Hypertension

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Prepared by md, PhD., Associate Professor Marta R. Gerasymchuk, pathophysiology department

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  • The systolic blood pressure reflects the rhythmic ejection of blood into the aorta (Fig. 1). As blood is ejected into the aorta, it stretches the vessel wall and produces a rise in aortic pressure. The extent to which the systolic pressure rises or falls with each cardiac cycle is determined by the amount of blood ejected into the aorta with each heart beat (i.e., stroke volume), the velocity of ejection, and the elastic properties of the aorta. Systolic pressure increases when there is a rapid ejection of a large stroke volume or when the stroke volume is ejected into a rigid aorta. The elastic walls of the aorta normally stretch to accommodate the varying amounts of blood that are ejected into the aorta; this prevents the pressure from rising excessively during systole and maintains the pressure during diastole. In some elderly persons, the elastic fibers of the aorta lose some of their elasticity, and the aorta becomes more rigid. When this occurs, the aorta is less able to stretch and buffer the pressure that is generated as blood is ejected into the aorta, resulting in an elevated systolic pressure.
    Diastolic Blood Pressure
    The diastolic blood pressure is maintained by the energy that has been stored in the elastic walls of the aorta during systole. The level at which the diastolic pressure is maintained depends on the elastic properties of the aorta and large arteries and their ability to stretch and store energy, the resistance of the arterioles that control the outflow of blood into the microcirculation, and the competency of the aortic valve. The small diameter of the arterioles contributes to their effectiveness as resistance vessels because it takes more force to push blood through a smaller vessel than a larger vessel. When there is an increase in peripheral vascular resistance, as with sympathetic stimulation, diastolic blood pressure rises. Closure of the aortic valve at the onset of diastole is essential to the maintenance of the diastolic pressure. When there is incomplete closure of the aortic valve, as in aortic regurgitation, the diastolic pressure drops as blood flows backward into the left ventricle, rather than moving forward into the arterial system.
    Pulse Pressure
    The pulse pressure is the difference between the systolic and diastolic pressures. It reflects the pulsatile nature of arterial blood flow and is an important component of blood pressure. During the rapid ejection period of ventricular systole, the volume of blood that is ejected into the aorta exceeds the amount that exits the arterial system. The pulse pressure reflects this difference. The pulse pressure rises when additional amounts of blood are ejected into the arterial circulation, and it falls when the resistance to outflow is decreased. In hypovolemic shock, the pulse pressure declines because of a decrease in stroke volume and systolic pressure. This occurs despite an increase in peripheral vascular resistance, which maintains the diastolic pressure.
    Mean Arterial Pressure
    The mean arterial blood pressure represents the average blood pressure in the systemic circulation. The mean arterial pressure can be estimated by adding one third of the pulse pressure to the diastolic pressure (i.e., diastolic blood pressure + pulse pressure/3). Hemodynamic monitoring equipment in intensive and coronary care units measures or computes mean arterial pressure automatically. Because it is a good indicator of tissue perfusion, the mean arterial pressure often is monitored, along with systolic and diastolic blood pressures, in critically ill patients.
  • Sympathetic Nervous System (4 Points)
    1. both cardiac output and TPR increased with SNS tone
    2. level of efferent SNS tone is set in CNS by medullary vasomotor center. stimulation of alpha2 adrenergic receptors in medulla lowers SNS tone and BP.
    3. inhibition of ganglionic transmission or NE release from post-ganglionic nerve fiber can reduce CO and TPR.
    4. alpha1 or beta1 adrenergic receptor blockade can reduce TPR and CO respectively.
  • Blood Pressure – influenced by 3 major factors
    Total peripheral resistance
    Baroreceptor (BR) and CNS Influences
    u BP r u BR firing rate r vasodilation r d BP
    d BP r d BR firing rate r u sympathetics r u BP
    Chemoreceptor influences
    dO2, u CO2, d pH r CNS stim. r vasoconstriction
    Circulating catecholamine influences
    E and NE have varying effects on TP
    E and NE usually activate a receptors r u TPR
    Fight or flight response
    Q
    Blood Volume
    Renin – Angiotensin system
  • Sympathetic Activity
    Noradrenaline and adrenaline, either from sympathetic neurons or epirenal medullar cells, interact with peripheral smooth cell-μ1 adrenergic receptors increasing vascular tone at pre-capillary level. They also increase heart rate and contractility through interaction with cardiac-β1 adrenergic receptors. The net effect of sympathetic stimulation is an increase in CO. Chronic adrenergic stimulation induces vascular remodelling and smooth muscular cells proliferation, thus increasing diastolic pressure, while arterial vessels thicken and stiffen due to lipid, calcium and collagen accumulation and deposition in vascular walls.
    Moreover, chronically increased vascular tone leads to increased myocardial mass (e.g., left ventricular hypertrophy) and oxygen consumption, which in turn can lead to chronic ischemia or acute myocardial infarction. At renal level, increased sympathetic activity enhances sodium and water retention, further contributing to maintain elevated blood pressure.
  • Short-Term Regulation
    The mechanisms for short-term regulation of blood pressure, those occurring over minutes or hours, are intended to correct temporary imbalances in blood pressure, such as occur during physical exercise and changes in body position. These mechanisms also are responsible for maintenance of blood pressure at survival levels during life-threatening situations. The short-term regulation of blood pressure relies mainly on neural and hormonal mechanisms, the most rapid of which are the neural mechanisms.
  • The renin-angiotensin-aldosterone system plays a central role in blood pressure regulation. Renin is an enzyme that is synthesized, stored, and released by the kidneys in response to an increase in sympathetic nervous system activity or a decrease in blood pressure, extracellular fluid volume, or extracellular sodium concentration. Most of the renin that is released leaves the kidney and enters the bloodstream, where it acts enzymatically to convert an inactive circulating plasma protein called angiotensinogen to angiotensin I (Fig. 5). Angiotensin I travels to the small blood vessels of the lung, where it is converted to angiotensin II by the angiotensin-converting enzyme that is present in the endothelium of the lung vessels. Although angiotensin II has a half-life of several minutes, renin persists in the circulation for 30 minutes to 1 hour and continues to cause production of angiotensin II during this time.
    Angiotensin II functions in both the short-term and longterm regulation of blood pressure. It is a strong vasoconstrictor, particularly of arterioles and to a lesser extent of veins. The vasoconstrictor response produces an increase in peripheral vascular resistance (and blood pressure) and functions in the shortterm regulation of blood pressure. A second major function of angiotensin II, stimulation of aldosterone secretion from the adrenal gland, contributes to the long-term regulation of blood pressure by increasing salt and water retention by the kidney. It also acts directly on the kidney to decrease the elimination of salt and water.
  • From lecture Doctor of medicine, professor Khara Mariya Romanivna
  • Hypertension as a diagnosis is considered when the average of TWO or more consecutive clinical visits documents a DBP of 90 mmHg or greater or a SBP of 140 mmHg or greater.
    Elevated SBP is the main contributor of target organ damage.
  • Age/ Loss of arterial elasticity, >65 years, increased collagen content, increased vascular resistance
    heredity-, Close relatives
    Sex/Race- men (female >55 yrs), African-Americans
    Obesity- central abdominal obesity- increases cardiac workload and strains the vessels
    Stimulants- Smoking/caffeine-vasoconstrictors
    Sodium- water retention causes volume expansion/ decreases effects of certain B/P meds
    Hyperlipidemia- plaque in the vessels
    Diabetes- elevated glucose, insulin, and lipoprotein metabolism
    Socioeconomic-lower and less educated
  • Renin is an enzyme released by the kidney to help control the body's sodium-potassium balance, fluid volume, and blood pressure.
