Cardiovascular System: Blood Pressure PDF

Cardiovascular System Learning Objectives: Cardiovascular System Anatomy and functional roles of the different types of blood vessels Name the different types of vessels found in the circulatory system, and briefly relate the structural features to the functions for each major vessel type. C...

Cardiovascular System Learning Objectives: Cardiovascular System Anatomy and functional roles of the different types of blood vessels Name the different types of vessels found in the circulatory system, and briefly relate the structural features to the functions for each major vessel type. Consider the impact of vessel characteristics on flow, pressure and resistance. Define vasoconstriction and vasodilation.  Part 1 Blood Vessel Structure and Function Blood vessels: delivery system of dynamic structures that begins and ends at heart – Work with lymphatic system to circulate fluids Arteries: carry blood away from heart; oxygenated except for pulmonary circulation and umbilical vessels of fetus Capillaries: direct contact with tissue cells; directly serve cellular needs Veins: carry blood toward heart; deoxygenated except for pulmonary circulation and umbilical vessels of fetus © 2016 Pearson Education, Ltd. Figure 19.1 The relationship of blood vessels to each other and to lymphatic vessels. Venous system Arterial system Large veins Heart (capacitance vessels) Elastic Large arteries lymphatic (conducting vessels arteries) Lymph node Muscular arteries Lymphatic (distributing system arteries) Small veins (capacitance vessels) Arteriovenous anastomosis Lymphatic capillaries Sinusoid Arterioles (resistance vessels) Terminal Postcapillary arteriole venule Thoroughfare Capillaries Precapillary Metarteriole channel (exchange sphincter vessels) © 2016 Pearson Education, Ltd.  Blood Vessel Structure and Function Structure Functions Arteries The walls (outer structure) of arteries Transport blood away from the contain smooth muscle fibre that contract heart and relax under the instructions of the Transport oxygenated blood only sympathetic nervous system. (except in the case of the pulmonary artery). Arterioles Arterioles are tiny branches of arteries Transport blood from arteries to that lead to capillaries. These are also capillaries under the control of the sympathetic Arterioles are the main regulators nervous system, and constrict and dialate, of blood flow and pressure. to regulate blood flow. Capillaries Capillaries are tiny (extremely narrow) Function is to supply the tissues of blood vessels, of approximately 5-20 the body with the components of micro-metres blood, and (carried by the blood), (one micro-metre = 0.000001metre) and also to remove waste from diameter. the surrounding cells... as There are networks of capillaries in most opposed to simply moving the of the organs and tissues of the body. blood around the body (in the These capillaries are supplied with blood case of other blood vessels) by arterioles and drained by venules. Exchange of oxygen, carbon Capillary walls are only one cell thick (see dioxide, water, salts, etc., diagram), which permits exchanges of between the blood and the material between the contents of the surrounding body tissues. capillary and the surrounding tissue. Veins The walls (outer structure) of veins consist Transport blood towards the of three layers of tissues that are thinner heart. and less elastic than the corresponding Transport deoxygenated blood layers of aerteries. only (except in the case of the Veins include valves that aid the return of pulmonary vein). blood to the heart by preventing blood from flowing in the reverse direction. © 2016 Pearson Education, Ltd.  Physiology of Circulation Flow, Pressure, and Resistance Definition of Terms Blood flow: volume of blood flowing through vessel, organ, or entire circulation in given period – Measured in ml/min, it is equivalent to cardiac output (CO) for entire vascular system – Overall is relatively constant when at rest, but at any given moment, varies at individual organ level, based on needs Blood pressure (BP): force per unit area exerted on wall of blood vessel by blood – Expressed in mm Hg – Measured as systemic arterial BP in large arteries near heart – Pressure gradient provides driving force that keeps blood moving from higher- to lower-pressure areas © 2016 Pearson Education, Ltd.  