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![PHYSIOLOGY OF CIRCULATION
Blood flow (BF) Volume of blood flowing through
vessel, organ, or entire circulation
in given period [ml/min]
Equivalent to cardiac output; constant at rest; local BF varies
between organs
Blood pressure
(BP)
Force per unit area exerted on wall
of blood vessel by blood [mm Hg]
Measured as systemic BP in the large arteries; proportional to
blood volume (BV); blood follows pressure gradient (∆BP)
Peripheral
resistance (PR)
Opposition to flow Amount of friction blood encounters with vessel walls, generally
in peripheral (systemic) circulation
FLOW, PRESSURE, AND RESISTANCE](https://image.slidesharecdn.com/cardiovascularsystem-170116174108/85/Cardiovascular-system-46-320.jpg)
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Cardiovascular system
- 1. HEART ANATOMY • ≈size of fist; 250-350 g; in mediastinum between 2nd rib and 5th intercostal space • On superior surface of diaphragm • Two-thirds of heart to left of midsternal line • Anterior to vertebral column, posterior to sternum • Base and apex; apical impulse – between fifth and sixth ribs, just below left nipple • Heart is covered with triple-layered pericardium • Superficial fibrous protects, anchors, prevents overfilling • Serous consists of parietal (outer) and visceral (surrounds heart) layers • These layers are separated by fluid-filled pericardial cavity (decreases friction) • Pericarditis is the inflammation of pericardium • Causes: viral or bacterial infection, heart attack, chest trauma, cancer • Inflammation roughens surface pericardial friction rub (heard with stethoscope) • Pericardial effusion/cardiac tamponade: excess fluid in the pericardial cavity • Compression of the heart ↓ pumping ability LOCATION. PERICARDIUM
- 2. THREE LAYERS OFTHE HEART WALL • Epicardium is visceral pericardium • Myocardium is cardiac muscle and cardiac skeleton (connective tissue) • Anchors muscle, supports valves, limits electrical signals • Myocarditis – inflammation of myocardium; can be caused by virus (e.g., Coxackie virus), bacteria (e.g., Borellia burgdorferi), protozoa (e.g., Trypanosoma cruzi ), helminths (e.g., Trichinella spiralis) • Endocardium is simple squamous epithelium inside the heart, continuous with vascular endothelium • Endocarditis – inflammation of the endocardium; damages valves; deposition of bacterial (S. pyogenes, rheumatic fever) or sterile (hypercoagulation state or lupus) vegetations HEART ANATOMY
- 3. CHAMBERS AND GREATVESSELS HEART ANATOMY • Atria are small, thin-walled receiving chambers • Separated by interatrial septum • Fossa ovalis – depression left after foramen ovale in the fetal heart • Auricles increase atrial volume • Pectinate muscles on the walls of right A. and in the left auricle • Superior vena cava, inferior vena cava, coronary sinus empty into right A. • Four pulmonary veins empty into left A. • Ventricles are large thick-walled pumping chambers • Right V. occupies most of anterior surface • Left V. occupies most of posteroinferior surface • Separated by interventricular septum • Associated sulci: coronary (between A. and V.), anterior interventricular (between V.) • Trabeculae carneae – irregular ridges of muscle • Chordae tendineae regulate valve opening • Papillary muscles anchor chordae tendineae • Right V. delivers blood into pulmonary trunk • Left V. delivers blood into aorta
- 4. HEART VALVES • Preventbackflow between chambers → blood flows in one direction through heart • Open and close in response to pressure changes in the chambers and great vessels • Two atrioventricular (AV) valves – tricuspid and mitral • Prevent backflow into atria during ventricular contraction • Anchored by chordae tendineae to papillary muscles • Two semilunar (SL) valves – aortic and pulmonary • Prevent backflow into ventricles during ventricular relaxation • Incompetent valve (does not close) causes blood to backflow heart repumps same blood (regurgitation) • Aortic, mitral and tricuspid are most common • Valvular stenosis is stiffening valves constrict opening increased resistance to pumping • Aortic and mitral are most common • Can be replaced with mechanical, animal, or cadaver valve HEART ANATOMY
