HYPERTENSION/high blood pressure- a lecture-1.pptx
EmmanuelIshioma
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May 27, 2024
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About This Presentation
Hypertension
Size: 99.59 KB
Language: en
Added: May 27, 2024
Slides: 33 pages
Slide Content
HYPERTENSION By DR MBADIWE NKEIRUKA C.
OUTLINE Introduction Definitions Classification Pathophysiology Management -symptoms and signs of HTN -Investigations - treatment complication
Introduction Epidemiology World wide, HBP is estimated to cause about 7.5 million deaths, and about 12.8 % of all total deaths. Globally, as at year 2022,an estimated 26% of the world’s population (972 million people) has HTN., and the prevalence is expected to increase to 29% by the year 2025. Across the WHO regions, the prevalence of HBP was highest in Africa, 46% for males and females combined.
Epidemiology contd. HTN is a major modifiable risk factor for stroke, MI, HF, ESRD, PVD, dementia, progressive atherosclerosis Uncontrolled hypertension is associated with serious end organ damage including heart disease, stroke, blindness and renal disease. 4
Definition of Hypertension HYPERTENSION is currently defined as persistent elevation of BP of ≥140 &/or /90 mmHg for adults ≥ 18 years who are not taking antihypertensive medication. BLOOD PRESSURE is the measurement of the force exerted against the wall of your arteries as your heart pumps blood around your body.
Types of hypertension Primary (essential) hypertension- no particular or specific cause is found. Secondary hypertension- due to a specific medical conditions with potential for cure. Also occur in children.
Risk factors for Essential Hypertension Modifiable and non modifiable Non m odifiable risk factors : Male gender Increasing age Ethnicity (African/afro American), Genetics, etc. Fetal factors -low birth weight
Risk factors for Essential Hypertension M odifiable risk factors: Diet: high Na salts, low k 0besity , Chronic stress, anxiety Alcohol, Smoking Sedentary life Diabetes Mellitus
Causes of secondary HBP RENAL : Glomerulonephritis , diabethic nephropathy Atherosclerosis, Renovascular disease, adult polycystic kidneys dx , chronic tubulointerstitial dx Endocrine: Hormone related dxs e.g. Hyperthyriodism , hypothyroidism, acromegaly,Cushing's syndrome, Pheochromocytoma , hyperparathyroidism etc.
WHO Classification of Hypertension Category Systolic BP (mmHg) Diastolic BP (mmHg) Optimal BP Normal High-Normal BP Hypertension: Grade 1 HT (mild) Grade 2 HT (moderate) Grade 3 HT (severe) Isolated Systolic HT <120 <130 130 – 139 140 - 159 and/or 160 – 179 and/or ≥180 and/or ≥140 <80 <85 85 – 89 90 – 99 100 – 109 ≥110 <90
The Nigerian Hypertension Society Classification Category Systolic BP (mmHg) Diastolic BP (mmHg) Optimal BP Normal High-Normal BP Grade 1 HT (mild) Grade 2 HT (moderate) Grade 3 HT (severe) Isolated Systolic HT <120 <130 130 – 139 140 - 159 and/or 160 – 179 and/or ≥180 and/or ≥ 140 <80 <85 85 – 89 90 – 99 100 – 109 ≥110 <90
TABLE 1. JOINT NATIONAL COMMITTEE – 7 (JNC-7 ) 2003 GUIDELINES Category Systolic BP (mmHg) Diastolic BP (mmHg) Normal Prehypertension Stage 1 Hypertension Stage 2 Hypertension <120 and 120 - 139 or 140 – 159 or ≥160 or <80 80 – 89 90 – 99 ≥100 Source: Arch Int. Med. 2006; 157:2413
Pathophysiology of HTN The actual pathogenesis of essential Hypertension is not very clear. However, certain pathophysiological mechanisms have been postulated: It is believed that in some young persons who become hypertensive, an early increase in cardiac output, together with an increased pulse rate leads to changes in the sensitivity of the baroreceptor, which cause it to operate at a higher level of blood pressure.
Cardiac changes: Resistance vessels , i.e the small arteries and arterioles show structural changes in hypertension, with increase in wall thickness and reduction in the diameter of the lumen of the vessels. This increases the peripheral vascular resistance which maintains the blood pressure at an elevated level. Also the vessels undergo rarefaction (reduction in density) and the entire mechs give rise to increase in overall total peripheral resistance.
