HYPERTENSION_ Hypertensive vacular disease REAL.pptx

Hypertensive vascular disease

1. KAMPALA INTERNATIONA UNIVERSITY HOIMA RRH TEACHING SITE HYPERTENSIVE VASCULAR DISEASE PRESENTED BY OPAKASI OBED ORENA 2020-08-00265

2. OVERVIEW DEFINITION Hypertension is defined as a chronic medical condition characterized by elevated blood pressure(BP) in the arteries with a systolic BP >/= 140mmHg and/or diastolic BP >/= 90mmHg, an average of 2 readings on 2 separate takings. EPIDEMIOLOGY Global prevalence: 1.13 billion people which is 26% of the global adult population it has an increasing trend with the number expected to be 1.5 billion by 2025 and is the leading cause of mortality: responsible for 17.9 million deaths worldwide annually

3. CONTINUATION OF EPIDEMIOLOGY The prevalence of Hypertension in Uganda stands at 26.4% with 34.6% being from urban areas and 23.4% from rural areas An increasing trend is projected to reach 42.1% by 2025 The highest prevalence is between 45 to 54 years(35.1%) 27.5% of the males in the population have hypertension and 25.3% of the females in the population have hypertension.

4. RISK FACTORS FOR HYPERTENSION These are variables or characteristics that when present, interact to increase the likelihood of the occurence of Hypertension. MODIFIABLE RISK FACTORS Obesity Physical Inactivity Heavy alcohol consumption High salt dietary intake Smoking Pre-existing vascular disease Type II Diabetes Mellitus Serum Cholesterol

5. NON MODIFIABLE RISK FACTORS Age: most especially above 45 years Sex: Male>female Race: people of African and Carribean descent Family history most especially first degree relatives

6. CLASSIFICATION OF HYPERTENSION According to the cause Essential or Primary Hypertension This has no specific cause but comes about as a result of the interaction of risk factors. 2. Secondary Hypertension This type of hypertension is common in people under 30 years of age and is sudden on onset, severe and usually refractory. The causes of secondary Hypertension include: Alcohol Obesity

7. CONTINUATION Pregnancy Renal disease ie Parenchymal disease(glomerulonephritis), renal artery stenosis Coarctation of the Aorta Drugs like oral contraceptives, steroids, cocaine Endocrine disease like: Phaechromocytoma( presents with paroxysmal headaches, sweating and palpitations) Primary Aldosteronism Hyperthyroidsm Hypothyroidism Cushing’s syndrome.(Increased cortisol> SNS activation)

8. CLASSIFICATION OF BLOOD PRESSURE CATEGORY SBP(mmHg) DBP(mmHg) NORMAL <120 <80 PRE-HYPERTENSION 120-139 80-89

9. GRADING OF HYPERTENSION GRADES SYSTOLIC BLOOD PRESSURE (mmHg) DIASTOLIC BLOOD PRESSURE (mmHg) GRADE 1/ MILD HYPERTENSION 140-159 90-99 GRADE 2/ MODERATE HYPERTENSION 160-179 100-109 GRADE 3/ SEVERE HYPERTENSION > OR = 180 > OR = 110

10. PATHOPHYSIOLOGY OF HYPERTENSION Increased activity of the sympathetic Nervous system which brings about Beta receptor activation >Increased Heart rate and cardiac output> increased BP Alpha 1 receptor activation> vasoconstriction>increased peripheral resistance> increased BP Increases renin production> activation of the RAAS and production of angiotensin II hence: 1) vasoconstriction (2) Aldosterone production> Na retention> Increased BP 3) Anti-Diuretic Hormone production and release> water retention> Increased BP

11. CONTINUATION 2. Endothelial damage and dysfunction This leads to reduced production of Nitric Oxide(NO), a potent vasodilator, reduced response to NO and production of endothelin-1, a vasoconstrictor. This causes increased peripheral vascular resistance and susequently, an increase in the blood pressure 3. Advanced age means an increase in collagen greater than smooth muscle. This reduces elasticity of arteries causing a loss in compliance. There’s increased vascular resistance and hence a rise in Blood pressure to counteract the resistance.

