CVS Note (2013) PDF
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Uploaded by LushRiemann9174
University of Ibadan
2013
Ajonijebu D. Chris
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Summary
This document provides notes on the cardiovascular system, covering heart physiology, functions, chambers, valves, and related topics. The document also discusses left vs. right heart functions, cardiac circuitry, and adaptations.
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CARDIOVASCULAR SYSTEM Heart Physiology Ajonijebu D. Chris Introduction CVS is a system of the body that sub- serves the function of transport of nutrients and other factors necessary for cell’s survival are adequately delivered to it and by products o...
CARDIOVASCULAR SYSTEM Heart Physiology Ajonijebu D. Chris Introduction CVS is a system of the body that sub- serves the function of transport of nutrients and other factors necessary for cell’s survival are adequately delivered to it and by products of cellular metabolism are taken away for excretion. Hence, CVS is also known as Circulatory system. Introduction CVS consists of: - The Heart: The muscular pump - The vascular system: Network of blood vessels. Functions of CVS Transport Respiratory Nutritive Excretory Regulatory/Homeostatic functions: Arterial blood pressure Body temperature Delivers regulatory hormones Adjusts to altered states such as hemorrhage, exercise, and changes in posture Protection Immunity Clotting Heart Chambers and Valves Each side of heart has 2 chambers: - Right Atrium and Right ventricle - Left Atrium and Left Ventricle Each side of heart has 2 valves: - Right: Tricuspid Valve and Pulmonic Valve - Left: Mitral Valve and Aortic Valve Left vs Right Heart The circulatory system forms two circuits in series with each other:- - Systemic circulation (greater circulation) - Pulmonary circulation (lesser circulation) Circuitry Functional adaptation of the Heart Specialized conducting System The components are: - SA node - AV node - Bundle of His (right and left branches) - Purkinje fibers Heart sounds First Heart Sound (S1) - Caused by sudden closure of the AV valves at onset of ventricular systole - Heard as ‘Lubb’ sound. Low and slightly prolonged. Second Heart Sound (S2) - Caused by closure of semilunar valves just after end of ventricular systole. - Heard as ‘dubb’ sound. Higher freq vibrations & of shorter duration. Read up 3rd and 4th heart sounds. Murmurs or Bruits Abnormal sounds; called bruits when heard outside the heart Often indicates valve disorder Causes: - Incompetent valve/Backflow - Stenosis; will cause accel. and turbulent flow - Congenital defects Defects in kids Unclosed opening in the interatrial Unclosed connection between the septum (Foramen ovale). pulmonary trunk and the aorta (Ductus arteriosus) Innervations of The Heart: Autonomic nerve supply 1- Sympathetic: increase activity of the whole heart. (increase heart rate and contractility) 2- Parasympathetic: comes through vagus nerve and decrease activity of atria only. (decrease heart rate) 09/07/2015 14 Autonomic Innervations of the heart 09/07/2015 15 Hemodynamics Principles that govern blood flow in cardiovascular system Concepts of flow, pressure, resistance, and capacitance Blood Vessels Blood vessels Blood move from the hearts to body organs by arteries, arterioles and capillaries. It return to the heart by venules and veins. Blood from the arterioles passes into the capillaries. Sometimes it passes from arterioles directly to venules by means of arteriovenous anastomoses. Histology of the blood vessels Both arteries and veins are composed of: 1. Inner endothelium 2. Elastic tissue 3. Smooth muscle 4. Loose fibrous connective tissue Blood capillary cell endothelium (one cell thick) lumen Comparison between the artery, vein and capillary Blood capillaries Due to constrictions of the arterioles and the presence of the precapillary Sphincter blood reach the capillaries in a decreased pressure. There are 3 types of capillaries: continuous capillaries, found in muscle and lungs. fenestrated capillaries, found in the kidney, endocrine glands and intestine. Discontinuous capillaries, found In the liver, bone marrow and spleen. Veins Most of the blood is kept in the veins because veins expand to occupy more coming blood. Blood moves in the veins by: 1. massaging action (skeletal muscle pump) and the one way venous valves. 