Definition of Terms (cont.) Resistance (peripheral resistance): opposition to flow – Measurement of amount of friction blood encounters with vessel walls, generally in peripheral (systemic) circulation – Three important sources of resistance Blood viscosity Total blood vessel length Blood vessel diameter © 2016 Pearson Education, Ltd.  Definition of Terms (cont.) – Blood viscosity The thickness or “stickiness” of blood due to formed elements and plasma proteins – The greater the viscosity, the less easily molecules are able to slide past each other Increased viscosity equals increased resistance – Total blood vessel length The longer the vessel, the greater the resistance encountered – Blood vessel diameter Has greatest influence on resistance Frequent changes alter peripheral resistance Viscosity and blood vessel length are relatively constant Resistance varies inversely with fourth power of vessel radius – If radius increases, resistance decreases, and vice-versa © 2016 Pearson Education, Ltd.  19.9 Control of Blood Flow Tissue perfusion: blood flow through body tissues; involved in: 1. Delivery of O2 and nutrients to, and removal of wastes from, tissue cells 2. Gas exchange (lungs) 3. Absorption of nutrients (digestive tract) 4. Urine formation (kidneys) Rate of flow is precisely right amount to provide proper function to that tissue or organ © 2016 Pearson Education, Ltd.  19.9 Control of Blood Flow – Example: redistribution of blood during exercise At rest, skeletal muscles receive about 20% of total blood in body, but during exercise, skeletal muscle can receive over 70% of blood Intrinsic controls: skeletal muscle arterioles dilate, increasing blood flow to muscle Extrinsic controls decrease blood flow to other organs such as kidneys and digestive organs – MAP is maintained despite dilation of skeletal muscle arterioles © 2016 Pearson Education, Ltd. Figure 19.13 Distribution of blood flow at rest and during strenuous exercise. 750 750 Brain 750 12,500 Heart 250 Skeletal 1200 muscles Skin 500 Kidneys 1100 Abdomen 1400 1900 Other 600 Total blood 600 flow at rest 600 5800 ml/min 400 Total blood flow during strenuous exercise 17,500 ml/min Cardiovascular System Learning Objectives: Cardiovascular System Regulation of cardiac output (CO), stroke volume (SV), and heart rate (HR) Name the different types of vessels found in the circulatory system, and briefly relate the structural features to the functions for each major vessel type. Consider the impact of vessel characteristics on flow. Define cardiac output (CO) and state its units of measurement. Explain how to calculate cardiac output (CO), given stroke volume (SV) and heart rate (HR). Predict how changes in heart rate (HR) and/or stroke volume (SV) affect cardiac output (CO). Explain how venous return, preload, and afterload each affect end diastolic volume (EDV), end systolic volume (ESV), and stroke volume (SV). Describe the role of the autonomic nervous system in the regulation of cardiac output.  18.7 Regulation of Pumping Cardiac output: amount of blood pumped out by each ventricle in 1 minute CO = heart rate (HR) × stroke volume (SV) HR = number of beats per minute Stroke volume: volume of blood pumped out by one ventricle with each beat – Correlates with force of contraction At rest: CO (ml/min) = HR (75 beats/min) × SV (70 ml/beat) = 5.25 L/min CO is affected by factors leading to: – Regulation of stroke volume – Regulation of heart rates © 2016 Pearson Education, Ltd.  Regulation of Stroke Volume Mathematically: SV = EDV − ESV – EDV is affected by length of ventricular diastole and venous pressure (∼120 ml/beat) – ESV is affected by arterial BP and force of ventricular contraction (∼50 ml/beat) – Normal SV = 120 ml − 50 ml = 70 ml/beat Three main factors that affect SV: – 1. Preload – 2. Contractility – 3. Afterload © 2016 Pearson Education, Ltd.  