1. HYPERTENSION
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2. Introduction Incidence Morbidity/Mortality 50 million Americans
1 in 5 Americans or 18%
Undiagnosed 15 million (30% of the 50 million)
1 in 18 Americans or 5%
Morbidity/Mortality
Gender – Male=49.7. Female=50.3
Death Rate (per 100,000) – White Males=14.4, Black Males=49.6, White Females=13.7, and Black Females=40.5.
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3. Define Systolic blood Pressure: Normal
Define Blood Pressure
Define Systolic blood Pressure: Normal
Define Diastolic Blood Pressure: Normal
What are blood pressure perimeters that indicate high pressure.
What are some factors that determine blood pressure. Formula
What factors may affect blood pressure determination.
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4. Blood Pressure Regulation Mechanisms
Autonomic Nervous System
Kidneys (Renin-Angiotensin-Aldosterone)
Endocrine System
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5. RENIN
An enzyme released by the kidney that stimulates production of angiotensin.
A protein secreted by the kidneys that raises blood pressure back to normal when it begins to fall.
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6. ALDOSTERONE
The main electrolyte-regulating hormone secreted by the adrenal cortex: primarily controls sodium and potassium balance.
Released by the adrenal glands that increases blood pressure by signaling the kidneys to retain sodium, which increases blood volume.
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7. Angiotensin
A peptide that is produced by a biochemical reaction caused by the enzyme Renin.
Hormone that has two forms: angiotensin I which is inactive and angiotensin II which is the active form. The latter raises blood pressure by causing arteries to constrict and triggering the release of aldosterone.
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8. Renin-Angiotensin KNOW THIS
Renin stimulates formation of angiotensin I:
Then converts to angiotensin II
Angiotensin II is a potent vasoconstrictor
Stimulates ADH secretion
Results in:
Reabsorption of sodium and water
Elevation in blood pressure
Activation of renin-angiotensin system
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9. ADH
ADH is a hormone released by pituitary gland but made elsewhere (in the hypothalamus). ADH has an antidiuretic action; it suppresses the rate of urine production. ADH is also known as vasopressin.
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10. Blood Pressure Regulation Mechanisms
Autonomic Nervous System
Baroreceptors – Measure stretch (heart, great vessels)
Chemoreceptor's – Measure hypoxemia, acidosis…pH & PO2 (carotid, aortic bodies)
Results in vessel dilation or constriction
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11. Blood Pressure Regulation Mechanisms
Kidneys (Renin-Angiotensin-Aldosterone)
Decreased BP
Renin secreted by kidneys. Works on angiotensinogen to produce angiotensin I
Angiotensin I converted to angiotensin II by angiotensin converting enzyme (ACE)
Vasoconstriction & secretion of aldosterone and ADH (AKA: Vasopressin)
Results in water and sodium retention and higher blood pressure
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12. Blood Pressure Regulation Mechanisms
Kidneys (Renin-Angiotensin-Aldosterone
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13. Sketch the Renin – Angiotensin –Aldosterone mechanism.
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14. Myocardial hypertrophy Starlings Law Peripheral Vascular Resistance
Define
Hypertrophy
Myocardial hypertrophy
Starlings Law
Peripheral Vascular Resistance
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15. CHF, HTN, & Renal Failure
Long term untreated HTN leads to hypertrophy (LV).
The Starling effect is compromised and the LV is not fully emptied during systole.
Decreased Stroke Volume (SV) and Cardiac Output (CO).
Blood backs up causing CHF
Less cardiac output = major organs (vessels, kidneys, brain, eyes) not adequately perfuse
Cells are then damaged, begin to fail, and die
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16. Hypertension Development Recognized Factors
CAD
Age
Heredity
Ethnicity
African-Americans, Puerto Ricans, Cubans, Hispanics
Diet
Cholesterol
Fats
Sodium
Weight
Obesity
Smokeless Tobacco Users
Stress/Type A Personalities
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17. Hypertension Etiology Primary Hypertension
No specific identifying cause
Arteriole wall vasoconstriction, wall damage
Many risk factors
Develops over years
May or may not be symptomatic
Treatment aimed at lowering BP through diet and medications
Patient Home Medications - Cardiac
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18. Hypertension Etiology Primary Hypertension
Patient Home Medications – Cardiac
Beta Blockers
Calcium Channel Blockers
Adrenergic Inhibitors
ACE Inhibitors
Diuretics
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19. Calcium Channel blockers ACE Inhibitors ACE? Diuretics
Describe the therapeutic actions for each class & identify several medications that are used.
