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

Prepared by md, PhD. 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 d O 2 , u CO 2 , 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- μ 1 adrenergic receptors increasing vascular tone at pre-capillary level. They also increase heart rate and contractility through interaction with cardiac- β 1 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-Barr e 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

Transcript

  • 1. Hypertension
  • 2. Actuality Arterial hypertension is a very common condition. Cerebral, coronary and renal vessels are mainly affected by the deleterious effect of this condition, and both acute and chronic organ failure may ensue. Exacerbation of underlying pathophysiologic conditions or new precipitating factors can lead to hypertensive crisis, either urgencies or emergencies. During hypertensive emergencies, a quick raise in arterial pressure may lead to acute and significant organ dysfunction, such as aortic dissection, acute myocardial infarction, intracranial bleeding or acute renal failure. Perioperative hypertension often takes the shape of a crisis and it can be related to hypothermia, pain, neuro-hormonal response to surgical trauma or antihypertensive drugs withdrawal.
  • 3. CONTENT• 1. Factors which predetermine the level of blood pressure for a man, basal tone of vessels.• 2. Pressor and depressor systems of organism, their description.• 3. Arterial hypertensions: kinds, classification. Degrees of high arterial pressure.• 4. Nephrogenic hypertensions: reasons, kinds, pathogenesis.• 5. Etiology and pathogenesis of endocrinal hypertension.• 6. A role of the sympathetic nervous system in pathogenesis of nerogenic hypertension.• 7. Salt hypertension: etiology, mechanisms of development.• 8. Etiology and pathogenesis of essential hypertension.• 9. Complication of essential hypertension.• 10. Reasons and mechanisms of arterial hypotension.
  • 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. Definitions• 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 ventricularrelaxation)• Mean Arterial Pressure (MAP) "average" pressure throughout the cardiac cycle against the walls of the proximal systemicarteries (aorta) • estimated as: .33(SBP - DBP) + DBP• Total Peripheral Resistance (TPR) - the sum of all forces that oppose blood flow • length of vasculature (L) TPR = ( 8 ) ( V ) ( L ) • blood viscosity (V) (  ) ( r4) • vessel radius (r)
  • 6. Physiological factors affecting Arterial Blood pressureAge: New born: 80/40 mmHg 4 years: 100/65 mmHg. Adults: 120/80 mmHg After that: Gradually increase due to increase elasticity of arteries.Sex: Children: have equal Blood pressure. Adults before 45 years: male more than female. Adults after 45 years: the diastolic B.P. is more in female than males.Race: ABP in oriental is less than in European and American.Gravity: B.P. in upper parts of the body is more than the lower parts especially during standing.Meals: Digestion increases the arterial blood pressure.Emotions and exercise: increase the arterial blood pressure.Sleep: Deep quiet sleep decrease A.B.P., while sleep with dreams increase A.B.P.
  • 7. Measurements of Blood Pressure1- Direct Method The most accurate means for measuring blood pressure is directly within an artery (intra-arterial) using a catheter. But because this method is invasive, it is neither practical nor appropriate for repeated measurements in non-hospital settings, or for large-scale public health screenings.2- The mercury-filled sphygmomanometer The usual method of measurement, therefore, is a noninvasive means that uses a sphygmomanometer, which includes either a column of mercury or pressure-registering gauge.
