• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Hypertension
 

Hypertension

on

  • 1,253 views

What is Blood Pressure. Components of Blood Pressure. Pressure of blood against the walls of the arteries;

What is Blood Pressure. Components of Blood Pressure. Pressure of blood against the walls of the arteries;

Statistics

Views

Total Views
1,253
Views on SlideShare
1,253
Embed Views
0

Actions

Likes
0
Downloads
121
Comments
0

0 Embeds 0

No embeds

Accessibility

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment
  • Let’s review
  • 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 tissue
  • Atherosclerosis- fatty deposits become hard with age Hardening of the arteries
  • 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
  • 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
  • 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 retake
  • Left ventricle becomes enlarged Inability to meet demands Heart Failure Left ventricle becomes enlarged When unable to meet demands =heart failure
  • Intermittent claudiation- Ischemic muscle pain precipitated by activity and relived with rest. Aortic Aneurysm pulsating mass
  • PMH- DM, HTN hyperlipidemia, CAD
  • Abnormal heart sounds: laterally displaced, sustained, forceful apical pulse
  • Uric acid provides a base line- if giving a diuretic these level will be elevated
  • KNOW side effects
  • Diet-low fat, low calorie, sodium reduction, limit alcohol Nicotine increases the heart rate and produces peripheral vasoconstriction

Hypertension Hypertension Presentation Transcript

  • HypertensionGeorge Ann Daniels MS, RN
  • What is Blood Pressure• Components of B/P • Systolic – Force while the heart – Pressure of blood pumps against the walls of the – Pressure as the heart pushes arteries the blood out to the body – Normal >130 – The elasticity of the artery walls • Diastolic – Force between heart pumps – The volume and – Pressure as the heart begins thickness of the blood to fill with blood – Normal >85 • Systolic over diastolic • 120/80
  • 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
  • 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
  • Classifications of Hypertension• Primary – Essential HTN • Slow onset • Asymptomatic – Malignant • Sudden onset • Rapid development of symptoms • Accelerated progression
  • Risk Factors R/T Primary Hypertension • Age/Heredity • Sex • Race • Obesity • Stimulants • Sodium • Alcohol • Stress • Hyperlipidemia • Diabetes • Socioeconomic Status
  • 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
  • Clinical Manifestation • Persistent hypertension • Fatigue • Reduced activity tolerance, • Palpation • Angina • Dyspnea
  • 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
  • • 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
  • 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
  • • Peripheral Vascular Disease (PVD) – Hypertension speeds up Atherosclerosis in the peripheral blood vessels • Aortic aneurysm • Aortic dissection • PVD – C/O • Intermittent claudication
  • • Nephrosclerosis – End stage renal disease – Renal dysfunction • Ischemia – Narrowed intrarenal vessel » Atrophy of tubules » Destruction of glomeruli » Death of nephron – Earliest symptom • nocturia
  • • 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
  • Nursing Assessment Data• Subjective Data FHP 6 – Past medical history/Family Cognitive/perception history Blurred vision – FHP 2 Nutrition • Alcohol use, salt and fat paresthesia intake, wt. gain/loss FHP 9 Sexual/Repro – FHP 3 Elimination Impotence • Nocturia – FHP 4 Activity/Exercise FHP 10 Coping/stress • Fatigue, Dyspnea on Stressful life events exertion, palpitation, angina, chest pain, Noncompliance intermittent claudication, knowledge deficit muscle cramps, smoking history, sedentary lifestyle financial
  • Objective Data• Cardiovascular • Musculoskeletal – Persisted elevated B/P – Truncal obesity – Orthostatic change in B/P – Abnormal waist-hip or pulse ratio – Retinal changes • Neurologic – Abnormal heart sounds – Diminished or absent – Mental status changes, peripheral pulses – Localized edema – Carotid, renal, ischial or femoral bruits – edema
  • Abnormal Diagnostic Test• Lab • ECG – UA, BUN, serum – Left Ventricular Creatinine hypertrophy • Renal involvement – Serum electrolytes • EEG • Potassium – Ischemic heart disease – Hyperaldosteronism – Blood Glucose – Serum cholesterol and triglycerides – Uric acid
  • Medications • Diuretics – Suppresses renal tubular re- absorption of sodium • Diuril – Loop diuretics • Bumex, Lasix, Demadex – Potassium supplement – Potassium sparing diuretic • Aldactone
  • • Beta Blockers – Blocks sympathetic • Peripheral Inhibitors stimulation, decreases renin – Relaxes smooth muscle, secretions, decreases cardiac decreases peripheral output. resistance, decreases • Tenormin, Lopressor, heart rate, and B/P Corgard, Inderal • Resperine• Alpha Inhibitors • Vasodilators – Decreases peripheral vascular – Relaxation of arteriolar resistance, smooth muscle, – Vasodilator vasodilatation, decreases • Catapres cardiac output, decreases• Central Inhibitors peripheral resistance – Decreases cardiac output, • Apresolilne, Nipride peripheral resistance, and heart rate • Aldomet, Tenex
  • • Calcium Channel • Angiotension- Blockers Converting Enzyme – Inhibits calcium into Inhibitors smooth muscle cells, – Decreases peripheral vasodilatation, decreases vascular resistance peripheral resistance, • Lotension, Captoen, increases cardiac output Vasotec, Prinivil, • Norvasc, Cardizem, Accupril Plendil
  • 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.
  • Plan of Care• Health Promotion • Teaching – Life style modifications – Hypertension • Diet • Family/patient • Regular physical activity – Correct technique for taking B/P • Avoid smoking and chewing – ID Risk factors and • Relaxation S& S techniques/stress – Screening programs management – Drug therapy • Drug Therapy • Recommendations for follow-up – Box 31-13
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • • Hypertensive Urgencies – Sit quietly for 20-30 minutes – Oral medications – Encourage patient to verbalize fears R/T hypertension – Follow up in 24 hours
  • 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
  • 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
  • The End