    Description
    When the kidneys release the enzyme renin in response to certain conditions (high blood potassium, low blood sodium, decreased blood volume), it is the first step in what is called the renin-angiotensin-aldosterone cycle. This cycle includes the conversion of angiotensinogen to angiotensin I, which in turn is converted to angiotensin II, in the lung. Angiotensin II is a powerful blood vessel constrictor, and its action stimulates the release of aldosterone from an area of the adrenal glands called the adrenal cortex. Together, angiotensin and aldosterone increase the blood volume, the blood pressure, and the blood sodium to re-establish the body's sodium-potassium and fluid volume balance. Primary aldosteronism, the symptoms of which include hypertension and low blood potassium (hypokalemia), is considered "low-renin aldosteronism."
  • Figure 1. Examples of Mild Hypertensive Retinopathy. Panel A shows arteriovenous nicking (black arrow) and focal narrowing (white arrow). Panel B shows arteriovenous nicking (black arrows) and widening or accentuation ("copper wiring") of the central light reflex of the arterioles (white arrows).
  • Causes of Secondary Hypertension
    Autonomic hyperactivity (spinal cord injury, Guillain-Barre syndrome, diabetes mellitus)
    • Intracranial hypertension and brain edema
    • Pheochromocytoma
    • Tumors secreting renin or aldosterone
    • Eclampsia and preeclampsia
    • Vasculitis and scleroderma
    • Parenchymal renal disease (e.g., acute glomerulonephritis)
    • Renal vascular disease (e.g., renal artery stenosis or thrombosis)
    • Drugs (e.g., cocaine, amphetamine, phencyclidine)
    • Drug interaction (e.g., monoamine oxydase inhibitor with tyramine, tryciclics antidepressants or sympathomimetics)
    • Abrupt withdrawal of anti-hypertensive drugs (e.g., clonidine)
    • Alcohol withdrawal
  • Gestational Hypertension. Gestational hypertension represents a blood pressure elevation without proteinuria that is detected for the first time after midpregnancy. It includes women with preeclampsia syndrome who have not yet manifested proteinuria, as well as women who do not have the syndrome. The final determination that a woman does not have the preeclampsia syndrome is made only postpartum. If preeclampsia has not developed and blood pressure has returned to normal by 12 weeks postpartum, the condition is considered to be gestational hypertension. If blood pressure elevation persists, a diagnosis of chronic hypertension is made.
  • Preeclampsia-Eclampsia. Preeclampsia-eclampsia is a pregnancyspecific syndrome. It is defined as an elevation in blood pressure and proteinuria developing after the 20th week of gestation. It is defined as an elevation in blood pressure (systolic >140 or diastolic >90 mm Hg) and proteinuria (≥0.3 g/24 hours) developing after the 20th week of gestation. The presence of systolic pressure ≥160 mm Hg, diastolic pressure ≥110 mm Hg; proteinuria (≥2.0 g/24 h); increased serum creatinine (>1.2 mg); platelet counts <100,000 cells/mm; elevated liver enzymes; persistent headache or cerebral or visual disturbances; and persistent epigastric pain serve to reinforce the diagnosis. Preeclampsia may occur in women who already are hypertensive, in which case the prognosis for the mother and fetus tends occurence, in a woman with preeclampsia, of seizures that cannot be attributed to other causes.
    Preeclampsia occurs primarily during first pregnancies and during subsequent pregnancies in women with multiple fetuses, diabetes mellitus, or coexisting renal disease. It is associated with a condition called a hydatidiform mole (i.e., abnormal pregnancy caused by a pathologic ovum, resulting in a mass of cysts). Women with chronic hypertension who become pregnant have an increased risk of preeclampsia and adverse neonatal outcomes, particularly when associated with proteinuria early in pregnancy.
    Pregnancy-induced hypertension is thought to involve a decrease in placental blood flow, leading to the release of toxic mediators that alter the function of endothelial cells in blood vessels throughout the body, including those of the kidney, brain, liver, and heart. The endothelial changes result in signs and symptoms of preeclampsia and, in more severe cases, of intravascular clotting and hypoperfusion of vital organs. There is risk for development of disseminated intravascular coagulation, cerebral hemorrhage, hepatic failure, and acute renal failure. Thrombocytopenia is the most common hematologic complication of preeclampsia. Platelet counts of less than below 100,000/mm3 signal serious disease. The cause of thrombocytopenia has been ascribed to platelet deposition at the site of endothelial injury. The renal changes that occur with preeclampsia include a decrease in glomerular filtration rate and renal blood flow. Sodium excretion may be impaired, although this is variable. Edema may or may not be present. Some of the most severe forms of preeclampsia occur in the absence of edema. Even when there is extensive edema, the plasma volume usually is lower than that seen in normal pregnancy. Liver damage, when it occurs, may range from mild hepatocellular necrosis with elevation of liver enzymes to the more ominous hemolysis, elevated liver function tests, and low platelet count (HELLP) syndrome that is associated with significant maternal mortality. Eclampsia, the convulsive stage of preeclampsia, is a significant cause of maternal mortality. The pathogenesis of eclampsia remains unclear and has been attributed to both increased coagulability and fibrin deposition in the cerebral vessels.
  • From lecture Doctor of medicine, professor Khara Mariya Romanivna
  • From lecture Doctor of medicine, professor Khara Mariya Romanivna
  • Hypertension

    1. 1. Hypertension
    2. 2. ActualityActuality  Arterial hypertension is a very commonArterial hypertension is a very common condition. Cerebral, coronary and renal vesselscondition. Cerebral, coronary and renal vessels are mainly affected byare mainly affected by the deleterious effect ofthe deleterious effect of this condition, and both acute and chronic organthis condition, and both acute and chronic organ failure may ensue.failure may ensue.  Exacerbation of underlyingExacerbation of underlying pathophysiologicpathophysiologic conditions or new precipitating factors can leadconditions or new precipitating factors can lead to hypertensive crisis, either urgencies orto hypertensive crisis, either urgencies or emergencies.emergencies.  During hypertensive emergencies, a quick raiseDuring hypertensive emergencies, a quick raise in arterial pressure may lead to acute andin arterial pressure may lead to acute and significant organ dysfunction,significant organ dysfunction, such as aorticsuch as aortic dissection, acute myocardial infarction,dissection, acute myocardial infarction, intracranial bleeding or acute renal failure.intracranial bleeding or acute renal failure.  PerioperativePerioperative hypertension often takes thehypertension often takes the shape of a crisis and it can be related toshape of a crisis and it can be related to hypothermia, pain, neuro-hormonal response tohypothermia, pain, neuro-hormonal response to surgical trauma or antihypertensive drugssurgical trauma or antihypertensive drugs withdrawal.withdrawal.
    3. 3. CONTENTCONTENT • 1. Factors which predetermine the level of blood pressure for a1. Factors which predetermine the level of blood pressure for a man, basal tone of vessels.man, basal tone of vessels. • 2. Pressor and depressor systems of organism, their description.2. Pressor and depressor systems of organism, their description. • 3. Arterial hypertensions: kinds, classification. Degrees of high3. Arterial hypertensions: kinds, classification. Degrees of high arterial pressure.arterial pressure. • 4. Nephrogenic hypertensions: reasons, kinds, pathogenesis.4. Nephrogenic hypertensions: reasons, kinds, pathogenesis. • 5. Etiology and pathogenesis of endocrinal hypertension.5. Etiology and pathogenesis of endocrinal hypertension. • 6. A role of the sympathetic nervous system in pathogenesis of6. A role of the sympathetic nervous system in pathogenesis of nerogenic hypertension.nerogenic hypertension. • 7. Salt hypertension: etiology, mechanisms of development.7. Salt hypertension: etiology, mechanisms of development. • 8. Etiology and pathogenesis of essential hypertension.8. Etiology and pathogenesis of essential hypertension. • 9. Complication of essential hypertension.9. Complication of essential hypertension. • 10. Reasons and mechanisms of arterial hypotension.10. Reasons and mechanisms of arterial hypotension.
