Microcirculation Handouts PDF

Specialised flow (skin) Guyton p868 12th ed, p912 13th ed Specialised flow (lungs) Decreased alveolar O2 reduces local alveolar blood flow – Opposite to effect observed in systemic vessels – Mediator unknown Specialised flow (kidney) Learning outcomes To identify the major routes across capil...

Specialised flow (skin) Guyton p868 12th ed, p912 13th ed Specialised flow (lungs) Decreased alveolar O2 reduces local alveolar blood flow – Opposite to effect observed in systemic vessels – Mediator unknown Specialised flow (kidney) Learning outcomes To identify the major routes across capillary membranes of fluids, solutes and larger molecules/proteins. To explain how Starling’s forces contribute to fluid homeostasis and the net transcapillary movement of water across capillary beds, including the importance of the lymphatic system. To describe the factors which affect venous return and consequently determine cardiac output and blood pressure. 6. Microcirculation, venous blood flow and venous return MD3001 Dr Alun Hughes 5 Cardiovascular physiology 1) 2) 3) 4) 5) 6) 7) 8) 9) Circulation of blood Physiological properties of the heart Cardiac contractility and the cardiac cycle Control of cardiac output Vasculature Microcirculation Control of blood pressure Control of blood volume Exercise and blood flow through special regions 6 Lecture overview Oncotic and hydrostatic pressures Balance of Starling forces Lymphatic drainage Venous return 7 Capillary diffusion Naish p614 Interstitium and interstitial fluid Interstitium • Collagen and proteoglycan filaments Interstitial fluid • Fluid trapped amongst filaments • “Tissue gel” • ~ 1% of water “free” • Diffusion occurs in gel ~95-99% as rapidly in free fluid Diffusion vs bulk flow / filtration Guyton p180 12th ed, p192 13th ed Transfer Crystalloids – Low mol. wt. solutes • e.g. Na+, Cl-, K+ Colloids – Plasma proteins Diffusion – Net movement of nutrients, oxygen and metabolic end products Bulk flow – Distribution of extracellular fluid Oncotic pressure (a.k.a. colloid osmotic pressure) Capillary wall is (generally) a barrier to proteins – Readily permeable to water and most solutes – Not a perfect filter • Permeability for albumin is 1/1000th that of water Oncotic pressure generated by plasma proteins – ~28mmHg – Predominately generated by albumin, lesser extent by globulins Plasma oncotic pressure draws fluid in to capillaries – Interstitial oncotic pressure is much lower (~5-8mmHg) Hydrostatic pressure Capillary hydrostatic pressure – Forces fluid out of the capillaries and in to the interstitium – Drops from arterial end to venous end • Pressure at arterial end ~30-40mmHg • Pressure at venous end ~10-15mmHg Interstitial hydrostatic pressure – Forces fluid in to the capillary when positive – Draws fluid in to the interstitium when negative Remember: flow to capillaries fluctuates – Changes in hydrostatic pressure follows, affects fluid flow – When averaged over time and capillaries, general observations hold true Starling forces Guyton p181 12th ed, p193 13th ed Starling forces Capillary Arteriole end Lymph duct Venule end Starling forces Naish p615 Lymphatic system Capillaries loose more water than they gain • Approx. 2-3L per day Lymphatic system • Large, fenestrated walls of capillaries • Drain via lymphatic vessels • Pass through lymph nodes Important in controlling: • Concentration of proteins in interstitial fluids • Volume of interstitial fluid • Interstitial fluid pressure • Also in immune response Rhoades p282 Figure 15.3 Systemic venous circulation Low pressure system – Between 3-18mmHg High volume system – Holds ~60% of total blood volume Venous return to the heart is a major determinant of cardiac output – Frank-Starling mechanism Guyton p158 12th ed, p170 13th ed 17 Venous return Sympathetic innervation Muscle pumps Inspiratory movements – Diaphragm descends • ↑ abdominal pressure • Transmitted passively to intraabdominal veins – ↓ Pressure in thorax • ↓ pressure in intrathoracic veins and right atrium – ↑pressure difference between peripheral veins and heart Blood volume – E.g. Hemorrhage, fluid challenge Sympathetic innervation Sympathetic innervation of veins increases venous return to the heart  increases cardiac output – Important in exercise, blood loss etc Guyton p202 12th ed p216 13th ed Postural effects Standing completely still – Pressure ↑ by 1mmHg for each 13.6mm below the surface • By feet +90mmHg – Mean arterial pressure at level of heart ~100mmHg – So, in feet ~190mmHg – Leg oedema • 10-20% of blood volume within 15-30min But… venous valves and ‘venous pump’ Guyton p185 Figure 15.10 Vein valves Guyton p174 12th ed p186 13th ed Muscle pumps Naish p618 Postural changes in hydrostatic pressure Orthostatic (postural) hypotension – Immediate effect in going from supine to upright • Around 500 ml of blood from the upper body to legs • ↓ venous return –  ↓ cardiac output –  ↓ blood pressure – Reflex vasoconstriction in legs and lower abdomen • Takes a few seconds to kick in Main points Fluid forces favour small amounts of loss into tissue space, reclaimed as lymph The venous system is high-volume, low pressure system Compliance of veins can be adjusted by sympathetic innervation Venous return limits cardiac output 24 Learning outcomes To identify the major routes across capillary membranes of fluids, solutes and larger molecules/proteins. To explain how Starling’s forces contribute to fluid homeostasis and the net transcapillary movement of water across capillary beds, including the importance of the lymphatic system. To describe the factors which affect venous return and consequently determine cardiac output and blood pressure.