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What is blood pressure?
- Force exerted by blood against artery wall during ventricular contraction (systolic) and ventricular relaxation (diastolic)
- Must be adequate to maintain tissue perfusion during activity and rest
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What are the two main factors that influence blood pressure?
- Cardiac Output
- Systemic Vascular Resistance
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What regulates blood pressure?
- Sympathetic nervous system (if BP is too low, the SNS is stimulated to release epi and norepi which stimulates beta receptors and alpha receptors, resulting in increased BP)
- Cardiovascular system
- Renal system (RAAS)
- Endocrine system (ADH)
- Stimulation of beta receptors increases HR and contractility
- Stimulation of alpha receptors causes vasocontriction
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How do you ensure accurate measurement of blood pressure?
- Recheck questionable readings and dynamap
- Correct cuff size? (too tight, reading will be too high; too loose, reading will be too low)
- Arm supported
- Release valve at steady even pace
- Beware of ausculatory gap
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How does the body recognize changes in blood pressure?
- Baroreceptors (carotid arteries and aortic arch)
- Play an important role in maintenance of BP stability
- In the presence of long-standing HTN, baroreceptors become adjusted to elevated levels of BP and recognize the level as "normal"
- Transmission to vasomotor center in the brainstem
- If BP rises, messages are sent to medulla to inhibit SNS activity. PNS (vagus nerve) assumes control and decreases HR, vasodilation occurs in arteries.
- If BP drops, SNS is activated by release of epi and norepi, HR increases and vasoconstriction occurs
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SNS effect on blood pressure
- Epi and norepi released at terminal end of nerve endings
- Specialized receptors (beta 1&2 and alpha 1&2) are stimulated in SA node, myocardium, and vascular smooth muscle
- Alpha-adrenergic receptors located in vasculature cause vasoconstriction when stimulated by norepi
- Beta-adrenergic receptors located in vasculature cause vasodilation
- Alpha receptors increase contractility
- Beta receptors increase HR and force of contraction
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Renal system and blood pressure
- RAAS activated in response to sympathetic stimulation, decreased blood flow to kidneys, and decreased serum NA concentration
- Renin is excreted by the kidneys and is converted to angiotensin I
- ACE converts angiotensin I to angiotensin II (potent vasoconstrictor) which increases BP and afterload
- Angiotensin II stimulates the adrenal gland to secrete aldosterone which causes sodium and water retention by the kidneys, resulting in increased blood volume, cardiac output, and preload
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What is hypertension?
- Sustained elevation of BP
- Systolic is > or = 140 mmHg and diastolic is > or = to 90 mmHg for extended periods of time
- Diagnosis based on 3 occasions of elevation within a several week period
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What effects does hypertension have on the body?
- High BP means the heart is working harder than normal, both heart and blood vessels are under strain
- Endothelial damage occurs
- Target organ damage
- Cardiomegaly
- Worsens atherosclerosis
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What are hypertensive patients at risk for?
- MI
- CHF
- CVA/stroke
- Renal failure
- PVD
- Retinal damage
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Who is at risk for HTN?
- Increased age
- African-Americans
- More prevalent in men than women
- Women after the age of 55
- Equal risk for men and women from 55-75 years of age and after 75 years of age more prevalent in women.
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What is Primary HTN?
- Elevated BP without an underlying disease
- Accounts for 90-95% of all cases of HTN
- Contributing factors: high sodium diets, obesity, sedentary lifestyles, increased SNS activity (stress, illness), high renin activity, high insulin concentration in bloodstream (stimulates SNS activity)
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What is Secondary HTN?
- Elevated BP with specific underlying cause (identifying and correcting underlying problem will usually correct HTN; ex: pheochromocytoma)
- Main cause of HTN in children (80%)
- Causes: hypokalemia, narrowing of the aorta, tachycardia, renal disease, meds (NSAID’s), neurologic disorders (brain tumors), endocrine disorders (hyperaldosteronism), obstructive sleep apnea
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What is isolated systolic hypertension?