2. Thoracic pump which sucks up blood from the abdomen Blood Vessels Arteries (aorta is largest) - Thick-walled, extensive elastic tissue, smooth muscle, and connective tissue - Under highest pressure - Stressed Volume—volume of blood contained in arteries Arterioles (smallest branches of the arteries) - Extensive smooth muscle in walls - Site of highest resistance to blood flow - Innervated by sympathetic adrenergic nerve fibers * α-Adrenergic receptors caused constriction of smooth muscle (resistance to blood flow) Found in skin and splanchnic vasculature * β2-Adrenergic receptors cause relaxation of smooth muscle (decrease resistance) Found in skeletal muscle Blood Vessels Capillaries - Lined by single layer of endothelial cells - Site where nutrients, gases, water, and solutes are exchanged between blood and tissues - Lipid-soluble substances (O2, CO2) diffuse across capillary wall - Water-soluble substances (ions) use pores to cross capillary wall - Not all capillaries are perfused with blood at all times * Selective perfusion is determined by degree of dilation or constriction of arterioles and precapillary sphincters Blood Vessels Venules and veins - Venules are thin-walled - Veins have modest amount of elastic tissue, smooth muscle, and connective tissue - Large capacitance (capacity to hold blood) - Contain largest percentage of blood in cardiovascular system - Unstressed volume—volume of blood contained in veins - Smooth muscle in walls of veins innervated by sympathetic nerve fibers * Increases in sympathetic nerve activity contracts veins lowering their capacitance and therefore reduces unstressed volume Velocity of Blood Flow V = Q/A V = velocity (cm/sec) Q= flow (ml/sec) A = cross- sectional area (cm2) of a vessel or group of vessels Velocity of Blood Flow Changes in diameter alter velocity of flow through a vessel - As vessel diameter increases, velocity of flow decreases - Blood flow at each level is the same - Velocity of blood flow is highest in aorta and lowest in capillaries * Low velocity in capillaries is advantageous because it maximizes the time for exchange across capillary wall Velocity of Blood Flow - Smallest vessel represents aorta, medium-sized vessel represents all arteries, and largest vessel represents all capillaries Blood Flow, Pressure, Resistance Blood flow is determined by 2 factors: - Pressure difference (driving force) b/w 2 ends of vessel - Resistance of vessel to blood flow Q = ΔP/R Q=Blood flow (ml/min) ΔP=Pressure difference (mm Hg) R=Resistance (mm Hg/ml/min) Major mechanism for changing blood flow is changing resistance in the arterioles Pressure Blood flows from high pressure to low pressure areas. Although, pressure required for blood flow is primarily generated by heart’s pumping action, but also aided by: Diastolic recoil of arterial wall Muscle pump(particularly during exercise) Negative thoracic pressure(during inspiration) Total Peripheral Resistance Resistance of the entire systemic vasculature Substitute cardiac output for flow (Q) and difference in pressure between aorta and vena cava for ΔP TPR = ΔP/Q Resistance R = (8ηl)/(πr4) When radius of a blood vessel decreases, its resistance increases (not linear) Viscosity Length of vessel Capacitance (Compliance) Volume of blood the vessel can hold at a given pressure C = V/P C=Compliance (ml/mm Hg) V=Volume (ml) P=Pressure (mm Hg) Higher the compliance of a vessel, the more volume it can hold at a given pressure Compliance Changes in Compliance Changing compliance of veins redistributes blood between veins and arteries - If compliance of veins decreases (venoconstriction), veins hold less volume so blood shifts from veins to arteries (unstressed volume decreases and stressed volume increases) - Such redistributions of blood between veins and arteries have consequences for arterial pressure Aging and Compliance With increasing age, arteries become stiffer, less compliant - Therefore, at a given arterial pressure, arteries hold less blood - In order for “old artery” to hold same volume as “young artery,” the pressure in the “old artery” must be higher than the pressure in the “young artery” ↓C=V/↑P Pressure Pressure differences between heart and blood vessels are driving force for blood flow Pressure is highest in large arteries and decreases progressively as blood flows from arteries to veins and back to heart Decrease in pressure occurs because energy is consumed in overcoming frictional resistances - Most significant drop occurs in arterioles because the arterioles constitute a high resistance to flow Q = ↑ΔP/↑R Pressure Summary of Hemodynamics Arterial Blood Pressure Definition: It is the lateral pressure exerted by blood on the walls of aorta and arteries. Ejection of blood into the aorta by the left ventricle results in a characteristic aortic pressure pulse. The peak of the aortic pressure pulse is termed the systolic pressure (SP). The lowest pressure in the aorta is termed the diastolic pressure(DP). PP = SP - DP The mean aortic pressure (MAP) is the average pressure (geometric mean) during the aortic pulse cycle Arterial BP Characteristic changes occur in SP,DP and MAP as the pressure pulse travels down the blood vessels. Away from heart, SP rises and DP falls. Also, MAP slightly declines due to resistance in the arteries. Arterial BP Hence, arterial pressure measured using a sphygmomanometer (i.e., blood pressure cuff) on the upper arm, that is pressure within the brachial artery, will be slightly different from the pressure measured in the aorta or the pressure measured in other distributing arteries. Measurement of Blood Pressure 1- Direct Method (Invasive) The most accurate means for measuring blood pressure directly within an artery (intra-arterial) using a catheter. But because this method is invasive, it is neither practical nor appropriate for repeated measurements in non-hospital settings, or for large-scale public health screenings. 