Hypertension

1. Hypertension George Ann Daniels MS, RN Let’s reviewLet’s review

2. What is Blood Pressure Components of B/P Pressure of blood against the walls of the arteries The elasticity of the artery walls The volume and thickness of the blood Systolic Force while the heart pumps Pressure as the heart pushes the blood out to the body Normal >130 Diastolic Force between heart pumps Pressure as the heart begins to fill with blood Normal >85 Systolic over diastolic 120/80

3. What is Hypertension Is the result of persistent high arterial blood pressure which may cause damage to the vessels and arteries of the Heart Brain Kidneys Eyes B/P > 140/90 Heart- works harder, damage the heart muscle- Heart failure-muscle is overused and loses its elascitity and the heart expands like a out of shape rubber band Heart arteries become blocked leading to MI Brain- arteries in the brain become blocked or the pressure will burst blood vessels in the brain=stroke Kidneys- tiny vessels in the kidneys become blocked. Kidney can no longer remove wastes, kidney failure body becomes toxic Eyes- blindness of impaired vision- tiny blood vessels rupture or become blocked, damaging the surrounding eye tissueHeart- works harder, damage the heart muscle- Heart failure-muscle is overused and loses its elascitity and the heart expands like a out of shape rubber band Heart arteries become blocked leading to MI Brain- arteries in the brain become blocked or the pressure will burst blood vessels in the brain=stroke Kidneys- tiny vessels in the kidneys become blocked. Kidney can no longer remove wastes, kidney failure body becomes toxic Eyes- blindness of impaired vision- tiny blood vessels rupture or become blocked, damaging the surrounding eye tissue

4. Damage to arteries HTN arterial walls thicken Narrowing the opening inside the artery and reduces/block blood flow Persistent HTN arterial walls become rough Easy for plaque is collect inside the artery Decreased/blocked blood flow Plaque can become mobile Fatty emboli Atherosclerosis- fatty deposits become hard with age Hardening of the arteriesAtherosclerosis- fatty deposits become hard with age Hardening of the arteries

6. Classifications of Hypertension Primary Essential HTN Slow onset Asymptomatic Malignant Sudden onset Rapid development of symptoms Accelerated progression

7. Risk Factors R/T Primary Hypertension Age/Heredity Sex Race Obesity Stimulants Sodium Alcohol Stress Hyperlipidemia Diabetes Socioeconomic Status Age/ Loss of arterial elasticity, >65 years, increased collagen content, increased vascular resistance heredity-, Close relatives Sex/Race- men (female >55 yrs), African-Americans Obesity- central abdominal obesity- increases cardiac workload and strains the vessels Stimulants- Smoking/caffeine-vasoconstrictors Sodium- water retention causes volume expansion/ decreases effects of certain B/P meds Hyperlipidemia- plaque in the vessels Diabetes- elevated glucose, insulin, and lipoprotein metabolism Socioeconomic-lower and less educated Age/ Loss of arterial elasticity, >65 years, increased collagen content, increased vascular resistance heredity-, Close relatives Sex/Race- men (female >55 yrs), African-Americans Obesity- central abdominal obesity- increases cardiac workload and strains the vessels Stimulants- Smoking/caffeine-vasoconstrictors Sodium- water retention causes volume expansion/ decreases effects of certain B/P meds Hyperlipidemia- plaque in the vessels Diabetes- elevated glucose, insulin, and lipoprotein metabolism Socioeconomic-lower and less educated

8. Secondary Hypertension Underlying cause that impairs peripheral blood flow, alters cardiac output, or increases blood viscosity Most common Renal failure Other causes Endocrine, Coarctation, neurological, sleep apnea, medications/stimulants, PIH Treat cause and hypertension resolves Coarctation- narrowing of aorta congential Endocrine-Cushing’s, Phenochromocytoma (deficiency in an enzyme essential to fat metabolism-lipoprotein, Hyperaldosteronism Neurological-brain tumors, quadriplegia, head injury Coarctation- narrowing of aorta congential Endocrine-Cushing’s, Phenochromocytoma (deficiency in an enzyme essential to fat metabolism-lipoprotein, Hyperaldosteronism Neurological-brain tumors, quadriplegia, head injury

