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hypertension Blood pressure (BP), sometimes it is called arterial blood pressure, is the pressure exerted by circulating blood upon the walls of blood vessel. During each heartbeat, blood pressure varies between a maximum (systolic) and a minimum (diastole) pressure. Hypertension - Introduction Silent Killer – painless complications It is the leading risk factor –MI, HF, CRF Stroke 25% of population Complications bring to diagnosis but late… hypertension Persistent SBP greater than 140mmhg , DBP greater than 90mmhg or current use of antihypertensive drugs Which means heart is working harder than normal ,putting both heart and blood vessels under strain Hypertension Arterial BP = Cardiac Output (CO) x Systemic vascular resistance (SVR) Cardiac Output = stroke volume x beats per min Systemic vascular resistance = force opposing the movement of blood within the blood vessels What is the effect on BP if SVR increased and CO remains constant? Mechanisms that Regulate BP Sympathetic Nervous System Vascular Endothelium Renal System Endocrine System Regulation of BP: BP = Cardiac Output x Peripheral Resistance Endocrine Factors Renin, Angiotensin, ANP, ADH, Aldosterone. Neural Factors Sympathetic & Parasympathetic Blood Volume Sodium, Mineralocorticoids, ANP Cardiac Factors Heart rate & Contractility. Sympathetic Nervous System (SNS) – Nor epinephrine released from sympathetic nerve endings Increases Heart Rate - chronoscopic Increased cardiac contractility - inotropic Produces widespread vasoconstriction in peripheral arterioles Promotes release of rennin from the kidney (SNS) –Sympathetic Vasomotor Center – located in the medulla Baroreceptors: specialized nerve cells the carotid arteries and the aortic arch Sensitive to BP changes: Increase: Inhibits SNS – peripheral vessel dilation. Decreased heart rate, and decreased contractility of the heart + increased parasympathetic activity (vagus nerve) decreased heart rate Decrease: Activates SNS – peripheral vessel constriction, increased heart rate, and increased contractility of the heart Hypertension SNS Receptors Influencing B/P Vascular Endothelium Single cell layer that lines the blood vessels Produce vasoactive substances: EDRF Endothelium-derive relaxing factor – Helps maintain low arterial tone at rest Inhibits growth of the smooth muscle layer Inhibits platelet aggregation Vasodilation – prostacyclin Endothelin (ET) potent vasoconstrictor Endothelial dysfunction may contribute to atherosclerosis & primary hypertension Renal System Control Na+ excretion & extracellular fluid volume Renal - Renin-angiotensin-aldosterone Renin converts angiotensinogen to angiotensin I Angiotensin-converting enzyme (ACE) converts I into angiotensin II Immediate: Vasoconstrictor – increased systemic vascular resistance Prolonged: Stimulates the adrenal cortex to secret Aldosterone – Na+ and Water retention Renal Medulla - Prostaglandins - vasodilator effect Hypertension Renin-Angiotensin Hypertension Renin-Angiotensin System Endocrine System Stimulates the SNS with Epinephrine – increases HR and contractility Activates B2-adrenergic receptors in peripheral arterioles of skeletal muscle = vasodilation Activates A1-adrenergic receptors in peripheral arterioles of skin and kidneys = vasoconstiction Adrenal Cortex – Aldosterone – stimulates kidneys to retain Na+ Increased Na+ stimulates posterior pituitary – ADH – reabsorbs ECF/water Aldosterone Mechanism Increased Aldosterone Increases sodium reabsorption Increases water reabsorption Increases blood volume Increases cardiac output MI , HF Renal stroke dx Hyper tension Pre hypertension SBP -- 120 to 139 mmhg DBP -- 80 to 89 mmhg epidemiology Before age of 55yrs – common in men After age of 55yrs – common in women Men with HTN is more chance of MI than stroke Women with HTN is more chance of stroke than MI classification TYPE SBP DBP NORMAL < 120 mmhg < 80 mmhg PRE HTN 120 – 19 mmhg 80 – 89 mmhg HTN stage I 140 – 159 mmhg 90 – 99 mmhg HTN stage II > 160 mmhg > 100 mmhg Category Optimal Normal High normal Systolic blood pressure Diastolic < 120 < 80 < 130 < 85 130-139 85-89 Hypertension Grade I (mild ) 140-159 90-99 Grade 2 (moderate) 160-179 100-109 Grade 3 (severe) ≥180 ≥110 Grade 1 140-149 < 90 Grade 2 ≥160 <90 Isolated subtypes Isolated Pseudo Isolated hypertension SBP greater than or equal to 140mmhg with average DBP less than 90 mmhg SBP = increases with aging DBP = increases untill 50 yrs and then declines Pseudo hypertension occur with advanced atherosclerosis sclerotic arteries don't collapse when cuff is fully inflated presenting high cuff pressures than actually exist within vessels OSLER SIGN Etiology Primary HTN – essential / idiopathic Elevated BP