Regulation of Stroke Volume (cont.) 1. Preload: degree of stretch of heart muscle – Preload: degree to which cardiac muscle cells are stretched just before they contract Changes in preload cause changes in SV – Affects EDV – Relationship between preload and SV called Frank-Starling law of the heart – Most important factor in preload stretching of cardiac muscle is venous return—amount of blood returning to heart Slow heartbeat and exercise increase venous return Increased venous return distends (stretches) ventricles and increases contraction force Venous → EDV → SV → CO Return Frank-Starling Law © 2016 Pearson Education, Ltd.  Regulation of Stroke Volume (cont.) 2. Contractility – Contractile strength at given muscle length Independent of muscle stretch and EDV – Increased contractility lowers ESV; caused by: Sympathetic epinephrine release stimulates increased Ca2+ influx, leading to more cross bridge formations Positive inotropic agents increase contractility – Thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca2+ – Decreased by negative inotropic agents Acidosis (excess H+), increased extracellular K+, calcium channel blockers © 2016 Pearson Education, Ltd.  Regulation of Stroke Volume (cont.) 3. Afterload: back pressure exerted by arterial blood – Afterload is pressure that ventricles must overcome to eject blood Back pressure from arterial blood pushing on SL valves is major pressure – Aortic pressure is around 80 mm Hg – Pulmonary trunk pressure is around 10 mm Hg – Hypertension increases afterload, resulting in increased ESV and reduced SV © 2016 Pearson Education, Ltd. Figure 18.21 Factors involved in determining cardiac output. Exercise (by Ventricular Bloodborne CNS output in sympathetic activity, filling time (due epinephrine, response to exercise, skeletal muscle and to heart rate) thyroxine, fright, anxiety, or respiratory pumps; excess Ca2+ blood pressure see Chapter 19) Venous Sympathetic Parasympathetic Contractility return activity activity EDV ESV (preload) Stroke volume (SV) Heart rate (HR) Initial stimulus Physiological response Cardiac output (CO = SV × HR) Result © 2016 Pearson Education, Ltd.  Regulation of Heart Rate Heart rate can be regulated by: – Autonomic nervous system – Chemicals Autonomic nervous system regulation of heart rate – Sympathetic nervous system can be activated by emotional or physical stressors – Norepinephrine is released and binds to β1-adrenergic receptors on heart, causing: Pacemaker to fire more rapidly, increasing HR – EDV decreased because of decreased fill time Increased contractility – ESV decreased because of increased volume of ejected blood – Parasympathetic nervous system opposes sympathetic effects Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels, which slows HR © 2016 Pearson Education, Ltd.  Regulation of Heart Rate (cont.) Chemical regulation of heart rate – Hormones Epinephrine from adrenal medulla increases heart rate and contractility Thyroxine increases heart rate; enhances effects of norepinephrine and epinephrine – Ions Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function – Imbalances are very dangerous to heart © 2016 Pearson Education, Ltd.  Clinical – Homeostatic Imbalance 18.7 Hypocalcemia: depresses heart Hypercalcemia: increases HR and contractility Hyperkalemia: alters electrical activity, which can lead to heart block and cardiac arrest Hypokalemia: results in feeble heartbeat; arrhythmias © 2016 Pearson Education, Ltd. Cardiovascular System Learning Objectives: Cardiovascular System Blood pressure and its functional interrelationships with cardiac output (CO), peripheral resistance, and hemodynamics Define total peripheral resistance (TPR), compare the relative contributions of systemic arteries, arterioles, capillaries, and veins to TPR, and identify which vessels are the primary site of variable (controlled) resistance to flow. Write and explain the equation relating mean arterial pressure (MAP) to cardiac output (CO) and total peripheral resistance (TPR). Predict and describe how mean arterial pressure (MAP) is affected by changes in total peripheral resistance (TPR), cardiac output (CO), heart rate (HR) and stroke volume (SV). Diagram or describe the anatomical components and steps of the baroreceptor reflex and explain how this reflex helps maintain blood pressure homeostasis when blood pressure changes. Predict the baroreceptor reflex response