  • 8. Cardiovascular Hemodynamic Basics Pressure (MAP) P aorta – P vena cava Flow (Q) = = Resistance (TPR) (8) (V) (L) () (r 4) Flow (Q) = () (Pa – Pv) (r 4) Normally Resting Q is about 5 - 6 liters / minute (8) (V) (L)V = viscosity of fluid (blood) flowing through the pipeL = length of pipe (blood vessel)r = radius of the pipe (blood vessel)Pa = aortic pressurePv = venous pressure BP = CO x PR
  • 9. The “Closed” Cardiovascular Mean arterial pressures in red Hemodynamic System PO2 = 160 LV PCO2 = .3 RV RA LUNGS LA AORTA PO2 = 100 (0) (13) PCO2 = 40 (3) (100) 9% of blood volume (7) Ohms Law: Flow (Q) = upstream pressure – downstream pressure SYSTEMIC (92) resistance ARTERIES low compliance VEINS 13% of blood volume (CAPACITANCE VESSELS) (20) high compliance (40) (2) 64% of blood volume CAPILLARY ARTERIOLES PO2 = 40 PCO2 = 46 BEDS 7% of blood volumeSystemic Circulation = 100 mmHg – 0 mmHg = 100 ml / sec = 6 liters / min Flow (Q) 1 mmHg sec / ml
  • 10. Blood Pressure Regulation Systemic arterial pressure is a function of stroke volume, heart rate, and total peripheral resistance The major organs involved in regulation of blood pressure are the heart (HR & SV), the SNS (TPR-total peripheral resistance), and the kidneys (ECF – extracellular fluid volume & secretion of renin). (Wynne, Woo, & Olyaei, 2007, p. 1093)
  • 11. Factors Influencing BP Cardiac •Heart rate •Inotropic state •Neural (pons and medulla) •Humoral (hormones) Cardiac Output Renal Fluid Volume Control •Renin–angiotensin •Aldosterone •Atrial natriuretic factor Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
  • 12. Regulative systemsSympathetic Nervous System Baroreceptors – Nerve cells in carotid artery & aortic arch – Maintain BP during normal activities – React to increases & decreases in BP BP – impulse to brain to inhibit SNS; HR & force of contraction; vasodilation of arterioles BP – activates SNS; vasoconstriction of arterioles; HR & heart contractility 1. Barroreceptors of aorta arch and sinus caroticus
  • 13. Sites ofCardiorespiratory Control
  • 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. THE BARORECEPTOR REFLEX - AN EXAMPLE CORRECTION OF POSTURAL HYPOTENSIONOn standing up venous return falls Effect of gravity on venous returnCardiac output diminishes Preload diminished - Starling’s LawArterial blood pressure is reduced Subject possibly feels faint as cerebral flow is reducedBaroreceptor afferent firing reduced Due to reduced arterial B.P.Medullary centres inhibition reducedIncreased sympathetic tone to Vasoconstriction Tend toarterioles restore Reduced vagal tone to s.a. Tachycardia arterial node bloodIncreased myocardial sympathetic tone Raised stroke work pressure
  • 16. Sympatetic activity Increases Increases Increases Induces heart rate vascular tone at sodium and vascular and precapillary water remodelling contractility level reabsorption Vasoconstriction Increased leftIncrease increasing ventricular Increase cardiac peripheral hypertrofy and diastolic output vascular oxygen pressure resistances consumption Chronic Increase BP Ischemia and AMI
  • 17. Blood pressure regulation by the renin-angiotensin system and the central roles of sodium metabolism in specific causes of inherited and acquired forms of hypertension. Components of the systemic renin-angiotensin system are shown in black. Genetic disorders that affect blood pressure by altering activity of this pathway are indicated in red; arrows indicate sites in the pathway altered by mutation. Genes that are mutated in these disorders are indicated in parentheses. Acquired disorders that alter blood pressure through effects on this pathway are indicated in blue. (From Lifton RP, et al: Molecular genetics of human blood pressure variation. Science 272:676, 1996.)
  • 18. Effect of renin-angiotensin system Renin 2. Renin–angiotensin systemon cardiovascular homeostasis Angiotensin II Vasoconstriction Alteration of renal on systemic and arterial and Aldosterone ADH renal vassels capillary vessels’ wall Increase left Sodium and ventricular Glomeruar ischemia, water renal wall parenchymal damage, retention tension proteinuria, end-stage renal failure Left ventricular Hypervolemia hypertrophy and myocardial Increase BP ischemia
  • 19. 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 inindividual renal cells in the thick ascending limb of the loop of Henle (TAL), distal convoluted tubule (DCT), and the corticalcollecting tubule (CCT) are indicated, along with the pathway of the renin-angiotensin system, the major regulator of renalsalt reabsorption. Single gene defects that manifest as inherited diseases affecting these pathways are indicated, withhypertensive disorders in red and hypotensive disorders in blue. Abbreviations: Al, angiotensin I; ACE, angiotensinconverting enzyme; All, angiotensin II; MR, mineralocorticoid receptor; GRA, glucocorticoid-remediable aldosteronism;PHA1, pseudohypoaldosteronism, type 1; AME, apparent mineralocorticoid excess; 11b-HSD2, 11b-hydroxysteroiddehydrogenase-2; and DOC, deoxycorticosterone. (From Lifton RP, et al: Molecular mechanisms of human hypertension.Cell 104:545, 2001.)
