Special Circulations PDF

Special Circulations systemic circulation cerebral coronary right left pulmonary heart heart skeletal cutaneous...

Special Circulations systemic circulation cerebral coronary right left pulmonary heart heart skeletal cutaneous others  Blood supply to the lungs the lungs have two circulations bronchial circulation – part of systemic circulation – meets the metabolic requirements of the lungs pulmonary circulation – blood supply to alveoli – required for gas exchange The pulmonary circulation must accept the entire cardiac output PULMONARY cardiac output at rest ~ 5 l/min RA LA maximum cardiac RV LV output ~ 20 -25 l/min (non athlete) SYSTEMIC  The pulmonary circulation works with low pressure and low resistance Pulmonary artery PULMONARY 15-30mmHg 4 -12mmHg left ventricle RA LA 100-140mmHg 0-8mmHg 1-10mmHg 1-10mmHg RV LV Aorta 100-140mmHg 60-90mmHg right ventricle 15-30mmHg SYSTEMIC 0 - 8mmHg Features of the pulmonary circulation low pressure – mean arterial pressure  12-15mmHg – mean capillary pressure  9-12mmHg – mean venous pressure  5mmHg low resistance – short, wide vessels – lots of capillaries (many parallel elements) – arterioles have relatively little smooth muscle  Adaptations to promote efficient gas exchange very high density of capillaries in alveolar wall – large capillary surface area short diffusion distance – very thin layer of tissue separating gas phase from plasma – combined endothelium & epithelium thickness is ~ 0.3 μm large surface area and short diffusion distance produce high O2 and CO2 transport capacity  Blood-gas barrier electron micrograph of alveolar septum alveolus type I pneumocyte (epithelial cell) endothelial cell capillary erythrocyte lumen From: Wheater’s Functional Histology (Young & Heath)  Ventilation – Perfusion ratio for efficient oxygenation need to match ventilation of alveoli with perfusion of alveoli divert blood from alveoli which are not well ventilated  Hypoxic pulmonary vasoconstriction ensures optimal ventilation perfusion ratio most important mechanism regulating pulmonary vascular tone alveolar hypoxia results in vasoconstriction of pulmonary vessels ensures that perfusion matches ventilation poorly ventilated alveoli are less well perfused helps to optimise gas exchange Chronic hypoxic vasoconstriction can cause right ventricular failure Chronic hypoxia can occur at altitude or as a consequence of lung disease such as emphysema. – chronic increase in vascular resistance - chronic pulmonary hypertension – high afterload on right ventricle - can lead to right ventricular heart failure  Low pressure pulmonary vessels are strongly influenced by gravity In the upright position (orthostasis) there is greater hydrostatic pressure on vessels in the lower part of the lung apex vessels collapse during diastole vessels continuously patent heart vessels distended by gravity  Effect of exercise on pulmonary blood flow increased cardiac output small increase in pulmonary arterial pressure opens apical capillaries increased O2 uptake by lungs as blood flow increases capillary transit time is reduced – at rest transit time ~ 1s – can fall to ~ 0.3s without compromising gas exchange  Low capillary pressure minimises the formation of lung lymph Interstitial oncotic pressure Hydrostatic pressure arterial end venous end Plasma oncotic pressure filtration ≈ reabsorption Oncotic pressure = osmotic pressure due to non-permeant molecules such as proteins  Increased capillary pressure causes more fluid to filter out → oedema Interstitial oncotic pressure arterial end venous end Hydrostatic pressure increased venous pressure Plasma oncotic pressure filtration > reabsorption  Low capillary pressure prevents pulmonary oedema Pulmonary capillary pressure is normally low (9 - 12mmHg) – only a small amount of fluid leaves the capillaries (lung lymph) Can get pulmonary oedema if capillary pressure increases – if the left atrial pressure rises to 20 - 25 mmHg Mitral valve stenosis Left ventricular failure  Pulmonary Oedema Pulmonary oedema impairs gas exchange Use diuretics to relieve symptoms Treat underlying cause  Cerebral Circulation The brain has a high O2 demand Receives about 15% of cardiac output – but only accounts for 2% of body mass O2 consumption of grey matter accounts for ~ 20% of total body consumption at rest Must provide a secure O 2 supply  How does the cerebral circulation meet the high demand for O2? high capillary density – large surface area for gas exchange – reduced diffusion distance ( 20 times in active muscle At rest only ~ ½ of capillaries are perfused at any one time – allows for increased recruitment  Increased flow due to metabolic hyperaemia Various agents are thought to act as vasodilators – ↑[K+] – ↑ osmolarity – Inorganic phosphates – Adenosine – ↑[H+] Adrenaline also acts as a vasodilator at arterioles in skeletal muscle – Acts through β2 receptors – Vasoconstrictor response via NA on α1 receptors  Cutaneous circulation Special role in temperature regulation Core temperature is normally maintained around 37oC Balance of heat production and heat loss Skin is the main heat dissipating surface – This is regulated by cutaneous blood flow Acral (apical) skin has specialised structures called artereovenous anastomoses (AVAs) AVAs regulate heat loss from apical skin Apical (acral) skin has a high surface area to volume ratio AVAs are under neural control – sympathetic vasoconstrictor fibres Not regulated by local metabolites Decrease core temperature increases sympathetic tone in AVAs – decreases blood flow to apical skin Increased core temperature opens AVAs AVAs regulate heat loss from apical skin reduced vasomotor drive to AVA’s allows them to dilate low resistance shunt to venous plexus allows skin temperature to rise so dissipating heat  Special Circulations Each circulation has a special task There are structural and functional adaptations to meet that task Clinical problems associated with some circulations