- SBP is elevated but DBP is normal
- Significant risk of stroke and other complications
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Elderly and hypertension
- BP increases as with age due to loss of tissue elasticity, decreased renal function, and increased peripheral vascular resistance
- Strongly familial
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Clinical manifestations of HTN
- May be asymptomatic, also known as “silent killer”, until it causes damage to target organs
- Secondary symptoms: fatigue, decrease in activity, dizziness, palpitations, angina, dyspnea, headache
- Important to teach patient about adherence to medications to control HTN
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Complications (target organ diseases): CAD
- HTN is major risk factor
- Exact mechanism unknown
- Thought to be caused by a disruption of coronary artery endothelium due to high pressures
- Assessment: ask patient if they have any exertional chest pain or dyspnea
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Complications (target organ diseases): Left Ventricular Hypertrophy
- Sustained high pressures increase cardiac workload
- Adaptive mechanism to increase CO by increasing contraction
- Heart failure occurs when the heart can no longer compensate for the increased pressures and demand to supply oxygen Enlarged heart on X-ray, SOB on exertion, fatigue, ECG changes (wide QRS, inverted T wave)
- Assessment: radiology tests, ECHO, Cardiomegaly (displacement of PMI)
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Complications (target organ diseases): CVD
- Atherosclerosis is the most common cause
- Risk for stroke is 4 times higher in people with HTN
- Atherosclerotic plaques in carotid arteries can break off and can travel to the brain causing a TIA or stroke
- Hypertensive encephalopathy may occur after prolonged HTN
- When BP remains high, the cerebral blood vessels dilate producing edema and marked loss of consciousness
- Death may occur from brain damage
- Assessment: neuro checks, history of headaches, stroke or TIA
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Complications (target organ diseases): PVD
- HTN speeds up the process of atherosclerosis in the peripheral blood vessels
- Classic symptom: intermittent claudication (ischemic muscle pain caused by activity, relieved with rest)
- Assessment: weak difficult to palpate pulses, circulatory changes, pain while walking, pale skin, fungus in nails
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Complications (target organ diseases): Nephrosclerosis
- HTN is the leading cause of end-stage renal disease
- Direct result of ischemia caused by the narrowed lumen of intrarenal blood vessels
- Leads to atrophy of the tubules, destruction of the glomeruli, and eventual death of the nephron itself
- Labs: BUN, creatinine, proteinuria, albuminuria, hematuria
- Nocturia is the earliest sign of renal dysfunction
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Complications (target organ diseases): Retinal damage
- The retina is the only place in the body where blood vessels can be directly visualized
- Includes blurring of vision, retinal hemorrhages, loss of vision
- Damage to the retina gives an indication of cardiac vessel damage
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Diagnostic studies for HTN
- Manual BP
- BUN
- Creatinine
- Urinalysis
- Electrolytes
- Blood glucose
- Cholesterol
- ECG (any past MI, conduction defects, LVH)
- ECHO (ejection fraction, heart failure, structural abnormalities)
- Sleep study (destructive sleep apnea)
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JNC-VII: Evidenced based care of HTN
- Important to control isolated systolic HTN
- Thiazide diuretics are first line for most patients
- Adequate control may require drug combinations
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What are the classifications of HTN?
- Normal: SBP < 120 DBP < 80 (encourage healthy lifestyle)
- Prehypertension: SBP 120-139 DBP 80-89 (strongly pursue lifestyle changes)
- Stage 1 HTN: SBP 140-159 or DBP 90-99 (initiate drug therapy, Thiazide = 1st line of treatment)
- Stage 2 HTN: SBP >160 or DBP > 100 (initiate two drug combination)
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AHA 2007 HTN Recommendations
- Target BP <130/80 for Diabetics, CAD, CKD, carotid disease, PAD
- Target BP <120/80 for heart failure patients
- First line agents: Thiazides, ACEI, ARBs, CCBs
- Beta blockers for CHF, angina, post MI
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Lifestyle modifications
- Dietary changes (DASH diet: high K, low Na, high fiber, more fruits and vegetables)
- Limit alcohol consumption (alcohol increases BP)
- Regular physical activity (decreases BP)
- Avoid tobacco use
- Stress management
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Low sodium diet teaching
- Ideal 2g or less per day
- Read labels
- Do not cook with salt
- Avoid using salt shaker
- Try using different spices
- Limit processed, pickled or cured foods
- Be cautious with canned soups, vegetables
- Avoid fast food and salty snacks
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What are the first line agents for HTN?