    4. 4. Determinants of Blood Pressure • Components of B/P – Pressure of blood against the walls of the arteries – The elasticity of the artery walls – The volume and thickness of the blood
    5. 5. • Systolic Blood Pressure (SBP) pressure measured in brachial artery during systole (ventricular emptying and ventricular contraction period) • Diastolic Blood Pressure (DBP) pressure measured in brachial artery during diastole (ventricular filling and ventricular relaxation) • Mean Arterial Pressure (MAP) "average" pressure throughout the cardiac cycle against the walls of the proximal systemic arteries (aorta) • estimated as: .33(SBP - DBP) + DBP • Total Peripheral Resistance (TPR) - the sum of all forces that oppose blood flow • length of vasculature (L) • blood viscosity (V) • vessel radius (r) Definitions TPR = ( 8 ) ( V ) ( L ) ( p ) ( r 4 )
    6. 6. Physiological factors affecting Arterial Blood pressurePhysiological factors affecting Arterial Blood pressure AgeAge::  New born: 80/40 mmHgNew born: 80/40 mmHg  4 years: 100/65 mmHg.4 years: 100/65 mmHg.  Adults: 120/80 mmHgAdults: 120/80 mmHg  After that: Gradually increase due to increase elasticity of arteries.After that: Gradually increase due to increase elasticity of arteries. SexSex::  Children: have equal Blood pressure.Children: have equal Blood pressure.  Adults before 45 years: male more than female.Adults before 45 years: male more than female.  Adults after 45 years: the diastolic B.P. is more in female than males.Adults after 45 years: the diastolic B.P. is more in female than males. RaceRace:: ABP in oriental is less than in European and American.ABP in oriental is less than in European and American. GravityGravity:: B.P. in upper parts of the body is more than the lower partsB.P. in upper parts of the body is more than the lower parts especially during standing.especially during standing. Meals:Meals: Digestion increases the arterial blood pressure.Digestion increases the arterial blood pressure. Emotions and exerciseEmotions and exercise:: increase the arterial blood pressure.increase the arterial blood pressure. SleepSleep:: Deep quiet sleep decrease A.B.P., while sleep with dreamsDeep quiet sleep decrease A.B.P., while sleep with dreams increase A.B.P.increase A.B.P.
    7. 7. Measurements of Blood PressureMeasurements of Blood Pressure 1- Direct Method1- Direct Method  The most accurate means for measuring bloodThe most accurate means for measuring blood pressure is directly within an artery (intra-arterial)pressure is directly within an artery (intra-arterial) using a catheter.using a catheter.  But because this method is invasive, it is neitherBut because this method is invasive, it is neither practical nor appropriate for repeated measurementspractical nor appropriate for repeated measurements in non-hospital settings, or for large-scale publicin non-hospital settings, or for large-scale public health screenings.health screenings. 2- The mercury-filled sphygmomanometer2- The mercury-filled sphygmomanometer  The usual method of measurement, therefore, is aThe usual method of measurement, therefore, is a noninvasive means that uses a sphygmomanometer,noninvasive means that uses a sphygmomanometer, which includes either a column of mercury orwhich includes either a column of mercury or pressure-registering gauge.pressure-registering gauge.
    8. 8. Cardiovascular Hemodynamic Basics Flow (Q) Pressure (MAP) P aorta – P vena cava = = Resistance (TPR) (8) (V) (L) (p) (r 4 ) Flow (Q) = () (Pa – Pv) (r 4 ) (8) (V) (L) V = viscosity of fluid (blood) flowing through the pipe L = length of pipe (blood vessel) r = radius of the pipe (blood vessel) Pa = aortic pressure Pv = venous pressure Normally Resting Q is about 5 - 6 liters / minute BP = CO x PRBP = CO x PR
    9. 9. RA RV LUNGS LA LV AORTA ARTERIOLES SYSTEMIC ARTERIES VEINS (CAPACITANCE VESSELS) (100) (92) (40) low compliance 13% of blood volume high compliance 64% of blood volume PO2 = 40 PCO2 = 46 (0) (2) PO2 = 100 PCO2 = 40 PO2 = 160 PCO2 = .3 CAPILLARY BEDS 7% of blood volume 9% of blood volume (7) (13) (3) Ohms Law: Flow (Q) = upstream pressure – downstream pressure resistance Systemic Circulation = 100 mmHg – 0 mmHg = 100 ml / sec = 6 liters / min Flow (Q) 1 mmHg sec / ml The “Closed” Cardiovascular Hemodynamic System Mean arterial pressures in red (20)
    10. 10. Blood Pressure RegulationBlood Pressure Regulation  Systemic arterial pressure is a function ofSystemic arterial pressure is a function of stroke volume, heart rate, and totalstroke volume, heart rate, and total peripheral resistanceperipheral resistance  The major organs involved in regulation ofThe major organs involved in regulation of blood pressure are the heart (HR & SV),blood pressure are the heart (HR & SV), the SNS (TPR-total peripheral resistance),the SNS (TPR-total peripheral resistance), and the kidneys (ECF – extracellular fluidand the kidneys (ECF – extracellular fluid volume & secretion of renin).volume & secretion of renin).  (Wynne, Woo, & Olyaei, 2007, p. 1093)(Wynne, Woo, & Olyaei, 2007, p. 1093)
    11. 11. Factors Influencing BPFactors Influencing BP CardiacCardiac •Heart rate •Inotropic state •Neural (pons and medulla) •Humoral (hormones) CardiacCardiac •Heart rate •Inotropic state •Neural (pons and medulla) •Humoral (hormones) Cardiac OutputCardiac Output Renal Fluid Volume ControlRenal Fluid Volume Control •Renin–angiotensin •Aldosterone •Atrial natriuretic factor Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
    12. 12. Regulative systemsRegulative systems Sympathetic Nervous SystemSympathetic Nervous System BaroreceptorsBaroreceptors – Nerve cells in carotid artery & aortic archNerve cells in carotid artery & aortic arch – Maintain BP during normal activitiesMaintain BP during normal activities – React to increases & decreases in BPReact to increases & decreases in BP BP – impulse to brain to inhibit SNS; HR &BP – impulse to brain to inhibit SNS; HR & force of contraction; vasodilation of arteriolesforce of contraction; vasodilation of arterioles BP – activates SNS; vasoconstriction ofBP – activates SNS; vasoconstriction of arterioles; HR & heart contractilityarterioles; HR & heart contractility 1. Barroreceptors of aorta arch and sinus caroticus
    13. 13. Sites of Cardiorespiratory Control
    14. 14.  Increased BP send inhibitory impulse to sympathetic vasomotor center in brainstem;  In long-standing hypertension, baroreceptors adjust to elevated BP and reads it as normal; doesn’t make adjustments; also becomes less responsive in some older adults
    15. 15. On standing up venous return fallsOn standing up venous return falls Cardiac output diminishesCardiac output diminishes Arterial blood pressure is reducedArterial blood pressure is reduced Baroreceptor afferent firing reducedBaroreceptor afferent firing reduced Medullary centres inhibition reducedMedullary centres inhibition reduced THE BARORECEPTOR REFLEX - AN EXAMPLETHE BARORECEPTOR REFLEX - AN EXAMPLE CORRECTION OF POSTURAL HYPOTENSIONCORRECTION OF POSTURAL HYPOTENSION Effect of gravity onEffect of gravity on venous returnvenous return Preload diminishedPreload diminished - Starling’s Law- Starling’s Law Subject possibly feels faintSubject possibly feels faint as cerebral flow is reducedas cerebral flow is reduced Due to reduced arterial B.P.Due to reduced arterial B.P. VasoconstrictionVasoconstriction TachycardiaTachycardia Raised stroke workRaised stroke work Tend to restore arterial blood pressure Increased sympathetic tone toIncreased sympathetic tone to arteriolesarterioles Reduced vagal tone to s.a.Reduced vagal tone to s.a. nodenode Increased myocardial sympathetic toneIncreased myocardial sympathetic tone
    16. 16. Sympatetic activitySympatetic activity Increase BP Increases heart rate and contractility Increase cardiac output Vasoconstriction increasing peripheral vascular resistances Increases sodium and water reabsorption Increases vascular tone at precapillary level Induces vascular remodelling Increase diastolic pressure Chronic Ischemia and AMI Increased left ventricular hypertrofy and oxygen consumption
    17. 17. Blood pressure regulation by the renin-angiotensin systemBlood pressure regulation by the renin-angiotensin system and the central roles of sodium metabolism in specificand the central roles of sodium metabolism in specific causes of inherited and acquired forms of hypertension.causes of inherited and acquired forms of hypertension. Components of theComponents of the systemic renin-angiotensinsystemic renin-angiotensin system are shown in black.system are shown in black. Genetic disorders thatGenetic disorders that affect blood pressure byaffect blood pressure by altering activity of thisaltering activity of this pathway are indicated inpathway are indicated in red;red; arrowsarrows indicate sitesindicate sites in the pathway altered byin the pathway altered by mutation. Genes that aremutation. Genes that are mutated in these disordersmutated in these disorders are indicated inare indicated in parentheses. Acquiredparentheses. Acquired disorders that alter blooddisorders that alter blood pressure through effectspressure through effects on thison this pathway arepathway are indicated in blue.indicated in blue. (From Lifton RP, et al: Molecular genetics of human blood pressure variation. Science 272:676, 1996.)
