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Clinics in Perinatology Sep 2016The physiology of the fetus is fundamentally different from the neonate, with both structural and functional distinctions. The fetus is well-adapted to the relatively... (Review)
Review
The physiology of the fetus is fundamentally different from the neonate, with both structural and functional distinctions. The fetus is well-adapted to the relatively hypoxemic intrauterine environment. The transition from intrauterine to extrauterine life requires rapid, complex, and well-orchestrated steps to ensure neonatal survival. This article explains the intrauterine physiology that allows the fetus to survive and then reviews the physiologic changes that occur during the transition to extrauterine life. Asphyxia fundamentally alters the physiology of transition and necessitates a thoughtful approach in the management of affected neonates.
Topics: Adaptation, Physiological; Ductus Arteriosus; Female; Fetus; Foramen Ovale; Heart; Humans; Infant, Newborn; Lung; Parturition; Pregnancy; Pulmonary Circulation
PubMed: 27524443
DOI: 10.1016/j.clp.2016.04.001 -
Critical Care (London, England) Sep 2016The primary role of the right ventricle (RV) is to deliver all the blood it receives per beat into the pulmonary circulation without causing right atrial pressure to... (Review)
Review
The primary role of the right ventricle (RV) is to deliver all the blood it receives per beat into the pulmonary circulation without causing right atrial pressure to rise. To the extent that it also does not impede left ventricular (LV) filling, cardiac output responsiveness to increased metabolic demand is optimized. Since cardiac output is a function of metabolic demand of the body, during stress and exercise states the flow to the RV can vary widely. Also, instantaneous venous return varies widely for a constant cardiac output as ventilatory efforts alter the dynamic pressure gradient for venous return. Normally, blood flow varies with minimal changes in pulmonary arterial pressure. Similarly, RV filling normally occurs with minimal increases in right atrial pressure. When pulmonary vascular reserve is compromised RV ejection may also be compromised, increasing right atrial pressure and limiting maximal cardiac output. Acute increases in RV outflow resistance, as may occur with acute pulmonary embolism, will cause acute RV dilation and, by ventricular interdependence, markedly decreased LV diastolic compliance, rapidly spiraling to acute cardiogenic shock and death. Treatments include reversing the causes of pulmonary hypertension and sustaining mean arterial pressure higher than pulmonary artery pressure to maximal RV coronary blood flow. Chronic pulmonary hypertension induces progressive RV hypertrophy to match RV contractility to the increased pulmonary arterial elastance. Once fully developed, RV hypertrophy is associated with a sustained increase in right atrial pressure, impaired LV filling, and decreased exercise tolerance. Treatment focuses on pharmacologic therapies to selectively reduce pulmonary vasomotor tone and diuretics to minimize excessive RV dilation. Owning to the irreversible nature of most forms of pulmonary hypertension, when the pulmonary arterial elastance greatly exceeds the adaptive increase in RV systolic elastance, due to RV dilation, progressive pulmonary vascular obliteration, or both, end stage cor pulmonale ensues. If associated with cardiogenic shock, it can effectively be treated only by artificial ventricular support or lung transplantation. Knowing how the RV adapts to these stresses, its sign posts, and treatment options will greatly improve the bedside clinician's ability to diagnose and treat RV dysfunction.
Topics: Cardiac Output; Heart Ventricles; Humans; Hypertension, Pulmonary; Pulmonary Circulation; Ventricular Dysfunction, Right
PubMed: 27613549
DOI: 10.1186/s13054-016-1440-0 -
Archivos de Cardiologia de Mexico 2022
Topics: Heart; History, Medieval; Pulmonary Circulation
PubMed: 34987236
DOI: 10.24875/ACM.M21000080 -
Current Topics in Membranes 2018
Topics: Cell Membrane; Endothelium, Vascular; Humans; Lung; Pulmonary Circulation; Vascular Diseases
PubMed: 30360785
DOI: 10.1016/S1063-5823(18)30049-8 -
Seminars in Respiratory and Critical... Oct 2010Aging is associated with a progressive deterioration in the structure and function of the pulmonary circulation. Remodeling of the pulmonary vasculature occurs from... (Review)
Review
Aging is associated with a progressive deterioration in the structure and function of the pulmonary circulation. Remodeling of the pulmonary vasculature occurs from maturity to senescence that is characterized by an increase in pulmonary vascular stiffness, pulmonary vascular pressures, and pulmonary vascular resistance along with increased heterogeneity of alveolar ventilation and pulmonary perfusion and decreased pulmonary capillary blood volume and membrane diffusing capacity that is consistent with a reduction in alveolar-capillary surface area. In theory, the aforementioned age-related changes in the pulmonary circulation may conspire to make elderly individuals more susceptible to gas exchange abnormalities during exercise. However, despite the erosion in ventilatory reserve with aging, the healthy older adult appears able to maintain alveolar ventilation at a level that allows maintenance of arterial blood gases within normal limits, even during heavy exercise. This ability to maintain adequate gas exchange likely occurs because age-related reductions in the maximal metabolic demand of exercise occur at a rate equal to or greater than the rate of deterioration in ventilatory reserve. A more prominent aspect of aging is the loss of lung elastic recoil that is associated with a modest reduction in the expiratory boundary of the maximal flow-volume envelope. This in turn increases the severity of expiratory airflow limitation and induces dynamic lung hyperinflation during exercise. The consequences of this age-associated decrease in elastic recoil on the pulmonary circulation are speculative, but an age-associated decline in elastic recoil may influence pulmonary vascular resistance and cardiac output, in addition to its impact on the work and oxygen cost of breathing.
