Done by Jamil Mourad Supervised by Dr. Sahar Shammah
Hypertension
Classification Determinants of BP Reg...
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Done by Jamil Mourad Supervised by Dr. Sahar Shammah
Hypertension
Classification Determinants of BP Regulation of BP Signs and symptoms Pathophysiology Etiology Treatment
Shock (Hypotension)
Classification Etiology Signs and symptoms Pathophysiology Treatment
Persistently high arterial blood pressure, defined as systolic blood pressure above 140 mm Hg and/or diastolic blood pressure above 90 mm Hg It is one of the most common cardiovascular diseases It is estimated that 50% of middle aged persons have hypertension
Practice guidelines for primary care physicians: 2003 ESH/ESC
1.Blood volume 2.Vascular resistance to pressure 3.Heart stroke volume
■
Amount of blood pumped by heart (vol/min)
■ Stroke volume times heart rate
■ Viscosity of blood ■ Width of vessels—(constriction or dilation) —controlled by muscle tone in vessel walls
Blood pressure
=
Cardiac output
Hypertension
=
Increased CO
x
Peripheral resistance
and/or
Increased PR
Vasoconstriction Preload
Contractility Heart rate
Fluid volume Sympathetic nervous system
Renal sodium retention Excess sodium intake
Genetic factors
Reninangiotensinaldosterone system
Asymptomatic in early stages
Initial signs vague and nonspecific ◦ Fatigue ◦ Dizziness ◦ Morning headache
The condition is discovered during routine screening or when patient seeks medical advice for its complications which may be fatal
That’s why hypertension is called “the silent killer”
Increased BP
Insidious onset, mild symptoms and signs
3 major categories ◦ Essential (primary) 90-95% No known cause Multifactorial nature
◦ Secondary Identified source Renal disease is the most common cause
◦ Malignant Pheochromocytoma, increased secretion of catecholamines from a chromaffin tumor
Develops when BP consistently over 140/90
Over long time, high BP damages arterial walls ◦ Sclerosis, decreased lumen ◦ Wall may dilate, tear Aneurysm
Areas most frequently damaged: ◦ Kidneys, brain, retina
End result of poorly controlled hypertension: ◦ ◦ ◦ ◦
Chronic renal failure Stroke Loss of vision CHF
Increases with age Males more frequent and severe Genetic factors High sodium ion intake Excessive alcohol Low K, Ca, Mg intake Obesity Prolonged, recurrent stress Lack of exercise
Genetic Factors in Hypertension
Heritability estimates for systolic and diastolic blood pressure range from 20% to 40%.
A number of genes responsible for rare hypertension syndromes have been identified
Genome scans have implicated regions that may contain genes that underlie susceptibility to essential hypertension.
Coarctation of the aorta
Renal abnormalities
Abnormalities of the renin-angiotensin system
Adrenal gland disorders
Neurologic disorders
Relation to insulin resistance
Treated in sequence of steps ◦ Life style changes ◦ Mild diuretics, ACE inhibitors ◦ One or more drugs added
Patient compliance is an issue
Prognosis depends on treating underlying problems and maintaining constant control of BP
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
Diuretics —Thiazides —Loop diuretics —Potassium-sparing diuretics
Beta blockers Alpha1 receptor blockers ACE inhibitors Angiotensin II receptor antagonists Calcium antagonists Direct vasodilators
Results from decreased circulating blood volume ◦ General hypoxia ◦ Low CO
Hypovolemic shock ◦ Loss of blood, plasma Burn pts, dehydration
Cardiogenic shock ◦ Associated with cardiac impairment
Distributive shock ◦ Blood relocated B/C vasodilation Anaphylactic shock Neurogenic shock
Septic shock ◦ Severe infection
1st signs ◦ Shock, thirst, agitation, restlessness ◦ Often missed
2nd signs ◦ Cool, moist, pale skin; tachycardia; oliguria ◦ Compensation ◦ Vasoconstriction
Direct effects ◦ Decrease BP and blood flow ◦ Acidosis
Prolonged ◦ Decreased responsiveness in body ◦ Compensated metabolic acidosis progresses to decompensated ◦ Acute renal failure
BP decreases when blood volume, heart contraction, or periph resistance fails Low CO, microcirculation ◦ = decreased oxygen, nutrients for cells
Compensation mechanism ◦ ◦ ◦ ◦ ◦
SNS, adrenal medulla stimulated Renin secreted Increased secretion of ADH Secretion of glucocorticoids Acidosis stimulates respiration
Complications of decompensation of shock ◦ Acute renal failure ◦ Adult respiratory distress syndrome (ARDS) ◦ Hepatic failures ◦ Hemorrhagic ulcers ◦ Infection of septicemia ◦ Decreased cardiac function
Primary problem must be treated Hypovolemic shock ◦ Whole blood, plasma, electrolytes, bicarbonate required
Anaphylactic shock ◦ Antihistamines, corticosteroids
Septic ◦ Antimicrobials, glucocorticoids
Maximize oxygen supply Epinephrine reinforces heart action and vasoconstriction Dopamine, dubutamine increase heart function Good prognosis in early stages Mortality increases as irreversible shock develops
Stephen J. MacPhee, MD. Pathophysiology of Disease, 5th ed. Appleton and Lange, 2006; 11: 316-325 Michael L. Bishop, MS, CLS, MT(ASCP). Clinical Chemistry, 5th ed. Lippincott Williams & Wilkins, 2005; Jorde Carey,PhD. Medical Genitecs, 3rd ed. Mosby, 2006; 12: 260-268 Cardiovascular Disorders. Chapter 18. Pgs 285-308 Medical Nutrition Therapy in Hypertension. Chapter 36 JORGE POLÓNIA. Hipertensão