    18. 18. Increase BPIncrease BP Renin Angiotensin II AldosteroneAldosterone VasoconstrictionVasoconstriction on systemic andon systemic and renal vasselsrenal vassels Left ventricularLeft ventricular hypertrophyhypertrophy andand myocardialmyocardial ischemiaischemia Increase leftIncrease left ventricularventricular wallwall tensiontension Alteration of renalAlteration of renal arterial andarterial and capillarycapillary vessels’ wallvessels’ wall Glomeruar ischemia,Glomeruar ischemia, parenchymal damage,parenchymal damage, proteinuria, end-stageproteinuria, end-stage renal failurerenal failure ADHADH Sodium andSodium and water renalwater renal retentionretention HHypervolemiaypervolemia Effect of renin-angiotensin systemEffect of renin-angiotensin system on cardiovascular homeostasison cardiovascular homeostasis 2.2. ReninRenin––angiotensinangiotensin systemsystem
    19. 19. Mutations altering blood pressure in humans.Mutations altering blood pressure in humans. A diagram of a nephron, the filtering unit of the kidney, is shown. The molecular pathways mediating NaCl reabsorption in individual renal cells in the thick ascending limb of the loop of Henle (TAL), distal convoluted tubule (DCT), and the cortical collecting tubule (CCT) are indicated, along with the pathway of the renin-angiotensin system, the major regulator of renal salt reabsorption. Single gene defects that manifest as inherited diseases affecting these pathways are indicated, with hypertensive disorders in red and hypotensive disorders in blue. Abbreviations: Al, angiotensin I; ACE, angiotensin converting enzyme; All, angiotensin II; MR, mineralocorticoid receptor; GRA, glucocorticoid-remediable aldosteronism; PHA1, pseudohypoaldosteronism, type 1; AME, apparent mineralocorticoid excess; 11b-HSD2, 11b-hydroxysteroid dehydrogenase-2; and DOC, deoxycorticosterone. (From Lifton RP, et al: Molecular mechanisms of human hypertension. Cell 104:545, 2001.)
    20. 20. Regulative systems 3. Renin–angiotensin-aldosteron system Renin Actination of suprarenal glangs (cortical layer) Na reabsorbtion in kidney increase Angiotensin 2 Aldosteron excretion Na concentration in blood increase, blood osmotic pressure increase Move of extravascular fluid inside the vessels Increase of circulative blood volume (CBV) CО increase
    21. 21. Mechanism of Action of AldosteroneMechanism of Action of Aldosterone Increases CO by increasing blood volume .
    22. 22. BP Regulation: EndotheliumBP Regulation: Endothelium Nitric oxideNitric oxide is secreted by endothelial cellsis secreted by endothelial cells which results in relaxation of blood vesselswhich results in relaxation of blood vessels It also produces local vasodilators, suchIt also produces local vasodilators, such asas prostacylcinprostacylcin andand endothelium-derivedendothelium-derived hyperpolarizing factorhyperpolarizing factor EndothelinEndothelin is an extremely potentis an extremely potent vasoconstrictor and also stimulatesvasoconstrictor and also stimulates vascular smooth muscle growthvascular smooth muscle growth (Wynne, Woo, & Olyaei, 2007, p. 1094)(Wynne, Woo, & Olyaei, 2007, p. 1094)
    23. 23. Healthy LifestyleHealthy Lifestyle Maintain a Healthy Blood Pressure: Blood PressureBlood Pressure ClassificationClassification Systolic BPSystolic BP (mm Hg)(mm Hg) Diastolic BPDiastolic BP (mm Hg)(mm Hg) NormalNormal < 120< 120 < 80< 80 PrehypertensionPrehypertension 120 – 139120 – 139 80 – 8980 – 89 Stage 1 HypertensionStage 1 Hypertension 140 – 159140 – 159 90 – 9990 – 99 Stage 2 HypertensionStage 2 Hypertension 160 – 179160 – 179 100 – 109100 – 109 Stage 3 HypertensionStage 3 Hypertension (Hypertensive crisis)(Hypertensive crisis) ≥≥ 180180 ≥≥ 110110 Source: Clinical Practice Guidelines Management of Hypertension, 3rd Ed. 2008 February;MOH/P/PAK/156.08(GU)
    24. 24. Hypertension:Hypertension: DefinitionDefinition Persistent elevation ofPersistent elevation of  Systolic bloodSystolic blood pressurepressure ≥140 mm Hg≥140 mm Hg oror  Diastolic blood pressureDiastolic blood pressure ≥90 mm Hg≥90 mm Hg  Worldwide an estimatedWorldwide an estimated 1 billion1 billion peoplepeople have hypertension; about 1 in 3have hypertension; about 1 in 3 Americans affectedAmericans affected  Direct relationship between hypertensionDirect relationship between hypertension and cardiovascular disease (CVD)and cardiovascular disease (CVD)
    25. 25. ClassificationClassification Arterial hypotensionArterial hypotension Arterial hypertensionArterial hypertension AcuteAcute ChronicChronic SecondarySecondary AP above 139/89 mm HgAP above 139/89 mm Hg PrimaryPrimary AP less than 100/60 mm HgAP less than 100/60 mm Hg
    26. 26. Primary HypertensionPrimary Hypertension ►Etiological TheoriesEtiological Theories ►Inability of kidneys to excrete sodiumInability of kidneys to excrete sodium ►Overactive renin/angiotensin systemOveractive renin/angiotensin system ►Overactive sympathetic nervous systemOveractive sympathetic nervous system ►Decreased vasodilatory reactionDecreased vasodilatory reaction ►Resistance to insulin actionResistance to insulin action ►Genetic Inheritance (polygenic)Genetic Inheritance (polygenic)
    27. 27. Risk Factors R/T PrimaryRisk Factors R/T Primary HypertensionHypertension Age/HeredityAge/Heredity SexSex RaceRace ObesityObesity StimulantsStimulants SodiumSodium AlcoholAlcohol StressStress HyperlipidemiaHyperlipidemia DiabetesDiabetes SocioeconomicSocioeconomic StatusStatus
    28. 28. Risk Factors forRisk Factors for -- Primary HypertensionPrimary Hypertension Age (>55) Alcohol Cigarette smoking Diabetes mellitus Elevated serum lipids Excess dietary sodium Gender – SBP rises with age Alcohol – excessive use strongly correlated to hypertension – Smoking – increases risk for CV disease ; vasoconstriction – Diabetes – along with hypertension greater risk for target organ disease and usually more severe – Hyperlipidemia elevated in people with hypertension; increases risk of atherosclerosis – Some pts Na sensitive Males have higher rates of hypertension <55 and increased in women>55
    29. 29. Risk Factors forRisk Factors for Primary HypertensionPrimary Hypertension Family historyFamily history ObesityObesity EthnicityEthnicity Sedentary lifestyleSedentary lifestyle StressStress
    30. 30. Primary HypertensionPrimary Hypertension  Water and sodium retentionWater and sodium retention • AA high sodium intake may resulthigh sodium intake may result in water retentionin water retention • Some people are Na sensitiveSome people are Na sensitive (about 20%) ; not everyone(about 20%) ; not everyone with high salt diet developswith high salt diet develops hypertensionhypertension
    31. 31. Pathophysiology ofPathophysiology of Primary HypertensionPrimary Hypertension  Water and sodium retentionWater and sodium retention  Certain demographics areCertain demographics are associated with “saltassociated with “salt sensitivity”sensitivity”  ObesityObesity  Increasing ageIncreasing age  African American ethnicityAfrican American ethnicity  People with diabetes, renalPeople with diabetes, renal diseasedisease