Topics: Aged; Aging; Exercise; Exercise Tolerance; Heart Failure; Humans; Lung; Pulmonary Circulation; Pulmonary Gas Exchange; Pulmonary Ventilation
PubMed: 20941654
DOI: 10.1055/s-0030-1265894 -
Physiological Reviews Oct 2010During the development of the pulmonary vasculature in the fetus, many structural and functional changes occur to prepare the lung for the transition to air breathing.... (Review)
Review
During the development of the pulmonary vasculature in the fetus, many structural and functional changes occur to prepare the lung for the transition to air breathing. The development of the pulmonary circulation is genetically controlled by an array of mitogenic factors in a temporo-spatial order. With advancing gestation, pulmonary vessels acquire increased vasoreactivity. The fetal pulmonary vasculature is exposed to a low oxygen tension environment that promotes high intrinsic myogenic tone and high vasocontractility. At birth, a dramatic reduction in pulmonary arterial pressure and resistance occurs with an increase in oxygen tension and blood flow. The striking hemodynamic differences in the pulmonary circulation of the fetus and newborn are regulated by various factors and vasoactive agents. Among them, nitric oxide, endothelin-1, and prostaglandin I(2) are mainly derived from endothelial cells and exert their effects via cGMP, cAMP, and Rho kinase signaling pathways. Alterations in these signaling pathways may lead to vascular remodeling, high vasocontractility, and persistent pulmonary hypertension of the newborn.
Topics: Fetus; Gene Expression Regulation, Developmental; Humans; Infant, Newborn; Lung; Pulmonary Circulation; Respiration
PubMed: 20959617
DOI: 10.1152/physrev.00032.2009 -
Annual International Conference of the... 2009Long-standing pulmonary hypertension causes significant peripheral and proximal arterial remodeling and right ventricular dysfunction. The clinical metric most often... (Review)
Review
Long-standing pulmonary hypertension causes significant peripheral and proximal arterial remodeling and right ventricular dysfunction. The clinical metric most often used to assess the progression of PH is the pulmonary vascular resistance (PVR). However, even when measured from multipoint pressure-flow curves, PVR provides information only on the peripheral arterial function, not the proximal arterial function and gives only an incomplete description of all the forces that oppose right ventricular (RV) flow output. Pulmonary vascular impedance spectra (PVZ) capture the impact of proximal and peripheral arterial structure and function on RV function. Analyses of ventricular-vascular coupling give insight into the efficiency of mechanical and metabolic interactions between the right ventricle and the pulmonary vasculature. Here we review techniques for measuring PVZ in humans and animal models and for determining RV function.
Topics: Algorithms; Animals; Blood Pressure; Blood Pressure Determination; Computer Simulation; Diagnosis, Computer-Assisted; Humans; Models, Cardiovascular; Pulmonary Artery; Pulmonary Circulation; Ventricular Function, Right
PubMed: 19964469
DOI: 10.1109/IEMBS.2009.5333835 -
Heart Failure Clinics Jul 2018Valvular heart disease (VHD) is frequently accompanied by pulmonary hypertension (PH). In asymptomatic patients, PH is rare, although the exact prevalence is unknown and... (Review)
Review
Valvular heart disease (VHD) is frequently accompanied by pulmonary hypertension (PH). In asymptomatic patients, PH is rare, although the exact prevalence is unknown and mainly stems from the severity of the VHD and the presence of diastolic dysfunction. PH can also be depicted during exercise echocardiography. PH either at rest or during exercise is also a powerful determinant of outcome and is independently associated with reduced survival, regardless of the severity of the underlying valvular pathology. Therefore, because PH is a marker of poor prognosis, assessment of PH in VHD is crucial for risk stratification and management of patients with VHD.
Topics: Echocardiography; Exercise; Heart Valve Diseases; Heart Ventricles; Humans; Hypertension, Pulmonary; Prognosis; Pulmonary Circulation; Ventricular Dysfunction, Right
PubMed: 29966640
DOI: 10.1016/j.hfc.2018.03.009 -
Kidney & Blood Pressure Research 2007Numerous uremic patients on hemodialysis have pulmonary hypertension attributable to the presence of arteriovenous fistulas, vascular calcification, and endothelial... (Review)
Review
Numerous uremic patients on hemodialysis have pulmonary hypertension attributable to the presence of arteriovenous fistulas, vascular calcification, and endothelial dysfunction due to alterations in the balance between vasoconstrictive and vasodilatory substances. For these reasons, the effects of recombinant human erythropoietin, a drug widely used in patients on dialysis, on the pulmonary circulation were studied. Some authors maintain that recombinant human erythropoietin has an antihypertensive effect, while others have observed that this hormone induces a reduction in pulmonary arterial pressure due to its vasoactive and stimulatory effects on endothelial and smooth muscle cell precursors.
Topics: Animals; Antihypertensive Agents; Erythropoietin; Humans; Hypertension, Pulmonary; Pulmonary Circulation; Recombinant Proteins; Renal Dialysis
PubMed: 17587864
DOI: 10.1159/000104443 -
American Journal of Physiology. Lung... Nov 2008
Topics: Animals; Diabetes Mellitus; Endothelium; Humans; Nitric Oxide; Pulmonary Circulation; Rats; Reactive Oxygen Species
PubMed: 18790989
DOI: 10.1152/ajplung.90482.2008