Cardiac Pathophysiology

Signs and symptoms
1-Chest pain Characters , Location, Radiation, Relation to exercise, stages and associated symptoms 2-Dyspnea, orthopenia, PND, Pulmonary edema 3-Palpitation 4-Diziness

Evaluation Components Medical history Physical examination Routine laboratory tests Optional tests

Medical History
Duration and classification of hypertension. Patient history of cardiovascular disease. Family history. Symptoms suggesting causes of hypertension. Lifestyle factors - Ethanol intake. Current and previous medications.

Physical Examination
Blood pressure readings (two or more). Verification in contralateral arm. Height, weight, and waist circumference. Funduscopic examination. Examination of the neck, heart, lungs, abdomen, and extremities. Neurological assessment.

Laboratory Tests Recommended Before Initiating Therapy Urinalysis Complete blood count Blood chemistry (potassium, sodium, creatinine, and fasting glucose) Lipid profile (total cholesterol and HDL cholesterol) 12-lead electrocardiogram

Optional Tests and Procedures
Creatinine clearance Microalbuminuria 24-hour urinary protein Serum calcium Serum uric acid Fasting triglycerides LDL cholesterol Glycosolated hemoglobin

Investigation History and examination Exclude secondary Hypertension Urea and electrolytes FBP and ESR ECG Lipid profile Chest x-ray no longer routinely indicated

The normal radial artery blood pressures in adults are: Systolic arterial pressure: 100 to 140 mmHg. Diastolic arterial pressure: 60 to 90 mmHg. These pressures are called Normal blood pressure or (normo-tensive pressure). Stage I hypertension: systolic (140-159 mmHg) and/or diastolic (90-99 mmHg). Stage II hypertension: systolic (•160 mmHg) and/or diastolic (• 100 mmHg).

BP = TPR * CO Where, BP: blood pressure; TPR: Total peripheral resistance; CO: cardiac output. Where, CO = SV * HR ; SV: stroke volume; HR: Heart rate.

Types of hypertension: ‡In more than 95% of cases a specific underlying cause of hypertension cause of hypertension cannot found. Such patients are said to have (essential hypertension). In reality the problem is probably multi-factorial. Hypertension in approximately 40-60% is explained by genetic factors. Important environmental factors including high salt intake, heavy consumption of alcohol, obesity, and impaired intra-uterine growth.

About 5% of cases, hypertension shown to be a consequence of a specific disease or abnormality leading to Na retention and/or peripheral vasoconstriction (secondary hypertension).

The possible causes : A. Alcohol. B. Pregnancy: Gestational hypertension: blood pressure elevation without protein-uria, that is detected for first time during mid-pregnancy and return to normal by 12 week post-partum Pre-eclampsia /eclampsia: pregnancy specific syndrome with elevated blood pressure that occurs after the first 20 weeks of pregnancy and accompanied by protein-uria and edema. C. Renal diseases: Renal vascular disease (renal artery stenosis) Parenchymal renal disease (glomerulonephritis) Polycystic kidney diseases. Most of the kidney diseases are associated with disorder of renninangiotensin- aldosterome system.

D. Endocrine diseases: 1.Phaechromocytoma: It is mostly benign tumor of the adrenal medulla with increase secretion of epinephrine and nor-epinephrine, so it causes paroxysmal hypertension but may be persist. 2.Cushing syndrome: elevated level of cortisol has mineralo-corticoid effect. 3.Primary hyper-aldosteroe-ism (Conn's syndrome). 4.Primary hypo-thyroid-ism: it is associated with atherosclerosis. 5.Thyrotoxicosis: high thyroid hormone associated with increase in systolic pressure due to increase activity of the heart (increase stroke volume and heart rate) and decrease diastolic pressure due to vasodilatation.

E. Drugs: example oral contraceptives containing estrogen, anabolic steroid, corticosteroids, NSAID, carbenoxolone (is a licensed drug for oesophageal ulceration and inflammation, and treatment of oral and perioral lesion), sympathomimetic agents.

Complications of hypertension: A. Blood vessels: 1.In large vessels (>1mm in diameter): the internal elastic lamina is thickened, smooth muscle hypertrophy, and fibrous tissue deposit. The vessel dilated and become tortuous and their wall become less complains (less elastic which means increase resistance). 2.Smaller arteries (<1mm in diameter): hyaline arteriosclerosis occurs in the wall, lumen narrows and may lead to coronary and/or cerebro-vascular disease. Particularly if risk factors (e.g. smoking, hyper-lipidemia) are present. These structural changes in vasculature often perpetuate and aggravate hypertension by increase peripheral vascular resistance, reduce renal function and induce renal artery stenosis. 3.Hypertension is implicated in the pathogenesis of aortic aneurysm and arotic dissection.