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- 18. PULMONARY AND SYSTEMICCIRCUITS • Right atrium receives oxygen-poor blood from systemic circuit and conveys it to right ventricle • Right ventricle pumps oxygen-poor blood into pulmonary circuit to enrich it with oxygen • Left atrium receives oxygen-rich blood from pulmonary circuit and conveys it to left ventricle • Left ventricle pumps the oxygen-rich blood into the systemic circuit to deliver oxygen to tissues • Valves direct the blood flow through the heart CIRCUITS
- 19. BLOOD FLOW THROUGHTHE HEART • Equal volumes of blood are pumped to pulmonary and systemic circuits • Mismatch in pumped volumes → congestive heart failure (discussed later) • Pulmonary circuit is short, has low resistance to flow and pressure • Systemic circuit is long, has high resistance to flow and pressure • Due to the higher resistance, left V. walls are 3x thicker than right V. CIRCUITS
- 20. CORONARY CIRCUIT • Deliversblood to the cardiac muscle only when heart relaxed • Coronary arteries arise from base of aorta • LCA interventricular septum, anterior ventricular walls, left A., posterior wall of left V. • RCA right atrium, most of right ventricle • Coronary sinus empties into right A. • Anterior cardiac veins empty into right A. anteriorly • Most blood supply goes to the left V. • Circuit varies among individuals; vessels are frequently connected via anastomoses • Anastomoses provide collateral blood flow around obstructed vessel; cannot compensate for coronary artery occlusion • Partial occlusion – angina pectoris; complete occlusion – myocardial infarction; cells die; replaced by connective tissue CIRCUITS
- 21. • Contractions areinvoluntary; do not require nervous stimulation (pacemaker cells) • Cells are striated, short, branched, 1-2 nuclei connected by gap junctions; many mitochondria; wide T tubules • Sarcoplasmic reticulum is simpler than in skeletal muscle • Endomysium connects to cardiac skeleton; many capillaries • Intercalated discs between cells contain desmosomes and gap junctions • Desmosomes hold cardiomyocytes together • Gap junctions electrically couple adjacent cells → functional syncytium • Mechanism of contraction is similar to the skeletal muscle ANATOMY OF A CARDIAC MUSCLE CARDIAC MUSCLE
- 22. ROLE OF CA2+ .SLIDING FILAMENTS • Ca2+ low: tropomyosin (TPM) blocks myosin (M.) -binding sites on actin (A.) → M. heads can’t attach → muscle fiber relaxed • Ca2+ high: Ca2+ binds troponin (TN) → TN shifts TPM away from M.-binding sites on A. → M. heads attach to A. → contraction • Ca2+ is pumped back into SR → contraction stops CARDIAC MUSCLE
- 23. Step Ion flowVoltage-gated Na+ channels Voltage-gated K+ channels Voltage-gated Ca+ channels Depolarization Na+ in Open Closed Closed Plateau Ca2+ in, K+ out Closed Open Open Repolarization K+ out Inactivated Open Closed PHYSIOLOGY OF CONTRACTION • Rapid influx of Na+ → depolarization of cardiomyocytes (1) • Depolarization closes Na+ voltage-gated channels (VGC), opens Ca2+ VGC • Influx of Ca2+ maintains depolarization (plateau on the pic, 2) • Plateau allows for extended contraction of the muscle • Ca2+ VGC close, K+ VGC open; efflux of K+ → repolarization • When Na+ VGC close at the peak, they are inactivated – nothing can open them → absolute refractory period • Prevents possible tetanic contractions • Metabolism is aerobic; little anaerobic ability • Can use multiple fuel sources (i.e., lactic acid) • Anaerobic respiration may cause damage to the cells CARDIAC MUSCLE • Ischemia anaerobic respiration lactic acid pH↓ Ca2+ ↑ mitochondrial damage decreased ATP production gap junctions close lack of connection fatal arrhythmias
