Review

Authors: Sarah U Morton, Dara Brodsky

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

Review

Authors: Michael R Pinsky

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

Review

Authors: Susan R Hopkins, Michael K Stickland

The pulmonary circulation is a low-pressure, low-resistance circuit whose primary function is to deliver deoxygenated blood to, and oxygenated blood from, the pulmonary capillary bed enabling gas exchange. The distribution of pulmonary blood flow is regulated by several factors including effects of vascular branching structure, large-scale forces related to gravity, and finer scale factors related to local control. Hypoxic pulmonary vasoconstriction is one such important regulatory mechanism. In the face of local hypoxia, vascular smooth muscle constriction of precapillary arterioles increases local resistance by up to 250%. This has the effect of diverting blood toward better oxygenated regions of the lung and optimizing ventilation-perfusion matching. However, in the face of global hypoxia, the net effect is an increase in pulmonary arterial pressure and vascular resistance. Pulmonary vascular resistance describes the flow-resistive properties of the pulmonary circulation and arises from both precapillary and postcapillary resistances. The pulmonary circulation is also distensible in response to an increase in transmural pressure and this distention, in addition to recruitment, moderates pulmonary arterial pressure and vascular resistance. This article reviews the physiology of the pulmonary vasculature and briefly discusses how this physiology is altered by common circumstances.

Topics: Humans; Vasoconstriction; Vascular Resistance; Lung; Pulmonary Circulation; Hypoxia; Blood Pressure

PubMed: 37816344
DOI: 10.1055/s-0043-1770059

Authors: Brian Fouty

Topics: Animals; Diabetes Mellitus; Endothelium; Humans; Nitric Oxide; Pulmonary Circulation; Rats; Reactive Oxygen Species

PubMed: 18790989
DOI: 10.1152/ajplung.90482.2008

Authors: Ma Del Carmen Lacy-Niebla

Topics: Heart; History, Medieval; Pulmonary Circulation

PubMed: 34987236
DOI: 10.24875/ACM.M21000080

Review

Authors: Yuansheng Gao, J Usha Raj

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

Authors: Patrick Belvitch, Steven Dudek

Topics: Cell Membrane; Endothelium, Vascular; Humans; Lung; Pulmonary Circulation; Vascular Diseases

PubMed: 30360785
DOI: 10.1016/S1063-5823(18)30049-8

Review

Authors: Laura Filippetti, Damien Voilliot, Michele Bellino...

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

Review

Authors: I S Anand

Topics: Adaptation, Physiological; Altitude; Altitude Sickness; Blood Pressure; Humans; Hypoxia; Pulmonary Artery; Pulmonary Circulation; Vasoconstriction

PubMed: 7974321
DOI: 10.1136/thx.49.suppl.s19

Authors: Robert Naeije

Topics: Exercise; Humans; Pulmonary Circulation; Ventricular Dysfunction, Right; Ventricular Function, Right

PubMed: 27151521
DOI: 10.1016/j.jcmg.2015.07.023