    32. 32. Pathophysiology ofPathophysiology of Primary HypertensionPrimary Hypertension • Stress and increased SNS activityStress and increased SNS activity – Produces increased vasoconstrictionProduces increased vasoconstriction – ↑↑ HRHR – ↑↑ Renin releaseRenin release – Angiotensin II causes direct arteriolarAngiotensin II causes direct arteriolar constriction, promotes vascularconstriction, promotes vascular hypertrophy and induces aldosteronehypertrophy and induces aldosterone secretionsecretion
    33. 33. Pathophysiology ofPathophysiology of Primary HypertensionPrimary Hypertension Insulin resistance & hyperinsulinemia High insulin concentration stimulates SNS activity and impairs nitric oxide–mediated vasodilation Not present in secondary hypertension and don’t improve when hypertension is treated
    34. 34. Risk factors and aetiological influences in hypertensionRisk factors and aetiological influences in hypertension Risk factor or aetiologicalRisk factor or aetiological influenceinfluence Possible rationale and commentPossible rationale and comment MajorMajor Family historyFamily history Inherited tendency – probably polygenicInherited tendency – probably polygenic Dietary Na highDietary Na high Fluid retention; vascular wall oedema; ion pump defectFluid retention; vascular wall oedema; ion pump defect ObesityObesity Possible artefact of measurement (problem with arm cuff)?Possible artefact of measurement (problem with arm cuff)? Greater perfusion demands of increased body massGreater perfusion demands of increased body mass Reducing weight can reverse borderline HPTReducing weight can reverse borderline HPT AlcoholAlcohol Unknown mechanism; possibly 30% of HPT related to alcohol abuseUnknown mechanism; possibly 30% of HPT related to alcohol abuse Sedentary lifeSedentary life Unknown mechanism; regular exercise lowers BPUnknown mechanism; regular exercise lowers BP Renal diseaseRenal disease Overt or occult renal disease often implicated: cause or effect?Overt or occult renal disease often implicated: cause or effect? MinorMinor AgeAge Stress or type A personalityStress or type A personality Overactive sympathetic nervous system → vasoconstriction and/or raised COOveractive sympathetic nervous system → vasoconstriction and/or raised CO Difficult to quantify; effect may have been exaggeratedDifficult to quantify; effect may have been exaggerated DietaryDietary  Ca, K, Mg ↓Ca, K, Mg ↓  Saturated fatSaturated fat  Animal productsAnimal products Some evidence,Some evidence, May induce vasoconstriction via endothelial interactionsespecially for KMay induce vasoconstriction via endothelial interactionsespecially for K Vegetarians may have lower BPVegetarians may have lower BP Glucose intoleranceGlucose intolerance Complex interaction between insulin resistance, hyperlipidaemia and HPTComplex interaction between insulin resistance, hyperlipidaemia and HPT RaceRace Increased average BP in urban Blacks: response to stress or dietary salt?Increased average BP in urban Blacks: response to stress or dietary salt? SmokingSmoking NoNo sustained effect on BP itself but greatly exacerbates atheroscleroticsustained effect on BP itself but greatly exacerbates atherosclerotic complicationscomplications BP, blood pressure; Ca, calcium; CO, cardiac output; HPT, hypertension; K, potassium; Mg, magnesium; Na, sodium.BP, blood pressure; Ca, calcium; CO, cardiac output; HPT, hypertension; K, potassium; Mg, magnesium; Na, sodium.
    35. 35. HypertensionHypertension Clinical ManifestationsClinical Manifestations  Referred to as the “silent killer”Referred to as the “silent killer”  Frequently asymptomatic until targetFrequently asymptomatic until target organ disease occursorgan disease occurs  Or recognized on routine screeningOr recognized on routine screening
    36. 36. HypertensionHypertension Clinical ManifestationsClinical Manifestations often secondary to target organ disease Can include: – Fatigue, reduced activity tolerance – Dizziness – Palpitations, angina – Dyspnea
    37. 37. Target Organ DamageTarget Organ Damage  Caused by damage to the body’s blood vesselsCaused by damage to the body’s blood vessels which particularly affect the following organs:which particularly affect the following organs:  Blood VesselsBlood Vessels  HeartHeart  KidneysKidneys  BrainBrain  EyesEyes
    38. 38. HypertensionHypertension ComplicationsComplications • Target organ diseases occur mostTarget organ diseases occur most frequently in:frequently in: – HeartHeart – BrainBrain – Peripheral vasculaturePeripheral vasculature – KidneyKidney – EyesEyes
    39. 39. Hypertension-Hypertension-ComplicationsComplications • Cerebrovascular diseaseCerebrovascular disease – Stroke • Peripheral vascular diseasePeripheral vascular disease • Nephrosclerosis • Retinal damageRetinal damage • AtherosclerosisAtherosclerosis most common cause of cerebrovascular disease; hypertension major risk factor for cerebral atherosclerosis and stroke • AtherosclerosisAtherosclerosis in peripheral blood vessels too; can lead to PVD, aortic aneurysm, aortic dissection • Hypertension one of leading causes of end-stage renal disease, esp. in African-Americans; some degree of renal dysfunction usual in person with even mild BP elevations • RetinaRetina is only place blood vessels can be directly visualized; if see damage there then indicates damage in brain, heart, & kidney too; Can cause blurring, retinal hemorrhage and blindness
    40. 40. Accelerated-malignant HTAccelerated-malignant HT • Fundoscopic changesFundoscopic changes – Retinal hemorrhagesRetinal hemorrhages – ExudatesExudates – PapilledemaPapilledema
    41. 41. Wong, T. Y. et al. N Engl J Med 2004;351:2310-2317 Examples of Mild Hypertensive Retinopathy AV nicking Focal narrowing AV nicking Copper wiring
    42. 42. Secondary HypertensionSecondary Hypertension ►It is caused by another diseaseIt is caused by another disease process such as:process such as: ►Renal FailureRenal Failure ►Diabetes MellitusDiabetes Mellitus ►Cushing’s SyndromeCushing’s Syndrome ►Primary AldosteronismPrimary Aldosteronism ►Coarctation of the AortaCoarctation of the Aorta ►PheochromocytomaPheochromocytoma ►Sleep ApneaSleep Apnea
    43. 43. Secondary hypertension representSecondary hypertension represent symptoms of such diseasessymptoms of such diseases • 1. Diseases of kidneys: glomerulonephritis (14 %), pielonephritis, interstitial nephritis due to abusing analgetics, hereditary nephritis (syndrome Alport’s), polycytosis kidney. • 2. Stenosis of renal artery (1 %). Hypertension arises not in each stenosis. The most often reason of stenosis, caused atherosclerotic platelits(at 70-80 of %), which damage usually proximal third of renal artery on the one hand. Other reason of stenosis with hypertension its fibromuscular hyperplasia of an average third of renal artery. It, as a rule, double-side and more often happens at the women. The mechanism of hypertension in stenosis of renal artery – hyperproduction of renin.
