Hypertension Coronary artery disease
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1 Hypertension Coronary artery disease 1
2 Problem Magnitude Hypertension( HTN) is the most common primary diagnosis. Worldwide prevalence estimates for HTN may be as much as 1 billion. Arterial hypertension affects % of adults in developed countries. Frequency of arterial hypertension suddenly increases after 50 years of life (>50% of this population). 2
3 Hypertension is an intermittent or a sustained elevation of diastolic or systolic blood pressure (BP). 3
4 Types of Hypertension Primary HTN: also known as essential HTN. Secondary HTN: less common cause of HTN ( 5%). accounts for 95% cases of HTN. secondary to other potentially rectifiable causes. no universally established cause known. 4
5 Secondary causes of AH : Renal parenchymal disease (most common cause) Renovascular hypertension (2nd most common cause) Pheochromocytoma Primary hyperaldosteronism Cushing s syndrome Obstructive sleep apnea Coarctation of aorta Drug induced hypertension 5
6 Definition A systolic blood pressure ( SBP) >139 mmhg and/or A diastolic (DBP) >89 mmhg. Based on the average of two or more properly measured, seated BP readings. On each of two or more office visits. 6
7 Accurate Blood Pressure Measurement The equipment should be regularly inspected and validated. The operator should be trained and regularly retrained. The patient must be properly prepared and positioned and seated quietly for at least 5 minutes in a chair. The auscultatory method should be used. Caffeine, exercise, and smoking should be avoided for at least 30 minutes before BP measurement. An appropriately sized cuff should be used. 7
8 BP Measurement At least two measurements should be made and the average recorded. Clinicians should provide to patients their specific BP numbers and the BP goal of their treatment. 8
9 Diagnostic procedures in arterial hypertension repeated BP measurements family and clinical history physical examination laboratory and instrumental investigation 9
10 Signs and symptoms Cerebral symptoms: headache, dizziness, buzzing in the ears and head, irritation (due to disorders of vessel tone, their widening is changed spasm. It results in disorders of cerebral circulation. There is an irritation of the cerebral vessels by increased BP). Cardiac symptoms: heart pain, palpitation and interruption of the heart bit General symptoms: fatigue, sleep disorders, decreasing work ability Visual examination: flush of the face and sclera. Pulse is hard, intense. 10
11 Definition and classification of blood pressure levels (mmhg) Category Systolic Optimal Normal High normal Grade 1 hypertension Grade 2 hypertension Grade 3 hypertension < Diastolic and <80 and/or and/or and/or and/or and/or
12 Prehypertension SBP >120 mmhg and <139mmHg and/or DBP >80 mmhg and <89 mmhg. Prehypertension is not a disease category rather a designation for individuals at high risk of developing HTN. 12
13 Pre HTN Individuals who are prehypertensive are not candidates for drug therapy but Should be firmly and unambiguously advised to practice lifestyle modification Those with pre HTN, who also have diabetes or kidney disease, drug therapy is indicated if a trial of lifestyle modification fails to reduce their BP to 130/80 mmhg or less. 13
14 Target Organs CVS (Heart and Blood Vessels) The kidneys Nervous system The Eyes 14
15 Effects On CVS Ventricular hypertrophy, dysfunction and failure. Arrhithymias Coronary artery disease, Acute MI Arterial aneurysm, dissection, and rupture. 15
16 Effects on The Kidneys Glomerular sclerosis leading to impaired kidney function and finally end stage kidney disease. Ischemic kidney disease especially when renal artery stenosis is the cause of HTN 16
17 Nervous System Stroke, intracerebral and subaracnoid hemorrhage. Cerebral atrophy and dementia 17
18 The Eyes Retinopathy, retinal hemorrhages and impaired vision. Vitreous hemorrhage, retinal detachment Neuropathy of the nerves leading to extraoccular muscle paralysis and dysfunction 18
