hypertension (PH) is a heterogenous disorder involving multiple pathophysiological processes that ultimately affect the vasculature within the lungs. Right heart catheterization (RHC) continues to be the benchmark for diagnosing PH. The use of provocation techniques during RHC can help sub-characterize the type of PH and thus assist in developing appropriate treatment strategies for the management of each PH subtype. This review examines proven and novel approaches for evaluating the pulmonary vasculature during RHC and aspires to provide an accurate, clinically relevant framework for using RHC to diagnose and manage PH. Further improvement in standardized protocols will help optimize the application of RHC in patients with PH.