12. CLINICAL MANIFESTATION Usually assymptomatic and diagnosis made during routine physical examination or when a complication arises. Symptoms Headache Dizziness Nosebleeds Easy fatiguability Chest pain Confusion Lower limb swelling Palpitations Vision changes(Blurry vision, double vision or loss of vision)

13. SIGNS OF HYPERTENSION These are indicative of the secondary causes of hypertension and will be noticeable during History taking and Physical Examination. Radio-femoral delay in coarctation of aorta Enlarged Kidneys in polycystic kidney disease Abdominal bruits in Renal artery stenosis Central obesity, characteristic face of Cushing’s syndrome Signs of left Ventricular Hypertrophy Added heart sounds Cotton wool exudates in retinopathy

14. COMPLICATIONS OF HTN CVS: Dissecting Aorta Aortic Aneurysm Dilatation of the blood vessels due to shear force Atherosclerosis with thrombi formation due to unstable plaques Coronary Artery Disease(CAD) Left Ventricular Hypertrophy. This together with CAD cause Atrial fibrillations Pulmonary edema> reduced filling of Left Ventricle Peripheral Artery Disease and claudication RENAL Renal failure from nephrosclerosis depicted by Hematuria and Albuminuria.

15. RETINA Viewed by fundoscopy Arterio-venule nicking and blind ending veins Microhemorrhages Infarction Swelling of the optic disc: Papilloedema CNS Beri aneurysm hence Sub-arachnoid Hemorrhage Posterior reversible encephalopathy from edema

16. KEITH-WAGNER-BARKER CLASSIFICATION OF HYPERTENSIVE RETINOPATHY   GRADE 1 MILD GENERALISED RETINAL ARTERIOLAR NARROWING GRADE 2 GRADE 1 PLUS ARTERIOVENOUS NIPPING GRADE 3 GRADE 2 PLUS EVIDENCE OF ISCHEMIA(BLOT HEMORRHAGES AND COTTON WOOL EXUDATES) GRADE 4 SEVERE GRADE 3 RETINOPATHY PLUS PAPILLEDEMA

17. C o t t on w o o l spots

18. BLOOD VESSELS In large blood vessels{>1mm in diameter} t he internal elastic lamina is thickened, smooth muscle is hypertrophied and fibrous tissue is deposited. The vessels dilate and become tortuous and their wall become less compliant. In smaller arteries[<1mm] hyaline arteriosclerosis occurs in the wall,the lumen narrows and aneurysms may develop . Widespread atheroma develop and may lead to coronary and/or cerebrovascular disease.

19. EXAMINATION OF A PATIENT WITH HYPERTENSION Introduce yourself, confrim the patient’s details and gain consent Adorn PPE and position your patient in a cardiac bed with the head of the bed elevated. General exam -Inspect for risk factors, signs of secondary causes and complications of hypertension -look for evidence of associated disease e .g; round face and truncal obesity of Cushings syndrome. -muscular development in upper extremity more than lower suggesting coarctation of aorta, acromegaly, stature of the patient. VITAL SIGNS Pulse –feel radial pulse for nature, examine for radio-femoral and radial radial synchronicity. Temperature- Hyperthyroidism

20. CONTINUATION OF THE EXAMINATION BP-with patient sitting with the arm supported at level of heart and also while standing. A rise in diastolic BP on standing occurs typically in essential HTN, a fall on standing may suggest a secondary cause. Take 2 readings at least 5 minutes apart.

21. CARDIOVASCULAR SYSTEM EXAMINATION Inspection of the chest for size, shape, symmetry, therapeutic scars, markings and swellings. Inspect for activity of the precordium. Inspect the neck for vein distension and also lower limb for swelling. Palpate for the position of the trachea, tenderness, apical beat, parasternal heaves, thrills. Take note of the chest expansion. Palpate the lower limb for edema and grade it Auscultate heart sounds and apex beat Identify added heart sounds if any Auscultate lung bases to rule in or rule out pulmonary edema

22. CONTINUATION OF EXAMINATION Taylor your examinations according to the complications the patients presents with and those you suspect or expect RENAL SYSTEM EXAMINATION FUNDOSCOPY CENTRAL NERVOUS SYSTEM EXAMINATION MUSCULOSKELETAL SYSTEM EXAM

23. INVESTIGATIONS Carried out to Confirm the diagnosis Identify causative factors Grade progression of disease or identify complications Monitor response to therapy Rule out differentials Identify comorbidities that influence the choice of antihypertensives.

24. CONTINUATION Blood Pressure measurement in sitting position with arm supported. Repeat after 5 minutes rest if the first reading is high. Ambulatory BP measurement is encouraged since it provides a wide profile Urinalysis especially for Blood, protein and glucose to check for nephropathy Blood urea, electrolytes and creatinine for renal function Blood glucose since Type II Diabetes Mellitus is a risk factor Serum total and HDL cholesterol Thyroid function Tests 12-lead ECG

25. OTHER INVESTIGATIONS(PATIENT DEPENDENT) CXR-to detect cardiomegaly,heart failure,coarctation of aorta. Echocardiogram-to detect or quantify left Ventricular hypertrophy Renal USS-To detect possible renal disease Renal angiography: To detect or confirm the presence of renal artery stenosis

26. CONTINUATION Urinary catechol amines(metanephrine): To detect possible phaechromocytoma. Urinary cortisol and dexamethasone suppression test: To detect possible Cushing’s syndrome Plasma renin activity and aldosterone: To detecct possible primary aldosteronism Head CT scan: Often shows hemorrhage in and around basal ganglia in hpertensive encephalopathy.