    44. 44. Secondary hypertension representSecondary hypertension represent symptoms of such diseasessymptoms of such diseases • 3. Primary aldosteronism (Cоnn syndrome)3. Primary aldosteronism (Cоnn syndrome) – in 1 %– in 1 % of cases. The reasons – unilateral adenomaof cases. The reasons – unilateral adenoma glomerular zone adrenal glands or double-sideglomerular zone adrenal glands or double-side diffuse hyperplasia of adrenal glands.diffuse hyperplasia of adrenal glands. • 4. Paraganglioma (1 %)4. Paraganglioma (1 %) – tumour from chromaffin– tumour from chromaffin cells of medullarcells of medullar layer adrenal glands or sympatheticlayer adrenal glands or sympathetic nerves, as a rule –nerves, as a rule – benighnbenighn. In paraganglioma is. In paraganglioma is increased both cardiac output, and peripheralincreased both cardiac output, and peripheral resistance.resistance. • 5. Coarctation of the aorta is an anatomic defect5. Coarctation of the aorta is an anatomic defect, in, in which aorta in pectoral or abdominal department iswhich aorta in pectoral or abdominal department is narrowed to such extend, that it represents seriousnarrowed to such extend, that it represents serious barrier for blood circulation. In all vessels, whichbarrier for blood circulation. In all vessels, which depart from the aorta proximal of narrowing, thedepart from the aorta proximal of narrowing, the resistance increases and is increased arterialresistance increases and is increased arterial pressure.pressure.
    45. 45. Pheochromocytoma • A pheochromocytoma is a tumor of chromaffin tissue, which containsA pheochromocytoma is a tumor of chromaffin tissue, which contains sympathetic nerve cells.sympathetic nerve cells. • The tumor is most commonly located in the adrenal medulla but canThe tumor is most commonly located in the adrenal medulla but can arise in other sites, such as sympathetic ganglia, where there isarise in other sites, such as sympathetic ganglia, where there is chromaffin tissuechromaffin tissue. Although only 0.1% to 0.5% of persons with. Although only 0.1% to 0.5% of persons with hypertension have an underlying pheochromocytoma, the disorder canhypertension have an underlying pheochromocytoma, the disorder can cause serious hypertensive crises.cause serious hypertensive crises. • Eight percent to 10% of the tumors are malignant.Eight percent to 10% of the tumors are malignant. • Like adrenal medullary cells, the tumor cells of a pheochromocytomaLike adrenal medullary cells, the tumor cells of a pheochromocytoma produce and secrete the catecholaminesproduce and secrete the catecholamines epinephrine andepinephrine and norepinephrine.norepinephrine. • TheThe hypertensionhypertension that develops is the result of a massive release ofthat develops is the result of a massive release of these catecholamines. Their release may be paroxysmal, rather thanthese catecholamines. Their release may be paroxysmal, rather than continuous, causing periodic episodes of headache, excessivecontinuous, causing periodic episodes of headache, excessive sweating, and palpitations.sweating, and palpitations. • HeadacheHeadache is the most common symptom and can be quite severe.is the most common symptom and can be quite severe. Nervousness, tremor, facial pallor, weakness, fatigue, and weight lossNervousness, tremor, facial pallor, weakness, fatigue, and weight loss occur less frequently. Marked variability in blood pressure betweenoccur less frequently. Marked variability in blood pressure between episodes is typical.episodes is typical. • Some persons with pheochromocytoma have paroxysmal episodes ofSome persons with pheochromocytoma have paroxysmal episodes of hypertension, sometimes to dangerously high levels; others may havehypertension, sometimes to dangerously high levels; others may have sustained hypertension; and some may even be normotensive.sustained hypertension; and some may even be normotensive.
    46. 46. Peripheral Arterial DiseasePeripheral Arterial Disease (PAD)(PAD) § PAD is equivalent in risk to ischemic heart disease.PAD is equivalent in risk to ischemic heart disease. § Any class of drugs can be used in most PAD patients.Any class of drugs can be used in most PAD patients. § Other risk factors should be managed aggressively.Other risk factors should be managed aggressively. § Aspirin should be used.Aspirin should be used.
    47. 47. Hypertension in OlderHypertension in Older PersonsPersons § More than two-thirds of people over 65 have HTN.More than two-thirds of people over 65 have HTN. § This population has the lowest rates of BP control.This population has the lowest rates of BP control. § Treatment, including those who with isolated systolic HTN,Treatment, including those who with isolated systolic HTN, should follow same principles outlined for general care ofshould follow same principles outlined for general care of HTN.HTN. § Lower initial drug doses may be indicated to avoid symptoms;Lower initial drug doses may be indicated to avoid symptoms; standard doses and multiple drugs will be needed to reach BPstandard doses and multiple drugs will be needed to reach BP targets.targets.
    48. 48. Postural HypotensionPostural Hypotension § Decrease in standing SBP >10 mmHg, when associatedDecrease in standing SBP >10 mmHg, when associated with dizziness/fainting, more frequent in older SBPwith dizziness/fainting, more frequent in older SBP patients with diabetes, taking diuretics, venodilators, andpatients with diabetes, taking diuretics, venodilators, and some psychotropic drugs.some psychotropic drugs. § BP in these individuals should be monitored in the uprightBP in these individuals should be monitored in the upright position.position. § Avoid volume depletion and excessively rapid doseAvoid volume depletion and excessively rapid dose titration of drugs.titration of drugs.
    49. 49. Hypertension in WomenHypertension in Women Hypertensive disorders complicate 6% to 8% ofHypertensive disorders complicate 6% to 8% of pregnancies.pregnancies. They are the second leading cause, after embolism, ofThey are the second leading cause, after embolism, of maternal mortality in the United States, accounting formaternal mortality in the United States, accounting for almost 15% of such deaths.almost 15% of such deaths. Hypertensive disorders also contribute to stillbirths andHypertensive disorders also contribute to stillbirths and neonatal morbidity and mortality.neonatal morbidity and mortality. The incidence of hypertensive disorders of pregnancyThe incidence of hypertensive disorders of pregnancy increases with maternal age and is more common inincreases with maternal age and is more common in African-American women.African-American women.
