The hemodynamic effects of mechanical ventilation can be grouped into three clinically relevant concepts. First, since spontaneous ventilation is exercise. In patients increased work of breathing, initiation of mechanical ventilatory support may improve O delivery because the work of breathing is reduced. Second, changes in lung volume alter autonomic tone, pulmonary vascular resistance, and at high lung volumes compress the heart in the cardiac fossa similarly to cardiac tamponade. As lung volume increases so does the pressure difference between airway and pleural pressure. When this pressure difference exceeds pulmonary artery pressure, pulmonary vessels collapse as they pass form the pulmonary arteries into the alveolar space increasing pulmonary vascular resistance. Hyperinflation increases pulmonary vascular resistance impeding right ventricular ejection. Anything that over distends lung units will increase their vascular resistance, and if occurring globally throughout the lung, increase pulmonary vascular resistance. Decreases in end-expiratory lung volume cause alveolar collapse increases pulmonary vasomotor tone by the process of hypoxic pulmonary vasoconstriction. Recruitment maneuvers that restore alveolar oxygenation without over distention will reduce pulmonary artery pressure. Third, positive-pressure ventilation increases intrathoracic pressure. Since diaphragmatic descent increases intra-abdominal pressure, the decrease in the pressure gradient for venous return is less than would otherwise occur if the only change were an increase in right atrial pressure. However, in hypovolemic states, it can induce profound decreases in venous return. Increases in intrathoracic pressure decreases left ventricular afterload and will augment left ventricular ejection. In patients with hypervolemic heart failure, this afterload reducing effect can result in improved left ventricular ejection, increased cardiac output and reduced myocardial O demand. This brief review will focus primarily on mechanical ventilation and intrathoracic pressure as they affect right and left ventricular function and cardiac output.
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http://dx.doi.org/10.21037/atm.2018.04.29 | DOI Listing |
Am J Physiol Heart Circ Physiol
January 2025
Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Increased blood pressure upon standing is considered a cardiovascular risk factor. We investigated the reproducibility of changes in aortic blood pressure, heart rate, stroke volume, cardiac output, and systemic vascular resistance during three passive head-up tilts (HUT) in 223 participants without cardiovascular medications (mean age 46 years, BMI 28 kg/m2, 54% male). Median time gap between the first and the second HUT was 9 weeks and the second and the third HUT 4 weeks.
View Article and Find Full Text PDFEgypt Heart J
January 2025
Department of Cardiology and Vascular Medicine, Faculty of Medicine, Sebelas Maret University, Surakarta, Indonesia.
Background: Precapillary pulmonary hypertension (PH) as complication in atrial septal defect (ASD) is closely related to right heart hemodynamics, such as right atrial pressure (RAP) and pulmonary vascular resistance (PVR). Right heart catheterization (RHC) as the gold standard for their measurement is invasive and not widely available in Indonesia. Electrocardiography (ECG) was proposed to be alternative in this matter.
View Article and Find Full Text PDFTransl Vis Sci Technol
January 2025
Yale Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Purpose: Alteration of visual acuity in wet age-related macular degeneration (AMD) is mostly driven by vascular endothelial growth factor A (VEGF-A)-induced edema from leaky newly forming blood vessels below the retina layers. To date, all therapies aimed at alleviation of this process have relied on inhibition of VEGF-A activity. Although effective in preventing vascular leak and edema, this approach also leads to the loss of normal vasculature and multiple related side effects.
View Article and Find Full Text PDFRheumatology (Oxford)
January 2025
The Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Objective: To explore the clinical characteristics and risk factors for adverse outcomes in patients with Sjögren's Syndrome-associated pulmonary arterial hypertension (SS-PAH).
Methods: A retrospective analysis was conducted on SS-PAH patients diagnosed by right heart catheterization (RHC) between March 2013 and March 2024 across four Chinese medical centers. Patients were categorized into primary SS-PAH (pSS-PAH) and overlap SS-PAH, based on the presence of additional autoimmune diseases.
Radiol Case Rep
March 2025
University of Maryland School of Medicine, Department of Diagnostic Radiology and Nuclear Medicine, Division of Vascular and Interventional Radiology, Baltimore, MD, USA.
Splenic steal syndrome (SSS) post liver transplant is a potential cause of graft dysfunction in the setting of peripheral hepatic arterial bed resistance and redirection of blood flow to a dominant splenic artery resulting in reduction of hepatic arterial inflow. We report utilization of balloon occlusion of the proximal splenic artery as an objective measure to confirm the diagnosis of SSS in a patient with orthotopic liver transplant followed by successful treatment with proximal splenic artery embolization using Gelfoam and Amplatzer vascular plug. Written informed consent for the publication of this case report was obtained from the patient.
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