Week 10- Hypertension PDF

Hypertension NURS 2055: Adult Illness Concepts I Chapter 35 Nursing Management: Hypertension Ainsley Miller, 2024  Hypertension High blood pressure One of the most important modifiable risk factors for cardiovascula...

Hypertension NURS 2055: Adult Illness Concepts I Chapter 35 Nursing Management: Hypertension Ainsley Miller, 2024  Hypertension High blood pressure One of the most important modifiable risk factors for cardiovascular disease (a modifier of diabetes- can cause severe cause of DKA, micro and macrovascular systems, retinopathy, neuropathy) (HYPER TENSION AND A HIGH A1C) As BP increases, so does risk of MI, heart failure, stroke, renal disease look at sodiumlevels hightension on the arteries and vital organs normal BP is 120 80 over magnytohing  Normal Regulation of Blood Pressure Blood pressure – force exerted by the blood against the walls of the blood vessel Must be adequate for tissue perfusion to be maintained during activity and rest WIT BP = CO x SVR howmuch blood your your pumpsinone heart minute Cardiac output g – volume of blood ejected from the heart per minute Stroke volume (amount of blood pumped out of left ventricle per beat) x HR (for 1 minute) Systemic vascular resistance – force opposing the movement of blood within the blood vessels no howhardit is foryourbloodtoflowthroughyourbloodvessels exwatertryingtoflowthroughasmallpipe Small change in radius of arterioles creates major change in SVR itisto the1819 1hesitate Regulation involves nervous, cardiovascular, renal and endocrine functions mightiest Short-term regulation (seconds) – sympathetic nervous system and vascular endothelium Yeighetwhhendp.EEFnedhesi ppaif.de yourbraintellsyourhearttobeatfasterandyourbloodvesse dogs y and hormonal processes regulating EEi esteady Long-term regulation (seconds to hours) – renal arteriolar resistance and blood volume nokidneysandhormonescontrolfluidandvesselsizeforlongertermbalance Factors Influencing Blood Pressure Sympathetic Nervous System Baroreceptors (specialized nerve cells) sense change in BP and transmitted to vasomotor centres in brainstem Located in external and internal carotid arteries and arch of aorta Sensitive to stretching Chronic hypertension causes baroreceptors to adjust to high BPs and consider them “normal” Musset Its like an elastic band, over time it will continue to be over-stretched and wear out. Go Will lose the ability to detect fluctuations of blood pressure once its worn out Reacts within seconds after decrease in arterial pressure Increases heart rate fightorflightF Activates sympathetic nervous system Increases cardiac contractility Widespread vasoconstriction in peripheral arterioles everything is Release of renin from kidneys Ultimately increases CO and SVR increased Sympathetic Nervous System Receptors Influencing Blood Pressure Adrenergic Receptor Location Response When Activated α1 loodvesselsanamamestheneart Vascular smooth muscle Vasoconstriction bigptea.se Heart Increased contractility α2 release Presynaptic membrane Inhibition of norepinephrine release thesystemreduces calms norepinephrine increases Vascular smooth muscle Vasoconstriction hvanabpsandnarrowsbiooonessel T.EE 1 and Heart Increased contractility nsteIiE.is55 Increased heart rate sympathetic Increased conduction Juxtaglomerular cells Increased renin secretion 2 an ii ii Smooth muscle of peripheral blood Vasodilation ie vessels in skeletal muscle, coronary arteries, lungs, kidneys, liver, islet Relaxation Gluconeogenesis cells, bladder Increase in secretion Dopaminergic receptors Primarily kidney and mesenteric Vasodilation blood vessels  Vascular Endothelium yuauumammmtmnnymnmn.n.MG Single cell layer that lines blood vessels Produces vasoactive substances and growth factors Nitric oxide – endothelium-derived relaxing factors Maintain low arterial tone at rest Inhibits growth of smooth muscle layer Inhibits platelet aggregation Endothelin – potent vasoconstrictor produced by endothelial cells Endothelial dysfunction contributes to atherosclerosis and primary hypertension keeps bloodflowingsmoothly makesasubstance stay nitricoxidethathelpsbloodvessels called clots stops prevents bloodausplate fit c g IitInd Fitting Is that block could blood your vessels blood make needed when tighten vessels butit be must careful this too nottodomuch size vessel Regulates itcanalso Renal System Mathew bathePressaby managing Kidneys contribute by controlling sodium excretion and ECF volume Sodium retention results in water ii retention → increased ECF volume Increases venous return to the heart iiiI III.it Increases stroke volume Elevates BP through an increase in CO Renin-angiotensin-aldosterone system (RAAS) EE Prostaglandins E and blood from outtheeffectsofRaas prevent p ressure balance blood can bythekidneysthatcanhelprelax which vessels produce gtheengemjcay.gg  stressor in fightorflightmode Endocrine System whenyourbodyisunder increasingbloodpressure Stimulation of SNS results in release of EpinephrineCat Increases COc by I increasing HR and myocardial