to a decrease in arterial blood pressure occurringupon standing (orthostatic hypotension). Describe the short-term and long term regulation of mean arterial pressure  Arterial Blood Pressure Systolic pressure: pressure exerted in aorta during ventricular contraction – Left ventricle pumps blood into aorta, imparting kinetic energy that stretches aorta – Averages 120 mm Hg in normal adult Diastolic pressure: lowest level of aortic pressure when heart is at rest Pulse pressure: difference between systolic and diastolic pressure Pulse: throbbing of arteries due to difference in pulse pressures, which can be felt under skin Mean arterial pressure (MAP): pressure that propels blood to tissues – Heart spends more time in diastole, so not just a simple average of diastole and systole MAP is calculated by adding diastolic pressure + 1/3 pulse pressure – Example: BP = 120/80; Pulse Pressure = 120 − 80 = 40; so MAP = 80 + (1/3)x40 = 80 + 13 = 93 mm Hg Pulse pressure and MAP both decline with increasing distance from heart © 2016 Pearson Education, Ltd.  Arterial Blood Pressure (cont.) Clinical monitoring of circulatory efficiency – Vital signs: pulse and blood pressure, along with respiratory rate and body temperature – Taking a pulse Radial pulse (taken at the wrist): most routinely used, but there are other clinically important pulse points Pressure points: areas where arteries are close to body surface – Can be compressed to stop blood flow in event of hemorrhaging © 2016 Pearson Education, Ltd. Figure 19.7 Body sites where the pulse is most easily palpated. Superficial temporal artery Facial artery Common carotid artery Brachial artery Radial artery Femoral artery Popliteal artery Posterior tibial artery Dorsalis pedis artery © 2016 Pearson Education, Ltd.  Arterial Blood Pressure (cont.) – Measuring blood pressure Systemic arterial BP is measured indirectly by auscultatory methods using a sphygmomanometer 1. Wrap cuff around arm superior to elbow 2. Increase pressure in cuff until it exceeds systolic pressure in brachial artery 3. Pressure is released slowly, and examiner listens for sounds of Korotkoff with a stethoscope Systolic pressure: normally less than 120 mm Hg – Pressure when sounds first occur as blood starts to spurt through artery Diastolic pressure: normally less than 80 mm Hg – Pressure when sounds disappear because artery no longer constricted; blood flowing freely © 2016 Pearson Education, Ltd.  19.8 Regulation of Blood Pressure Maintaining blood pressure requires cooperation of heart, blood vessels, and kidneys – All supervised by brain Three main factors regulating blood pressure – Cardiac output (CO) – Peripheral resistance (PR) – Blood volume Blood pressure varies directly with CO, PR, and blood volume © 2016 Pearson Education, Ltd.  19.8 Regulation of Blood Pressure Recall that CO = SV × HR, so if MAP = CO × PR, then MAP = SV × HR × PR Anything that increases SV, HR, or TPR will also increase MAP – SV is effected by venous return (EDV) – HR is maintained by medullary centers – PR (systemic resistance) is effected mostly by vessel diameter © 2016 Pearson Education, Ltd. Figure 19.9 Major factors determining MAP. Stroke Heart Diameter of Blood Blood volume rate blood vessels viscosity vessel length Cardiac output Peripheral resistance Mean arterial pressure (MAP) © 2016 Pearson Education, Ltd.  19.8 Regulation of Blood Pressure Factors can be affected by: – Short-term regulation: Neural mechanisms Vasomotor center Reflex Control- – Baroreceptor Reflexes – Chemoreceptor Reflexes Hormonal Control Higher order brain centers – Long-term regulation: renal controls © 2016 Pearson Education, Ltd.  21-3 Cardiovascular Regulation  Neural mechanisms – Cardiovascular (CV) center of the medulla oblongata Consists of cardiac centers and vasomotor center – Cardiac centers Cardioacceleratory center increases cardiac output Cardioinhibitory center reduces cardiac output  Vasomotor center – Control of vasoconstriction Controlled by adrenergic nerves (NE) Stimulate contraction in arteriole walls – Control of vasodilation Controlled by cholinergic nerves (NO) Relax smooth muscle 30 © 2018 Pearson Education, Ltd. Short-Term Regulation Baroreceptor reflexes – Located