  • 20. Regulative systems 3. Renin–angiotensin-aldosteron systemRenin Angiotensin 2 Actination of suprarenal glangs (cortical layer)Na concentration in Na reabsorbtion Aldosteron blood increase, in kidney increase excretion blood osmotic pressure increaseMove of extravascular Increase of circulative CО increase fluid inside the blood volume vessels (CBV)
  • 21. Mechanism of Action of Aldosterone Increases CO by increasing blood volume .
  • 22. BP Regulation: EndotheliumNitric oxide is secreted by endothelial cellswhich results in relaxation of blood vesselsIt also produces local vasodilators, suchas prostacylcin and endothelium-derivedhyperpolarizing factorEndothelin is an extremely potentvasoconstrictor and also stimulatesvascular smooth muscle growth(Wynne, Woo, & Olyaei, 2007, p. 1094)
  • 23. Healthy LifestyleMaintain a Healthy Blood Pressure: Blood Pressure Systolic BP Diastolic BP Classification (mm Hg) (mm Hg)Normal < 120 < 80Prehypertension 120 – 139 80 – 89Stage 1 Hypertension 140 – 159 90 – 99Stage 2 Hypertension 160 – 179 100 – 109Stage 3 Hypertension ≥ 180 ≥ 110(Hypertensive crisis)Source: Clinical Practice Guidelines Management of Hypertension, 3rd Ed. 2008February;MOH/P/PAK/156.08(GU)
  • 24. Hypertension: DefinitionPersistent elevation of  Systolic blood pressure ≥140 mm Hg or  Diastolic blood pressure ≥90 mm Hg Worldwide an estimated 1 billion people have hypertension; about 1 in 3 Americans affected Direct relationship between hypertension and cardiovascular disease (CVD)
  • 25. Classification Arterial hypertension AP above 139/89 mm Hg Primary SecondaryAP less than 100/60 mm Hg Arterial hypotension Acute Chronic
  • 26. Primary Hypertension►Etiological Theories► Inability of kidneys to excrete sodium► Overactive renin/angiotensin system► Overactive sympathetic nervous system► Decreased vasodilatory reaction► Resistance to insulin action► Genetic Inheritance (polygenic)
  • 27. Risk Factors R/T Primary HypertensionAge/HereditySexRaceObesityStimulantsSodiumAlcoholStressHyperlipidemiaDiabetesSocioeconomicStatus
  • 28. Risk Factors for - Primary HypertensionAge (>55)AlcoholCigarette smokingDiabetes mellitusElevated serum lipidsExcess dietary sodiumGender – 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. Risk Factors for Primary HypertensionFamily historyObesityEthnicitySedentary lifestyleStress
  • 30. Primary Hypertension Water and sodium retention • A high sodium intake may result in water retention • Some people are Na sensitive (about 20%) ; not everyone with high salt diet develops hypertension
  • 31. Pathophysiology of Primary Hypertension Water and sodium retention  Certaindemographics are associated with “salt sensitivity”  Obesity  Increasing age  African American ethnicity  People with diabetes, renal disease
  • 32. Pathophysiology of Primary Hypertension• Stress and increased SNS activity – Produces increased vasoconstriction – ↑ HR – ↑ Renin release – Angiotensin II causes direct arteriolar constriction, promotes vascular hypertrophy and induces aldosterone secretion
  • 33. Pathophysiology of Primary 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. Risk factors and aetiological influences in hypertension Risk factor or aetiological Possible rationale and comment influenceMajorFamily history Inherited tendency – probably polygenicDietary Na high Fluid retention; vascular wall oedema; ion pump defectObesity Possible artefact of measurement (problem with arm cuff)? Greater perfusion demands of increased body mass Reducing weight can reverse borderline HPTAlcohol Unknown mechanism; possibly 30% of HPT related to alcohol abuseSedentary life Unknown mechanism; regular exercise lowers BPRenal disease Overt or occult renal disease often implicated: cause or effect?MinorAgeStress or type A personality Overactive sympathetic nervous system → vasoconstriction and/or raised CO Difficult to quantify; effect may have been exaggeratedDietary Ca, K, Mg ↓ Some evidence, Saturated fat May induce vasoconstriction via endothelial interactionsespecially for K Animal products Vegetarians may have lower BPGlucose intolerance Complex interaction between insulin resistance, hyperlipidaemia and HPTRace Increased average BP in urban Blacks: response to stress or dietary salt?Smoking No sustained effect on BP itself but greatly exacerbates atherosclerotic complicationsBP, blood pressure; Ca, calcium; CO, cardiac output; HPT, hypertension; K, potassium; Mg, magnesium; Na, sodium.
