Unit 6 Physiology of CVS PDF

Unit 6 : Physiology of the Cardiovascular System-CVS 1  Outlines Functions of CVS – Excitation of the heart Components of CVS – ECG – C...

Unit 6 : Physiology of the Cardiovascular System-CVS 1  Outlines Functions of CVS – Excitation of the heart Components of CVS – ECG – Cardiac cycle Heart – Heart sound – Introduction – Cardiac output – Division of circulation – Blood pressure – Blood supply to the Hypertension heart Shock – Cardiac muscle E-C coupling Myocardial action potential 2  FUNCTIONS OF THE CVS 1. Transport of materials to and from all parts of the body Substances transported by CVS can be divided Nutrients, water, and gases that enter the body from the external environment – Oxygen from the lungs and nutrients from GIT Materials that move from cell to cell within the body – Wastes from some cells to the Liver for processing – Immune cells,antibodies,clotting proteins delivered to any cell that needs them – Hormones frome endocrine cells to target cells Wastes that the cells eliminate – Metabolic wastes from all cells to Kidneys – Heat from all cells to Skin 3 – Carbon dioxide from all cells to Lungs  Cont’d 2. Sensory and endocrine functions :regulate blood pressure and blood volume 3.Vital role in reproduction - hydraulic mechanism for penile erection 4  Components of the CVS CVS composed of: heart,blood vessels,blood 1.Heart: Pumping centre – Atria :receives blood returning to the heart from the blood vessels – Ventricle :pumps blood out into the blood vessels 2.Blood vessels Arteries:conducting blood to the various organs (Distributing system) Capillaries: Major sites of nutrient, metabolic end product, and fluid exchange between blood and tissues (Exchange system) Veins:conduits for blood flow back to the heart( Collecting system) 3.Blood :a fluid that circulates around the body, carrying materials to and from the cells. 5  Cont’d Division of the Circulation In the CVS, blood passes through two (double) circulations: Pulmonary circulation: Circulation of blood from the right ventricle to the lungs and to the left atrium  RV →Pulmonary arteries → Pulmonary capillaries →Pulmonary veins → LA. Systemic circulation: Circulation of blood from the left side of the heart to the tissues and back to the right side of the heart  LV→ Aorta → Systemic arteries →Systemic capillaries →Veins →vena cava→RA 6 Pathway of Blood Through the Heart and Lungs 7 Pulmonary Circulation 1. Low Resistance 2. Low Pressure (25/9 mmHg) Systemic Circulation 1. High Resistance 2. High Pressure (120/80 Mmhg) Parallel Subcircuits on Different Organs Unidirectional Flow 8 Cont’d Pathway of blood through the heart and lungs Left atrium  bicuspid valve  left ventricle  aortic semilunar valve  aorta  systemic circulation  vena cava  right atrium  tricuspid valve  right ventricle  pulmonary semilunar valve  pulmonary arteries  lungs  pulmonary veins left atrium 9 10  Blood supply to the heart The heart receives arterial blood from the coronary artery, which is the branch of ascending aorta. Resting coronary blood flow = 250 ml/min, 5% CO Ascending Aorta R. Coronary L. Coronary artery artery Supplies R. Atrium Posterior Circumflex a. Anterior ventricles Supplies descending a  R ventricle L.Atrium Supplies L ventricle L ventricle R ventricle L ventricle 11 Coronary Circulation: Arterial Supply 12  The Heart Heart is the hollow, muscular organ that plays a central pumping role. Located centrally in the thoracic cavity It is surrounded by a membranous sac called the pericardium, – which contains pericardial fluid that lubricates the heart The heart wall consists of three layers – Epicardium an outer layer of connective tissue – Myocardium a middle layer of cardiac muscle – Endothelium an inner layer of epithelial cells Vertically divided into left & right sides by a structure called septum 13  Cont’d The heart has four chambers – 2 atria(right atria and left atria) and 2 ventricles(right ventricle and left ventricle) RA receives blood from venae cavae and sends to RV RV receives blood from RA and sends to the lungs LA receives blood from the lung and sends