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Pulmonary Lymph and Lymphatics
Published in Waldemar L. Olszewski, Lymph Stasis: Pathophysiology, Diagnosis and Treatment, 2019
The entire cardiac output passes through the pulmonary arteries, and a small amount of blood enters the lungs through the bronchial arteries. Some fluid passes from the vascular system to the pulmonary interstitium and the pulmonary lymphatics as determined by the Starling equation. The Starling equation defines the rate of trans vascular fluid flux across a capillary membrane. Under normal conditions, fluid fluxing across the pulmonary vascular endotheium according to the forces in Starling’s equation is subsequently drained from the interstitium by the efficient action of the lung lymphatics.
The Adult Respiratory Distress Syndrome and the Microcirculation
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
The physiologic basis for filtration of liquid and protein across any semipermeable barrier was proposed by Starling in 1986.14 Starling’s equation has been used extensively in the last 25 years for both experimental and clinical purposes to understand the pathophysiologic basis for the pulmonary edema that occurs in ARDS. The Starling equation predicts that the net flow of liquid across a semipermeable barrier is the product of the driving pressure (both hydrostatic and osmotic pressures) and the conductance, or permeability, of the barrier. The equation is:
Circulation of fluid between plasma, interstitium and lymph
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
As we shall see, the Starling equation is central to understanding disorders such as oedema, inflammatory swelling and posthaemorrhagic fluid absorption. However, it must be remembered that ni is a rough substitute for the true factor πg, and in some circumstances the distinction is important (Section 11.6).
Emerging therapeutic targets for cerebral edema
Published in Expert Opinion on Therapeutic Targets, 2021
Ruchira M. Jha, Sudhanshu P. Raikwar, Sandra Mihaljevic, Amanda M. Casabella, Joshua S. Catapano, Anupama Rani, Shashvat Desai, Volodymyr Gerzanich, J. Marc Simard
The Monro-Kellie doctrine, described over two centuries ago, outlines the principle that a rigid skull necessitates a fixed sum of intracranial components (blood, CSF/interstitial fluid, brain tissue) whereby an increase in one causes a reciprocal decrease in one (or more) of the others. Once these compensatory reserves are exhausted, ICP rises and can cause herniation and death. The threshold at which this occurs varies between individuals and is a function of intracranial elastance and compliance [8]. Conceptually, this has provided the basis for several current approaches to edema including CSF diversion (external ventricular drain, EVD), reduction in metabolic demand and CBF (sedation, hypothermia), and hyperosmotic agents (mannitol, hypertonic saline). At a local level, the modified Starling equation [quantifies the net flow (Jv) of water across membranes by leveraging differences in capillary (c) vs. interstitial (i) hydrostatic (P) and oncotic (p) pressures [8,18]. This principle explains the action/benefit of hyperosmotic therapies whereby water moves from the brain interstitium and intracellular compartments into the vasculature. The phenomenon of rebound edema can be observed with repeated administration of mannitol or hypertonic saline; it is related to breakdown of the blood–brain barrier (BBB) and accumulation of the hyperosmolar agent within the interstitium/outside an intact vasculature creating a reverse-osmolar gradient.
Phases of fluid management and the roles of human albumin solution in perioperative and critically ill patients
Published in Current Medical Research and Opinion, 2020
Endothelial functions including inflammation and permeability are determined by the glycocalyx, a network of proteoglycans and glycoproteins that coats the luminal surface of vascular endothelium (Figure 1)74,75. The predominant proteoglycans of the glycocalyx are the transmembrane-bound-syndecan and the membrane-bound glypican, bound to which are glycosaminoglycan side chains, mostly heparan sulfate but also others such as hyaluronic acid and chondroitin sulfate. Diverse glycoproteins are found in the glycocalyx, including the cell adhesion molecules as well as receptors involved in intercellular signaling, fibrinolysis, and coagulation. Also incorporated into the glycocalyx scaffold network are various other molecules derived from the endothelium or plasma, including serum albumin76. Understanding the effects of the glycocalyx on oncotic pressure differences across blood vessel walls led to the “revised” or “extended” Starling equation of transvascular fluid exchange77,78, although Hahn et al. noted that this principle may not fully account for the dynamic nature of the circulatory system and clinical observations in fluid therapy studies79.
Recognition and management of idiopathic systemic capillary leak syndrome: an evidence-based review
Published in Expert Review of Cardiovascular Therapy, 2018
Noor Ul-Ain Baloch, Marvi Bikak, Abdul Rehman, Omar Rahman
At a molecular level, capillaries are the relay between arterial and venous circulations. Flow into the capillary beds is controlled by periarteriolar muscular sphincters, which contract and relax serving as a valve to forward flow. Moreover, exchange of particles at the molecular level is governed by the differences in hydrostatic and oncotic pressures of the capillary and interstitium (Starling equation). A delicate balance of chemical mediators is responsible for maintaining normal flow to the capillary bed and ensuring normal exchange of substances at the molecular level without promoting capillary leak. Patients with SCLS have unexplained episodes of capillary leakage [15] that may or may not be preceded by a clear precipitant. In the cohort of Kapoor et al. (2010), 56% of patients reported a flu-like illness prior to the development of hypotension and shock [9]. In a few recent reports, influenza A virus infection was implicated as a possible precipitant of capillary leakage in patients with SCLS [16,17]. In the published literature, reports of capillary leakage following administration of general anesthesia [18], gemcitabine [19], trastuzumab [20], and filgrastim [21] have been described.