9. Clinical Manifestation Persistent hypertension Fatigue Reduced activity tolerance, Palpation Angina Dyspnea Past thinking: epitaxis, vertigo, lightheadedness, occipital headache, are not increased in hypertension than in the general population. White Coat syndrome- elevated blood pressure. Rest 20-30 minutes then retakePast thinking: epitaxis, vertigo, lightheadedness, occipital headache, are not increased in hypertension than in the general population. White Coat syndrome- elevated blood pressure. Rest 20-30 minutes then retake

10. Complications Hypertensive Heart Disease Coronary Artery Disease Hypertension is a major risk factor for CAD Left Ventricular Hypertrophy (LVH) Increased resistance in the arteries Stiffness and narrowing of vessels Left heart works harder pumping against higher pressure Increases myocardial work and 02 consumption Left ventricle becomes enlarged Inability to meet demands Heart Failure Left ventricle becomes enlarged When unable to meet demands =heart failureLeft ventricle becomes enlarged Inability to meet demands Heart Failure Left ventricle becomes enlarged When unable to meet demands =heart failure

11. Heart Failure Heart can no longer pump enough blood to meet the metabolic needs of the body Contractility depressed Stroke volume and cardiac output decreases C/O SOB on exertion, paroxysmal nocturnal dyspnea and fatigue

12. Complications Con’t Cerebrovascular Disease (CVA) Most common cause Atherosclerosis Portions of plaque or a blood clot (forms on plaque) breaks off Thromboembolism Travels to intracerebral vessels Stops the flow of blood to parts of the brain Aneurysms burst R/T increased pressure Hemorrhage Brain tissue damage

13. Peripheral Vascular Disease (PVD) Hypertension speeds up Atherosclerosis in the peripheral blood vessels Aortic aneurysm Aortic dissection PVD C/O Intermittent claudication Intermittent claudiation- Ischemic muscle pain precipitated by activity and relived with rest. Aortic Aneurysm pulsating massIntermittent claudiation- Ischemic muscle pain precipitated by activity and relived with rest. Aortic Aneurysm pulsating mass

14. Nephrosclerosis End stage renal disease Renal dysfunction Ischemia Narrowed intrarenal vessel Atrophy of tubules Destruction of glomeruli Death of nephron Earliest symptom nocturia

15. Retinal Damage Red flag Damage to retinal vessels may indicate vessel damage in the heart, brain, and kidney C/O Blurred vision Retinal hemorrhage Loss of vision

16. Nursing Assessment Data Subjective Data Past medical history/Family history FHP 2 Nutrition Alcohol use, salt and fat intake, wt. gain/loss FHP 3 Elimination Nocturia FHP 4 Activity/Exercise Fatigue, Dyspnea on exertion, palpitation, angina, chest pain, intermittent claudication, muscle cramps, smoking history, sedentary lifestyle FHP 6 Cognitive/perception Blurred vision paresthesia FHP 9 Sexual/Repro Impotence FHP 10 Coping/stress Stressful life events Noncompliance knowledge deficit financial PMH- DM, HTN hyperlipidemia, CADPMH- DM, HTN hyperlipidemia, CAD

17. Objective Data Cardiovascular Persisted elevated B/P Orthostatic change in B/P or pulse Retinal changes Abnormal heart sounds Diminished or absent peripheral pulses Carotid, renal, ischial or femoral bruits edema Musculoskeletal Truncal obesity Abnormal waist-hip ratio Neurologic Mental status changes, Localized edema Abnormal heart sounds: laterally displaced, sustained, forceful apical pulse Abnormal heart sounds: laterally displaced, sustained, forceful apical pulse

18. Abnormal Diagnostic Test Lab UA, BUN, serum Creatinine Renal involvement Serum electrolytes Potassium Hyperaldosteronism Blood Glucose Serum cholesterol and triglycerides Uric acid ECG Left Ventricular hypertrophy EEG Ischemic heart disease Uric acid provides a base line- if giving a diuretic these level will be elevatedUric acid provides a base line- if giving a diuretic these level will be elevated

19. Medications Diuretics Suppresses renal tubular re-absorption of sodium Diuril Loop diuretics Bumex, Lasix, Demadex Potassium supplement Potassium sparing diuretic Aldactone