- 24. PACEMAKER CELLS • Heartcan contract without nervous stimulation • Heartbeat is coordinated by gap junctions and noncontractile autorhythmic (pacemaker) cells • Pacemaker cells have unstable resting membrane potential ELECTROPHYSIOLOGY OF THE HEART Step Ion flow Na+ VGC K+ VGC Ca+ VGC Pacemaker potential Na+ in Open Closed Closed Depolarization Ca2+ in Open Closed Open Repolarization K+ out Closed Open Inactivated
- 25. Structure Location FunctionInherent rate SA node Right atrial wall Pacemaker; sends impulses across atria to AV node 100 bpm AV node Inferior atrial septum Small fibers, fewer junctions → impulse delayed ≈0.1 sec; atria contract prior to ventricles 50 bpm AV bundle Superior interventricular septum Electrical connection b/w atria and ventricles (no gap junctions!) 30-40 bpmBundle branches Interventricular septum Pathways towards apex Purkinje fibers Ventricular walls Pathways into ventricular walls; ventricular contraction follows from apex towards atria INTRINSIC CONDUCTION SYSTEM ELECTROPHYSIOLOGY OF THE HEART SINOATRIAL NODE ATRIOVENTRICULAR NODE ATRIOVENTRICULAR BUNDLE SUBENDOCARDIAL CONDUCTING NETWORK (PURKINJE FIBERS) RIGHT AND LEFT BUNDLE BRANCHES
- 26. • All actionpotentials generated by nodal and contractile cells at given time • P wave – depolarization of the SA node atrial depolarization • QRS complex – ventricular depolarization and atrial repolarization • T wave – ventricular repolarization • P-R interval: start of atrial depolarization to the start of ventricular depolarization • S-T segment: entire ventricular myocardium depolarized • Q-T interval: start of ventricular depolarization to the end of ventricular repolarization NORMAL ELECTROCARDIOGRAM ELECTROPHYSIOLOGY OF THE HEART
- 27. • Cardioinhibitory (parasympathetic)center in medulla oblongata (MO) • Normally inhibits SA, AV nodes via vagus nerve → normal heart rate (HR) @ 70 bpm • Cardioacceleratory (sympathetic) center in MO stimulates SA, AV nodes via sympathetic nerves →↑ HR REGULATION OF HEART RATE ELECTROPHYSIOLOGY OF THE HEART Tachycardia Fast heart rate (>100 bpm) EKG normal otherwise; causes: •fever (10 bpm per 1°C ↑) •sympathetic stimulation •toxins •blood loss Bradycardia Slow heart rate (<60 bpm) EKG normal otherwise; causes: •athletic training •parasympathetic stimulation (carotid sinus syndrome – extremely sensitive baroreceptors in carotid sinuses)
- 28. BLOCK OF INTRACARDIALPATHWAYS ELECTROPHYSIOLOGY OF THE HEART SA block Signal is blocked at SA node before it enters atrial muscle; no P waves; ventricles set the rhythm (slower, 40- 60 bpm – junctional rhythm) AV block Decreased rate of impulse conduction or complete blockage via AV bundle •1st degree – extended P-R interval (delay of conduction) •2nd degree – dropped beat (AP sometimes can’t get through) •3rd degree – complete block; rhythm originates in AV node or AV bundle •Too slow (30-40 bpm), pacemaker needed
- 29. ECTOPIC FOCI. FIBRILLATIONELECTROPHYSIOLOGY OF THE HEART Premature atrial contraction Ectopic focus is in the atria; extended interval between contractions is compensatory pause; can be observed in healthy people; caffeine, nicotine, lack of sleep can be a cause AV nodal /bundle premature contraction Impulse travels to ventricles and backwards to atria; P wave is superimposed on the QRS-T complex; same importance and causes as premature atrial contractions Ventricular premature contraction QRS complex is prolonged, with higher voltage; T wave has inverted electrical polarity; can have same causes as previous two; sign for higher risk for ventricular fibrillation Atrial fibrillation Uncoordinated contractions of atrial muscle; ↓pumping for 20-30%; may be caused by atrial enlargement due to the defective valves Ventricular fibrillation Uncoordinated contractions of ventricular muscle resulting in no pumping of blood; caused by electric shock or ischemia • Ectopic focus – pacemaker out of SA node; may be due local ischemia, calcifications, or chemicals (caffeine, nicotine, drugs)