to LV LV receives blood from the RA sends to all tissues except lung The heart has four valves Prevent back flow of blood(Ensure one-way flow in the heart) Atrioventricular valves(inlet valves)-between atria and ventricles – Tricuspid valve:between RA and RV – Mitral valve:between LA and LV Semilunar valves (outlet valves)–between ventricles and arteries – Aortic valve:between LV and aorta – Pulmonary valve:between RV and pulmonary artery 14 Cont’d The heart can be functionally separated into left and right halves: The atria and ventricles are separated by a wall called the septum. – Between RA &LA- interatrial septum – Between RV&RV- interventricular septum Septum prevents blood in the left heart from mixing with blood in the right heart. The heart also has a “top” and a “bottom.” – The wider upper pole (end) of the heart is known as the base – T he narrower lower pole is the apex. 15  Cont’d Functional Anatomy of the heart 16 17  Cardiac muscle (myocardium) There are two types of cardiac muscles A. Contractile muscles -99% 1. The atrial muscle 2. The ventricular muscle – Typical striated muscle, with contractile fibers organized into sarcomeres B. Authorhythmic cells -1% – are smaller and contain few contractile fibers. – Because they do not have organized sarcomeres, Do not contribute to the contractile force of the heart Two types 1.Pacemakers -Initiate action potentials spontaneously – Establish the heart rhythm 2. Conduction fibers – Transmit AP through the heart 18  Cont’d Cardiac muscle cells are Smaller than skeletal muscles Striated Mono-nucleated Connect to each other through intercalated disks that include desmosomes and gap junctions. Has many mitochondria and utilizes most of the O2. 19  Cont’d Differences b/n Cardiac muscle and skeletal muscle Cardiac muscles are Are much smaller than skeletal muscle fibers and usually have a single nucleus per fiber. Are branched and neighboring cells joined end-to-end by cell junctions, known as intercalated disks. – Intercalated disks have two components:desmosomes and gap junctions – Desmosomes are strong connections that tie adjacent cells together, allowing force created in one cell to be transferred to the adjacent cell. – Gap junctions electrically connect cardiac muscle cells to one another. Allow waves of depolarization to spread rapidly from cell to cell, so that all the heart muscle cells contract almost 20 simultaneously.  Cont’d Have larger t-tubules than skeletal muscle, and they branch inside the myocardial cells. SR is smaller than that of skeletal muscle Cardiac muscle depends on extracellular Ca2+ to initiate contraction. Mitochondria occupy about one-third of its cell volume 21  Excitation-contraction coupling in cardiac muscle The mechanism by which the action potential causes the myofibrils of muscle to contract. Action potential originates spontaneously in the heart’s pacemaker cells and spreads into the contractile cells through gap junctions. When the myocardial cell is excited → Na+ influx → depolarization of the sarcolemma → depolarization of the T-tubules → Ca2+ influx through slow calcium channels in the membrane → Ca2+ enters the cell and opens ryanodine receptor Ca2+ release channels (RyR) in the SR →Ca2+ binds to troponin C → myocardial cell contracts 22 Ca2+ signaling in cardiac muscle Inhibited by digitalis & ouabain; indirectly Affected by epinephrine () and ACh () 1 Ca2+ out for Na+/Ca2+ inside Entry of Ca2+ during 3 Na+ in action potential 23 Differences on excitation contraction coupling of cardiac and skeletal muscle In cardiac muscle Ca2+ comes from both the ECF and SR. Only SR is the source of ca2+ for skeletal muscle to contract. Differences in relaxation in cardiac muscle and skeletal muscle In skeletal muscle, Ca2+ is transported back into the SR with the help of a Ca2+-ATPase. In cardiac muscle , Ca2+ is also removed from the cell in exchange for Na+ via the Na+-Ca2+ exchanger (NCX).  Ca2+ moves out of the cell in exchange for 3 24 Na+.  