CVS Physiology Part 2 PDF

Physiology of the Cardiovascular System (Part II) Dr. Rozlin Abd Rahman  Question What effect does increase venous return have on stroke volume?  Question How would increased sympathetic stimulation of the heart aff...

Physiology of the Cardiovascular System (Part II) Dr. Rozlin Abd Rahman  Question What effect does increase venous return have on stroke volume?  Question How would increased sympathetic stimulation of the heart affect stroke volume? increase, increase Blood vessels and hemodynamics Revisit: Structure and function of blood vessels ▪ 5 main types ▪ Arteries – carry blood AWAY from the heart ▪ Arterioles ▪ Capillaries – site of exchange ▪ Venules ▪ Veins – carry blood TO the heart  Basic structure TUNICA INTERNA: Endothelium Basement membrane Valve Internal elastic lamina TUNICA MEDIA: Smooth muscle External elastic lamina TUNICA EXTERNA Lumen Lumen (a) Artery (b) Vein  Arteries Internal elastic lamina External elastic lamina Tunica externa can stretch Lumen with blood cells Tunica interna Tunica media Connective tissue LM 200x Transverse section through an artery  Connective tissue Red blood cell Capillary endothelial cells LM 600x Red blood cells passing through a capillary Arterioles ▪ Abundant microscopic vessels ▪ Metarteriole has precapillary sphincter which monitors blood flow into capillary ▪ Sympathetic innervation and local chemical mediators can alter diameter and thus blood flow and resistance ▪ Resistance vessels – resistance is opposition to blood flow ▪ Vasoconstriction can raise blood pressure  Capillaries Lumen Basement Endothelium membrane Capillary Types of Capillaries 3 types 1.Continuous ▪ Endothelial cell membranes from continuous tube 2.Fenestrated ▪ Have fenestrations or pores 3.Sinusoids ▪ Wider and more winding ▪ Unusually large fenestrations Capillary Networks Figure 21-5 Capillary exchange ▪ Movement of substances between blood and interstitial fluid ▪ 3 basic methods 1. Diffusion most important method in capillary exchange e.g CO2, H2O 2. Transcytosis small quantity of component ?? 3. Bulk flow cannot diffuse to blood capillary, digested by endocytosis Veins ▪ Same 3 layers ▪ Tunica interna thinner than arteries ▪ Tunica media thinner with little smooth muscle ▪ Tunica externa thickest layer ▪ Not designed to withstand high pressure ▪ Valves – folds on tunica interna forming cusps ▪ Aid in venous return by preventing backflow Hemodynamics  Factors affecting blood flow ▪ Blood flow – volume of blood that flows through any tissue in a given period of time (in mL/min) ▪ Total blood flow is cardiac output (CO) CO = SV x HR ▪ Distribution of CO depends on ▪ Pressure differences that drive blood through tissue ▪ Resistance to blood flow in specific blood vessels  Blood Pressure ▪ Contraction of ventricles generates blood pressure TOP ▪ Systolic BP – highest pressure BOTTOM attained in arteries during systole ▪ Diastolic BP – lowest arterial pressure during diastole ventricles relax ▪ Blood pressure also depends on total volume of blood ▪ BP= CO x TPR total peripheral resistance highest pressure = AORTA  Blood Pressure ▪ Systolic pressure ▪ Pressure during contraction phase of heart ▪ Normal value: 90 – 120 mmHg ▪ Diastolic pressure ▪ Pressure during relaxation phase of heart ▪ Normal value: 60 – 80 mmHg  Blood Pressure ▪ Mean arterial pressure (MAP) ▪ Average pressure in the arterial system over a given time during single cardiac cycle ▪ Normal value: 80 – 100 mmHg min. value = 60  Blood Pressure X will not be asked ▪ Mean arterial pressure MAP = Diastolic BP + 1/3 (systolic BP – diastolic BP) A MAP of approximately 60 mmHg is necessary to perfuse coronary arteries, brain, kidneys. stress to heart since need to push harder to push against resistance Abnormal Blood Pressure ▪ Hypertension: ▪ abnormally high blood pressure: repeat to 3 consecutive days, at the same time ▪ greater than 140/90 ▪ Hypotension: old age ▪ abnormally low blood pressure  