Beta Blockers
Calcium Channel blockers
ACE Inhibitors ACE?
Diuretics
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20. Hypertension Etiology Secondary Hypertension
Often has an identifying cause
10% of hypertension cases
Abrupt onset
Commonly renal in origin
Renal artery stenosis
Polycystic disease
Fibro-muscular disease of renal artery
Adrenal tumors
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21. Anatomical Damage from Hypertension
Vessels
Kidney
Brain
Heart
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22. Anatomical Damage from Hypertension
Vessels
Large vessels – Sclerosis (hardened)
Narrowed lumen – tunica media hypertrophy, tunica intima with endothelium damage (allows vascular content leakage)
Lose of elasticity
Decreased blood flow
Occlusion, tear, rupture (aneurysm)
Increased PVR
Aorta – Weakens and leads to aneurysms
Small vessels
Damage to intima layer
Scar tissue
Fibrin strands/clot formation
Obstruction
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23. Anatomical Damage from Hypertension
Kidney
Poor perfusion leads to organ damage
Decreased function…failure
In many cases, leads to renal dialysis
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24. Anatomical Damage from Hypertension
Brain
Stroke/CVA – Cerebral Vascular Accident
TIA – Trans Ischemic Attack
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25. Anatomical Damage from Hypertension
Heart
As described earlier
AMI
Vessel obstruction from poor blood flow (coronaries)
Hypertrophy
Outgrows blood supply
Smaller chamber size
Decreased CO – Incomplete LV emptying
CHF – Congestive Heart Failure (result of increased PVR)
Poor perfusion of other organs, related to CO
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26. Pre-hospital Hypertensive Crisis
Pathophysiology can cause intercerebral or subarchnoid bleeding and cerebral infarcts
Cerebral edema
BP generally greater than 100 mmHg diastolic
Other key organs can be damaged as well
Common cause is sudden discontinuation of HTN medications
Pregnancy Induced Hypertension is a common cause (5% of pregnancies)
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27. Pre-hospital Hypertensive Crisis
Signs/Symptoms – Marked BP Elevation
Headache
Nausea
Vomiting
Confusion
Restless
Seizure
Stroke
Coma
Frequent LOC checks
AMI
Arrhythmias
EKG monitoring
Nosebleeds
Airway issues
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28. Pre-hospital Hypertensive Crisis Management
Rapid lowering of BP can be dangerous
Slow lowering (2-6 hours) of BP is preferred
Ischemia and infarct is possible
Nitroprusside
Nitroglycerine is not preferred in the EMS environment
Pre-hospital therapies:
Airway control, as needed
Calm, reassure patient
Oxygenation & Ventilation
IV – TKO
EKG Monitoring
LOC reassessment
Vital signs
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29. Long Term Treatment of Hypertension
Slight decrease (5%) in BP will decrease the risk of stroke by 35-40%
Adequate treatment of high blood pressure will decrease:
Heart failure 52% (Higher risk for CHF)
Often develops into CHF 91%
Stroke 38%
LV Hypertrophy 35%
Cardiovascular Mortality 21%
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30. Hypertension Prevention & EMS Role
EMS has a role in educating the public
Prevention Programs
On-scene Education
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31. Hypertension Prevention & EMS Role
What to educate:
Lifestyle early age
Good diet
Reduce cholesterol, lipids, and triglyceride levels
Exercise
Avoid tobacco
Take prescribed medications
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32. Hypertension Prevention & EMS Role
EMS Activities
FD station BP checks, educate as needed
Organized healthcare screenings, educate as needed
On-scene treatment and education
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33. REVIEW
Hypertension
Signs
&
Symptoms
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