    50. 50. Classification of High Blood Pressure inClassification of High Blood Pressure in PregnancyPregnancy Classification Description GestationalGestational hypertensionhypertension Blood pressure elevation, without proteinuria, that isBlood pressure elevation, without proteinuria, that is detected for the first time during midpregnancy anddetected for the first time during midpregnancy and returns to normal by 12 weeks postpartum.returns to normal by 12 weeks postpartum. ChronicChronic hypertensionhypertension Blood pressure ≥140 mm Hg systolic or ≥90 mm HgBlood pressure ≥140 mm Hg systolic or ≥90 mm Hg diastolic that is present and observable before the 20thdiastolic that is present and observable before the 20th week of pregnancy. Hypertension that is diagnosed forweek of pregnancy. Hypertension that is diagnosed for the first time during pregnancy and does not resolvethe first time during pregnancy and does not resolve after pregnancy also is classified as chronicafter pregnancy also is classified as chronic hypertension.hypertension. Preeclampsia-Preeclampsia- eclampsiaeclampsia Pregnancy-specific syndrome of blood pressure elevationPregnancy-specific syndrome of blood pressure elevation (blood pressure >140 mm Hg systolic or >90 mm Hg(blood pressure >140 mm Hg systolic or >90 mm Hg diastolic) that occurs after the first 20 weeks ofdiastolic) that occurs after the first 20 weeks of pregnancy and is accompanied by proteinuria (urinarypregnancy and is accompanied by proteinuria (urinary excretion of 0.3 g protein in a 24-hour specimen).excretion of 0.3 g protein in a 24-hour specimen). PreeclampsiaPreeclampsia superimposedsuperimposed on chronicon chronic hypertensionhypertension Chronic hypertension (blood pressure ≥140 mm Hg systolicChronic hypertension (blood pressure ≥140 mm Hg systolic or ≥90 mm Hg diastolic prior to 20th week ofor ≥90 mm Hg diastolic prior to 20th week of pregnancy) with superimposed proteinuria and with orpregnancy) with superimposed proteinuria and with or without signs of the preeclampsia syndromewithout signs of the preeclampsia syndrome
    51. 51. 1st period functional violations (heart hypertrophy) 2d period Pathological changes in arteries and arterioles (dystrophy): - Arterioles sclerosis - Arteriole’s wall infiltration by plasma (leads to dystrophy) - Arterioles necrosis (hypertonic crisis arises in clinic) - Vein’s wall thickening Arterial hypertension after-effects
    52. 52. 33dd periodperiod Secondary changes in organs and systemsSecondary changes in organs and systems KidneyKidney ((nephrosclerosisnephrosclerosis andand chronicchronic kidneykidney insufficiencyinsufficiency)) KidneyKidney ((nephrosclerosisnephrosclerosis andand chronicchronic kidneykidney insufficiencyinsufficiency)) CNSCNS –– brain hypoxiabrain hypoxia –– neurons destructionneurons destruction –– apoplexyapoplexy ((because vessels destruction and rupturebecause vessels destruction and rupture leads toleads to brain hemorrhagesbrain hemorrhages and brainand brain destructiondestruction)) CNSCNS –– brain hypoxiabrain hypoxia –– neurons destructionneurons destruction –– apoplexyapoplexy ((because vessels destruction and rupturebecause vessels destruction and rupture leads toleads to brain hemorrhagesbrain hemorrhages and brainand brain destructiondestruction)) HeartHeart Decompensate heart failureDecompensate heart failure HeartHeart Decompensate heart failureDecompensate heart failure Organs of visionOrgans of vision - retinopathyretinopathy ((retina’sretina’s vessels injuryvessels injury)) - hemorrhages and separation (exfoliation) ofhemorrhages and separation (exfoliation) of retinaretina,, that leads to blindnessthat leads to blindness Organs of visionOrgans of vision - retinopathyretinopathy ((retina’sretina’s vessels injuryvessels injury)) - hemorrhages and separation (exfoliation) ofhemorrhages and separation (exfoliation) of retinaretina,, that leads to blindnessthat leads to blindness Endocrine systemEndocrine system Glands atrophy and sclerosisGlands atrophy and sclerosis Endocrine systemEndocrine system Glands atrophy and sclerosisGlands atrophy and sclerosis Arterial hypertension after-effectsArterial hypertension after-effects
    53. 53. Hypertensive crisisHypertensive crisis  DefinitionDefinition  Severe elevation in BP ( >220/120 mmHg)Severe elevation in BP ( >220/120 mmHg)  Sub classified into emergency and urgencySub classified into emergency and urgency  Hypertensive emergencyHypertensive emergency  Require an immediate reduction in BP ( 1 hr )Require an immediate reduction in BP ( 1 hr )  Rx IV therapy and in ICURx IV therapy and in ICU  Hypertensive urgencyHypertensive urgency  No evidence of progressive end-organ injuryNo evidence of progressive end-organ injury  Require only gradual reduction in BP in 24-48 hrRequire only gradual reduction in BP in 24-48 hr
    54. 54. Laboratory TestsLaboratory Tests § Routine Tests • Electrocardiogram • Urinalysis • Blood glucose, and hematocrit • Serum potassium, creatinine, or the corresponding estimated GFR, and calcium • Lipid profile, after 9- to 12-hour fast, that includes high- density and low-density lipoprotein cholesterol, and triglycerides § Optional tests • Measurement of urinary albumin excretion or albumin/creatinine ratio § More extensive testing for identifiable causes is not generally indicated unless BP control is not achieved
    55. 55. Collaborative CareCollaborative Care Lifestyle ModificationsLifestyle Modifications  Wt. reduction  10 kg (22 lb) loss; SBP by 5-20 mm Hg  DASH eating plan (dietary approaches to stop hypertension)  Na reduction  <2.4 g of sodium/day  Moderate alcohol intake  Men: 2 drinks/day or less  Women: 1 drink/day or less
    56. 56. Collaborative CareCollaborative Care Lifestyle ModificationsLifestyle Modifications Physical activity:Physical activity: – Regular physical (aerobic) activity,Regular physical (aerobic) activity, – At least 30 min, most days of weekAt least 30 min, most days of week Avoidance of tobacco productsAvoidance of tobacco products Stress managementStress management
    57. 57. ExperimentalExperimental models of arterialmodels of arterial hypertensionhypertension..  Models confirming a role of the nervous factor in increase ofModels confirming a role of the nervous factor in increase of arterial pressure:arterial pressure:  1.1. Arterial hypertension owing to an irritation ofArterial hypertension owing to an irritation of hypothalamus nucleuseshypothalamus nucleuses. The irritation of a back nucleus. The irritation of a back nucleus frequently resultsfrequently results toto hypertension, connected with increasehypertension, connected with increase of cardiac output. The irritation of a central nucleus causesof cardiac output. The irritation of a central nucleus causes hyperensionhyperension due todue to of peripheral resistance increase.of peripheral resistance increase. Electricity stimulation ventro-medial nucleus givesElectricity stimulation ventro-medial nucleus gives hypertension, which depends from simultaneoushypertension, which depends from simultaneouslyly increaseincrease of cardiac output and peripheral resistance.of cardiac output and peripheral resistance.  2.2. Arterial hypertension from double-side damage nucleusArterial hypertension from double-side damage nucleus tractus solitarii totractus solitarii to medullamedulla oblongoblongataata of rats, where areof rats, where are located primary synapsis of sinuaorticus baroreceptors.located primary synapsis of sinuaorticus baroreceptors. Arterial pressure is increased immediately without changeArterial pressure is increased immediately without change of frequency of cardiac rof frequency of cardiac rateate. The reason of hypertension is. The reason of hypertension is the sharp increase of peripheral resistancethe sharp increase of peripheral resistance  3.3. Reflexogenic hypertensionReflexogenic hypertension,, inin dogs and rabbits adogs and rabbits affterffter section depressor nerve Ludvig-Cion or sinus nerves Heringsection depressor nerve Ludvig-Cion or sinus nerves Hering ..