Cont’d Myocardial Action Potentials The main difference between the action potential of the myocardial contractile cell and those of skeletal muscle fibers – Is that the myocardial cell has a longer action potential due to Ca2+ entry. Phases of myocardial contractile cell action potential 1.Resting membrane potential= -90 mV. 2. Depolarization: the result of Na+ entry 3. Initial repolarization: Na+ channels close, K+ cannel open , K+ leaves, the cell begins to repolarize. 4. The plateau phase: a decrease in K+ permeability and an increase in Ca2+ permeability. 5. Rapid repolarization: Ca2+ channels close 25 and K+ permeability increase  Cont’d Functions of the plateau phase – Prevents tetanic contraction – Allow ventricular filling 26  Excitation of the heart Electrical communication in the heart begins with an action potential in an autorhythmic cell The depolarization spreads rapidly to adjacent cells through gap junctions. The depolarization wave is followed by a wave of contraction that passes across the atria, then moves into the ventricles – The conduction system causes a wave of excitation to move first through the atria, causing them to depolarize and then contract as a unit. – Next, the wave of excitation moves through the ventricles, causing them to depolarize and then contract as a unit Sequence of Excitation 1.Sino-atrial node (SA-node) Autorhythmic cells in the right atrium that serve as the main pacemaker of the heart. The discharge rate of the SA node determines the heart rate 27  Cont’d 2.Internodal pathways: Conduct impulse from the SA-node to the Atrioventricular node (AV-node) 3.AV-node: Autorhythmic cells located at the base of the right atrium. Links atrial depolarization to ventricular depolarization Delays the propagation of action potential for 0.1 sec. – Allows atrial contraction to be completed before ventricular excitation occurs – Important for complete filling of ventricles. 28  Cont’d 4.Av bundle (bundle of His): Conducts impulse from the atria to the ventricle. The AV node and the bundle of His constitute the only electrical connection between the atria and the ventricles. 5.Left and right bundle branches conduct impulses to the left and right ventricles 6.Purkinje fibers Conduct cardiac impulse to the ventricles. 29  Cont’d Various automatic cells have different 'rhythms': SA node: usually 60 - 100 per minute) AV node : 40 - 60 per minute AV bundle: 35-40 per min Bundle branches & Purkinje fibers: 20 - 40 per minute. 30 31  Conduction of the Impulse Action potentials from the SA node spread very quickly. At a rate of 0.8 to 1.0 (m/sec)—across the myocardial cells of both atria. The impulse spreads at moderate velocity through the atria. The conduction rate then slows considerably as the impulse passes into the AV node(0.03 to 0.05 m/sec). Impulse delayed more than 0.1 second in the A-V nodal region before appearing in the ventricular septal A-V bundle. The conduction rate increases greatly in the atrioventricular bundle and reaches very high velocities (4 m/sec) in the Purkinje fibers. Ventricular contraction begins 0.1 to 0.2 32  Factors affecting autorhythmicity 1. ANS SyNS: Innervates SA-node, AV-node, conductive and contractile muscles ↑rhythmicity, +ve chronotropic effect Mechanism: increases the slope of pacemaker potential of SA-node by decreasing K+ permeability PSNS: Innervates SA-node, AV-node, atrial muscles Inhibits autorhythmicity, -ve chronotropic effect Strong vagal stimulation leads to cardiac arrest Mechanism: decreases the slope of pacemaker potential by increasing K+ conductance in the SA- node 2.Temperature: ↑BT by 1oC, ↑HR by 20 beats/min 33 ↑BT increases SA- nodal discharge  Cont’d 3. Drugs: AD, NAD, T3/T4 increase cardiac rhythmicity they have +ve chronotropic effect Cholinergic drugs: Ach, pilocarpin→ -ve chronotropic effect 4. Electrolytes: Hyperkalemia ([K+] 5-9 meq/L) increases membrane excitability Hypokalemia leads hyperpolarization 34  The Electrocardiogram(ECG) Is a tool for evaluating the electrical events within the heart. It is recorded by placing electrodes on the surface of the skin. Electrical activity generated in muscle tissue spreads through the body because body fluids function as conductors. Differences between action potential and ECG An AP is one electrical event in a single cell recorded using an intracellular electrode. – An upward deflection represents depolarization and a downward one represents repolarization. – The action potential has much greater amplitude because it is being recorded close to the source of the signal. The ECG is an extracellular recording that represents the sum of multiple action potentials taking place in many heart muscle cells. 