Regulation of Blood Pressure PDF

THE CARDIOVASCULAR SYSTEM REGULATION OF BLOOD PRESSURE PM DR SATIRAH ZAINALABIDIN After completion of this topic, students should be able to:  Define blood pressure and the factors determining it.  Explain the regulation of blood pressure.  Discuss about the cardiovascular compensa...

THE CARDIOVASCULAR SYSTEM REGULATION OF BLOOD PRESSURE PM DR SATIRAH ZAINALABIDIN After completion of this topic, students should be able to:  Define blood pressure and the factors determining it.  Explain the regulation of blood pressure.  Discuss about the cardiovascular compensation in special conditions: exercise, change of posture and hemorrhage. HEMODYNAMICS: FACTORS AFFECTING BLOOD FLOW The means by which blood flow is altered and distributed and by which blood pressure is regulated. Blood flow is defined as the quantity blood passing through any tissue in the circulation in a given period (in ml/min) Overall blood flow in the total circulation of an adult is about 5000 ml/min → the cardiac output Blood pressure (BP) is the pressure exerted on the walls of a blood vessel; in clinical use, BP refers to pressure in arteries. More explanation - Regulation of Cardiac Output and Mean Arterial Pressure relationships. https://www.youtube.com/watch?v=ecXJ7to6Lb4 Hemodynamics Factors affecting circulation – pressure differences that drive the blood flow velocity of blood flow volume of blood flow blood pressure – resistance to flow – venous return An interplay of forces result in blood flow RELATIONSHIP OF CARDIAC OUTPUT WITH BLOOD PRESSURE  As cardiac output is made up of heart rate and stroke volume - at rest these are relatively constant.  With exercise the heart beats faster - more blood is pumped out with each beat contributing to a rise in BP.  Changes in the volume of blood within the cardiovascular system will also affect BP.  A person was severely dehydrated or lost a large quantity of blood through a wound, there would be less blood for the heart to pump, thereby reducing cardiac output and BP. Ventricular contraction Ventricular relaxation  Arterial Blood Pressure (mm Hg) Pressure in the aorta varies with the cardiac cycle. Two pressure readings: ▪ Systolic blood pressure = maximum pressure ▪ Due to ejection of blood into aorta ▪ Diastolic blood pressure = minimum pressure ▪ Not zero due to elastic recoil of aorta ▪ Normal BP 120/80 mm Hg ▪ Higher than normal= hypertension ▪ Lower than normal= hypotension How BP works https://www.youtube.com/watch?v=Ab9OZsDECZw  BLOOD PRESSURE Pressure exerted by blood on walls of a vessel – caused by contraction of the ventricles – highest in aorta 120 mm Hg during systole & 80 during diastole If heart rate increases cardiac output, BP rises Pressure falls steadily in systemic circulation with distance from left ventricle – 100 mmHg after leaving the heart – 35 mmHg entering the capillaries – 0 mmHg entering the right atrium If decrease in blood volume is over 10%, BP drops Water retention increases blood pressure Must overcome total peripheral resistance (TPR) → the resistance of entire cardiovascular system  Pulse pressure = Systolic pressure – Diastolic pressure  Mean arterial pressure (MAP): MAP = diastolic pressure + 1/3 pulse pressure  A pulse is a rhythmic pressure occillation that accompanies each heartbeat What is the importance of the high vs low pressure? Which one has higher compliance?  What is Pulse pressure (PP) for? Normal PP ~ 25% of the systolic pressure. Low/narrow PP - in patients with a low SV in congestive heart failure, stenosis of the aortic valve, or severe blood loss. High/wide PP - common in healthy people doing strenuous exercise (resting PP 30–40 mmHg vs exercising PP up to 100 mm Hg as stroke volume increases). A persistent high pulse pressure >100 mm Hg may indicate excessive resistance in the arteries → can degrade the heart, brain, and kidneys. Mean arterial pressure (MAP) Normal: 70–110 mm Hg. If the value 60 mm Hg CO = MAP TPR Normal ratio is 3:2:1 -- systolic/diastolic/pulse pressure CO = SV x HR Systemic Vascular Resistance (SVR) the resistance to blood flow offered by all of the systemic vasculature Also called as total peripheral resistance (TPR). SVR is therefore determined by factors that influence vascular resistance (friction between blood and vessel walls) in individual vascular beds. SVR is primarily determined by changes in: (a) blood vessel diameters Vasoconstriction → R high, BP high Vasodilation → R low, BP low R increases exponentially as vessel diameter decreases (Poiseuille’s law) -- R α 1/r4 R=resistance, r=radius Systemic Vascular Resistance (SVR) (b) adult vessel length is constant  The longer the vessel, the larger surface area, the more friction happens -obese people have hypertension because additional blood vessel within the adipose tissue increase total blood vessel length (c) blood viscosity (thickness) ratio of red blood cells to plasma volume Whole blood viscosity is about 5 times that of water, so it needs higher pressure to flow Increase in viscosity increase resistance eg. dehydration, polycythemia Decrease in viscosity eg. anemia, haemorrhage  MAP and pulse pressure decrease with distance from heart  Blood pressure decreases with friction  Pulse pressure decreases due to elastic rebound (the arteries recoil to their original dimensions) Capillaries vs arterioles, who has the highest resistance?  