in carotid sinuses, aortic arch, and walls of large arteries of neck and thorax – If MAP is high: Increased blood pressure stimulates baroreceptors to increase input to vasomotor center Inhibits vasomotor and cardioacceleratory centers Stimulates cardioinhibitory center Decrease cardiac output Cause peripheral vasodilation Results in decreased blood pressure – When blood pressure falls, CV centers Increase cardiac output Cause peripheral vasoconstriction 19.8 Regulation of Blood Pressure What happends when you stand up? → blood pools in veins → ↓ venous return (↓EDV) → ↓ SV → ↓ CO → ↓ MAP → baroreceptors sense the decreased BP → ↑ sympathetic discharge → ↑ HR → ↑ contractility (SV) → ↑ arteriolar resistance (vasoconstriction) → ↑ CO & ↑ TPR → MAP returned to normal Figure 19.10 Baroreceptor reflexes that help maintain blood pressure homeostasis. Slide 6 3 Impulses from baroreceptors stimulate cardioinhibitory center (and inhibit cardioacceleratory center) and inhibit vasomotor center. 4a Sympathetic impulses to heart cause HR, contractility, and CO. 2 Baroreceptors in carotid sinuses and aortic arch are stimulated. 4b Rate of vasomotor impulses allows vasodilation, 5 CO and R causing R. return blood 1 Stimulus: pressure to Blood pressure homeostatic range. (arterial blood Homeostasis: Blood pressure in normal range pressure rises above normal range). 1 Stimulus: Blood pressure (arterial blood pressure falls below 4b Vasomotor normal range). 5 CO and R return blood fibers stimulate pressure to vasoconstriction, homeostatic causing R. range. 2 Baroreceptors in carotid sinuses and aortic arch are inhibited 4a Sympathetic impulses to heart Cause HR, contractility, and 3 Impulses from baroreceptors CO. activate cardioacceleratory center (and inhibit cardioinhibitory center) and stimulate vasomotor center. © 2016 Pearson Education, Ltd.  Short-Term Regulation Chemoreceptor reflexes – Aortic arch and large arteries of neck detect increase in CO2, or drop in pH or O2 – Cause increased blood pressure by: Signaling cardioacceleratory center to increase CO Signaling vasomotor center to increase vasoconstriction © 2016 Pearson Education, Ltd.  Short-Term Regulation Influence of higher brain centers – Reflexes that regulate BP are found in medulla – Hypothalamus and cerebral cortex can modify arterial pressure via relays to medulla – Hypothalamus increases blood pressure during stress – Hypothalamus mediates redistribution of blood flow during exercise and changes in body temperature © 2016 Pearson Education, Ltd.  Short-Term Mechanisms: Hormonal Controls Hormones regulate BP in short term via changes in peripheral resistance or long term via changes in blood volume Adrenal medulla hormones – Epinephrine and norepinephrine from adrenal gland increase CO and vasoconstriction Angiotensin II stimulates vasoconstriction ADH: high levels can cause vasoconstriction Atrial natriuretic peptide decreases BP by antagonizing aldosterone, causing decreased blood volume © 2016 Pearson Education, Ltd.  Long-Term Mechanisms: Renal Regulation Long-term mechanisms control BP by altering blood volume via kidneys Kidneys regulate arterial blood pressure by: 1. Direct renal mechanism 2. Indirect renal mechanism (renin-angiotensin- aldosterone) © 2016 Pearson Education, Ltd.  Long-Term Mechanisms: Renal Regulation (cont.) Direct renal mechanism – Alters blood volume independently of hormones Increased BP or blood volume causes elimination of more urine, thus reducing BP Decreased BP or blood volume causes kidneys to conserve water, and BP rises © 2016 Pearson Education, Ltd. Figure 19.11 Direct and indirect (hormonal) mechanisms for renal control of blood pressure. Direct renal mechanism Indirect renal mechanism (renin-angiotensin-aldosterone) Initial stimulus Arterial pressure Arterial pressure Physiological response Result Inhibits baroreceptors Sympathetic nervous system activity Filtration by kidneys Angiotensinogen Renin release from kidneys Angiotensin I Angiotensin converting enzyme (ACE) Angiotensin II Urine formation ADH release by Thirst via Vasoconstriction; Adrenal cortex posterior pituitary hypothalamus peripheral resistance Secretes Aldosterone Blood volume Sodium reabsorption Water reabsorption Water intake by kidneys by kidneys Blood volume Mean arterial pressure Mean arterial pressure © 2016 Pearson Education, Ltd.  