35  Cont’d The ECG contains waves ,intervals and segments – Waves appear as deflections above or below the baseline. – Segments are sections of baseline between two waves. – Intervals are combinations of waves and segments. Different waves of the ECG reflect depolarization or repolarization of the atria and ventricles. Three major waves can be seen on a normal ECG P wave –represents atrial depolarization QRS complex-represents ventricular depolarization 36 T wave-represents ventricular repolarization.  Cont’d Segments P-R segment: an isoelectric line that represents conduction through AV node. S-T segment: it indicates the end of ventricular depolarization Intervals P-R interval: represents atrial depolarization and conduction through AV node. Q-T interval: represents ventricular depolarization and repolarization 37 Cont’d 38 Heart Physiology: Sequence of Excitation 39 59 o 40  Electrocardiography 1 mV ECG T P Repolarization of ventricles Q S Depolarization of ventricles Depolarization of atria 41 Heart Excitation Related to ECG 42 Cont’d 43 44  Cardiac cycle Events that occur from the beginning of one beat to the beginning of the next beat. Includes all the events associated with the flow of blood through the heart during a single complete heartbeat. Can be divided into two major stages: – Diastole, the period of ventricular relaxation. – Systole, the period of ventricular contraction. Total duration of cardiac cycle(0.8 second) is a reciprocal of heart rate. Systole comprises about 40% (0.3 second) ,diastole comprises 60%(0.5 second) of the entire cardiac cycle. 45  Cont’d Phases of the cycle 1.Rapid ventricular filling Blood returning to the heart via the systemic and pulmonary veins enters the relaxed atria. Atrial pressure become slightly higher than ventricular pressure. The AV valve is held open by the pressure difference – blood entering the atrium from the pulmonary veins continues on into the ventricle. 80% of the ventricle fills when the atria is relaxed. 2. Atrial systole Completion of ventricular filling – The last 20% of filling is accomplished when the atria contract and push blood into the ventricles. Atrial systole begins following depolarization of the atria. Atrial pressure increases and pushes blood into the 46 ventricles  Cont’d The amount of blood in the ventricle at the end of diastole is called the end-diastolic volume ( EDV ). EDV = about 120 ml 3. Isovolumetric contraction At the beginning of systole the ventricles contract, which raises the pressure within them. When ventricular pressure exceeds atrial pressure the AV valves close. – The semilunar valves remain closed because ventricular pressure is not yet high enough to force them open. No blood flows into or out of the ventricles because all the valves are closed. The volume of blood within them remains constant. 47  Cont’d 4. Ventricular ejection Blood is ejected into the aorta and pulmonary arteries through the open semilunar valves – Ventricular pressure exceeds aortic pressure – Semilunar valves held open – Blood exits from the ventricles in to pulmonary artery and aorta. The volume of blood ejected from the ventricle per contraction is called stroke volume. – Stroke volume (SV): SV = EDV – ESV=70 ml End systolic volume (ESV): The volume of blood that remains in the ventricle at the end of ventricular systole – ESV = 50 ml Cardiac output: the volume of blood ejected from the heart per minute. 