Blood flow smooth  Slowest flow near the walls; fastest at the center  Swirling action that disturbs smooth flow of liquid, increases resistance  Occurs in heart chambers and great vessels, but not in small vessels  Atherosclerotic plaques cause abnormal turbulence Blood flow can either be laminar or turbulent Darcy’s law for radial flow: F = P R F = Flow = cardiac output = CO  P = mean arterial pressure = MABP R = total peripheral resistance = TPR CO = MAP TPR MAP = CO x TPR Blood Pressure Measurement One of the critical basic parameters measured on patients. The technique used today was developed in 1905 by a Russian physician Dr. Nikolai Korotkoff. Turbulent blood flow through the vessels can be heard as a soft ticking while measuring blood pressure; these sounds are known as Korotkoff sounds. The technique of measuring blood pressure requires the use of a sphygmomanometer (a blood pressure cuff attached to a measuring device) and a stethoscope. Measuring your BP https://www.youtube.com/watch?v=bNApnYMR16w  Goal of cardiovascular regulation is to ensure that these blood flow changes occur:  At an appropriate time  In the right area  Without drastically altering blood pressure and blood flow to vital organs  Factors involved in regulation of cardiovascular function include:  Local factors  Neural mechanisms  Endocrine factors Cardiovascular Responses  Control cardiac output and blood pressure: 1. Autoregulation (intrinsic control):  Local factors change the pattern of blood flow within capillary beds  causes immediate, localized homeostatic adjustments  If autoregulation fails, neural/endocrine are activated 2. Neural mechanisms (extrinsic control):  respond to pressure/blood gas quickly at specific sites 3. Endocrine mechanisms (extrinsic control):  Releases hormone that enhance short-term /direct long- term changes Cardiovascular: Controlling Arteriole Resistance https://www.youtube.com/watch?v=2I4Mw3fR_8g  The ability of a tissue to automatically adjust its own blood flow to match its metabolic demand for supply of O2 and nutrients and removal of wastes  Intrinsic control mechanisms that automatically control blood flow to local tissues → ultimate goal: maintain blood flow  Cardiac output stays the same  important for tissues that have major increases in activity (brain, cardiac & skeletal muscle) Vasodilation 1. Physical changes o Warming – vasodilation, Cold – vasoconstriction o Myogenic response o The response to pressure changes o VSM contracts when stretched o VSM dilates when stress is reduced o Scenario – loss of blood? ? ? ? ? o Scenario – laying to standing? What happens if failure to compensate? 2. Local vasodilator & vasoconstrictor o Vasodilator – accelerate blood flow o Vasoconstrictor – restrict blood flow o Due to local chemicals or changes of O2 level  Examples of local vasodilators include: ❑ Low O2 or high CO2 levels  Eg. (↑ CO2 → vasodilation→↑ blood flow) Metabolic ❑ Low pH (acids) eg. Lactic acid product ❑ High K+ or H+ concentrations ❑ Carbon monoxide from heme ❑ Nitric oxide (NO) from endothelium ❑ Chemicals released by inflammation or trauma (histamine, prostaglandin, bradikinin) ❑ Elevated local temperature  Examples of local vasoconstrictors: ❑ prostacyclin from endothelium ❑ Thromboxane A2 from arachidonic acid (COX pathway) ❑ Endothelins by damaged tissues – from endothelium ❑ Cold temperature Autoregulation https://www.youtube.com/watch?v=RZo5yjfynIE  Cardiovascular (CV) centers:  cardiac and vasomotor centers of medulla oblongata  adjust cardiac output and blood vessel diameter (peripheral resistance)  CV centers detect changes in tissue by monitoring:  arterial blood (especially BP)  pH  dissolved gas concentrations  Cardioacceleratory center:  increases cardiac output through sympathetic  Cardioinhibitory center:  reduces cardiac output through parasympathetic Input to the Cardiovascular Center Higher brain centers such as cerebral cortex, limbic system & hypothalamus anticipation of competition increase in body temperature Proprioceptors –input during physical activity Baroreceptors –changes in pressure within blood vessels Chemoreceptors – monitor concentration of chemicals in the blood (pH & dissolved gasses) Output from the Cardiovascular Center Heart – parasympathetic (vagus nerve) decrease heart rate – sympathetic (cardiac accelerator nerves) cause