contractility heartstrength Activates beta 2-adrenergic receptors in peripheral arterioles of skeletal muscle (ex. lungs) Causing vasodilation Blgodvesseismakingit Fas ñdy.ie Norepinephrineincreaseshrandblood constriction vessels blood raise pressure neping Aldosterone remainingc'iyasagaterinkidneysmoresodiumandwaterinyour bloodstream Retention of sodium and water Increases BP by increasing CO Antidiuretic hormone Reabsorption of water in the kidneysbesttiteaterwhich i ncreases Increase in blood volume results in increase in BP  Sympathetic Nervous System In healthy persons, these regulatory mechanisms function in response to the Vascular demands of the body. Renal Endothelium When hypertension System develops, one or more of the BP-regulating mechanisms are defective Endocrine System Hypertension (KNOW THE NUMBERS AND MOST APPROPRIATE APPROACH) ios Normal BP is SBP < 120 mm Hg and DBP < 80 mm Hg Hypertension – sustained elevation of systemic arterial blood pressure SBP ≥ 140 mm Hg or DBP ≥ 90 mm Hg Stage 1 hypertension SBP 140-159 mm Hg or DBP 90-99 mm Hg Stage 2 hypertension SBP > 160 mm Hg or DBP > 100 mm Hg Hypertensioncrisis Hypertension + diabetes mellitus SBP ≤ 130 mm Hg and DBP ≤ 80 mm Hg Hypertension High BP most significant modifiable risk factor for cardiac disease Small changes in SBP and DBP have direct effect on mortality Hypertension known as “silent killer” Pre-hypertension no a bithigherthannormalBP High-normal BP Annual BP assessment Subtypes of Hypertension Isolated Systolic Hypertension (ISH) than mm Hg with a DBPless 90 mm HgXp Ideal body weight Beingoverweight Family history Excessive alcohol intake Sedentary lifestyle notexersing Subtypes of Hypertension has a reason and can be identified and Secondary Hypertension treated Elevated BP with a specific cause that can be identified and corrected 5-10% hypertension in adults > 80% hypertension in children more commoninchildren Possible causes Coarctation or congenital narrowing of the aorta makes it harder forbloodtoflow Renal disease such as renal artery stenosis and parenchymal disease Endocrine disorders such as Cushing’shighcortisollevels syndrome highaldosterone and hyperaldosteronism Neurological disorders such as brain tumours, quadriplegia and head injury Sleep apnea Medications likebirthcontrolpillsorsteriods develops Pregnancy-induced hypertension that Treatment → eliminate underlying cause 111gBlgeurg  f Pathophysiology of Primary Hypertension For arterial pressure to rise, there must be an increase in either cardiac output or systemic vascular resistance Five's's Bessment m'iitgIthearaeeforPii odor ir 1 Risk factors for primary hypertension catosing Advancing age highbloodpressure Heavy alcohol consumption Cigarette smoking Glucose intolerance (diabetes mellitus) Elevated serum lipids High dietary sodium intake Gender Family history Obesity Ethnicity Sedentary lifestyle Socioeconomic status Psychosocial stress Clinical Manifestations Frequently asymptomatic until severe silent killer Severe hypertension symptoms results from increased workload on heart Fatigue Reduced activity tolerance Dizziness Palpitations Angina Dyspnea  Complications Site of Injury Mechanism of Injury Potential Pathological Effect Myocardium Increased workload combined with diminished blood flow Left ventricular hypertrophy, myocardial ischemia, left through coronary arteries heart failure Coronary arteries Accelerated atherosclerosis (CAD) bind ofplagueitnhe arteries Myocardial ischemia, myocardial infarction, sudden up highblood canaccelerateatherosclerosis pressure death Aorta Weakened vessel wall increase the weakens pressure walls Aneurysms, acute aortic syndromes Kidneys Renin and aldosterone secretion stimulated by reduced Retention of sodium and water, leading to increased blood flow blood volume and perpetuation of hypertension Inflammation and ischemia Tissue damage that comprises filtration High pressures in renal arterioles Nephrosclerosis leading to renal failure Brain Reduced blood flow and oxygen supply; weakened vessel Transient ischemic attack, cerebral thrombosis, walls, accelerated atherosclerosis aneurysm, hemorrhage, acute brain infarction Eyes (retinas) Reduced blood flow Retinal vascular sclerosis High arteriolar pressure Exudation, hemorrhage Arterial vessels of Reduced blood flow and high pressures in arterioles, Intermittent claudication, arterial thrombosis, lower extremities accelerated atherosclerosis gangrene Diagnostic Studies Not based on a single elevated reading Tched Urinalysis ins Requires several BP readings over several weeks Laboratory tests albumin canbeasignorkianeyiss.es Blood chemistry (potassium, sodium, creatinine, blood urea and nitrogen) Fasting blood glucose tocheckfordiabetes Fasting total cholesterol, HDL, LDL, triglyceridesghepgggsh.esshealthandrisk Urinary albumin excretion in patients with diabetes highlevelscan kidney indicate d amage 12-lead ECG natestthatrecordsthe activityotfheheart electrical  Interprofessional Care Risk stratification Periodic monitoring of BP Home BP monitoring