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بسم هللا الرحمن الرحيم ﴿و ما أوتيتم من العلم إال قليال﴾ صدق هللا العظيم االسراء اية 58 Dr abdelaziz Husssein, Mansoura Faculty of Medicine By Dr. Abdel Aziz M. Hussein Lecturer of Medical Physiology Member of American Society of Physiology Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine • The pulmonary circulation is concerned with passage of blood from the Rt ventricle, through the lungs and then to the lt atrium. • The pulmonary circulation time is about 7 seconds at rest. • It receives all the COP from the right ventricle. Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine a) Pulmonary arteries: The lungs are supplied with blood from 2 sources: i) Pulmonary artery: •It transmits venous blood from the Rt ventricle to the lungs. •It branches finally to capillaries around the alveoli→ exchange of gases ( ) alveolar air and pulmonary blood. ii)Bronchial arteries: •They arise from the aorta and supply mainly the bronchi and bronchioles. •There are many anastomosis ( ) the bronchial and pulmonary arteries. Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine b) Pulmonary veins: The blood leaves the lungs by 2 ways; i) 4 pulmonary veins: • They transmit oxygenated blood from the lung to the left atrium. ii) Bronchial veins: • They transmit venous blood from the bronchi and bronchioles to the pulmonary veins, and finally to the left atrium. Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine 1) Transport of blood from the right side of the heart to the left side→ low resistance pathway for blood transport through the lungs. 2) Arterializations of venous blood during its passage through the lungs→ removal of CO2 and receiving O2 Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine Value: Dr abdelaziz Husssein, Mansoura Faculty of Medicine Value: Dr abdelaziz Husssein, Mansoura Faculty of Medicine Intrinsic (autoregulation) Extrinsic mechanism 1. Nervous regulation Hypoxic V.C. 2. Chemical regulation 3. Mechanical regulation Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine ◊ Def. • It is the automatic control of local pulmonary blood flow distribution. ◊ Mechanism: • When the alveolar O2 concentration becomes very low, the adjacent blood vessels slowly constrict within 3 to 10 minutes. • It is opposite to what happens in systemic vessels that respond to low PO2 by VD. • It is believed that hypoxia leads to release of some VC substances from the lung tissues that promote Dr abdelaziz Husssein, Mansoura Faculty of Medicine VC. VD VC ↑ PO2 ↓ PO2 Significance: Shift of blood to areas of the lungs that are better Dr abdelaziz Husssein, Mansoura aerated or ventilated. Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine • Pulm. BF equals COP, so factors affecting COP, affect the pulmonary BF. • ↑ed COP (as in exercise) →↑es the pulmonary BF with slight ↑ in pulmonary BP. • COP should be ↑ed 4 times before ↑ pulmonary BP because: a)Pulmonary blood vessels dilate passively b)The outflow of blood from pulmonary veins ↑es due to ↑ed HR (by Bainbridge reflex) Significance: •It ↑es pulmonary gas exchange with COP (in exercise) without over work of the heart. Dr abdelaziz Husssein, Mansoura Faculty of Medicine • Pulmonary circulation can change its capacity to buffer excess changes in pulmonary BP because the pulmonary vessels are highly distensible a) Removal of one lung → all COP of the Rt ventricle is pumped to one lung →↑ in pulmonary capacity→ prevents much ↑ in pulmonary BP. b) Haemorrhage → pulmonary vessels constrict → ↓ pulmonary capacity → prevent much drop in pulmonary BP Dr abdelaziz Husssein, Mansoura Faculty of Medicine c) Left side heart failure → stagnation and congestion of blood in lungs occur→↑ pulmonary capacity → prevent excessive ↑ in pulmonary BP to certain limit. • When pulmonary capacity exceeds this limit → ↑ pulmonary BP. d) Posture (gravity) → capacity is greater in recumbent position than in sitting or standing due to ↑ed VR caused by absence of the effect of gravity. e) Respiration •During inspiration→ pulmonary capacity ↑ es (due to VD) and pulmonary BP ↓es. •During expiration→Dr abdelaziz the capacity ↓es (due to VC) and Husssein, Mansoura Faculty of Medicine pulmonary BP ↑es. ◊ Value: • It equals l/6 systemic PR •An ↑ in pulmonary PR (e.g. in mitral stenosis, emphysema, fibrosis, and embolism) produces much ↑ in pulmonary PB→ Rt ventricle dilates to ↑ the power of contraction (Starling's law). • If the ↑ in pulmonary BP persists → Rt ventricular hypertrophy and failure. Dr abdelaziz Husssein, Mansoura Faculty of Medicine •Pulmonary peripheral resistance is ↑ed in: 1.Mitral stenosis due to back pressure in lungs and reflex VC by hypoxia. Pulmonary PR and BP. 2.Emphysema: bad ventilation produces generalized hypoxia and VC of pulmonary blood vessels Pulmonary PR and BP. 3.Pulmonary fibrosis and embolism: blocking of pulmonary blood vessels and reflex VC from hypoxia Pulmonary PR and BP. Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine a) Vagal stimulation → VD of pulmonary blood vessels and ↓es pulmonary BP. b) Sympathetic stimulation → VC of pulmonary blood vessels and ↑es pulmonary BP. However, the nervous effect is weak on pulmonary BP. Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine a) Ach and certain prostaglandins dilate the pulmonary arterioles. b) Catecholamines, angiotensin II constrict the pulmonary arterioles. c) Serotonin and histamine constrict the pulmonary venules. d) Nitric oxide (NO) dilate the pulmonary arterioles → its deficiency in pulmonary vessels leads to pulmonary hypertension. Dr abdelaziz Husssein, Mansoura Faculty of Medicine 1) It is distensible low pressure circulation, so the pressure in it is low (1/6 of ABP) • Pulmonary PR is 1/6 systemic PR because: a) Pulmonary artery → is thin, 1/3 thickness of the aortic wall. b) Small pulmonary arteries and arterioles → short with large diameter and with little smooth ms fibers→ accommodate large amount of blood. c) Pulmonary capillaries→ are wide, have many anastomoses around alveoli, highly permeable and have high exchangeable surface area. d) Pulmonary veins → are short, distensible and act as blood reservoir. Dr abdelaziz Husssein, Mansoura Faculty of Medicine 2. There is very little fluid formation in the alveoli, but the lungs are richly supplied by lymphatics to keep the alveoli dry. Dr abdelaziz Husssein, Mansoura Faculty of Medicine Dr abdelaziz Husssein, Mansoura Faculty of Medicine ◊ Def, •It is a pathological accumulation of fluid in the lung alveoli or in the pulmonary interstitial spaces. •It is dangerous (even fatal) because it prevents gas exchange in the lungs. Formation and drainage interstitial fluid in lungs Dr abdelaziz Husssein, Mansoura Faculty of Medicine Formation and drainage interstitial fluid in lungs o Thus the net mean filtration pressure = 29-28 = 1 mmHg→ slight continual flow of fluid from the pulmonary capillaries into the interstitial spaces. o This fluid is drained to the circulation through the pulmonary lymphatic system. ◊ Causes: a) Marked ↑ of pulmonary capillary B.P., as in patients with left sided heart failure due to lung congestion. b) ↑ed permeability of pulmonary capillary membrane caused by infectious diseases or poisons as some war gases. Dr abdelaziz Husssein, Mansoura Faculty of Medicine ◊ Pulmonary edema safety factors: a) Low capillary pulmonary pressure (7 mmHg) (filtering force). b) High osmotic pressure of plasma proteins (28 mmHg) (reabsorbing force), so any filtered fluid will be immediately reabsorbed. - Safety factor against pulmonary edema is 28 -7 =21 mmHg Dr abdelaziz Husssein, Mansoura Faculty of Medicine THANKS Dr abdelaziz Husssein, Mansoura Faculty of Medicine