- 30. THE CARDIAC CYCLE •Cardiac cycle describes blood flow through the heart during one complete heartbeat with all accompanying electrical events, pressure changes, opening and closing of valves • Systole is the contraction, and diastole is relaxation (of atria or ventricles) • Mid-to-late diastole; AV valves open; SL valves closed; Pa > Pv < Pvessel • 80% of blood passively flows into ventricles • Atrial systole delivers remaining 20% • End diastolic volume (EDV): volume of blood in the ventricle at the end of diastole • Atria relax; ventricles contract • Isovolumetric contraction : all valves closed; Pa < Pv < Pvessel • Ejection : AV valves closed, SL valves open; Pa < Pv > Pvessel • End systolic volume (ESV): volume of blood in the ventricle after systole • Ventricles relax • Isovolumetric relaxation: all valves closed; Pa < Pv < Pvessel • Backflow of blood in aorta → dicrotic notch (spike in BP) • Goes back to ventricular filling CARDIAC CYCLE
- 31. • Valves close,produce two sounds (lub-dup) • First as AV valves close; beginning of ventricular systole • Second as SL valves close; beginning of ventricular diastole • Pause – heart relaxation • Heart murmurs - abnormal heart sounds; usually indicate incompetent or stenotic valves
- 32. CARDIAC OUTPUT • Volumeof blood pumped by each ventricle in one minute: CO = heart rate (HR) × stroke volume (SV) • HR = number of beats per minute; SV = volume of blood pumped out by one ventricle with each beat CARDIAC OUTPUT ↑CARDIAC OUTPUT ↑ ARTERIAL PRESSURE ↓ARTERIAL PRESSURE ↓ FORCE OF CONTRACTION ↑FORCE OF CONTRACTION ↑ LENGTH OF DIASTOLELENGTH OF DIASTOLE VENOUS RETURN/PRESSUREVENOUS RETURN/PRESSURE SYMPATHETIC STIMULATION ↑SYMPATHETIC STIMULATION ↑ HEART RATE ↑HEART RATE ↑ STROKE VOLUME ↑STROKE VOLUME ↑ EDV ↑EDV ↑ ESV ↓ESV ↓ CARDIAC CYCLE CO HR SV EDV ESV Increased if… Increased Increased Increased Decreased Decreased if… Decreased Decreased Decreased Increased • SV = EDV – ESV • CO = HR × (EDV – ESV) • CO at rest (ml/min) = HR (75 beats/min) × SV (70 ml/beat) = 5.25 L/min • COmax = 4–5x COrest in nonathletic people; 7x in trained athletes; cardiac reserve (CR) = COmax - COrest Volume Increased by Decreased by EDV Long diastole, ↑ venous pressure Short diastole, ↓ venous return/pressure ESV ↑ blood pressure, ↓ contractility ↓ BP, ↑ contractility
- 33. REGULATION OF STROKEVOLUME • Preload (1): increased degree of stretch of cardiac muscle increases the force of contraction (Frank-Starling law) • Cardiac muscle exhibits a length-tension relationship (like a coil) – shorter at rest than optimal length • Cardiac muscle is stretched by the blood returning from vein (venous return = EDV) • Slow heartbeat and exercise increase EDV and venous return • Contractility (2) is the force of contraction at the given muscle length – independent of muscle stretch and EDV • Increased by sympathetic stimulation (increased Ca2+ influx more cross bridges); parasympathetic – almost no effect • Thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca2+ → ↑ contractility; called positive ionotropic agents • Acidosis, ↑ extracellular K+ , Ca2+ channel blockers → ↓contractility; called negative inotropic agents • Afterload (3) – ventricles work against aortic blood pressure • Hypertension increases afterload → ↑ ESV and ↓ SV 1 2 3 CARDIAC CYCLE
- 34. • Atrial reflex:↑ venous return → ↑ atrial filling → ↑ stretch of atrial walls → SA node stimulation ↑ HR • Also stimulates atrial stretch receptors → sympathetic reflexes • Parasympathetics dominate at rest (vagal tone) • Ion concentrations (e.g., Ca2+ and K+ ) must be maintained for normal heart function Stimulation Sympathetic Parasympathethic Neurotransmitter Norepinephrine Acetylcholine Mechanism Binds to β1-adrenergic receptors ↑ frequency of pacemaker firing Ach hyperpolarizes pacemaker cells by opening K+ channels Effects on HR Increases Decreases Agents that exhibit effect Positive chronotropic Negative chronotropic Norepinephrine, epinephrine, thyroxine, extracellular calcium, young age, female gender, exercise, increased temperature Acetylcholine, extracellular potassium, male gender, decreased temperature REGULATION OF HEART RATE CARDIAC CYCLE Ion High (hyper) Low (hypo) Calcium Increased HR and contractility Depressed HR Potassium Hyperpolarization heart block, cardiac arrest Feeble heartbeat; arrhythmias
