1. 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
  2. What are the two main factors that influence blood pressure?
    • Cardiac Output
    • Systemic Vascular Resistance
  3. 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
  4. 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
  5. 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
  6. 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
  7. 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
  8. 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
  9. 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
  10. What are hypertensive patients at risk for?
    • MI
    • CHF
    • CVA/stroke
    • Renal failure
    • PVD
    • Retinal damage
  11. 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.
  12. 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)
  13. 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
  14. What is isolated systolic hypertension?
    • SBP is elevated but DBP is normal
    • Significant risk of stroke and other complications
  15. Elderly and hypertension
    • BP increases as with age due to loss of tissue elasticity, decreased renal function, and increased peripheral vascular resistance
    • Strongly familial
  16. 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
  17. 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
  18. 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)
  19. 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
  20. 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
  21. 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
  22. 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
  23. 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)
  24. 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
  25. 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)
  26. 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
  27. 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
  28. 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
  29. 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
  30. What effect do diuretics have on preload, afterload, and contractility?
    • Decreases preload (offloading volume)
    • Monitor fluids and electrolytes
    • No effect on afterload or contractility
  31. 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
  32. 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
  33. 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
  34. 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
  35. 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)
  36. 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
  37. What are reasons for non-adherance with HTN meds?
    • Cost
    • Side Effects (sexual dysfuntion, fatigue, frequent urination)
    • Knowledge Deficit
    • Lack of Symptoms
  38. 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
  39. 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
  40. What is Hypertensive Encephalopathy?
    • Changes in capillary permeability causing cerebral edema
    • Symptoms: headache, N/V, seizures, confusion, coma
  41. 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
  42. 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)
  43. 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?
  44. 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)
Card Set
HTN Med-Surg I Quiz 3