without identified cause Contributing factors Secondary HTN – elevated BP with specific cause Medications = Pheochromocytoma Cirrhosis Endocrine disorders COA = PIH Renal dx Risk factors Age Life style stress DM obesity Gender alcohol Socio economicity smoking genetic Sr.lipids diet White-coat hypertension blood pressure measurements taken in a doctor's office may not correctly characterize their typical blood pressure.In up to 25% of patients, the office measurement is higher than their typical blood pressure Cardiovascular Heart - Increased workload on left ventricle Left ventricular hypertrophy left ventricular failure. - Greater thickness of left ventricle decreased perfusion and ischemia of subendocardial region of myocardium. Arteries - Accelerated atherogenesis. - risk of developing aortic dissecting aneurism. Arterioles: Arteriolosclerosis - Benign HT: Deposition of eosinophilic (‘hyaline’) material in vessel walls due to influx of plasma proteins. - Malignant HT: Thickening of intima. Necrosis of vessel walls ('fibrinoid' necrosis) and formation of micro-aneurisms (of Bouchard) in brain. CNS - Rupture of micro-aneurisms of small penetrating arteries Intracerebral haemorrhage. - Risk of cerebral infarction due to atherosclerosis of circle of Willis. - Acute malignant HT: ‘Hypertensive encephalopathy’ due to cerebral oedema (headache, nausea and vomiting, visual disturbances, seizures and disturbances of consciousness). Renal complications Arteriolosclerosis Ischemic sclerosis of glomeruli and tubular atrophy. Proteinuria and microscopic haematuria, especially in malignant HT . Clinical features CARDIAC RENAL EYE LVF Proteinuria Retinopathy MI , angina Microalbuminuria Papiledema CAD Nephrosclerosis HF > sr.creatinine – 1.5mg palpitation PERIPHERAL VASCULAR CEREBRO VASCULAR Aneurysm TIA Claudication stroke Bruit / thrill Decreased or absent PP Nose bleed Headache , dizziness Decreased activity tolerance Hypertensive Retinopathy: Grade I – Thickening of arterioles. Grade II – Focal Arteriolar spasms. Vein constriction. Grade III – Hemorrhages (Flame shape), dot-blot and Cotton wool and hard waxy exudates. Grade IV Papilloedema EXAMINATION Elevated blood pressure is usually the only abnormal sign. Signs of an underlying cause should be sought, such as renal artery bruits in renovascular hypertension, or radiofemoral delay in coarctation of the aorta. The cardiac examination may also reveal features of left ventricular hypertrophy and a loud aortic second sound. If cardiac failure develops, there may be a sinus tachycardia and a third heart sound. Drug therapy DIURETICS – inhibit Nacl reabsorption Eg … metalazone , hydrochlorthiazide(thiazide) torsemide (loop) amiloride (k spar) spirinolactone , eplerenone(aldos recep block) – C/I in ? DIRECT VASODILATORS Hydralazine : minoxidil ( C/I in pheo) = direct arterial vasodilatation NTG = relax arterial , venous smooth muscle SNP = direct arterial vasodilatation , reduce SVR , BP ,, thiocynate toxicity GANGLIONIC BLOCKERS Interrupt adrenergic control of artery trimethapan ACE INHIBITORS Inhibit ACE and prevent conversion of A I to A II C/I in renal imparement , reno vascular dx Eg : captopril, enalpril, lisnopril vasotec A/E – inc K , angioedema, cough ANGIOTENSIN RECEPTOR BLOCKERS II Prevent the action of A II and vasodilating effect and sodium , water reabsorption Eg : losartan, valsartan, telmisartan, olmesartan ADRENERGIC INHIBITORS Centrally acting alpha adrenergic antagonist = decrease the sympathetic outflow from CNS ..(clonidine , methyl dopa) Peripherally acting – prevent release of nor epinephrine - resperine Alpha adrenergic blockers – block alpha 1 receptors – (prazosin , terazosin) Beta adrenergic blockers – block beta 1,2 receptor , decrease renin release, bronchospasm , conduction block. Combined alpha , beta adrenergic blockers carvidelol CALCIUM CHANNEL BLOCKERS Non dihydropyridines – diltiazem , verapamil Dihydropyridines – amlodipine , nife and nicardipine Blocks the extracellular calcium movement into the cells – dec H.R , Contractility , SVR, vaso dilating effect C/I – sick sinus syndrome, HF, AV block COMBINATION THERAPY ACEI + DIURETICS ARB + DIURETICS BETA ADRENERGIC BLOCKERS + DIURETICS CENTRALLY ACTING DRUGS + DIURETICS DIURETICS + DIURETICS ACEI + CALCIUM CHANNEL BLOCKERS DASH DIET = DIETARY APPROACH TO STOP HYPERTENSION HYPERTENSIVE CRISIS Severe abrupt elevation of BP , esp DBP > 140mmhg RISK FACTORS Exacerbation of chronic hypertension Renovascular hypertension Pre eclampsia / Eclampsia Pheochromocytoma , coccine use Rebound Htn , head injury Aortic dissection HYPERTENSIVE EMERGENCY HYPERTENSIVE URGENCY Developed over hours to day Over days to weeks in Patient BP severely elevated ( > 180 / > 120 mmhg) with