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PNUR 1700 FA 2024 Week 4 HTN and Atherosclerosis MI.pptx

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The Cardiovascula r System Erin K. Smith Friesen RN, BScN, MN(NP) Thompson Rivers University Hypertension 1 in 5 adult Canadians has high blood pressure Persistent elevation of: Systolic blood pressure ≥140 mm Hg or Diast...

The Cardiovascula r System Erin K. Smith Friesen RN, BScN, MN(NP) Thompson Rivers University Hypertension 1 in 5 adult Canadians has high blood pressure Persistent elevation of: Systolic blood pressure ≥140 mm Hg or Diastolic blood pressure ≥90 mm Hg or Current use of antihypertensive medication(s) Hypertension (cont’d) Prevalence increases with age Canadians of African descent and Indigenous people have a higher prevalence of stroke, heart disease and end-stage renal disease South Asians have a risk three times higher than the general population of developing HTN More prevalent in men than women until age 55; after Blood Pressure Classification Hypertension: Subtypes Isolated systolic hypertension Sustained elevation of SBP ≥ 140 mmHg and a DBP < 90 mmHg Common in older adults related to loss of elasticity in large arteries Pseudohypertension Can occur with sclerosis of the large arteries Osler’s sign Hypertension: Etiology Primary 90-95% of clients Focus on primary related to prevalence in clinical practice Secondary 5-10% in adults; > 80 % in children Many causes; treatment aimed at eliminating the underlying cause Primary Hypertension Primary (essential) hypertension Contributing factors: ↑ SNS activity ↑ Sodium retaining hormones and vasoconstrictors Diabetes mellitus > Ideal body weight ↑ Sodium intake Excessive alcohol intake Primary Hypertension: Risk Factors Age Alcohol & cigarette smoking Diabetes mellitus Elevated serum lipids Excess dietary sodium Gender & Family History Obesity Ethnicity Sedentary life style Socioeconomic Primary Hypertension: Heredity Pathophysiology Water and sodium retention Altered renin-angiotensin mechanism Stress and increased sympathetic nervous system activity Insulin resistance and hyperinsulinemia Endothethelial cell dysfuntion Primary Hypertension Clinical Manifestations Referred to as the Symptoms are “silent killer” often secondary because clients to target organ are frequently disease and can asymptomatic include until target organ Fatigue, reduced disease occurs activity tolerance Dizziness Palpitations, angina Dyspnea Hypertension: Target-Organ Diseases Most common complications are target-organ diseases Complete details in textbook: Hypertensive heart disease Cerebrovascular disease Peripheral vascular disease Nephrosclerosis Retinal damage Hypertension: Diagnostic Studies Several readings over several weeks Basic laboratory studies – table in textbook Serum electrolytes, especially potassium, important in detecting hyperaldosteronism, cause of secondary hypertension Other: Blood glucose, serum cholesterol, triglyceride, ECG Hypertension: Collaborative Care Encourage proper monitoring Annual assessment including cardiac risk Lifestyle modifications “Treat to target” Combination of drugs (textbook) & lifestyle changes Regular monitoring Focus on adherence Primary Hypertension: Planning Overall goals: Achieve & maintain target BP Therapeutic plan Minimal or no unpleasant side effects Confident of ability to manage and cope with condition Hypertension: Age-Related Considerations Isolated systolic hypertension (ISH) is the most common form of hypertension in individuals age 50+ The lifetime risk of developing hypertension is approximately 90% for middle-aged (age 55 to 65) and older (age 65+) normotensive men and women Hypertension: Age-Related Considerations Older adults(cont ’d) to have are more likely “white coat” hypertension Often 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 Consequently, orthostatic hypotension occurs often especially in clients with ISH Hypertensive Severe, abrupt Crisis increase in DBP (defined as >140 mm Hg) Rate