Long-Term Mechanisms: Renal Regulation (cont.) Indirect mechanism – The renin-angiotensin-aldosterone mechanism Decreased arterial blood pressure causes release of renin from kidneys Renin enters blood and catalyzes conversion of angiotensinogen from liver to angiotensin I Angiotensin-converting enzyme, especially from lungs, converts angiotensin I to angiotensin II Angiotensin II acts in four ways to stabilize arterial BP and ECF: Stimulates aldosterone secretion Causes ADH release from posterior pituitary Triggers hypothalamic thirst center to drink more water Acts as a potent vasoconstrictor, directly increasing blood pressure © 2016 Pearson Education, Ltd. © 2016 Pearson Education, Ltd. Cardiovascular System Learning Objectives: Cardiovascular System Application of homeostatic mechanisms Provide specific examples to demonstrate how the cardiovascular system maintains blood pressure homeostasis in the body. Predictions related to disruption of homeostasis Given a factor or situation (e.g., left ventricular failure), predict the changes that could occur in the cardiovascular system and the consequences of those changes (i.e., given a cause, state a possible effect).  Summary of Blood Pressure Regulation Goal of blood pressure regulation is to keep blood pressure high enough to provide adequate tissue perfusion, but not so high that blood vessels are damaged – Example: If BP to brain is too low, perfusion is inadequate, and person loses consciousness – If BP to brain is too high, person could have stroke © 2016 Pearson Education, Ltd. Figure 19.12 Factors that increase MAP. Activity of Release Fluid loss from Crisis stressors: Vasomotor tone; Dehydration, Body size muscular of ANPP hemorrhage, exercise, trauma, bloodborne high hematocrit pump and excessive body chemicals respiratory sweating temperature (epinephrine, pump NE, ADH, angiotensin II) Conservation Blood volume Blood pH of Na+ and Blood pressure O2 water by kidneys CO2 Blood Baroreceptors Chemoreceptors volume Venous Activation of vasomotor and cardio- return acceleratory centers in brain stem Diameter of Blood Blood vessel Stroke Heart blood vessels viscosity length volume rate Cardiac output Peripheral resistance Initial stimulus Physiological response Mean arterial pressure (MAP) Result © 2016 Pearson Education, Ltd.  Homeostatic Imbalances in Blood Pressure (cont.) Circulatory shock – Condition where blood vessels inadequately fill and cannot circulate blood normally Inadequate blood flow cannot meet tissue needs – Hypovolemic shock results from large-scale blood loss – Vascular shock results from extreme vasodilation and decreased peripheral resistance – Cardiogenic shock results when an inefficient heart cannot sustain adequate circulation © 2016 Pearson Education, Ltd.  Figure 19.18 Events and signs of hypovolemic shock. Initial stimulus Acute bleeding (or other events that reduce blood volume) leads to: Physiological response 1. Inadequate tissue perfusion Signs and symptoms resulting in O2 and nutrients to cells Result 2. Anaerobic metabolism by cells, so lactic acid accumulates 3. Movement of interstitial fluid into blood, so tissues dehydrate Chemoreceptors activated Baroreceptor firing reduced Hypothalamus activated Brain (by in blood pH) (by blood volume and pressure) (by blood pressure) Major effect Minor effect Respiratory centers Cardioacceleratory and Sympathetic nervous ADH Neurons activated vasomotor centers activated system activated released depressed by pH Intense vasoconstriction Heart rate (only heart and brain spared) Central nervous system depressed Renal blood flow Kidneys Renin released Adrenal cortex Angiotensin II produced in blood Aldosterone Kidneys retain Water released salt and water retention Rate and Tachycardia; Skin becomes Urine output Thirst Restlessness Coma depth of weak, thready cold, clammy, (early sign) (late sign) breathing pulse and cyanotic Blood pressure maintained; CO2 blown if fluid volume continues to off; blood decrease, BP ultimately pH rises drops. BP is a late sign. © 2013 Pearson Education, Inc.