evidence of acute organ damage of esp. CNS severely but no evidence of Encephalopathy , CNS hemorrhage , acute LVF with pulmonary edema , MI , renal failure , dissecting aneurysm which patient BP is elevated organ damage GOAL TO DECREASE MAP BY NO MORE THAN 25% IN ONE HOUR BP = 160 / 100 mmhg over 2 – 6 hrs I.V – SNP ,NTG , Labetolol, esmolol , vasotec Life style modifications BP REDUCE BY WEIGHT REDUCTION BMI : 18.5 – 24.9/kg/m2 5 – 20 mm / 10 Kg ADOPT DASH Fruit , vegetables , low fat ,dietary products 8 – 14 mmhg DIET SODIUM RESTRICTION 100 mmol / day 2 -8 mmhg PHYSICAL ACTIVITY Aerobic – 30 mn /day 4 – 9 mmhg Summary • Hypertension is the commonest cause of major morbidity, but less than a quarter of patients are adequately treated. • A reduction in cardiovascular disease mortality and morbidity can be achieved through improved treatment and control of hypertension. • A greater choice of drugs are available for hypertension than for other chronic diseases. • Rational choice of single and combination drugs facilitated by understanding their effects on the renin system, but systematic trial and error may still be necessary. A client is scheduled for a cardiac catherization using a radiopaque dye. Which of the following assessments is most critical before the procedure? Intake and output Baseline peripheral pulse rates Height and weight Allergy to iodine or shellfish A client is wearing a continuous cardiac monitor, which begins to sound its alarm. A nurse sees no electrocardiogram complexes on the screen. The first action of the nurse is to: Check the client status and lead placement Press the recorder button on the electrocardiogram console. Call the physician Call a code blue A client who has been receiving heparin therapy also is started on warfarin. The client asks a nurse why both medications are being administered. In formulating a response, the nurse incorporates the understanding that warfarin: Stimulates the breakdown of specific clotting factors by the liver, and it takes 2-3 days for this to exert an anticoagulant effect. Inhibits synthesis of specific clotting factors in the liver, and it takes 34 days for this medication to exert an anticoagulant effect. Stimulates production of the body’s own thrombolytic substances, but it takes 2-4 days for this to begin. Has the same mechanism of action as Heparin, and the crossover time is needed for the serum level of warfarin to be therapeutic. 2. Warfarin works in the liver and inhibits synthesis of four vitamin K-dependent clotting factors (X, IX, VII, and II), but it takes 3 to 4 days before the therapeutic effect of warfarin is exhibited. A 60-year-old male client comes into the emergency department with complaints of crushing chest pain that radiates to his shoulder and left arm. The admitting diagnosis is acute myocardial infarction. Immediate admission orders include oxygen by NC at 4L/minute, blood work, chest x-ray, an ECG, and 2mg of morphine given intravenously. The nurse should first: Administer the morphine Obtain a 12-lead ECG Obtain the lab work Order the chest x-ray 1. Although obtaining the ECG, chest x-ray, and blood work are all important, the nurse’s priority action would be to relieve the crushing chest pain. The nurse teaches the client with angina about the common expected side effects of nitroglycerin, including: Headache High blood pressure Shortness of breath Stomach cramps 1. Because of the widespread vasodilating effects, nitroglycerin often produces such side effects as headache, hypotension, and dizziness. The client should lie or shit down to avoid fainting. Nitro does not cause shortness of breath or stomach cramps. Which of the following arteries primarily feeds the anterior wall of the heart? Circumflex artery Internal mammary artery Left anterior descending artery Right coronary artery 3. The left anterior descending artery is the primary source of blood flow for the anterior wall of the heart. The circumflex artery supplies the lateral wall, the internal mammary supplies the mammary, and the right coronary artery supplies the inferior wall of the heart. When do coronary arteries primarily receive blood flow? During inspiration During diastolic During expiration During systole Although the coronary arteries may receive a minute portion of blood during systole, most of the blood flow to coronary arteries is supplied during diastole. Breathing patterns are irrelevant to blood flow Which of the following parameters is the major determinate of diastolic blood pressure? Baroreceptors Cardiac output Renal function Vascular resistance Vascular resistance is the impedance of blood flow by the arterioles that most predominantly affects the diastolic pressure. Cardiac output determines systolic blood pressure.