27. DIFFERENTIAL DIAGNOSES OF HYPERTENSION Whitecoat hypertension: is a phenomenon whea person’s blood pressure(BP) is elevated when measured in a clinical setting ie doctor’s office but normal when measured in a non-clinical setting like home. Masked Hypertension: a condition where a patient’s blood pressure(BP) readings are normal in a clinical setting but elevated when measured out of the clinical setting ie at home or using Ambulatory BP measurement

28. MANAGEMENT OF HYPERTENSION Objectives of Management Reduce the blood pressure Prevent target organ damage for say the kidneys, retina, heart and brain among others Reduce the risk of cardiovascular events like heart failure, strokes, heart attacks Improve quality of life Prevent complications

29. NON PHARMACOLOGICAL THERAPY These mainly comprise of lifestyle changes DASH—Dietary Approaches to Stop Hypertension like increased fruit and vegetable consumption Reduce alcohol intake Quit smoking Regular physical exercise Restricting salt dietary intake Correcting obesity

30. PHARMACOLOGICAL THERAPY These comprise of those used to treat primary disease and drugs used to manage complications. Commonly used groups of drugs to lower Blood pressure include: Angiotensin converting enzyme inhibitors (ACEI) Angiotensin receptor blockers (ARBs) Beta-blockers (BBs) Calcium channel blockers (CCBs) Diuretics

31. DIURETICS MOA:-They lower BP by 1)Decreasing plasma volume via renal excretion of Na and water therefore reducing cardiac output. 2)Reduction of peripheral vascular resistance Thiazide diuretics eg hydrochlorothiazide one tab Once daily are slower and take upto one month to produce results. 3) Loop diuretics eg furosemide 40mg/day and Bumetanide(1mg/day) are better. 4)Potassium sparing diuretics eg amiloride and triamterene can be combined with other diuretics. 5) Spironolactone is a particularly useful addition in treatment of resistant hypertension.

32. BETA BLOKERS MOA: Decrease heart rate and cardiac output by competitive inhibition of the effects of catecholamines at beta adrenergic receptors. A lso inhibit renin Are not First line except in Angina patients that are Hypertensive. Non cardioselective beta blockers: -They block both beta-1 and beta-2 receptors therefore also cause bronchospasm and cold extremities.eg propanolol-,timolol, and nadolol are non selective beta blockers. Labetalol and Carvedilol block both alpha and beta receptors

33. Cardioselective beta blockers: DRUG INITIAL DOSE DOSAGE RANGE atenolol 25mg od 200-1200 metoprolol 50mg in 1-2 doses 50-200 in 1-2 doses bisoprolol 5mg once daily 2.5-10mg od

34. CALCIUM CHANNEL BLOCKERS MOA: Decrease BP by arteriolar vasodilation by selectively blocking the slow inward calcium channels in the vascular smooth mu sc le cells. Dihydropyridines like amlodipine(5-10mg/day), nifedipine(30-90mg/day) and are useful in older people Side effects include flushing, palpitations. Rate limiting and Non-selective CCBs ie Verapamil, Diltiazem. They may cause bradycardia. The major side effect of Verapamil is constipation.

35. ANGIOTENSIN CONVERTING ENZYME INHIBITORS -”prils” and are well tolerated MOA: They block the conversion of angiotensin I to Angiotensin II(a vasoconstrictor)producing arterial and venous dilatation. Used with care in impaired renal function/ renal artery stenosis because they lower GFR and precipitate renal failure Side effects include: first dose hypotension, cough, rash, hyperkalemia. -captopril 25mg daily -enalapril 5mg od -lisinopril 5-10mg od -fosinopril 10mg od

36. ANGIOTENSIN RECEPTOR BLOCKERS sartans ie valsartan and losartan better tolerance than ACE inhibitors They don’t cause cough since there isn’t breakdown of bradykinin

37. ALPHA 1 RECEPTOR ANTAGONISTS They act on vascular smooth muscle causing relaxation Prazocin 1mg before sleep(0.5-20mg) Terazocin 1 mg before sleep(25-100mgbd) Doxazocin 1mg before sleep.(1-16mg daily) OTHERS Centrally acting drugs eg methyldopa(initial dose 250mg tds) and clonidine(0.05-0-1mg tds) r effective but cause fatigue and r ussually poorly tolerated. Drugs that act directly on vascular sm mm eg hydralazine 25-100mg bdand minoxidil 10-50mg daily.