Venous Return ▪ Amount of blood arriving at right atrium each minute ▪ Determined by venous pressure ▪ Transient changes in venous return can occur in response to several factors such as: ▪ Muscle contraction. ▪ Decreased venous compliance. ▪ Respiratory activity. ▪ Vena cava compression ▪ Gravity paralysis = slow venous return Vascular resistance ▪ Opposition to blood flow due to friction between blood and walls of blood vessels hydrated = resistance more = BP ▪ Depends on high 1. Size of lumen 2. Blood viscosity darah pekat = high resistance 3. Total blood vessel length longer blood vessel = greater resistance Control of blood pressure and blood flow Heart Rate Blood Stroke Volume Volume Syst. Vascular Resistance  How our body control the pressure of the blood? Autonomic Nervous system Humoral System Neural Control Neural regulation of blood pressure ▪ Negative feedback loops from 2 types of reflexes: HR HIGH, CONTRACTION HIGH, VASOCONSTRICTION HIGH 1. Baroreceptor reflexes ▪ Pressure-sensitive receptors ▪ Most important baroreceptor reflexes: ▪ Carotid sinus reflex ▪ Aortic reflex reduced firing, action potential slow ▪ When blood pressure falls, baroreceptors stretched less, slower rate of impulses to cardiovascular centre (CVC) ▪ CVC decreases parasympathetic stimulation and increases sympathetic stimulation  Location of baroreceptors Baroreceptors sense stretch and rate of stretch by generating action potentials (voltage spikes) Located in highly distensible regions of the circulation to maximise sensitivity  Baroreceptors During High Arterial Pressure HIGH BP: - more stretching of baroreceptor - fire more action potential VASODILATION Neural regulation of blood pressure 2. Chemoreceptor reflexes ▪ Monitor O2 the chemical composition of blood. CO2 Hydrogen ▪ Detect hypoxia, hypercapnia, acidosis CO2, O2, pH level ▪ CV increases sympathetic stimulation to arterioles and veins, producing vasoconstriction ▪ Receptors also provide input to respiratory center to adjust breathing rate Role of CV Center in BP Homeostasis 3 main types of sensory receptors ▪ Proprioceptors – monitor movements of joints and muscles to provide input during physical activity ▪ Baroreceptors – monitor pressure changes and stretch in blood vessel walls ▪ Chemoreceptors – monitor concentration of various chemicals in the blood ▪ Output from CV flows along neurons of ANS ▪ Sympathetic (stimulatory) opposes parasympathetic (inhibitory) Humoral Control  HumoralVasoconstriction  Sympathetic and adrenal release of norepinephrine and epinephrine.  Angiotensin II  Vasopressin (ADH) – very potent vasoconstrictor secreted by the posterior pituitary. Also increases renal H2O reabsorption.  Endothelin A – released from damaged vessels.  HumoralVasodilation  Bradykinin – powerful arteriolar dilation and increased permeability of the capillaries. vasodilation  Histamine – released from damaged or inflamed tissue; also during an allergic reaction. Also causes arteriolar dilation and increased permeability of the capillaries. constriction  Ions and Other Chemical Factors  Ca2+ ions – vasoconstriction.  K+ ions – vasodilation.  Mg2+ ions – vasodilation (often inhibits the actions of Ca2+ ions).  H+ ions – increase cause vasodilation, aciditic decrease causes constriction.  Anions High CO2 in blood, bad respiratory – acetate and citrate cause failure Slow breathing vasodilation.  CO2 – vasodilation, particularly important in the brain.  