Ambulatory BP monitoring measuringover24hrperiod Every 3-6 months once BP is stabilized Nutritional therapy Dietary Approaches to Stop Hypertension (DASH) diet is Fruits, vegetables, low-fat dairy products, dietary and soluble fibre, whole grains, protein Restricted sodium intake (reduce to 2000mg/day) Restricted intake of cholesterol and saturated fats Maintenance of adequate intake of potassium, calcium and magnesium Interprofessional Care Weight management Regular, moderate physical activity Tobacco cessation Moderation in alcohol consumption Stress management Antihypertensive medications Patient and caregiver teaching Primary Hypertension Drug Therapy  Hypertension – Medication Therapy Type Example Action Diuretics waterpill Mechanism of action on sodium/chloride - Thiazide and related diuretics Metalazone, indapamide concentrations causing fluid shifts (water loss) - Loop diuretics Furosemide helpyourbodyget rie.gengrtfettigEierbisoo - Potassium-sparing diuretics Spironolactone pressure Alpha 1-Adrenergic Blockers Doxazosin mesylate; prazosin; Block alpha 1-adrenergic receptors → peripheral phentolamine mesylate vasodilation (decrease SVR + BP)relax blood vessels Beta-Adrenergic Blockers Atenolol, metoprolol, propranolol, Antagonizing beta 1-adrenergic receptors → slowstheheartdown esmolol, carvedilol decrease contractility, HR, conduction, renin Combined alpha and beta-adrenergic Labetalol Alpha 1, beta 1 and beta 2-adrenergic blocking blocker → peripheral vasodilation, decreased HR, CO, SVR, BP Direct vasodilators decreaseBP Hydralazine, nitroglycerin Reduce SVR by arterial vasodilation Angiotensin inhibitors Inhibit ACE - Angiotensin-converting enzyme (ACE) Ramipril, enalapril, perindopril inhibitors Prevent action of A-II → vasodilation - Angiotensin II receptor blockers (ARB) Candesartan, irbesartan, losartan Calcium channel blocker (CCB) Amlodipine, diltiazem, verapamil Block movement of extracellular CA into cells → calciumcalms heart controls vasodilation and decreased SVR  Nursing Implementation Health Promotion Primary prevention of hypertension → lifestyle modifications Majority of hypertension diagnosed on routine screening Take BP 2-3 times, at least 2 minutes apart Record average pressure Ensure proper size BP cuff used for accurate measurement Measure both arms to detect any differences Arm uncovered and placed at level of the heart Nursing Implementation Ambulatory and Home Care Adherence to treatment plan Patient and family teaching Nutritional therapy Medication therapy Physical activity (30 min, moderate intensity, daily) Home monitoring of BP Tobacco cessation Stress management Detecting and reporting of adverse treatment effects Age-Related Considerations Hypertension is common in individuals age 60+. Age-related changes Loss of tissue elasticity Increased collagen content and stiffness of the myocardium Increased peripheral vascular resistance Decreased β-adrenergic receptor sensitivity Blunting of baroreceptor reflexes Decreased kidney function Decreased renin response to sodium and water depletion Age-Related Considerations Often there is a wide gap between the first Korotkoff sound and subsequent beats, called the auscultatory gap. Failure to inflate the cuff high enough may result in seriously underestimating the SBP. Older adults have varying degrees of impaired baroreceptor reflex mechanisms. Start to getworn out and think the highbloodpressure is normal Consequently, orthostatic hypotension occurs often.  so Hypertensive Crisis Severe and abrupt elevation in BP DBP > 120-130 mm Hg Rate of the rise of BP is more important than absolute value in determining the need for emergency treatment Occurs most commonly in patients with a history of hypertension who have failed to adhere to their prescribed medication regimen or who have been undermedicated Can occur from illicit substance use (cocaine, amphetamines, LSD) Hypertensive Crisis Hypertensive emergency = evidence of acute target organ damage Hypertensive encephalopathy Cerebral hemorrhage Acute renal failure Myocardial infarction Acute left ventricular failure with pulmonary edema Dissecting aortic aneurysm Hypertensive urgency = BP severely elevated but there is no clinical evidence of target-organ damage Hypertensive Crisis Clinical Manifestations Manifested as hypertensive Renal insufficiency encephalopathy Minor impairment Headache Complete renal shutdown Nausea Rapid cardiac decompensation Vomiting Unstable angina to infarction Seizures Pulmonary edema Confusion Aortic dissection Stupor Chest and back pain Coma Diaphoresis Blurred vision Loss of pulses in extremity Transient blindness Nursing and Interprofessional Management Hypertensive Crisis Patient assessment extremely important Look at elevated BP in combination with end-organ symptoms Neurological dysfunction Retinal damage Heart failure Pulmonary edema Renal failure Hospitalization required – parenteral administration of antihypertensive medications (vasodilators) and critical care monitoring Determine cause Education to prevent future crisis