- 35. SUMMARY OF CARDIACOUTPUT REGULATION CARDIAC CYCLE
- 36. CONGESTIVE HEART FAILURE •Progressive condition; CO is low → inadequate blood supply to the tissues • Weak myocardium due to the coronary atherosclerosis, high BP, myocardial infarcts, dilated cardiomyopathy (DCM) • Pulmonary congestion (left side failure) • Blood backs up in lungs → pulmonary edema • Heart failure cells in the lungs (macrophages laden with hemosiderin after consumption of RBC) • Peripheral congestion (right side failure) • Blood pools in body organs edema • Congestive hepatomegaly, cardiac sclerosis and cirrhosis; congestive splenomegaly • Pleural, pericardial, peritoneal effusions • Pulmonary and portal hypertension • Failure of either side ultimately weakens other • Treat by removing fluid, reducing afterload, increasing contractility • Mechanical assisting devices, stem cell therapy to improve myocardial function A. Left ventricular hypertrophy due to the ventricular outflow obstruction. B. Normal heart is in the center. Hypertrophied heart without dilation (increased mass and thickness) – left. Hypertrophied heart with dilation (increased mass and normal thickness) - right. C. Normal myocardium. D. Hypertrophied myocardium. Myocytes and their nuclei are increased in size. CARDIAC CYCLE
- 37. DDEVELOPING HEART. LEFT-TO-RIGHTSHUNTS • Embryonic heart chambers: sinus venosus (1), atrium (2), ventricle (3), bulbus cordis (4) • Fetal heart structures bypass pulmonary circulation; foramen ovale connects atria (fossa ovalis in adults) • Ductus arteriosus connects pulmonary trunk to aorta (ligamentum arteriosum in adults); close after birth CONGENITAL HEART DISEASE Left-to-right shunts Atrial septal defect (ASD) Ventricular septal defect (VSD) Patent ductus arteriosus (PDA) Pulmonary hypertension, cyanosis, heart failure, embolization, altered hemodynamics with dilation or hypertrophy
- 38. LEFT-TO-RIGHT SHUNTS. OBSTRUCTIONS Right-to-left shunts Tetralogyof Fallot (VSD, subpulmonary stenosis, aorta overrides VSD, RV hypertrophy) Transposition of great arteries (simultaneous shunts are frequent) Cyanosis Complete separation of circuits (incompatible with life), TV hypertrophy, LV hypotrophy Obstructions Coarctation of aorta Aortic stenosis or atresia (blockade) Cyanosis, high BP in upper extremities and low BP in lower extremities, arterial insufficiency LV hypoplasia (atresia) or hypertrophy (stenosis) CONGENITAL HEART DISEASE
- 39. AGING HEART CARDIACDISEASE
- 40. WALL LAYERS • Arteriescarry blood away from heart, veins carry blood toward heart; capillaries is the site of exchange in the tissues Vessels Tunics Consist of… Arteries and veins intima Endothelium (reduces friction, regulates vasomotor responses), basal lamina media Smooth muscle (vasodialtion/constriction), elastic fibers externa Collagen fibers (protection and structure), lymphatics, nerve fibers, vasa vasorum (blood supply for the walls of large vessels) Capillaries Endothelium and basal lamina (rapid exchange between blood and tissues) BLOOD VESSELS
- 41. ARTERIES Elastic Largest (aortaand branches); elastin in all tunics; large lumen = low resistance; no active vasomotor responses; pressure reservoir (expand and recoil) Muscular Distal to elastic; deliver blood to organs; thick t. media; active vasomotor responses Arterioles Smallest; deliver blood to tissues; active in vasoconstriction BLOOD VESSELS