48 CO = SV x HR =5-6 L/min  Cont’d 5. Isovolumetric relaxation At the end of ventricular ejection, the ventricles begin to repolarize and relax. – ventricular pressure decreases. – Semilunar valves closed Once ventricular pressure decreases to less than atrial pressure – Permitting the AV valves to open again – blood enters the ventricles from the atria. This marks the beginning of diastole 49 Cardiac cycle 50 Cont’d 51  Heart sound Heart sounds are made by the closure of valves and vibrations 1. First heart sound(S1)  Due to closure of AV valves  Occurs at beginning of systole( isovolumetric cntraction).  Sounds like LUB 2. Second heart sound(S2) Closure of Semilunar valves (Aortic & Pulmonic valves ). Occur at the beginning of diastole ( isovolumetric relaxation) Sounds like DUB 3.Third heart sound(S3) Occurs at the beginning of middle third diastole(rapid 52 ventricular filling).  Abnormal heart sounds(Murmur) Abnormal heart sounds (murmurs) are usually associated with valvular diseases. Valvular diseases results in stenotic valve or insufficient valve Valve stenosis & insufficiency are caused by rheumatic fever an autoimmune disease triggered by a streptococcus bacterial infection. 53  Cont’d Stenotic valve: –Stiff/narrowed valve that doesn’t open completely. –“Whistling” sound is heard when such problem exists. –Eg mitral stenosis,aortic stenosis Insufficient valve: –Valves can’t close completely due to valve edges scarred. –Blood flows back ward because of leaky valves, & opposite direction movement of blood creates“Swishing” (gurgling) murmur due to regurgitation of blood –Eg mitral regurgitation,aortic regurgitation 54  Cardiac output (CO) and its regulation The volume of blood pumped by one ventricle in a given period of time. CO is determined by SV & HR. – Cardiac output = heart rate * stroke volume – CO = HR * SV Control of HR 1.Neural control 2. Hormonal control  Sympathetic Epinephrine  Parasympathetic TH,insulin ,glucagon SV is determined by 3 factors 1. Preload/VR/EDV VR=venous return 2. Ventricular contractility 3. After load 55  1.Control of HR A.Neural The HR iscontrol determined by the rate of discharge of impulse from the SA- node. Sympathetic Control SA node receive direct input from –Speeds up heart rate the autonomic nervous system Mechanisms Parasympathetic control Release norepinephrine, –Slows HR which binds to β1 adrenergic receptors on Mechanisms the SA nodal cells Releases Acetylcholine w/h –Increased permeability activates muscarinic cholinergic to Na+ and Ca2+ receptors during the pacemaker I. Increases k+ permeability, potential phase hyperpolarizing the cell. –Speeds up II.Decreases Ca2+ permeability, depolarization and slows the rate at which the heart rate pacemaker potential depolarizes 56 Cont’d 57 Cont’d 58  Cont’d B.Hormonal control Epineprine –Increases action potential frequency at the SA node –Increases the velocity of action potential conduction through cardiac muscle fibers TH,Insulin,Glucagon –Increase the force of myocardial contraction, –Glucagon also promotes increased heart rate 59  Cont’d 2.Control of stroke volume(SV) SV is the volume of blood each ventricle ejects during each contraction. Factors influence SV 1. End-diastolic volume(preload) Is the volume of blood in the ventricles just before contraction. The relationship between SV and EDV is known as the Frank–Starling mechanism Frank–Starling mechanism Is a length–tension relationship – The greater the EDV, the greater the stretch and the more forceful the contraction SV increases as EDV increases. EDV is determined by venous return, – The amount of blood that enters the heart from the venous 60 circulation.  Cont’d Three factors affect venous return: – Contraction of veins returning blood to the heart (the skeletal muscle pump) – Pressure changes in the abdomen and thorax during breathing (the respiratory pump) – Sympathetic innervation of veins. The Frank–Starling mechanism stated as : – At any given HR, an increase in the venous return , increases CO by increasing EDV and, therefore, SV. 61  Cont’d 2. Ventricular contractility Is a measure of the ventricles’ capacity for generating force. Any factor that causes the ventricles to contract will increase SV, which will in turn increase CO. Any chemical that affects contractility is called an inotropic agent , and its influence is called an inotropic effect If a chemical increases the force of contraction, it is said to have a positive inotropic effect. – Eg the catecholamines -epinephrine and norepinephrine Any chemical that decrease force of contraction is said to have a negative inotropic effect. 