Hypertension and Shock Overview Guide
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JamilHypertension and Shock Overview Guide
Uploaded by
JamilDone by
Jamil Mourad
Supervised by
Dr. Sahar Shammah
Hypertension Shock (Hypotension)
Classification Classification
Determinants of BP Etiology
Regulation of BP Signs and symptoms
Signs and symptoms Pathophysiology
Pathophysiology Treatment
Etiology
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 x Peripheral resistance
Hypertension = Increased CO and/or Increased PR
Vasoconstriction
Preload Contractility
Heart rate
Fluid volume
Sympathetic Renin-
nervous angiotensin-
Renal sodium aldosterone
system
retention system
Excess Genetic
sodium factors
intake
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 Prolonged
◦ Shock, thirst, agitation, ◦ Decreased
restlessness responsiveness in body
◦ Often missed ◦ Compensated metabolic
2nd signs acidosis progresses to
decompensated
◦ Cool, moist, pale skin;
tachycardia; oliguria ◦ Acute renal failure
◦ Compensation
◦ Vasoconstriction
Direct effects
◦ Decrease BP and blood
flow
◦ Acidosis
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