- 42. VEINS • Large lumens→ little resistance; venous valves prevent backflow • Blood goes back to the heart easy despite the low pressure Venules Post-capillary (smallest, porous, fluid and WBC transport, no SMC); SMC appear as size increases (venules converge) Veins Larger lumens, thinner walls, and lower BP compared to arteries; thin t. media (weak vasomotor responses); capacitance vessels (60% of blood is in venules any given time) Venous sinuses Flattened veins with extremely thin walls (e.g., coronary sinus of the heart and dural sinuses of the brain) BLOOD VESSELS
- 43. CAPILLARIES • Smallest bloodvessels • Endothelium and basal lamina • Pericytes control stability and permeability • Diameter of a single cell • Walls of thin tunica intima • Not found in cartilage, epithelia, cornea, eye lens • Direct access to almost every cell • Exchange of gases, nutrients, wastes, hormones, etc., between blood and interstitial fluid BLOOD VESSELS
- 44. TYPES OF CAPILLARIES TypeLocation Features Continuous Skin, muscles, brain Tight junctions b/w endothelial cells; intercellular clefts (passage of fluids and small molecules); blood-brain barrier in the brain Fenestrated Small intestine, endocrine glands, kidneys More permeable; fenestrations; absorption or filtration Sinusoid Liver, bone marrow, spleen, adrenal medulla Few tight junctions; fenestrations; large clefts and lumens; slow blood flow; effective exchange; macrophages in the lining BLOOD VESSELS
- 45. BLOOD FLOW THROUGHCAPILLARY BEDS • Microcirculation: ≈ 95% vessels are microvessels (Ø <100 µm) • Networks of capillaries between arterioles and venules – capillary bed; different properties in different organs • First signs of disease appear in microvessels before signs are apparent in large vasculature • Terminal arteriole → metarteriole → capillaries and thoroughfare channel → postcapillary venule • Thoroughfare channel is vascular shunt (anastomose) • Can be arterial (e.g., coronary circulation), venular (frequent), or arteriovenular (thoroughfare channel) • 10 to 100 exchange vessels per capillary bed • Branch from metarteriole and return to thoroughfare channel • Precapillary sphincters regulate capillary blood flow • Blood flow through the capillary bed is regulated by local chemical cues, hormones, and nerves
- 46. PHYSIOLOGY OF CIRCULATION Bloodflow (BF) Volume of blood flowing through vessel, organ, or entire circulation in given period [ml/min] Equivalent to cardiac output; constant at rest; local BF varies between organs Blood pressure (BP) Force per unit area exerted on wall of blood vessel by blood [mm Hg] Measured as systemic BP in the large arteries; proportional to blood volume (BV); blood follows pressure gradient (∆BP) Peripheral resistance (PR) Opposition to flow Amount of friction blood encounters with vessel walls, generally in peripheral (systemic) circulation FLOW, PRESSURE, AND RESISTANCE
- 47. BLOOD FLOW INTHE SYSTEMIC CIRCUIT • Heart pumps blood → BF is generated • BF is opposed by PR →BP is generated • Systemic pressure is highest in aorta, declines through the circuit, lowest in the right atrium • Steepest BP drop in arterioles (resistance vessels) • Arterial pressure depends on the elasticity of and blood volume in the large arteries (aorta etc.) • BP near heart is pulsatile • Systolic (≈120 mm Hg), diastolic (≈70-80 mm Hg) • Pulse pressure (PP) = SBP – DBP (this is pulse) • Mean arterial pressure (MAP) propels blood to tissues; MAP = DBP + 1/3 PP • Ex. BP = 120/80; MAP = 93 mm Hg • PP and MAP decrease away from heart • Capillary from 17 to 35 mm Hg; lower is better • Otherwise may cause damage and edema • Venous is almost constant (≈15 mm Hg); low due to the low PR • Venous return is amount of blood coming back to the heart from veins • Muscular pump: contraction of skeletal muscles "milks" veins • Respiratory pump: pressure changes during breathing • Squeeze abdominal veins, expand thoracic veins • Valves prevent backflow; venoconstriction is possible PHYSIOLOGY OF CIRCULATION