62 Contractility: the Ventricular Function Curve +ve inotropic agents -Sympathetic stimul. -Hypercalcemia -Hyperkalemia -Glucagon, T3/T4 -Digitalis, ‒ve inotropic agents Xanthenes Parasympathetic --Cathecolamines stim. CHANGES IN --Hypocalcemia CONTRACTILITY -Acidosis -Toxins -Heart diseases 63  Cont’d Sympathetic Nervous Control of Ventricular Contractility – Causes the atria to contract with more force, which raises atrial pressure and increases the volume of blood the atria pump into the ventricles – As sympathetic activity increases, ventricular contractility increases , which tends to raise cardiac output. Mechanism of sympathetic nervous system – Increasing the flow of calcium into the cell during an action potential. – Enhance the release of calcium from the SR. – Increase the rate of the myosin ATPase, thereby increasing the speed of crossbridge cycling. – Enhance the rate of Ca2+-ATPase activity on the SR, which increases calcium reuptake thereby increasing the rate of relaxation of the contractile cell There is little or no parasympathetic influence on ventricular contractility 64 Cont’d 65  Cont’d Hormonal Control of Ventricular Contractility –Ventricular contractility is increased by epinephrine,insulin, glucagon, and thyroid hormones –Catecholamines increase Ca2+ entry and storage and exert their positive inotropic effect Contractility increases as the amount of calcium available for contraction increases. Increasing ventricular contractility, increases SV& CO. 66  Cont’d 3. Afterload A term used to describe how hard the heart must work to eject blood. The arterial pressures against which the ventricles pump. Increases in arterial pressure tend to cause stroke volume to decrease. – Because arterial pressure places a load on the myocardium after contraction starts, it is called afterload. For the left ventricle, afterload is determined by the pressure in the aorta during the ejection period. Afterload increases as mean arterial pressure rises. When afterload increases, the ventricle must increase its force of contraction. 67 Cont’d 68 Factors affecting CO... 69 Factors Involved in Regulation of CO 70  Blood Pressure Blood pressure is the pressure exerted by circulating blood upon the walls blood vessels i.e arteries. Determined primarily by: 1.Cardiac output 2.Resistance 3.Blood volume. 71  Cont’d Pressure is measured in millimeters of mercury (mm Hg). Blood pressure is recorded as two numbers, such as 120/80(systolic/diastolic) Systolic blood pressure Systolic pressure is the maximum pressure exerted by the blood against the artery walls. It results when the ventricles contract. Normally, it measures 120 mm Hg Diastolic blood pressure Diastolic Pressure is the lowest pressure in the artery. It result when the ventricles are relaxed and is usually around 80 mm Hg. 72  Controlling Blood Pressure Is subject to : – local, neural & hormonal controls Are either for the short-term or long-term. – Short-term control Affecting cardiac output (heart rate & stroke volume) & peripheral resistance. – Long-term control Accomplished via changes in blood volume. 73  Local Control of BP Refers to the regulation of blood flow at the level of individual blood vessels and specific tissues or organs. Ability of tissues to regulate their own blood supply is an example of autoregulation. If tissue is inadequately perfused (insufficient blood flow);  Hypoxia &  Metabolites (CO2,K+, H+,lactate&adenosine) 74 can accumulate.  Neural Control of BP The CNS coordinates the reflex control of blood pressure and distribution of blood to the tissues. The main integrating center is in the medulla oblongata. Neural regulation of blood pressure is achieved through the role of cardiovascular centers and baroreceptor stimulation. Stretch sensitive mechanoreceptors known as baroreceptors are located in the walls of the carotid arteries and aorta – can monitor the pressure of blood flowing to the brain (carotid baroreceptors) and to the body (aortic baroreceptors). 