Hormonal regulation of blood pressure ▪ Renin-angiotensin-aldosterone system (RAAS) kidney releases angiotensin ▪ Renin and angiotensin converting enzyme (ACE) act on substrates to produce active hormone angiotensin II ▪ Raises BP by vasoconstriction and secretion of aldosterone (increases water reabsorption in kidneys to raise blood volume and pressure)  Reduced renal Renin-angiotensin-aldosterone system LOW BP blood flow Increased blood volume in the kidney, sense Juxtaglomerular LV filling pressure) change in BP apparatus Increased J.A release Fluid re-absorption Renin pre-load into the blood stream (LV pressure Angiotensinogen Sodium retention beginning of systole) Renin Increased convert bawah ni jadi after-load Angiotensin I ACE converts atas jadi stimulate Increased aldosterone bawah secretion and ADH Angiotensin II Veins Vasoconstriction total peripheral resistance HIGH >> BP high Arteries  Hormonal regulation of blood pressure ▪ Epinephrine and norepinephrine ▪ Adrenal medulla releases in response to sympathetic stimulation ▪ Increase cardiac output by increasing rate and force of heart contractions CO INCREASE ▪ Antidiuretic hormone (ADH) or vasopressin ▪ Response to dehydration or decreased blood volume ▪ Causes vasoconstriction which increases blood pressure Atrial natriuretic peptide (ANP) ◼Released by cells of atria ◼Lowers blood pressure by causing vasodilation ◼Promotes loss of salt and water in urine ◼Reduces blood volume  Hormone that Reduces Blood Pressure - ANP ANP - triggered ADH causes vasoconstriction Autoregulation of blood pressure ▪ Ability of tissue to automatically adjust its blood flow to match metabolic demands ▪ 2 general types of stimuli 1. Physical – temperature changes, myogenic response 2. Vasodilating and vasoconstricting chemicals alter blood vessel diameter tissue to adjust to the blood flow e.g low temperature, blood vessels vasoconstrict Circulation ▪ Important difference between pulmonary and systemic circulation in autoregulatory response ▪ Systemic blood vessel walls dilate in response to low O2 to increase O2 delivery ▪ Walls of pulmonary blood vessels constrict under low O2 to ensure most blood flows to better ventilated areas of lung  Aging and the Cardiovascular System ▪ Age-related changes occur in: ▪ blood ▪ heart ▪ blood vessels Age-Related Changes in Blood measure % RBC proportion by volume (percentage) high hematocrit = high RBC 1. Decreased hematocrit 2. Blood clots (thrombus) not efficiently contractable as they are young prone to thrombus formation 3. Blood-pooling in legs ▪ due to venous valve deterioration arent contractable compared to younger risk of thrombus is HIGH with aging  Age-Related Changes in the Heart 1. Reduced maximum cardiac output 2. Changes in nodal and conducting cells 3. Reduced elasticity of fibrous skeleton 4. Progressive atherosclerosis 5. Replacement of damaged cardiac muscle cells by scar tissue  Age-Related Changes in Blood Vessels 1. Arteries become less elastic: ▪ pressure change can cause aneurysm bulge/balloon at wall of blood vessel 2. Calcium deposits on vessel walls: vessels hardened = risk of stroke ▪ can cause stroke or infarction death of tissue due to low blood supply 3. Thrombi can form: ▪ at atherosclerotic plaques Disorder in Blood Flow Regulation  Shock  Severe circulatory failure. heart does not contract efficiently to produce CO  low CO and falling peripheral BP.  Arise from multiple causes: ▪ failure of the heart to maintain normal CO ▪ Decreased circulating blood volume very severe dehydration ▪ Bacterial toxin ▪ Anaphylactic shock   As tissue perfusion falls below the level needed to maintain adequate oxygen supply, the cells begin to sustain damage from inadequate oxygen and build up of metabolic wastes.  Once damage occur, a positive feedback cycle begins.  It become worse until it become irreversible → mortality tissue lack of O2 >> cell damaged from low O2 >> accumulating metabolic wastes  Stroke  It is the loss of brain function due to a disturbance in the blood supply to the brain.  This disturbance is due to either ischemia (lack of blood flow) or hemorrhage.  As a result, the affected area of the brain cannot function normally, which might result in an inability to move one or more limbs on one side of the body, failure to understand or formulate speech, or a vision impairment of one side of the visual field paralysed, impairment in speech usual - blockage from blood clot blood leaking from a ruptured