  • 35. Hyper tensionClinical Manifestations  Referred to as the “silent killer”  Frequently asymptomatic until target organ disease occurs  Or recognized on routine screening
  • 36. HypertensionClinical Manifestations often secondary to target organ disease Can include: – Fatigue, reduced activity tolerance – Dizziness – Palpitations, angina – Dyspnea
  • 37. Target Organ Damage Caused by damage to the body’s blood vessels which particularly affect the following organs:  Blood Vessels  Heart  Kidneys  Brain  Eyes
  • 38. Hypertension Complications• Target organ diseases occur most frequently in: – Heart – Brain – Peripheral vasculature – Kidney – Eyes
  • 39. Hypertension-Complications• Cerebrovascular disease – Stroke• Peripheral vascular disease• Nephrosclerosis• Retinal damage• Atherosclerosis most common cause of cerebrovascular disease; hypertension major risk factor for cerebral atherosclerosis and stroke• Atherosclerosis 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• Retina 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. Accelerated-malignant HT• Fundoscopic changes – Retinal hemorrhages – Exudates – Papilledema
  • 41. Examples of Mild Hypertensive Retinopathy AV nicking Focal narrowing Copper wiring AV nicking Wong, T. Y. et al. N Engl J Med 2004;351:2310-2317
  • 42. Secondary Hypertension► Itis caused by another disease process such as:► Renal Failure► Diabetes Mellitus► Cushing’s Syndrome► Primary Aldosteronism► Coarctation of the Aorta► Pheochromocytoma► Sleep Apnea
  • 43. Secondary hypertension represent symptoms 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. Secondary hypertension represent symptoms of such diseases• 3. Primary aldosteronism (Cоnn syndrome) – in 1 % of cases. The reasons – unilateral adenoma glomerular zone adrenal glands or double-side diffuse hyperplasia of adrenal glands.• 4. Paraganglioma (1 %) – tumour from chromaffin cells of medullar layer adrenal glands or sympathetic nerves, as a rule – benighn. In paraganglioma is increased both cardiac output, and peripheral resistance.• 5. Coarctation of the aorta is an anatomic defect, in which aorta in pectoral or abdominal department is narrowed to such extend, that it represents serious barrier for blood circulation. In all vessels, which depart from the aorta proximal of narrowing, the resistance increases and is increased arterial pressure.
  • 45. Pheochromocytoma• A pheochromocytoma is a tumor of chromaffin tissue, which contains sympathetic nerve cells.• The tumor is most commonly located in the adrenal medulla but can arise in other sites, such as sympathetic ganglia, where there is chromaffin tissue. Although only 0.1% to 0.5% of persons with hypertension have an underlying pheochromocytoma, the disorder can cause serious hypertensive crises.• Eight percent to 10% of the tumors are malignant.• Like adrenal medullary cells, the tumor cells of a pheochromocytoma produce and secrete the catecholamines epinephrine and norepinephrine.• The hypertension that develops is the result of a massive release of these catecholamines. Their release may be paroxysmal, rather than continuous, causing periodic episodes of headache, excessive sweating, and palpitations.• Headache is the most common symptom and can be quite severe. Nervousness, tremor, facial pallor, weakness, fatigue, and weight loss occur less frequently. Marked variability in blood pressure between episodes is typical.• Some persons with pheochromocytoma have paroxysmal episodes of hypertension, sometimes to dangerously high levels; others may have sustained hypertension; and some may even be normotensive.