- Thiazide diuretics (#1)
- ACE inhibitors (prevents conversion of angiotensin I to II, reducing the resultant vasoconstriction)
- ARBs (prevents angiotensin II from binding to receptors in the walls of blood vessels)
- Calcium channel blockers (increases sodium excretion and cause arteriolar vasodilation by preventing movement of extracellular calcium into the cells)
- Beta blockers for certain indications (CAD, CHF, MI; can mask the signs of hypoglycemia and cause bronchospasm so monitor airway/breathing)
- Drug choice influenced by cost, presence of other medical conditions (diabetics should be on ACE inhibitors because protects kidneys), and side effects
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What effect do diuretics have on preload, afterload, and contractility?
- Decreases preload (offloading volume)
- Monitor fluids and electrolytes
- No effect on afterload or contractility
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What effect do beta blockers have on preload, afterload, and contractility?
- Decreases contractility and HR
- Slightly decreases afterload
- Monitor for bradycardia, bronchospasm, and masked symptoms of hypoglycemia
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What effect do calcium channel blockers have on preload, afterload, and contractility?
- Decreases contractility
- Decreases afterload
- Prevents vasoconstriction in periphery
- Monitor for headache, edema, CHF
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Types of calcium channel blockers
- Nondihydroperidines (Verapamil, Diltiazem) - have a direct effect on HR and contractility
- Dihydroperidines (drugs that end in "pine") - decrease contractility and afterload but not HR
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What effect do ACE Inhibitors have on preload, afterload, and contractility?
- Decreases afterload
- Decreases preload
- Blocks vasoconstriction; retains less fluid
- Monitor renal function, potassium, cough, and angioedema
- Drug of choice for diabetics
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Nursing considerations of drug therapy
- Always monitor BP and pulse prior to administration
- Beware of orthostatic hypotension
- Diuretics - monitor for fluid and electrolytes
- Beta blockers - monitor for bradycardia, bronchospasm (caused when beta 2 receptors are blocked), blood glucose (masks hypoglycemia; stimulation of SNS)
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Reasons for lack of responsiveness to drug therapy
- Nonadherence to therapy (ask patient how they are taking their meds, when they take them, why they stopped taking them)
- Drug related causes
- Secondary hypertension
- Pseudohypertension
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What are reasons for non-adherance with HTN meds?
- Cost
- Side Effects (sexual dysfuntion, fatigue, frequent urination)
- Knowledge Deficit
- Lack of Symptoms
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What is Hypertensive Crisis?
- Severe abrupt elevation in BP
- Diastolic > 140 mm Hg
- Etiology: non-compliance (meds, lifestyle modification), drug side effect, rapid withdrawal of antihypertensives (beta blockers, clonidine), ecclampsia, street drugs (cocaine, amphetamines, PCP, LSD)
- Mean arterial pressure (MAP) = SBP + 2(DBP)/3
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What is Hypertensive Emergency?
- Evidence of organ damage
- MI
- Angina
- TIA/CVA
- Encephalopathy (vessels under pressure, causes fluid to leak, cerebral edema)
- Renal Failure
- Aortic Dissection
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What is Hypertensive Encephalopathy?
- Changes in capillary permeability causing cerebral edema
- Symptoms: headache, N/V, seizures, confusion, coma
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Nursing care for hypertensive emergency
- Admit to ICU
- Continuous Monitoring (A-line, Tele, CVP monitor)
- IV nitroprusside via pump (potent vasodilator on venous and arterial side; decreases preload & afterload; titrate to BP)
- Alternative to nitroprusside: Cleviprex (IV calcium channel blocker)
- Gradually reduce MAP: 25% in one hour (too rapid can cause CVA)
- Monitor for signs of target organ damage (frequent neuro exams, EKG, cardiac enzymes, urine output, BUN, Cr)
- Patient education when crisis resolved
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What is Hypertensive Urgency?
- Very high BP with no symptoms
- Treated inpatient, ED or outpatient:
- Monitor response to treatment
- Patient can go home if BP stabilizes
- Requires follow-up within 24 hours
- Can be given oral drugs (Clonidine or Captopril)
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What questions should you ask the patient to determine etiology of a hypertensive crisis?
- Use of illicit substances?
- Use of meds?
- When was last dose?
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Hypertensive Nursing Care
- D - Daily weights
- I - I&O
- U - Urine output
- R - Response of BP
- E - Electrolytes
- T - Take pulses
- I - Ischemic episodes (TIA)
- C - Complications (4 C's: CAD, CRF, CVA, CHF)
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