75  Cont’d Baroreceptor Reflex Primary reflex pathway for homeostatic control of arterial blood pressure. Baroreceptors are stretch sensitive mechanoreceptors located – in the walls of the carotid arteries and aorta Are tonically active stretch receptors that fire action potentials continuously at normal blood pressures When arterial blood pressure increases – The baroreceptor membrane stretches – The firing rate of the receptor increases. If blood pressure falls, the firing rate of the receptor decreases. 76  Cont’d If blood pressure changes, the frequency of action potentials traveling from the baroreceptors to the medullary cardiovascular control center changes. The CVCC integrates the sensory input and initiates an appropriate response. As blood pressure increases – Baroreceptors increase their firing rate and Activating the medullary CVCC. – The CVCC increases parasympathetic activity and decreases sympathetic activity to slow down the heart and dilate arterioles. 77 Cont’d 78 Cont’d 79 Cont’d 80  Hormonal Controls of BP  Adrenal Medulla Hormones – In response to environmental stress, adrenal glands release epinephrine (85%) & norepinephrine (15%) into bloodstream. – Bind to vascular smooth muscle & cause vasoconstriction, ↑peripheral resistance & blood pressure. – Bind to heart muscle & nodal tissue ↑heart rate & stroke volume =↑cardiac output & blood pressure.  Antidiuretic Hormone (ADH) – Produced by hypothalamus & subsequently released via posterior pituitary gland in response to;low BP or high plasma osmolarity. – Prevents diuresis (urination),to conserve blood volume & prevents further BP decline. – Is a potent vasoconstrictor, there by increases resistance  Angiotensin II – Promoting vasoconstriction,reducing urine output by the kidney and stimulating thirst 81  Cont’d Long Term Blood Pressure Control Kidneys alter blood volume by renin-angiotensin- aldosterone mechanism. Renin-Angiotensin-Aldosterone System ↓BP prompts kidneys to release enzyme renin. Renin catalyze series of reactions that culminates with production of protein, angiontensin II. – Angiotensin II is potent vasoconstrictor, – causes secretion of steroid hormone aldosterone from the adrenal cortex and ADH from the hypothalamus. Aldosterone ↓urine output – prevents further ↓in blood volume by conserving water. 82 RAAS … 83  Hypertension  Chronic resting BP >140/90, may be primary or secondary.  Primary (essential ) – 90% of hypertension is essential hypertension, no underlying cause has been identified.  Secondary. – 10% (2ndry hypertension) is due to identifiable disorders (known causes), such as: excess rennin secretion by the kidneys artheriosclerosis, or hyperthyroidism. 84  Types of hypertension Primary hypertension Secondary Essential/idiopathic hypertension (90-95%). 5-10%. Cause is unknown, but Definite causes can be established in 4 there is strong genetic categories: tendency. – Cardiovascular Contributing factors hypertension include: – Renal hypertension obesity, stress, – Endocrine smoking & excessive hypertension ingestion of salt. – Neurogenic hypertension 85  Cont’d  Cardiovascular hypertension is due to chronically elevated resistance(atherosclerosis) Deposits of fatty substances, cholesterol, wastes, calcium… build up (plaque) in inner lining of artery presence of plaque ↑resistance & ↓blood flow attract platelets & increase likelihood of coagulation.  Renal hypertension Due to occlusion of renal arteries or unable to eliminate salt load  Increase blood volume ,then increasing BP. Endocrine hypertension due to endocrine disorder – Pheochormocytoma = adrenal tumor ↑ epinephrine & norepinephrin. – Conn’s syndrome =↑aldosterone due to hyper secreting Neurogenic hypertension occurs as a result of neural lesions due to  defect in cardiovascular control center or baroreceptors  occurs as a compensatory response to reduction in cerebral blood flow. 86.  Cont’d Methods for treating hypertension include; Hypotension – Weight loss. Blood pressure