- 48. REGULATION OF BLOODPRESSURE • Depends on and regulated by the changes in CO (heart), PR (blood vessels), BV (kidneys) • Neural, chemical, and hormonal short-term mechanisms alter CO and PR; renal long-term responses – BV PHYSIOLOGY OF CIRCULATION
- 49. NERVOUS, CHEMICAL, HORMONAL,HYPOTHALAMUS • Baroreceptors (mechanoreceptors) sense ↑or ↓ stretch of the vessel wall and then respectively • Signals to cardioinhibitory or cardioacceleratory centers in the medulla → ↓ or ↑ CO → ↓ or ↑ BP • Cardiac inhibition is parasympathetic, acceleration is sympathetic • Signals to vasomotor center in the medulla → vasodilation or vasoconstriction (entirely sympathetic) • Chemoreceptors in aortic arch and large arteries of neck detect ↑CO2, or ↓ pH or O2 • To cardioacceleratory center ↑ CO → BP ↑ • To vasomotor center ↑ vasoconstriction • Altogether BF ↑, chemistry of the blood restored • Hypothalamus can increase BP during stress (involves cortical regulation) and during exercise • Relaying signals through medulla oblongata • (Nor)EPI ↑ BP via ↑ CO, vasoconstriction • Angiotensin II, ADH ↑ BP via ↑ vasoconstriction • ANP ↓ BP via ↓ BV (aldosterone antagonist) SHORT-TERM CONTROLS
- 50. RENAL • Baroreceptors quicklyadapt to chronic BP changes • BP controlled by altering BV via kidneys • DIRECT MECHANISM (hormone-independent): • ↑ BP or blood volume → ↑ urination → ↓ BP • ↓ BP or blood volume → ↓ urination → ↑ BP • INDIRECT MECHANISM (renin-angiotensin- aldosterone system, RAAS) ∀ ↓ BP → ↑ renin • Renin converts angiotensinogen (liver) to angiotensin I • Angiotensin converting enzyme (ACE) (lungs) conversts angiotensin I to angiotensin II • Angiotensin II → ↑ aldosterone and ADH • Result: ↑ BV, thirst, vasoconstriction → ↑ BP LONG-TERM CONTROLS • ACE inhibitors are used to treat hypertension and heart failure • First predecessor – from the venom of the South American pit viper • Cushman and Ondetti studied structure of the first inhibitor • Eventually developed captopril – the first ACE inhibitor drug • Lasker Award 1999
- 51. SUMMARY OF BLOODPRESSURE CONTROL PHYSIOLOGY OF CIRCULATION
- 52. MEASURING OF CIRCULATORYPARAMETERS AND BP • Vital signs: pulse, blood pressure, respiratory rate, body temperature • Pulse: pressure wave caused by expansion and recoil of arteries • Pressure points where arteries are close to body surface; usually at the wrist (radial artery) • Systemic BP measured by auscultation (via sphygmomanometer) • Cuff pressure > systolic pressure in brachial artery • As pressure decreases, Korotkoff sounds examined by stethoscope • Systolic BP: blood spurts through artery, sound appears • Diastolic BP: blood flows freely, sound disappears BLOOD PRESSURE
- 53. ALTERATIONS IN BP •Transient changes: changes in posture, exercise, stress, fever • Age, sex, weight, race, mood → variations in BP • Hypertension: sustained BP > 140/90 mm Hg • Prehypertension: elevated BP • Often persistent in obesity, diabetes • Hypertension → heart failure, vasculopathy, renal failure, atherosclerosis, cardiomyopathy, stroke • Primary hypertension: 90% of HT • Risk factors: genetics, diet, obesity, age, diabetes mellitus, stress, and smoking • No cure, can be controlled: ↓ salt, ↑ exercise, ↓ weight, XXX smoking, antihypertensive drugs • Secondary hypertension is less common • Causes; obstructed renal arteries, kidney disease, endocrine disorders (hyperthyroidism, Cushing's) • Treatment focuses on correcting underlying cause • Hypotension: BP < 90/60 mm Hg; usually not a concern; only if BF to tissues become inadequate • Orthostatic hypotension: temporary low BP and dizziness when standing up • Chronic hypotension: hint of poor nutrition, Addison's disease, hypothyroidism • Acute hypotension: circulatory shock BLOOD PRESSURE
- 54. Circulatory Shock • Inadequatetissue perfusion and circulation • Hypovolemic shock: extreme blood loss CIRCULATORY SHOCK • Vascular shock: vasodilation and ↓ PR • Cardiogenic shock: cardiac insufficiency → inadequate circulation