    58. 58. ExperimentalExperimental models of arterial hypertensionmodels of arterial hypertension.. Models, which confirm participation renals factor in occurrence andModels, which confirm participation renals factor in occurrence and stabilization of arterial hypertension:stabilization of arterial hypertension: 1.1. Vasorenal hypertensionVasorenal hypertension, which is caused by narrowing renals arteries., which is caused by narrowing renals arteries. Conditions of reproduction: а) arteries should be narrowed only partially,Conditions of reproduction: а) arteries should be narrowed only partially, instead of are blocked completely;instead of are blocked completely; bb) the narrowing should be double-) the narrowing should be double- side; c) the variant is possible(probable): narrowing arteries of one kidneyside; c) the variant is possible(probable): narrowing arteries of one kidney plusplus removalremoval of the other kidney.of the other kidney. 2.2. Renoprival hypertensionRenoprival hypertension it arises afterit arises after removelremovel both kidneys andboth kidneys and spendingspending ofof animal on dialysisanimal on dialysis.. Models confirming a role of adrenal glands in fixing arterialModels confirming a role of adrenal glands in fixing arterial hypertension:hypertension: 1.1. Mineral-corticoids hypertensionMineral-corticoids hypertension –– in the casein the case ofof longlong introduction ofintroduction of aldosteron with simultaneousaldosteron with simultaneouslyly purpose of solution NaCl instead of water.purpose of solution NaCl instead of water. 2.2. Salty hypertensionSalty hypertension. Sodium chlorids in a fair quantity even without. Sodium chlorids in a fair quantity even without additional hormonal effects is capable to cause hypertension.additional hormonal effects is capable to cause hypertension. Model confirming role of the hereditary factor in etiology ofModel confirming role of the hereditary factor in etiology of hypertonic disease.hypertonic disease. Exists genetic (spontaneous) hypertension in rats.Exists genetic (spontaneous) hypertension in rats. InIn the animal withthe animal with spontaneous hypertension is revealed higher, than in normal animals,spontaneous hypertension is revealed higher, than in normal animals, permeability ions channels in membranes smoothmusclepermeability ions channels in membranes smoothmuscle cellscells of arteries.of arteries. These membrane defects can have some significance in increase ofThese membrane defects can have some significance in increase of arteries tonus and regulation of volume extracellular liquid. They can bearteries tonus and regulation of volume extracellular liquid. They can be considered as one of the factors pathogenesis hypertonic disease.considered as one of the factors pathogenesis hypertonic disease.
    59. 59. ReferencesReferences 1.1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia:General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia: Nova Knuha Publishers – 2011. – P.Nova Knuha Publishers – 2011. – P. 478478––489489.. 2.2. Russell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinicalRussell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical pharmacy practice / Russell J. Greene, Norman D. Harris // Published by thepharmacy practice / Russell J. Greene, Norman D. Harris // Published by the Pharmaceutical Press An imprint of RPS Publishing 1 Lambeth High Street, LondonPharmaceutical Press An imprint of RPS Publishing 1 Lambeth High Street, London SE1 7JN, UK 100 South Atkinson Road, Suite 200, Greyslake, IL 60030-7820, 3rdSE1 7JN, UK 100 South Atkinson Road, Suite 200, Greyslake, IL 60030-7820, 3rd edition, USA. – 2008. – Chapter 4. – P. 208–234.edition, USA. – 2008. – Chapter 4. – P. 208–234. 3.3. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing.Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P. 372–387.– 2010. – P. 372–387. 4.4. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova //Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide for medical students and practitioners.Study guide for medical students and practitioners. Edited by prof. Zaporozan, OSMU. –Edited by prof. Zaporozan, OSMU. – OdessaOdessa.. – 200– 20055. – P.. – P. 222222––229229.. 5.5. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams &Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback (2003)Wilkins), Trade paperback (2003) // Carol Mattson Porth, Kathryn J. Gaspard. –ChapterCarol Mattson Porth, Kathryn J. Gaspard. –Chapter 16 – P. 274–290.16 – P. 274–290. 6.6. SilbernaglSilbernagl S.S. Color Atlas of PathophysiologyColor Atlas of Pathophysiology / S./ S. SilbernaglSilbernagl, F., F. LangLang //// ThiemeThieme.. StuttgartStuttgart.. New YorkNew York. –. – 20002000. – P. 206–215.. – P. 206–215. 7.7. Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition.Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition. Copyright ВCopyright В.. – Lippincott Williams & Wilkins – 2008. –– Lippincott Williams & Wilkins – 2008. – Chapter 13. – P. 399–412, 426–Chapter 13. – P. 399–412, 426– 427, 431–435.427, 431–435. 8.8. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L.Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc. – 2010. – P. 374Banasic // Elsevier Inc. – 2010. – P. 374––395.395. 9.9. Robbins and Cotran Pathologic Basis of DiseaseRobbins and Cotran Pathologic Basis of Disease 88th edition./ Kumar, Abbas, Fautoth edition./ Kumar, Abbas, Fauto. –. – 20020077.. – Chapter 11. – P. 398–400.– Chapter 11. – P. 398–400. 10.10. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin.Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin. – New York, Milwaukee. – 2009. – P. 50–532.– New York, Milwaukee. – 2009. – P. 50–532.
    60. 60. ReferencesReferences 1.1. Donofrio, J., Haworth, K, Schaeffer, L. & Thompson, G., (Eds.). (2005).Donofrio, J., Haworth, K, Schaeffer, L. & Thompson, G., (Eds.). (2005). Cardiovascular careCardiovascular care made incredibly easy.made incredibly easy. Ambler, PA: Lippincott Williams & Wilkins.Ambler, PA: Lippincott Williams & Wilkins. 2.2. Herman, A. (2010). Hypertension: The pressure’s on.Herman, A. (2010). Hypertension: The pressure’s on. Nursing Made Incredibly Easy, 8Nursing Made Incredibly Easy, 8(4), 40-(4), 40- 53.53. 3.3. McCance, K. L., & Huether, S. E. (2006).McCance, K. L., & Huether, S. E. (2006). Pathophysiology: The biologic basis for disease inPathophysiology: The biologic basis for disease in adults and children,adults and children, (5(5thth ed.). Philadelphia, PA: Elsevier Mosby.ed.). Philadelphia, PA: Elsevier Mosby. 4.4. Moser, D. K., & Riegel, B. (2008).Moser, D. K., & Riegel, B. (2008). Cardiac nursing: A companion to braunwald’s heartCardiac nursing: A companion to braunwald’s heart disease.disease. Saunders Elsevier: St. Louis, MO.Saunders Elsevier: St. Louis, MO. 5.5. Smeltzer, S. C., Bare, B. G., Hinkle, J. L., & Cheever, K. H. (2008).Smeltzer, S. C., Bare, B. G., Hinkle, J. L., & Cheever, K. H. (2008). Brunner and suddarth’sBrunner and suddarth’s textbook of medical-surgical nursing,textbook of medical-surgical nursing, (11(11thth ed.). Philadelphia, PA: Lippincott Williams &ed.). Philadelphia, PA: Lippincott Williams & Wilkins.Wilkins. 6.6. Smithburger, P. L. et al. (2010) Recent advances in the treatment of hypertensive emergency.Smithburger, P. L. et al. (2010) Recent advances in the treatment of hypertensive emergency. Critical Care Nurse, 30Critical Care Nurse, 30(5),(5), 24-30.Woods, S. L., Froelicher, E. S., Underhill Motzer, S., &24-30.Woods, S. L., Froelicher, E. S., Underhill Motzer, S., & Bridges, E. J. (2005).Bridges, E. J. (2005). Cardiac nursing,Cardiac nursing, (5(5thth ed.). Philadelphia, PA: Lippincott Williams &ed.). Philadelphia, PA: Lippincott Williams & Wilkins.Wilkins. 7.7. Wynne, A. L., Woo, T. M., & Olyaei, A. J. (2007).Wynne, A. L., Woo, T. M., & Olyaei, A. J. (2007). Pharmacotherapeutics for nurse practitionerPharmacotherapeutics for nurse practitioner prescribers,prescribers, (2(2ndnd ed.). Philadelphia, PA: F. A. Davis Company.ed.). Philadelphia, PA: F. A. Davis Company. 8.8. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation,The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VII)and Treatment of High Blood Pressure (JNC-VII) 9.9. American Heart Association WebsiteAmerican Heart Association Website

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