increase in contractility & rate (SAN) Blood vessels – sympathetic vasomotor nerves controlled by adrenergic nerves (NE) increased stimulation produces constriction & increased BP Output from the Cardiovascular Center – sympathetic vasomotor nerves continual stimulation to arterioles in skin & abdominal viscera producing vasoconstriction (vasomotor tone) Produced by constant action of sympathetic vasoconstrictor nerves – tonic contraction - sufficient to keep the arterioles partially constricted Blood flow occurs in pulses rather than a steady & constant stream → blood flow in capillary beds to constantly change routes  Vasodilation:  controlled by ACh (cholinergic nerves) → Nitric oxide (NO)  relaxes smooth muscle Innervation of the Heart Speed up the heart with sympathetic stimulation Slow it down with parasympathetic stimulation (X) Sensory information from baroreceptors (IX)  Monitor degree of stretch receptors in walls of:  carotid sinuses:  maintain blood flow to brain  Very sensitive to maintain sufficient blood flow to the brain  aortic sinuses:  monitor start of systemic circuit  right atrium:  monitor end of systemic circuit (at vena cava & right atrium wall)  Send signal to the vasomotor center in the medulla oblongata  Initiate baroreceptor reflexes  Autonomic reflexes that adjust CO and peripheral resistance to maintain normal arterial pressures  When blood pressure rises, CV centers:  decrease cardiac output (parasymp. activation)  cause peripheral vasodilation (inhibition of excitatory neurons in the vasomotor centres) When blood pressure falls, CV centers: – increase cardiac output (sympathetic – cardioacceleratory) – cause peripheral vasoconstriction (stimulation of symphatetic vasoconstrictors) Baroreceptor https://www.youtube.com/watch?v=X3BCFOlk1oQ Carotid Sinus Massage & Syncope Carotid sinus massage can slow heart rate in paroxysmal superventricular tachycardia Stimulation (careful neck massage) over the carotid sinus lowers heart rate – paroxysmal superventricular tachycardia tachycardia originating from the atria anything that puts pressure on carotid sinus Pulse points – tight collar or hyperextension of the neck – may slow heart rate & cause carotid sinus syncope or fainting  In carotid bodies and aortic bodies:  monitor pH, O2, and CO2 concentrations in the blood (hypoxia, hypercapnia or acidosis) causes stimulation of cardiovascular center increases sympathetic stimulation to arterioles & veins vasoconstriction and increase in blood pressure  Also changes breathing rates as well Further explanation - Baro & Chemoreceptor https://www.youtube.com/watch?v=QvHdjYKi1N0 Chemoreceptor Reflexes  On cardiovascular centers:  thought processes and emotional states (anxiety, fear, rage) can elevate blood pressure by cardiac stimulation and vasoconstriction  Provides both short term and long term regulation  E and NE immediately stimulate CO, increase HR and peripheral vasoconstriction  Antidiuretic hormone (ADH), angiotensin II, erythropoietin (EPO), and natriuretic peptides (ANP)  Affect long term regulation of blood volume 1. Epinephrine & Norepinephrine In response to sympathetic increases heart rate & force of contraction causes vasoconstriction in skin & abdominal organs (alpha-adrenergic) vasodilation in coronary arteries & skeletal muscle (beta-adrenergic) – Why? 2. Renin-angiotensin-aldosterone system In response to decrease in BP or decreased blood flow to kidney release of renin / results in formation angiotensin II (ANG II) → systemic vasoconstriction, stimulates thirst causes release aldosterone (H2O & Na+ reabsorption) 3. Antidiuretic hormone (ADH) released from the pituitary → causes water reabsorption → increase blood volume (hence antidiuretic hormone) At pathological condition, it can cause vasoconstrictor (hence vasopressin) 4. Erythropoietin  Released at kidneys  Responds to low blood pressure, low O2 content → Stimulates red blood cell production, thereby increasing the volume and viscosity of the blood → improving O2 capacity Hormonal Regulation during decreased BP & BV  Atrial natriuretic factor (ANF):  produced by cells in right atrium in response to excessive stretching during diastole  Brain natriuretic peptide (BNP):  produced by ventricular muscle cells  Lower blood volume and blood pressure by:  Increasing Na+ excretion at the kidneys (natriuresis)  Promoting water losses by increasing the volume of urine produced (diuresis)  Reducing thirst (blocking ADH)  Blocking the release of renin → ANG II, aldosterone  Blocking the release of E & NE  Stimulating peripheral vasodilatation  As blood volume decline, stresses on the walls of hearts are removed & natriuretic peptide production ceases. Hormonal Regulation during increased BP & BV Check your pulse point, either on your wrist (radial artery) or on your neck (carotid artery). Can you figure out your heart rate?