Specific Circulations Notes

NOTES NOTES SPECIFIC CIRCULATIONS CEREBRAL CIRCULATION osms.it/cerebral-circulation ▪ Cerebral circulation: managed almost entirely by local (intrinsic) control (autoregulation; active, reactive hyperemia) ▫ ↑ pCO2 (↑H+, ↓pH) → arteriolar vasodilation → ↑ blood flow → CO2 removal (most vasoactive metabolites too big to cross blood-brain barrier → do not affect cerebral tissue ▫ Hyperventilation works by same mechanism → ↓ pCO2 → vasoconstriction (used to reduce swelling in situations of cerebral edema) CEREBRAL BLOOD SUPPLY SEGMENTATION ▪ Cerebral blood supply separated into anterior, posterior segments ▪ Anterior, posterior circulatory segments join via arterial posterior communicating arteries, form circle of Willis ▫ Back-up circulation in case of blood vessel occlusion 152 OSMOSIS.ORG Anterior segment ▪ Supplied by internal carotid arteries ▪ Enter skull in carotid canal, branch out ▫ Ophthalmic arteries: supply eyes, orbits, forehead, nose ▫ Anterior cerebral artery: medial part of frontal, parietal lobes; anastomoses with counterpart via anterior communicating artery (part of circle of Willis) ▫ Middle cerebral artery: supplies lateral sides of temporal, parietal, frontal lobes Posterior segment ▪ Supplied by vertebral arteries ▪ Enter skull through foramen magnum, branch out ▫ Right, left vertebral arteries fuse in skull → basilar artery which supplies brainstem, cerebellum, pons ▫ Posterior cerebral arteries: supply occipital lobes, inferior parts of temporal lobes

Chapter 21 Cardiovascular Physiology: Specific Circulations CORONARY CIRCULATION osms.it/coronary-circulation ▪ Coronary arteries: blood vessels delivering oxygenated blood to heart (myocardium) ▪ Cardiac veins: blood vessels retrieving deoxygenated blood from heart CORONARY ARTERIES ▪ Two coronary arteries emerge from base of aorta, surround heart in coronary sulcus Left coronary artery ▪ Two branches; supplies left atrium, left ventricle, interventricular septum ▫ Circumflex artery: supplies left atrium, posterior wall of left ventricle ▫ Anterior interventricular artery: supplies interventricular septum, anterior walls of ventricles Right coronary artery ▪ Two branches; supplies right atrium, right ventricle, part of left ventricle, electrical conduction system ▫ Right marginal artery: supplies lateral right side of heart, superficial parts of ventricle ▫ Posterior interventricular artery: supplies interventricular septum, posterior walls of ventricles CORONARY CIRCULATION CONTROL ▪ Coronary circulation managed primarily by local (intrinsic) control, secondarily by sympathetic nervous system ▪ ↑ oxygen demand → ↑ blood flow ▪ Active hyperemia via local (intrinsic) control triggers ▫ Hypoxia → build-up of metabolites ADP, AMP → degraded to adenosine (potent vasodilator) → binds to coronary vascular smooth muscle → ↓ calcium influx into cells → vasodilation → ↑ blood flow, oxygen delivery ▪ Other intrinsic control of vascular tone provided by endothelial factors ▫ Endothelium-derived nitric oxide: relaxes arterial smooth muscle ▫ Prostacyclin: vasodilator ▫ Endothelium-derived hyperpolarizing factor (EDHF): vasodilator ▫ Endothelin 1: vasoconstrictor ▪ Reactive hyperemia ▫ Brief arterial occlusion period during systole → ↓ blood flow → ↑ O2 debt → vasodilation during diastole → ↑ blood flow → O2 demands are met OSMOSIS.ORG 153

CONTROL OF BLOOD FLOW CIRCULATION osms.it/blood-flow ▪ Blood flow regulation ▫ Intrinsic (local): humoral, myogenic control ▫ Extrinsic (systemic): hormonal, neural LOCAL (INTRINSIC) BLOOD FLOW CONTROL Mechanisms ▪ Humoral: mediated by vasoactive substances ▫ Histamine, nitric oxide (arteriole dilation) ▫ Endothelin, serotonin ▪ Autoregulation: maintains constant blood flow via direct control of arterial resistance ▫ Present in organs such as kidneys, brain, heart, skeletal muscle (e.g. ↓ coronary artery pressure → compensatory arteriole vasodilation → ↓ vessel resistance → constant blood flow) ▪ Active hyperemia: ↑ blood flow directed to organ/tissue associated with ↑ metabolic activity (e.g. ↑ blood flow in active skeletal muscle) ▪ Reactive hyperemia: temporary ↑ blood flow following ischemia (↓ blood flow) in organ (e.g. arterial occlusion → ↓ blood flow → ↑ O2 debt → vasodilation, ↑ blood flow) ▪ Myogenic hypothesis for autoregulation ▫ Focus on arteriolar resistance: vascular smooth muscle contracts upon stretching (↑ wall tension) and vice versa ▫ ↑ blood flow → arteriole stretching → contraction → ↑ resistance → constant blood flow ▫ ↓ blood flow → ↓ arteriole stretching → relaxation → ↓ resistance → constant blood flow ▫ Explained by law of Laplace: ↑ pressure (P) + ↓ radius (r) → tension (T) remains constant (T=P x r) 154 OSMOSIS.ORG ▪ Metabolic hypothesis for autoregulation, active, reactive hyperemia ▫ O2 distribution changes in response to O2 consumption via altering arteriolar resistance ▫ ↑ metabolism → ↑ vasodilating metabolites (CO2, H+, K+, lactate, adenosine) → arteriole vasodilation → ↓ resistance → ↑ blood flow, O2 distribution ▫ Certain tissues more susceptible to certain metabolites (coronary circulation—PO2, adenosine; cerebral circulation—PCO2) NEURAL & HORMONAL (EXTRINSIC) CONTROL ▪ Neural: sympathetic nervous system acts on vascular smooth muscle ▫ ɑ1: vasoconstriction → skin, intestines ▫ β2: vasodilation → lungs, skeletal muscles ▪ Hormonal: vasopressin released from anterior pituitary → vasoconstriction