2- The mercury-filled sphygmomanometer It is the usual method of measurement. Therefore, is a noninvasive means that uses a sphygmomanometer which includes either a column of mercury or pressure- registering gauge. The process is known as Sphygmomanometry. Using this apparatus, BP can be measured in two ways: By palpitation By auscultation Average BP = 120/80 Arterial surge in pressure = Pulse Pulse rate usually = heart rate Average adult pulse = 60-80 BPM Physiological factors affecting Arterial BP Age: New born: 80/40 mmHg; 4 years: 100/65 mmHg. Adults: 120/80 mmHg Both SP and DP gradually increase with aging due to stiffness of arteries. Sex: Children: have equal Blood pressure. Adults before 45 years: males more than females. Adults after 45 years: the diastolic B.P. is more in females than males. Race: ABP in oriental(Japan, China or other countries in E.Asia) is less than in Europeans and Americans. Gravity: B.P. in upper parts of the body is more than the lower parts especially during standing. Meals: Digestion increases the arterial blood pressure. Emotions and exercise: increases the arterial blood pressure. Sleep: Deep quiet sleep decreases A.B.P., while sleep with dreams increases A.B.P. Factors that Affect Blood Pressure Blood pressure is affected by several factors: 1- Cardiac output. 2- Peripheral resistance 3- Vessel elasticity 4- Blood volume 1- Cardiac Output Definition: It is the volume of blood ejected by each ventricle per minute. Usually, CO from both ventricles are equal. It is about 5L/min in adults. Though, increases tremendously in exercise or other conditions demanding increase blood supply to tissues. CO/m2 of body surface area is called cardiac index. 3L/min/m2 in males & about 10% lower in females. Cardiac Output ↑CO results in increased BP. Also, anything that will cause ↓CO will ↓BP, because of less pressure on the vessel walls. CO = Heart Rate X Stroke Volume Anything that affects HR or SV will affect CO and thus blood pressure. Stroke Volume Volume of blood ejected in one ventricular contraction Difference in volume before ejection (end-diastolic volume) and after ejection (end-systolic volume) Normal = 70ml Stroke Volume = EDV – ESV Ejection Fraction Effectiveness of ventricles in ejecting blood Indicator of contractility (Intrinsic ability of myocardium to pump in absence of changes in preload and after load) Fraction of EDV that is ejected in one SV Normal = 55% Ejection Fraction = SV/EDV Sample Problem A man has an EDV of 140 ml, an ESV of 70 ml, and a heart rate of 75 beats/min - What is his stroke volume? - His cardiac output? - His ejection fraction? Heart rate Is the number of beats per minute – an intrinsic function of SA node. About 72beats/min in normal adults Diminishes by 10-20/min during sleep & may ↑ to more than 100/min during exercise or emotional excitement. The rate is about 50/min in a well-trained athletes at rest. Heart rate It is modified by autonomic NS (almost exclusively), humoral, mechanical and local factors Enhanced vagal activity ↓HR & sympathetic activity↑HR CO is directly proportional to HR Regulation of Heart Rate Autonomic influence - SA node is under tonic influence of ANS - whereas, propranolol(β-blocker) blocks sympathetic activity, hence cause a slight slowing of the heart. - In adults, blockade of both parasymp. & sympathetic nerves will cause HR to ↑to about 100beats/min. This is known as intrinsic HR. Influence by Higher centres Effects of reflexes Baroreceptor reflex ↑ BP ↑ BR in carotid sinus & aortic arch Sinus nerve & Aortic nerve IX & X nerve N. solitarius ↑ vagal tone ↓ HR Bainbridge reflex Venous engorgement of atria & great veins Stimulation of stretch receptors X nerve CVS center medulla ↓ Vagal tone ↑ HR Chemoreceptor reflex ↓pO2 ↑ pCO2 & ↓pH ↑ CR in carotid body & aortic arch Sinus nerve & Aortic nerve IX & X nerve ↑ Respiratory centre ↑ ventilatory drive Regulation of Stroke volume Nervous stimuli End-diastolic length of cardiac fibres. Measurement of CO In man, CO is measured indirectly and two most commonly used methods are: Fick-method Indicator-dilution method Regulation of CO The CO is regulated by two forces: Intrinsic regulation Extrinsic regulation Intrinsic Regulation Changes in the end-diastolic length of myocardial fibres. This is called