B. Central nervous system: Stroke: is common complication of hypertension and may be due to: cerebral hemorrhage or infarction Carotid atheroma and transient ischemic attack subarachnoid hemorrhage. Hypertensive encephalopathy: it is rare condition characterized by high blood pressure and neurological symptoms including transient disturbance of speech and vision, paraesthesiae, disorientation.

C. Heart: left ventricular hypertrophy atrial fibrillation left ventricular failure. D. Kidney: renal disease may result be result of hypertensive damage to renal vessels. Long standing hypertension may cause protein-uria, and progressive renal failure. E. Retina: hypertensive retino-pathy: long standing hypertension results in compensatory thickening of arterial wall, which effectively reduces capillary perfusion pressure. With sudden increase of blood pressure hemorrhage is likely to occur.

F. Malignant or accelerating hypertension: This rare complicate hypertension of any etiology and is characterized by accelerated micro-vascular damage with necrosis in the wall of small arteries and arterioles (fibrinoid necrosis) and intra-vascular thromosis. The diagnosis is based on evidence of high blood pressure and rapidly progressive end-organ damage such as retino-pathy, renal failure and/or hypertensive encephalo-pathy. Left ventricular failure may occur, and if this is untreated, death occurs within months.

‡Weight reduction and regular aerobic exercise (e.g., walking): ‡Reducing dietary sugar. ‡Reducing sodium (salt) in the body ‡Additional dietary changes beneficial to reducing blood pressure include the DASH diet (dietary approaches to stop hypertension) ‡Discontinuing tobacco use ‡Vasodialators such as niacin. ‡Limiting alcohol intake ‡Reducing stress, for example with relaxation therapy, ‡Increasing omega 3 fatty acids can help lower hypertension. Fish oil is shown to lower blood pressure in hypertensive individuals. The fish oil may increase sodium and water excretion.

Treatment Lifestyle modifications
‡ Lose weight if overweight ‡ Limit alcohol ‡ Increase physical activity ‡ Decrease sodium intake ‡ Keep potassium intake at adequate levels ‡ Take in adequate amounts of calcium and magnesium ‡ Decrease intake of saturated fat and cholesterol ‡ Stop smoking

‡Thiazide diuretics. Diuretics, sometimes called "water pills," are medications that act on your kidneys to help your body eliminate sodium and water, reducing blood volume. Thiazide diuretics are often the first ² but not the only ² choice in high blood pressure medications. If you're not taking a diuretic and your blood pressure remains high, talk to your doctor about adding one or replacing a drug you currently take with a diuretic.

‡Beta blockers. These medications reduce the workload on your heart and open your blood vessels, causing your heart to beat slower and with less force. When prescribed alone, beta blockers don't work as well in blacks or in the elderly ² but they're effective when combined with a thiazide diuretic.

‡Angiotensin-converting enzyme (ACE) inhibitors. These medications help relax blood vessels by blocking the formation of a natural chemical that narrows blood vessels.

‡Calcium channel blockers. These medications help relax the muscles of your blood vessels. Some slow your heart rate. Calcium channel blockers may work better for blacks and older adults than do ACE inhibitors or beta blockers alone. A word of caution for grapefruit lovers, though. Grapefruit juice interacts with some calcium channel blockers, increasing blood levels of the medication and putting you at higher risk of side effects. Talk to your doctor or pharmacist if you're concerned about interactions.

‡Central-acting agents. These medications prevent your brain from signaling your nervous system to increase your heart rate and narrow your blood vessels. ‡Vasodilators. These medications work directly on the muscles in the walls of your arteries, preventing the muscles from tightening and your arteries from narrowing.

Orthostatic (or postural) hypotension (a fall in blood pressure of • 20/10 mmHg from lying to standing position): 1.It is an abnormal drop in blood pressure on assumption of standing position. It is caused by: 1. Reduced blood or fluid volume: as in excessive use of diuretics, loss of GIT fluid (diarrhea and vomiting), and loss of fluid in prolong bed rest. 2. Drugs induce hypotension: anti-hypertensive drugs and psychotropic drugs. 3. Aging: weakness and dizziness on standing are common complaints of elderly persons. Postprandial (after meal) blood pressure often decreases in elderly persons especially after a high-carbohydrate meal.

4. Bed rest and immobility: Prolonged bed rest promotes a reduction in plasma volume, a decrease in venous tone, failure of peripheral vasoconstriction, and weakness of skeletal muscles that support the veins and assist in returning blood to the heart. 5. Disorder of autonomic nervous system function: The sympathetic nervous system plays an essential role in adjustment to upright position. Orthostatic hypotension caused by altered autonomic function is common in peripheral neuro-pathyies associated with diabetes mellitus, after injury or disease of spinal cord, or as result of cerebral vascular accident in which sympathetic outflow from the brain disrupt and finally Parkinson disease with autonomic failure.

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