Chapter 21 Cardiovascular Physiology: Specific Circulations MICROCIRCULATION & STARLING FORCES osms.it/microcirculation-starling-forces ▪ Microcirculation: vascular network involving capillaries, lymphatic vessels Capillaries ▪ Vessels: thin walls lined with endothelial cells ▪ Arterioles → metarterioles → capillaries → venules → veins ▫ Metarterioles end in precapillary sphincters → smooth muscle ring controls blood flow/capillary exchange rate by constricting/relaxing ▫ Capillary blood flow regulated by intrinsic (local), extrinsic (systemic) control CAPILLARY EXCHANGE ▪ Capillaries: exchange sites for nutrients, waste, fluids between interstitial, vascular space ▫ Afferent blood: capillaries → interstitial space → tissue ▫ Efferent blood: tissue → interstitial space → capillaries Capillary exchange types ▪ Simple diffusion: substance exchange through lipid bilayer/between capillary wall’s epithelial cells ▫ Depends on driving force (partial pressure gradient), available diffusion area ▫ Driving force: substances move across their own partial pressure gradient (towards ↓ concentration area) ▫ Lipid soluble substances (O2, CO2) pass through lipid bilayer ▫ Water soluble substances (ions, glucose, amino acids) pass between endothelial cells through fluid-filled intercellular clefts/fenestrations ▪ Vesicular transport: large molecule exchange (proteins) via pinocytic vesicles (caveolae) ▫ In some tissues (kidney, intestine) proteins pass through capillary fenestrations ▪ Osmosis: if capillary wall has aqueous pores, pressure gradient across membrane, driven by Starling forces STARLING FORCES ▪ Capillary filtration/absorption depend on Starling forces: hydrostatic, colloid osmotic (oncotic) pressure ▫ Filtration: fluid movement from capillaries → interstitium ▫ Absorption: fluid movement from interstitium → capillaries Hydrostatic pressure ▪ Pressure exerted by fluid against capillary wall ▪ Capillary hydrostatic pressure (Pc) ▫ Favors filtration: tends to move fluid out of capillaries ▫ Blood pressure ↓ throughout capillary beds → arterial (37mmHg) > venous (17mmHg) pressure ▪ Interstitial fluid hydrostatic pressure (Pi) ▫ Opposes filtration: pressure exerted outside capillary wall ▫ Tends to move fluid into capillary ▫ Contains very little fluid → Pi considered zero, slightly positive/slightly negative (1mmHg) Colloid osmotic pressure (oncotic pressure) ▪ Pressure gradient: large non-diffusible molecules (e.g. plasma proteins) ▫ Capillary oncotic pressure (πc) (25mmHg): created by plasma proteins (primarily albumin; reflection coefficient = 1.0); opposes filtration OSMOSIS.ORG 155

▫ Interstitial oncotic pressure (πi) (0mmHg): contains very little protein; favors filtration Flow direction ▪ Arterial end of capillary ▫ Blood pressure’s outward driving force > inwardly directed oncotic pressure force → fluid moves out of vessel ▪ Venous end of capillary ▫ Oncotic pressure inward driving force > outwardly directed hydrostatic pressure → fluid moves into vessel ▪ Most fluid leaving capillary at arterial end reenters capillary before leaving venous end ▪ Fluid remaining in interstitial space recovered by lymphatic vessels ▪ Fluid movement through capillary wall is dependent on Starling force Starling equation ▪ Jv = Kf [( Pc - Pi) - (πc - πi)] ▫ Jv = fluid movement (mL/min) ▫ Kf = hydraulic conductance (wall to water permeability; depends on tissue, wall structure—e.g. fenestrated, nonfenestrated) 156 OSMOSIS.ORG LYMPH ▪ Lymphatic capillaries drain excess fluid + some proteins from interstitial space into venous system ▫ Lymphatic capillaries → lymphatic vessels → thoracic duct/right lymphatic duct → subclavian vein ▫ One way valves → unidirectional flow Edema ▪ Abnormal buildup of fluid in interstitial space ▪ Causes ▫ Imbalance of Starling forces ▫ ↑ hydrostatic capillary pressure (↑ volume—e.g. heart failure; obstruction; e.g. thrombosis) ▫ ↓ oncotic capillary pressure (↓ plasma protein —e.g. liver failure, malnourishment, nephrotic syndrome ▫ ↑ capillary permeability (burns/ inflammation) ▫ Impaired drainage (immobility; lack of/ irradiated lymphatic nodes; parasitic infections of lymphatic nodes—e.g. filariasis)