Hypertension For Ems Providers
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HYPERTENSION
Paramedic Class 108
Introduction •
Incidence
• 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.
Group 1 Assignment • • • • • •
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.
Blood Pressure Regulation Mechanisms •
•
•
Autonomic Nervous System Kidneys (ReninAngiotensinAldosterone) Endocrine System
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.
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.
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.
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
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.
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
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
Blood Pressure Regulation Mechanisms •
Kidneys (Renin-Angiotensin-Aldosterone
Group 2 Assignment •
Sketch the Renin – Angiotensin –Aldosterone mechanism.
Group 3 Assignment Define • • • •
Hypertrophy Myocardial hypertrophy Starlings Law Peripheral Vascular Resistance
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
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
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
Hypertension Etiology Primary Hypertension •
Patient Home Medications – Cardiac • Beta Blockers • Calcium Channel Blockers • Adrenergic Inhibitors • ACE Inhibitors • ARBS • Diuretics
Group 4 Assignment Home Medications Describe the therapeutic actions for each class & identify several medications that are used. • Beta Blockers • Calcium Channel blockers • ACE Inhibitors ACE? • ARBS –ARBB? • Diuretics
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
Anatomical Damage from Hypertension
Vessels • Kidney • Brain • Heart •
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
Anatomical Damage from Hypertension •
Kidney • Poor perfusion leads to organ damage • Decreased function…failure • In many cases, leads to renal dialysis
Anatomical Damage from Hypertension •
Brain • Stroke/CVA – Cerebral Vascular Accident • TIA – Trans Ischemic Attack
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
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)
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
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
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%
Hypertension Prevention & EMS Role •
EMS has a role in educating the public • Prevention Programs • On-scene Education
Hypertension Prevention & EMS Role •
What to educate: • Lifestyle changes @ early age • Good diet • Reduce cholesterol, lipids, and triglyceride levels • Exercise • Avoid tobacco • Take prescribed medications
Hypertension Prevention & EMS Role •
EMS Activities • FD station BP checks, educate as needed • Organized healthcare screenings, educate as needed • On-scene treatment and education
Group 5 Assignment Scenario: 58 yo female c/o HA dizzy. Ran out of Meds . Propranolol, captopril, valsartan, furosmide, nitroglycerin Are the medications cardiac related? VS. 198/110 92 irreg. 16 non labored Patient History? Your Treatment?
REVIEW Hypertension Signs & Symptoms
QUESTIONS?
Paramedic Class 108
Introduction •
Incidence
• 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.
Group 1 Assignment • • • • • •
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.
Blood Pressure Regulation Mechanisms •
•
•
Autonomic Nervous System Kidneys (ReninAngiotensinAldosterone) Endocrine System
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.
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.
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.
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
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.
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
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
Blood Pressure Regulation Mechanisms •
Kidneys (Renin-Angiotensin-Aldosterone
Group 2 Assignment •
Sketch the Renin – Angiotensin –Aldosterone mechanism.
Group 3 Assignment Define • • • •
Hypertrophy Myocardial hypertrophy Starlings Law Peripheral Vascular Resistance
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
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
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
Hypertension Etiology Primary Hypertension •
Patient Home Medications – Cardiac • Beta Blockers • Calcium Channel Blockers • Adrenergic Inhibitors • ACE Inhibitors • ARBS • Diuretics
Group 4 Assignment Home Medications Describe the therapeutic actions for each class & identify several medications that are used. • Beta Blockers • Calcium Channel blockers • ACE Inhibitors ACE? • ARBS –ARBB? • Diuretics
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
Anatomical Damage from Hypertension
Vessels • Kidney • Brain • Heart •
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
Anatomical Damage from Hypertension •
Kidney • Poor perfusion leads to organ damage • Decreased function…failure • In many cases, leads to renal dialysis
Anatomical Damage from Hypertension •
Brain • Stroke/CVA – Cerebral Vascular Accident • TIA – Trans Ischemic Attack
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
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)
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
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
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%
Hypertension Prevention & EMS Role •
EMS has a role in educating the public • Prevention Programs • On-scene Education
Hypertension Prevention & EMS Role •
What to educate: • Lifestyle changes @ early age • Good diet • Reduce cholesterol, lipids, and triglyceride levels • Exercise • Avoid tobacco • Take prescribed medications
Hypertension Prevention & EMS Role •
EMS Activities • FD station BP checks, educate as needed • Organized healthcare screenings, educate as needed • On-scene treatment and education
Group 5 Assignment Scenario: 58 yo female c/o HA dizzy. Ran out of Meds . Propranolol, captopril, valsartan, furosmide, nitroglycerin Are the medications cardiac related? VS. 198/110 92 irreg. 16 non labored Patient History? Your Treatment?
REVIEW Hypertension Signs & Symptoms
QUESTIONS?
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