2 . Large vessel changes : Thickening of the media occurs with increase in collagen and secondary deposition of calcium. These changes result in loss of arterial compliance, which in turn leads to more pronounced arterial pressure wave. 3. Pulse wave velocity : This is a measure of arterial stiffness, and is inversely related to its distensibility .
Usually, with each systolic contraction, a pulse wave travels down the arterial wall before the flow of blood. The more rigid the vessel, the faster the pulse wave travels. The interaction of these mechanical stresses and low growth factors leads to development of Atheroma in the large arteries. There is also endothelial dysfunction with alterations in certain agents like Nitric Oxide, and endothelins .
Left Ventricular Hypertrophy: Results from increased peripheral vascular resistance and ↑ left ventricular load. 5. Renal Changes : Changed renal vasculature eventually leads to ↓ renal perfusion, ↓ glomerular filtration & sodium and water excretion. Decreased renal perfusion may → activation of the renin-angiotensin system with increased secretion of aldosterone and further salt and water retention.
6. Cerebral Changes: Changes in small vessels cause lacunae ( lacunar or small infarcts) and reversible neurological deficits which will not show abnormalities in imaging such as CT Scan or MRI. These however may eventually lead to dementia or stroke.
Symptoms of High BP No symptoms, incidental finding, silent killer. Headaches , Insomnia visual blurring, dizziness, nausea. Vomiting, confusion etc.
Signs of High BP For acute stage of HTN, i.e. f or new onset HTN, there may be no signs. But for long standing HTN, signs include: - Thickened radial arterial wall - locomotor brachialis - displaced, heaving apex beat. - Xray evidence of aortic unfolding and cardiomegaly - Retinopathy -seen on fundoscopy .
Lab investigations Chest X-Ray Electrocardiogram, Echocardiogram Fundoscopy FBC Urinalysis FBG, (Glucose tolerance test if FBG is >5.6mmol/L or 100 mg/dl). SEUC Fasting Lipids profile
Aim of Treatment of hypertension : Control BP down to target Prevent target organ damage Stop further organ damage Reverse organ damage where possible
Treatment modalities 1. Non pharmacological- -Life style change: Exercise, Weight reduction Stop smoking, reduce alcohol consumption Diet modification- low Na salt, ↑K, low cholesterol 2. Pharmacological - use of antihypertensive drugs
Classes of drugs used in Rx of HTN Alpha-blockers : E.g. Doxazosin , Indoramin , Phenoxybenzamine , Phentolamine . Aldosterone antagonists : E.g. Spironolactone , Eplerenone . Angiotensin -converting enzyme inhibitors : E.g. Enalapril , Lisinopril , Perindopril , Ramipril . Angiotensin II receptor blockers : E.g. Losartan , Candesartan , Valsartan , Olmesartan , Telmisartan . Beta-blockers: E.g. Atenolol , Bisoprolol , Nebivolol , Carvedilol , Labetalol .
Classes of drugs in Rx of HTN contd . Calcium channel blockers : E.g. Amlodipine , Nifedipine (long acting), Diltiazem (long acting), Verapamil . Centrally acting : E.g. Methldopa , Moxonidine . Diuretics : E.g. Hydrochlorthiazide , Bendroflumethiazide , Chlortalidone , Furosemide . Renin inhibitors : E.g. Aliskiren . Vasodilators: E.g. Hydralazine , Minoxidil , Sodium Nitroprusside .
Complications of Hypertension Brain - Strokes, dementia. Eyes - Hypertensive retinopathy, blindness. Heart –Long standing HTN can lead to the following Hypertensive heart Diseases(HHDs): 1. Left ventricular hypertrophy, 2. I schaemic heart disease/coronary artery disease, 3. heart failure, 4. conduction defects(heat blocks), 5. arrhythmias Kidney - Hypertensive nephrosclerosis , CKD. Peripheral vessels/ Vascular - peripheral vascular disease, aortic aneurysm etc.
Acute Complications of Hypertension Hypertensive Emergencies Acute Strokes, Subarachnoid haemorrhage etc. Acute Myocardial infarction etc. Aortic aneurysm dissection
Acute Complications of Hypertension Hypertensive Emergencies: Refer to a spectrum of clinical presentations in which uncontrolled blood pressure leads to progressive or impending end-organ damage, and requires aggressive lowering of blood pressure, over minutes to hours. This usually entails the use of parenteral route of antihypertensive drug administration.