  • 46. Peripheral Arterial Disease (PAD)§ PAD is equivalent in risk to ischemic heart disease.§ Any class of drugs can be used in most PAD patients.§ Other risk factors should be managed aggressively.§ Aspirin should be used.
  • 47. Hypertension in Older Persons§ More than two-thirds of people over 65 have HTN.§ This population has the lowest rates of BP control.§ Treatment, including those who with isolated systolic HTN, should follow same principles outlined for general care of HTN.§ Lower initial drug doses may be indicated to avoid symptoms; standard doses and multiple drugs will be needed to reach BP targets.
  • 48. Postural Hypotension§ Decrease in standing SBP >10 mmHg, when associated with dizziness/fainting, more frequent in older SBP patients with diabetes, taking diuretics, venodilators, and some psychotropic drugs.§ BP in these individuals should be monitored in the upright position.§ Avoid volume depletion and excessively rapid dose titration of drugs.
  • 49. Hypertension in WomenHypertensive disorders complicate 6% to 8% of pregnancies.They are the second leading cause, after embolism, of maternal mortality in the United States, accounting for almost 15% of such deaths.Hypertensive disorders also contribute to stillbirths and neonatal morbidity and mortality.The incidence of hypertensive disorders of pregnancy increases with maternal age and is more common in African-American women.
  • 50. Classification of High Blood Pressure inPregnancy Classification DescriptionGestational Blood pressure elevation, without proteinuria, that is hypertension detected for the first time during midpregnancy and returns to normal by 12 weeks postpartum.Chronic Blood pressure ≥140 mm Hg systolic or ≥90 mm Hg hypertension diastolic that is present and observable before the 20th week of pregnancy. Hypertension that is diagnosed for the first time during pregnancy and does not resolve after pregnancy also is classified as chronic hypertension.Preeclampsia- Pregnancy-specific syndrome of blood pressure elevation eclampsia (blood pressure >140 mm Hg systolic or >90 mm Hg diastolic) that occurs after the first 20 weeks of pregnancy and is accompanied by proteinuria (urinary excretion of 0.3 g protein in a 24-hour specimen).Preeclampsia Chronic hypertension (blood pressure ≥140 mm Hg systolic superimposed or ≥90 mm Hg diastolic prior to 20th week ofon chronic pregnancy) with superimposed proteinuria and with or hypertension without signs of the preeclampsia syndrome
  • 51. Arterial hypertension after-effects 1st period functional violations (heart hypertrophy) 2d periodPathological 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
  • 52. Arterial hypertension after-effects 3d periodSecondary changes in organs and systems CNS CNS ––brain hypoxia brain hypoxia ––neurons destruction neurons destruction ––apoplexy (because vessels destruction and rupture apoplexy (because vessels destruction and rupture Kidney Kidney leads to brain hemorrhages and brain leads to brain hemorrhages and brain(nephrosclerosis and chronic (nephrosclerosis and chronic destruction) ) destruction kidney insufficiency) ) kidney insufficiency Organs of vision Organs of vision - - retinopathy (retina’s vessels injury) ) retinopathy (retina’s vessels injury - - hemorrhages and separation (exfoliation) of hemorrhages and separation (exfoliation) of Heart retina, ,that leads to blindness retina that leads to blindness Heart Decompensate heart failure Decompensate heart failure Endocrine system Endocrine system Glands atrophy and sclerosis Glands atrophy and sclerosis
  • 53. Hypertensive crisis Definition  Severe elevation in BP ( >220/120 mmHg)  Sub classified into emergency and urgency Hypertensive emergency  Require an immediate reduction in BP ( 1 hr )  Rx IV therapy and in ICU Hypertensive urgency  No evidence of progressive end-organ injury  Require only gradual reduction in BP in 24-48 hr
  • 54. Laboratory 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. Collaborative CareLifestyle 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. Collaborative Care Lifestyle ModificationsPhysical activity:– Regular physical (aerobic) activity,– At least 30 min, most days of weekAvoidance of tobacco productsStress management
  • 57. Experimental models of arterial hypertension . Models confirming a role of the nervous factor in increase of arterial pressure: 1. Arterial hypertension owing to an irritation of hypothalamus nucleuses. The irritation of a back nucleus frequently results to hypertension, connected with increase of cardiac output. The irritation of a central nucleus causes hyperension due to of peripheral resistance increase. Electricity stimulation ventro-medial nucleus gives hypertension, which depends from simultaneously increase of cardiac output and peripheral resistance. 2. Arterial hypertension from double-side damage nucleus tractus solitarii to medulla oblongata of rats, where are located primary synapsis of sinuaorticus baroreceptors. Arterial pressure is increased immediately without change of frequency of cardiac rate. The reason of hypertension is the sharp increase of peripheral resistance 3. Reflexogenic hypertension, in dogs and rabbits affter section depressor nerve Ludvig-Cion or sinus nerves Hering .