Starling’s law of the heart. i.e ↑EDV = ↑stretching of cardiac muscle = ↑strength of cardiac contraction and ↑SV Frequency-induced regulation i.e ↑freq. of stimulation of myocardium = ↑force of contraction. This is known as staircase or Treppe phenomenon. Extrinsic Regulation Nervous control Humoral control Blood gases Control of CO 2- Peripheral Resistance Blood cells and plasma encounter resistance when they contact blood vessel walls. Increase in resistance requires more pressure to keep blood moving 3 main sources of peripheral resistance: a. Blood vessel diameter b. Blood viscosity c. Total vessel length a- Vessel Diameter ↑diameter, same volume→ less pressure ↓diameter, same volume→ more pressure Actively regulated by vasomotor fibers (sympathetic nerve fibers that innervate the vessel’s smooth muscle layer) Vasomotor fibers release NE, a powerful vasoconstrictor. Vessel diameter is also regulated by blood borne vasoconstrictors e.g Epinephrine, Angiotensin II, Vasopressin etc NB: Vasoconstriction raises BP b- Viscosity of blood Viscosity is related to the thickness of a fluid. The greater the viscosity, the less easily molecules slide past one another and the more difficult it is to get the fluid moving and keep it moving. Because of this greater resistance to flow, a greater pressure is required to pump the same volume of viscous fluid. The more viscous the blood, the greater resistance it encounters and the higher the blood pressure. c- Vessel Length Total vessel length affects PR. Increased fatty tissue requires more blood vessels to service it and adds to the total vessel length in the body. The longer the total vessel length, the greater the resistance encountered, and the greater the blood pressure. 3 - Vessel Elasticity It affects both PR and BP A healthy elastic artery expands absorbing shock of systolic pressure The elastic recoil of the vessel then maintains the continued flow of blood during diastole. Arteries become calcified and rigid in arteriosclerosis, so they can't expand when the pulse wave of systolic pressure passes through them 4 - Blood Volume ↑Blood volume → ↑BP and vice-versa ↓BV (for example due to excessive sweating) reduces BP short term. Long term homeostatic mechanisms compensate bringing BV and BP back up to normal levels ↑BV(for example due to water retention from excessive salt intake) increases BP short term. Long term homeostatic mechanisms compensate restoring normal levels. Regulation of arterial BP BP is maintained at a constant level within a narrow limit to ensure an adequate flow of blood to the tissues especially the vital organs e.g. heart, brain and kidney. Thus the regulation of arterial BP depend upon the previous two factors (CO & PR) thru two mechanisms: o Nervous o hormonal Regulatory mechanisms 1- Short term acting mechanisms 2- Long term acting mechanisms. Short acting mechanisms Starts: minutes to hours Mechanism: - Stimulation of baroreceptors in the aortic arch or carotid sinus by changes in BP between 60mmHg and 200mmHg blood pressure. - Stimulation of chemoreceptors in the aortic body or carotid body by changes of blood pressure between 40mmHg and 60mmHg blood pressure. Short term Baroreceptors in cardiac sinus & Aortic arch Cardiopulmonary baroreceptors Arterial chemoreceptors Vasoconstrictor effect of Angiotensin II immediately acting mechanisms Control of blood pressure 2- Long term acting mechanisms Starts: within half an hour. Lasts: days, months, or even years. Type: hormonal. Mechanisms: - 1- Renin mechanism. - 2- Aldosterone mechanism. - 3- Antidiuretic hormone mechanism. SHORT-TERM CONTROL OF ARTERIAL BP THE SENSORY ARM Arterial BP is controlled by a negative feedback process Carotid sinus and aortic arch baroreceptors respond to changes of blood pressure. Afferent nerve firing reflects both the rate of change of blood pressure during the pulse and the mean level SHORT-TERM CONTROL OF ARTERIAL BP THE EFFERENT ARM Medullary cardiovascular centres Receptor Medullary regulate the efferent arm afferents cardiovascular via the ANS centres When activated: sympathetic parasympathetic Sympathetic fibres innervate Arterioles - vasoconstriction The SA node - Tachycardia Myocardium - positive inotropy Parasympathetic (vagal) fibres innervate The SA node - bradycardia 84 NB: Vagal tone to the SA node predominates THE BARORECEPTOR REFLEX - AN EXAMPLE CORRECTION OF POSTURAL HYPOTENSION On standing up venous return falls Effect of gravity on VR Cardiac output diminishes Preload diminished - Starling’s Law Arterial blood pressure is reduced Subject possibly feels faint as cerebral flow is Baroreceptor afferent firing reduced reduced Due to reduced arterial Medullary centres inhibition reduced B.P. Tend to ↑sympathetic tone to arterioles Vasoconstriction restore Tachycardia arterial ↓vagal tone to SA node Raised stroke work BP ↑myocardial sympathetic tone