- 55. TISSUE PERFUSION • Deliveryof O2 and nutrients, removal of CO2 and wastes • Gas exchange (lungs), nutrient absorption of nutrients (digestive tract), urine formation (kidneys) • Flow matches tissue requirements • Different in different tissues • Inversely related to total cross-sectional area • Fast in arteries; slow in capillaries (exchange); faster in veins BLOOD FLOW THROUGH THE TISSUES
- 56. REGULATION OF TISSUEPERFUSION • Tissue perfusion (TP) adjusts to tissue needs • Organs control TP by altering arteriolar diameter • Local control – independent of systemic BP regulation (should be at the constant level) • Regulates via metabolic AND myogenic controls • METABOLIC CONTROLS • Metabolically active tissues: ↑ CO2, ↓ pH, ↓ O2 • ↑ K+ , adenosine, prostaglandins • Arterioles dilate, precapillary sphincters relax • Endothelial cells release NO (vasodilator) • NO acts on SMC, overcoming endothelin-mediated vasoconstriction • Inflammatory mediators also cause vasodilation (e.g., kinins, prostaglandins, adenosine) • MYOGENIC CONTROLS • Balance changes in the systemic BP • SMC respond to stretch • ↑ stretch (↑ BP) → vasoconstriction → ↓ BF • ↓ stretch → vasodilation → ↑ BF • LONG-TERM REGULATION • Angiogenesis: BF does not match tissue needs in the long-term perspective • Number of vessels ↑, existing vessels enlarge • Heart (coronary circuit), adaptation to high altitude, cancer BLOOD FLOW THROUGH THE TISSUES
- 57. MUSCLES. BRAIN. SKIN Muscles• At rest, myogenic and neural mechanisms predominate (~ 1L /minute) • Exercise hyperemia – blood flow increases in direct proportion to metabolic activity • Metabolic controls override sympathetic vasoconstriction; can increase 10× Brain • BF constant (neurons cannot survive without O2), ≈750 ml/min • Metabolic controls: ↓ pH, ↑ CO2 → vasodilation • Myogenic controls: ↓ BP → vasodilation → ↑ BF; ↑ BP) → vasoconstriction → ↓ BF (see pic) • BP < 60 mm Hg → syncope (fainting); BP > 160 mm Hg → cerebral edema Skin • BF to subcutaneous venous plexuses regulates body temperature • Varies from 50 ml/min to 2500 ml/min • Controlled by sympathetic reflexes (initiated by thermoreceptors) • Hypothalamus → ↓ vasomotor center • Vasodilation, heat dissipates • Sweat contains bradykinin → vasodilation Lungs • Arterial resistance and pressure are low (24/10 mm Hg) • Metabolic regulation is opposite: ↓ O2 → vasoconstriction; ↑ O2 → vasodilation • Blood flows to O2-rich areas of lung (ventilation-perfusion coupling) Heart • Systole: coronary vessels are compressed, myocardial BF ↓, O2 from myoglobin • Diastole: pressure from aorta forces blood through coronary circulation • At rest ~ 250 ml/min; myogenic control • Strenuous exercise: coronary vessels dilate (chemical regulation), BF ↑ 3x BLOOD FLOW THROUGH THE TISSUES
- 58. CAPILLARY FLOW • Capillaryflow is slow and intermittent • Diffusion of O2, CO2, nutrients, and wastes (b/w tissue and blood) • Lipid-soluble – simple diffusion; water-soluble – clefts, fenestrations (smaller molecules), pinocytosis (e.g., proteins) • Fluid leaves capillaries at arterial end, comes back at venular end • Creates permanent fluid flow through the tissues BLOOD FLOW THROUGH THE TISSUES
- 59. CAPILLARY PRESSURES Pressure Mechanismand direction Numbers Capillary hydrostatic pressure (HPc) Forces fluid through the capillary walls into the tissue Arterial end: 35 mm Hg Venular end: 17 mm Hg Interstitial fluid hydrostatic pressure (HPif) Forces fluid through the capillary walls into the blood Assumed to be 0 due to the lymphatic drainage Capillary colloid osmotic pressure (OPc) Fluid goes towards plasma proteins; pulled towards the blood 26 mmHg Interstitial fluid osmotic pressure (OPif) Fluid goes towards (low) proteins in the IF; pulled into the tissues 1 mmHg BLOOD FLOW THROUGH THE TISSUES
- 60. NET FILTRATION PRESSURE:ARTERIAL END BLOOD FLOW THROUGH THE TISSUES
- 61. NET FILTRATION PRESSURE:VENULAR END BLOOD FLOW THROUGH THE TISSUES