  • 58. Experimental models of arterial hypertension. Models, which confirm participation renals factor in occurrence and stabilization of arterial hypertension:1. Vasorenal hypertension, which is caused by narrowing renals arteries. Conditions of reproduction: а) arteries should be narrowed only partially, instead of are blocked completely; b) the narrowing should be double- side; c) the variant is possible(probable): narrowing arteries of one kidney plus removal of the other kidney.2. Renoprival hypertension it arises after removel both kidneys and spending of animal on dialysis. Models confirming a role of adrenal glands in fixing arterial hypertension:1. Mineral-corticoids hypertension – in the case of long introduction of aldosteron with simultaneously purpose of solution NaCl instead of water.2. Salty hypertension. Sodium chlorids in a fair quantity even without additional hormonal effects is capable to cause hypertension. Model confirming role of the hereditary factor in etiology of hypertonic disease.Exists genetic (spontaneous) hypertension in rats. In the animal with spontaneous hypertension is revealed higher, than in normal animals, permeability ions channels in membranes smoothmuscle cells of arteries. These membrane defects can have some significance in increase of arteries tonus and regulation of volume extracellular liquid. They can be considered as one of the factors pathogenesis hypertonic disease.
  • 59. References1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia: Nova Knuha Publishers – 2011. – P. 478–489.2. Russell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical pharmacy practice / Russell J. Greene, Norman D. Harris // Published by the Pharmaceutical Press An imprint of RPS Publishing 1 Lambeth High Street, London SE1 7JN, UK 100 South Atkinson Road, Suite 200, Greyslake, IL 60030-7820, 3rd edition, USA. – 2008. – Chapter 4. – P. 208–234.3. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P. 372–387.4. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide for medical students and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005. – P. 222–229.5. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. –Chapter 16 – P. 274–290.6. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. Stuttgart. New York. – 2000. – P. 206–215.7. Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition. Copyright В. – Lippincott Williams & Wilkins – 2008. – Chapter 13. – P. 399–412, 426– 427, 431–435.8. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc. – 2010. – P. 374–395.9. Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar, Abbas, Fauto. – 2007. – Chapter 11. – P. 398–400.10. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin. – New York, Milwaukee. – 2009. – P. 50–532.
  • 60. References1. Donofrio, J., Haworth, K, Schaeffer, L. & Thompson, G., (Eds.). (2005). Cardiovascular care made incredibly easy. Ambler, PA: Lippincott Williams & Wilkins.2. Herman, A. (2010). Hypertension: The pressure’s on. Nursing Made Incredibly Easy, 8(4), 40- 53.3. McCance, K. L., & Huether, S. E. (2006). Pathophysiology: The biologic basis for disease in adults and children, (5th ed.). Philadelphia, PA: Elsevier Mosby.4. Moser, D. K., & Riegel, B. (2008). Cardiac nursing: A companion to braunwald’s heart disease. Saunders Elsevier: St. Louis, MO.5. Smeltzer, S. C., Bare, B. G., Hinkle, J. L., & Cheever, K. H. (2008). Brunner and suddarth’s textbook of medical-surgical nursing, (11th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.6. Smithburger, P. L. et al. (2010) Recent advances in the treatment of hypertensive emergency. Critical Care Nurse, 30(5), 24-30.Woods, S. L., Froelicher, E. S., Underhill Motzer, S., & Bridges, E. J. (2005). Cardiac nursing, (5th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.7. Wynne, A. L., Woo, T. M., & Olyaei, A. J. (2007). Pharmacotherapeutics for nurse practitioner prescribers, (2nd ed.). Philadelphia, PA: F. A. Davis Company.8. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VII)9. American Heart Association Website