38. OTHER DRUGS USED TO TREAT COMPLICATIONS Aspirin : an antiplatelet. It decreases the risk of Cardiovascular events in patients above 50 years of age. Carries risk of intracranial hemorrhage Statins Treating hyperlipidemia can produce a substantial reduction in the risk of occurence of cardiovascular disease Attach a catheter and urine bag to monitor urine output

39. FACTORS AFFECTING THE CHOICE OF HYPERTENSIVE Cost Age Ethnicity Convenience The response to initial treatment Freedom from side effects Comorbid conditions

40. HYPERTENSIVE CRISIS HYPERTENSIVE URGENCY Accelerated hypertension. Hypertension is severe :systole>180mmHg and diastole >120mmHg with no organ damage. BP must be reduced within a 48 to 72 hours . Patient is managed ACE inhibitors or ARBs and CCBs with or without diuretics. Parenteral drug therapy is not required if there is no end organ damage.

41. HYPERTENSIVE EMERGENCY Systolic BP>/= 180mmHg and Diastolic BP>/=120mmHg with target organ damage For say: Neural deficits Renal failure Acute Kidney Injury Palpitations Retinopathy Rails over lung bases on Auscultation Shortness of breath

42. MANAGEMENT OF HYPERTENSIVE CRISIS Parenteral therapy is indicated in most emergencies esp if encephalopathy is present. BP should be reduced not more than 25% over a period of 1-2hrs And achieve BP level of 160/100mmHg wthin 2-6hrs. Rapid fall in BP causes cerebral damage including blindness and may precipitate coronary,cerebral or renal insufficiency.

43. CONTINUATION OF MANAGEMENT Hydralazine, Labetalol and Sublingual nifedipine Na nitroprusside iv infusion: -is a direct acting arterial and venous vasodilator -Its ac ti on is rapid,easily titrable and short lived when discontinued. It carries a risk of causing lactic acidosis. .Nitroglycerine IV infusion:when Na nitroprusside is c/I eg.in severe coronary insufficiency,advanced renal or hepatic d’se. -given as continous iv infusion at a rate of 5-100ug/min.

44. ACCELERATED/MALIGNANT HYPERTENSION A rare complication of both primary and secondary hypertension There’s microvascular damage and fibrinoid necrosis of small arteries and arterioles There’s High BP coupled with retinopathy, renal dysfunction and hypertensive encephalopathy. It also presents with Left Ventricle Heart failure

45. MANAGEMENT OF MALIGNANT HYPERTENSION Avoid fast lowering of BP. 150/90 mmHg in 24 to 48 hours is ideal. IV/IM Labetalol- 2mg/min to max of 200mg IV GTN(0.6 to 1.2 mg/hr) IV Hydralazine( 5 or 10 mg aliquotsin 30 minutes) IV Sodium Nitroprusside(0.3 to 1.0 micrograms per kg body weight per minute) The patient requires careful supersivion.

46. REFRACTORY HYPERTENSION Causes of treatment failure include: -non-compliance -Inadequate therapy -Failure to recognize secondary causes of hptn -Use of antagonist drugs e.g.-NSAIDS,steroids,cocaine and thyroxine. -Increased alcohol intake

47. ISOLATED SYSTOLIC HYPERTENSION ISH (systolic >160 and diastolic <90mmHg) Common in elderly affecting , affecting around 50% of people older than 70 years old Isolated systolic hypertension is associated with increased cardiovascular risk Treating ISH  reduce both stroke and ischemic heart disease Thiazides and Calcium antagonists are drugs of choice Mechanism of ISH: It is thought to result from large artery stiffening , which is determined by structural components within the vasculature but also by functional factors including NO and endothelin-1 . ISH in elderly: decreased arterial elasticity and increased stiffness → decreased  arterial compliance

48. ISH secondary to increased  cardiac output: Anemia Hyperthyroidism Clinical features : Often asymptomatic Signs of increased  pulse pressure : e.g., head pounding, rhythmic nodding, bobbing of the head in synchrony with heartbeats Symptoms of hypertension

49. Treatment :  thiazide diuretics OR dihydropyridine  calcium antagonists Prognosis :  high risk of cardiovascular events ( MI ,  stroke , renal dysfunction)

50. REFERENCES UpToDate 2024 DAVIDSON’S PRINCIPLES AND PRACTICES OF MEDICINE. 24TH EDITION by Ian D Penman, Stuart H Ralston, Mark W.J Strachan and Richard P Hobson. Oxford handbook of cardiology