19 Retina Normal and Hypertensive Retinopathy A B C Normal Retina Hypertensive Retinopathy A: Hemorrhages B: Exudates (Fatty Deposits) C: Cotton Wool Spots (Micro Strokes) 19
20 Classification and clinical presentation of the essential hypertension: I stage episodic elevation of BP with cerebral, cardiac and general symptoms without any other signs except high BP ІІ stage: Permanent symptoms and signs of affect of the target organs without their failure: Heart left ventricle hypertrophy ( sings, ECG, Ehocardiography, X Ray) Eye - hypertensive retinopathy I II Kidney proteinuria, increased blood creatinine (male mcmol/l or 1,3 1,5 mg/dl, female mcmol/l or 1,2 1,4 mcmol/l) ІІІ stage Permanent symptoms and signs of affect of the target organs with their failure (complicated stage) Heart myocardial infarction, heart failure ІІ ІІІ st. Brain - cerebrovascular accident, chronic hypertensive encephalopathy ІІІ st. and vassel dementia Eye - hypertensive retinopathy III IV Kidney proteinuria, increased blood creatinine (male >133 mcmol/l or >1,5 mg/dl, female >124 mcmol/l or >1,4 mcmol/l), chronic renal failure Vessels aortic dissecting aneurysm 20
21 Impact of High Normal BP on Risk of Major CV Events* in Men 16 Cumulative Incidence (%) of Major CV Events 14 High-normal BP 12 ( /85-89 mm Hg) 10 Normal BP 8 ( /80-84 mm Hg) 6 Optimal BP (<120/80 mm Hg) Time (y) * Defined as death due to CV disease; recognized myocardial infarction (MI), stroke, or congestive heart failure (CHF). Adapted from Vasan RS. N Engl J Med. 2001;345:
22 Aim of antihypertensive therapy The primary goal of treatment is to achieve maximum reduction in the long term total risk of CV disease For this reason lowering BP therapy (at least < 140/90 mm Hg) and treatment of all reversible risk factors are indicated In diabetes and in high and very high risk patients BP target should be at least < 130/80 mmhg 22
23 Benefits of Treatment Reductions in stroke incidence, averaging percent Reductions in MI, averaging percent Reductions in HF, averaging >50 percent. 23
24 Lifestyle changes smoking cessation weight reduction reduction of excessive alkohol intake physical exercise reduction of salt intake increase in fruit and vegetables intake decrease in saturated and total fat intake 24
25 Coronary artery disease (Ischemic heart disease) 25
26 Definition " Ischaemia " refers to an insufficient amount of blood. The coronary arteries are the only source of blood for the heart muscle. If these coronary arteries are blocked, the blood supply will reduce. 26
27 Risk Factors Uncontrollable Controllable Sex High blood pressure Hereditary High blood cholesterol Race Age Smoking Physical activity Obesity Diabetes Stress and anger 27
28 28
29 Key Concepts Ischemic heart disease (IHD): caused by coronary atherosclerotic plaque formation which leads to imbalance between O2 supply & demand results in myocardial ischemia Chest pain: cardinal symptom of myocardial ischemia caused by coronary artery disease (CAD) 29 29
30 Why would there be an insufficient blood supply to the heart? Remember that the coronary arteries are the only source of fuel to the heart The coronary arteries may become partially/completely occluded: Atherosclerotic Plaques 30
31 Atherosclerotic Plaque: Definition and Formation Focal accumulation of smooth muscle cells, foam cells, cholesterol crystals and lipid under the endothelium of the artery (within the Tunica Intima) Given time, this plaque can protrude into the lumen of the vessel reducing blood flow Often develops at branch points or curves within the vasculature blood is slowed and/or turbulent 31
32 Atherosclerotic Plaque Where does the plaque begin? within the Tunica Intima, the innermost wall of the artery What is a plaque made of? Superficial fibrous cap made of smooth muscle cells, collagen, elastin and proteins Also contains Macrophages, Foam Cells, T Cells Foam cells are one of the first cells found at the site of the fatty streak, which is the beginning of atherosclerotic plaque formation in vessels Necrotic Center of cholesterol crystals, lipids, Apolipoprotein B LDL 32