20. Beta Blockers Blocks sympathetic stimulation, decreases renin secretions, decreases cardiac output. Tenormin, Lopressor, Corgard, Inderal Alpha Inhibitors Decreases peripheral vascular resistance, Vasodilator Catapres Central Inhibitors Decreases cardiac output, peripheral resistance, and heart rate Aldomet, Tenex Peripheral Inhibitors Relaxes smooth muscle, decreases peripheral resistance, decreases heart rate, and B/P Resperine Vasodilators Relaxation of arteriolar smooth muscle, vasodilatation, decreases cardiac output, decreases peripheral resistance Apresolilne, Nipride

21. Calcium Channel Blockers Inhibits calcium into smooth muscle cells, vasodilatation, decreases peripheral resistance, increases cardiac output Norvasc, Cardizem, Plendil Angiotension-Converting Enzyme Inhibitors Decreases peripheral vascular resistance Lotension, Captoen, Vasotec, Prinivil, Accupril KNOW side effectsKNOW side effects

22. Expected Outcomes Patient will achieve and maintain desired B/P Patient will understand, accept, and implement the therapeutic plan for B/P Patient will experience minimal or no side effects from therapy Patient will exhibit a confident ability to manage and cope with hypertension.

23. Plan of Care Health Promotion Life style modifications Diet Regular physical activity Avoid smoking and chewing Relaxation techniques/stress management Drug Therapy Teaching Hypertension Family/patient Correct technique for taking B/P ID Risk factors and S& S Screening programs Drug therapy Recommendations for follow-up Box 31-13 Diet-low fat, low calorie, sodium reduction, limit alcohol Nicotine increases the heart rate and produces peripheral vasoconstrictionDiet-low fat, low calorie, sodium reduction, limit alcohol Nicotine increases the heart rate and produces peripheral vasoconstriction

24. Hypertensive Crisis Severe and abrupt elevation in B/P Diastolic of 120-130 Non-compliant patients Cocaine or crack users PCP, LSD Causes listed in table 31-15

25. Types of Hypertensive Crisis Hypertensive Emergency Develops over hours to days Evidence of damage to acute target organ CNS Hypertensive encephalopathy, intracranial or subarachnoid hemorrhage, acute left ventricular failure with pulmonary edema, myocardial infarction, renal failure, and dissecting aortic aneurysm Hypertensive Urgency Develops over days to weeks No evidence of target organ damage

26. Assessment data Sudden rise in arterial pressure seen in Hypertensive Encephalopathy HA, Nausea, Vomiting, Seizures, Confusion, Stupor, Coma Other common Blurred vision and transient blindness Renal insufficiency Minor to complete renal shut down Rapid cardiac decomposition Unstable angina to MI Pulmonary edema Chest pain and dyspnea Neurological Change in LOC

27. Diagnostic Mean arterial pressure (MAP) DBP plus pulse pressure(SBP minus DBP) MAP = DBP + 1/3 Pulse Pressure Goal decrease MAP 10-20% in the first 1-2 hours Patients with aortic dissection, unstable angina, or sign of MI Must have SBP lowered to l00-120 mm Hg asap

28. Medications IV Meds for Hypertensive Emergency Vasodilators Nipride (most effective), Nitroglycerin, Hyperstat, Apresoline Alpha Inhibitors Regitine, Normodyne, Brevibloc Ace Inhibitors Vasotec Meds for Hypertensive Urgency Oral agents Capoten, Catapres

29. Plan of Care Hypertensive Emergency Administer IV meds with rapid onset of action B/P Q 2-3 minutes Medication is titrated according to B/P Prevent hypotension Stroke, MI, visual changes Monitor ECG Hourly output Bedrest Neurochecks

30. Hypertensive Urgencies Sit quietly for 20-30 minutes Oral medications Encourage patient to verbalize fears R/T hypertension Follow up in 24 hours

31. Pediatric Considerations Most common secondary to a structural abnormality or underlying pathologic process Manifestations Adolescents/older children Frequent HA, dizziness, visual changes Infants/young children Irritability, head banging/head rubbing, wake up screaming at night

32. Treatment Diagnosis of underlying cause Surgery correction Life style changes Low salt diet, wt loss, exercise, avoid stress, avoid smoking Avoidance of BCP Education Orthostatic hypotension Take drug as prescribed Awarness of side effects and what to do Avoid alcohol Stay on diet

33. The End