of increase in BP is more important than the absolute value Often occurs in clients with a history of HTN who have failed to comply with medications or who Hypertensive Crisis: Clinical Manifestations Hypertensive emergency = evidence of acute target organ damage: Hypertensive encephalopathy, cerebral hemorrhage Acute renal failure Myocardial infarction Heart failure with pulmonary edema Hypertensive Crisis: Nursing and Collaborative IV drug therapy: Management Titrated to mean arterial pressure Monitor cardiac and renal function Neurological checks Determine cause Education to avoid future crises VIDEO: Crash Course - HTN https://www.youtube.com/ watch?v=ZVklPwGALpI Occlusive CV Arteriosclerosis Disorders Artery walls lose elasticity Part of normal aging Atherosclerosis Formation of plaques within arteries Damage to endothelial walls- inflammation-lipids, platelets, clotting factors accumulate Atherosclerosis https://www.youtube.com/watch? v=fLonh7ZesKs Risk Factors: Atherosclerosis Non-modifiable Age Gender Ethnicity Genetics Modifiable DM HTN Smoking Sedentary lifestyle Excessive alcohol intake Angina Ischemia Increased cardiac workload- increased cardiac oxygen demand-narrowed arteries unable to comply-ischemia- chest pain Angina Stable Variant (Prinzmetal’s) Unstable Silent Ischemia Stable Acute Coronary Prinzmetal Unstable Infarction Angina Angina Angina Syndromes temporary is- Vasospasm, Advanced Irreversible chemia/exerti with or reversible ischemia on without ischemia atherosclerosi s normal, Transient ST normal, Irreversible, transient ST elevation transient ST abnormal, depression/T depression/T pronounced Q wave wave waves inversion inversion Labs neg Labs neg Labs neg CPK_MB fraction, LDH, SGOT, AST elevation, Troponins Rest and Nitro, BB, CCB BB, CCB, anti- Morphine, nitro, BB, CCB coag’s ASA, thrombolytics, ACEI’s, BB, Statins, surgery Angina: non- pharmacological Smoking cessation treatment Stress reduction Supervised exercise program Decrease cholesterol and saturated fat intake Weight reduction Avoid cold and other stressors that cause vasoconstriction Myocardial Infarction Partial or complete blockage of coronary arteries-death of cardiac tissue Changes the way that the heart contracts/relaxes Occurs over period of hours MI: Signs and Chest pain Symptoms Shortness of Breath Dizziness Nausea Diaphoresis Poor colour Crackles/wheezes with auscultation Rapid pulse Extra heart sound Diagnostics ECG Echocardiogram Exercise Stress Testing Nuclear Cardiovascular imaging MI: ECG Changes Lab Tests/Cardiac Biomarkers Substances released into blood when cardiac muscle is damaged Current biomarker of choice: troponin Other less specific biomarkers: CK, CK-MB Lab Tests/Cardiac Biomarkers Substances released into blood when cardiac muscle is damaged Current biomarker of choice: troponin Other less specific biomarkers: CK, CK-MB MI: Treatment OXYGEN!!!! Aspirin/Ticlopidine/Clopidogrel Morphine Nitrates Thrombolytics: streptokinase, t- PA Anticoagulants: heparin Beta blockers: “olol’s” ACEI’s: “pril’s” Statins Surgical Interventions Percutaneous coronary intervention (PCI) http://youtu.be/36_qHWLFzI0 Coronary artery bypass grafting (CABG) http://youtu.be/3Nf6Q2skGOM Complications “ACT RAPID” Arrhythmias Congestive Heart Failure Tamponade / Thromboembolic disorder Rupture (Ventricle, septum, papillary muscle) Aneurysm (Ventricle) Pericarditis Infection Death Arrhythmias Arrhythmias are the most common complication after acute MI. They are related to the formation of re-entry circuits at the confluence of the necrotic and viable myocardium. PVCs ~ 90% - Vfib ~ 2 - 4% Supraventricular ~ 10% Bradyarrhythmias – common with inferior MI Complete AV Block ~ 20% with RV infarct Cardiac tamponade http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001245 / Aneurysm Left Pseudoaneurys ventricular m aneurysm: The Truth on Fat https://www.youtube.com/watch? v=dgiaISd4AHo&list=PLq-xxxa90 dh9Lh9E7pZVgejgd1PRI4scX&ind ex=24&t=0s

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