33 Continued As the plaque within the coronary arteries enlarges, the blood flow to the heart decreases and therefore so does the O2 supply The heart is not in danger of hypoxia until 50% of the vessel is occluded As the heart senses a decrease in O2, there is attempted compensation: Increase Heart Rate Increase Blood Pressure Aggravation/Worsening of the atheroma When 70% of the artery is occluded, Angina Pectoris will occur 33
34 Ischemic Heart Disease Classification of the CAD: Sudden coronary death Angina pectoris: - Stable angina causes pain that's predictable in frequency and duration and can be relieved with nitrates and rest. - Unstable angina causes pain that in creases in frequency and duration. It's more easily induced. - Prinzmetal s angina causes unpredictable coronary artery spasm. III. Myocardial infarction (MI) 34
35 Angina Pectoris At least 70% occlusion of coronary artery resulting in pain. What kind of pain? Chest pain Radiating pain to: Left shoulder Jaw Left or Right arm Usually brought on by physical exertion as the heart is trying to pump blood to the muscles, it requires more blood that is not available due to the blockage of the coronary artery(ies) Is self limiting usually stops when exertion is ceased 35
36 Angina Pectoris Continued Angina Pectoris can be Stable or Unstable: Stable: The pain and pattern of events is unchanged over a period of time (months years) Unstable: The pain and pattern is changing, be it in duration, intensity or frequency A Myocardial Infarction waiting to happen 36
37 Additional diagnostic measures include the following: Electrocardiography (ECG) during angina may show ischemia (ST depression; flat or inverted T waves) or may be normal; it may also show arrhythmias, such as premature ventricular contractions. The ECG is apt to be normal when the patient is pain free. Treadmill or bicycle exercise test may provoke chest pain and ECG signs of myocardial ischemia (ST segment depression). The patient undergoes a graduated, treadmill exercise test, with continuous 12 lead ECG and blood pressure monitoring. 37
38 Ambulatory ECG monitoring (Holter) Continuous ECG monitoring for 24h may be used to detect ST segment depression, either symptomatic (to prove angina), or to reveal 'silent' ischaemia (predictive of re infarction or death soon after Ml). Coronary angiography reveals narrowing or occlusion of the coronary artery, with possible collateral circulation. 38
39 Acute myocardial infarction (AMI) One of the most common diagnosis in hospitalized patients in industrialized nations Mortality of acute MI is 30% and one half of these deaths occur before hospitalization Mortality after admission has decreased by 30% in last 2 decades 1 in 25 pts (4%) who survive till hospital discharge die within one year 39
40 Signs and symptoms The cardinal symptom of MI is persistent, crushing substernal pain that may radiate to the left arm, jaw, neck, or shoulder blades. Such pain is often described as heavy, squeezing, or crushing and may persist for 12 hours or more. However, in some MI patients particularly older adults or diabetics pain may not occur at all; in others, it may be mild. 40
41 Stages of MI I acutest stage some first hours 1 day II acute stage 2 day till 2 weeks III subacute stage till 2 3 months IV scarring stage till6 month 41
42 ECG Total occlusion of infarct related artery leads to ST elevation (STEMI) and subsequent evolution of Q waves Partial occlusion/early recanalization/rich collaterals leads to NSTEMI (non ST elevation MI) 42
43 43
44 44
45 ECG: STEMI hyperacute (tall) T waves, ST elevation occur within hours of MI (I st.) T wave inversion and the development of pathological Q waves follow over hours to days (II st.) pathological Q, Inversion T wave and ST isoelectrically till 2 3 month (III st.) if patient has scar only pathological Q can be on ECG (IV st.) NSTEMI: ST depression, T wave inversion, non specific changes. 45
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