NRSG311 Week 4 Cardiac I PDF

Cardiovascular System: Part I NRSG311 – Week 4 R. Stent Winter 2025; adapted from K. Curtis-Harford Content Covered: Hypertension Coronary Artery Disease Angina Acute Coronary Syndrome Heart Failu...

Cardiovascular System: Part I NRSG311 – Week 4 R. Stent Winter 2025; adapted from K. Curtis-Harford Content Covered: Hypertension Coronary Artery Disease Angina Acute Coronary Syndrome Heart Failure Chapter 35: Hypertension Chapter 36: Coronary Artery Disease R. Stent Winter NRSG 311 2 2025  Objectives Understand primary hypertension etiology, clinical manifestations, and complications Explain collaborative care of the older adult with primary hypertension Describe and prioritize interprofessional care and nursing management of the patient with hypertension Explain the collaborative care of the patient with a hypertensive crisis Understand etiology, clinical manifestations, and complications of coronary artery disease, angina, and acute coronary syndrome Identify risk factors, clinical manifestations, interpersonal care, and nursing management of patients with coronary artery disease and acute coronary syndromes Explain diagnostic study results for coronary artery disease and acute coronary syndrome Understand medication therapy commonly used in treating patients with coronary artery disease and acute coronary syndrome Describe precipitating factors, clinical presentation, and collaborative care of patients who are at risk for or have experienced sudden cardiac death Describe the nursing role in prevention and promotion of therapeutic lifestyle changes related to cardiovascular health Describe key components to include in rehabilitation of patients recovering from acute coronary syndrome and coronary revascularization procedures R. Stent Winter 2025 3  Normal Regulation of Blood Pressure (BP) Normal BP Systolic BP (SBP) < 120mmHg Diastolic BP (DBP) < 80 mmHg What is BP 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 Maintaining Integration of both systemic factors and local peripheral vascular effects BP requires Arterial BP Arterial BP = Cardiac Output (CO) x Systemic Vascular Resistance (SVR) Mechanisms Can affect CO, SVR, or both regulating BP Complex Involves nervous, cardiovascular, renal, and endocrine functions process Regulated by short-term (seconds-hours) and long-term (days-weeks) R. Stent Winter 2025 mechanisms NRSG 311 4 Factors Influencing Blood Pressure R. Stent Winter 2025 NRSG 311 5  Cardiac Output (CO) Amount of blood pumped by ventricle in one minute Reflects heart’s mechanical ability Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)/min Impacted by factors that affect HR or SV Preload: volume of blood in ventricles at end diastole, before next contraction Contractility: the more fibers stretched (i.e. greater preload), greater force of contractility Afterload: peripheral resistance against which left ventricle must pump Atrial Kick: occurs during final phase of atrial systole, atria contract and eject bolus of blood into ventricles Cardiac Reserve: heart’s ability to respond to demands by increasing cardiac output R. Stent Winter 2025 NRSG 311 6 Systemic Vascular Resistance (SVR) Force opposing the movement of blood within vessels Determined principally by radius of small arteries and arterioles Small change in radius creates major change in SVR If SVR increases and CO remains constant or increases, arterial BP will increase R. Stent Winter 2025 NRSG 311 7  Defined as: Hypertension (HTN) Systolic BP (SBP) > 140 mmHg Sustained elevation of systemic arterial Diastolic BP (DBP) > 90 mmHg blood pressure (BP) One of most important modifiable risk Stage 1 Hypertension: factors of cardiovascular disease and SBP 140-159 or DBP 90-99 mortality in Canada mmHg Increased BP  increased risk for Stage 2 Hypertension: myocardial infarction (MI), heart failure (HF), stroke, renal disease, and death SBP 160 or DBP 100 mmHg WHO identifies HTN as “silent killer” Increased awareness and early detection Target for those with HTN and crucial DM: Measure BP in all adult patients, at all SBP < 130 mmHg appropriate visits, to determine cardiovascular DBP < 80 mmHg risk and monitor antihypertensive treatment R. Stent Winter 2025 NRSG 311 8  Primary vs. Secondary Hypertension Primary (Essential) Secondary Hypertension Hypertension Majority of HTN cases 5-10% of HTN in adults and >80% in Exact cause not identified children (complex interaction of Specific cause identified and corrected genes, environment) Clinical findings: unprovoked hypokalemia, Potential contributing factors: abdominal bruit, variable pressures with increased SNS activity, history of tachycardia, sweating, tremor, increased sodium intake, family history of renal disease overproduction of sodium- Potential causes: congenital condition of retaining hormones and aorta; renal disease; endocrine disorders; vasoconstrictors, increased neurological disorders; sleep apnea; body weight, DM, excess medications; pregnancy alcohol intake Treatment: eliminate underlying cause R. Stent Winter 2025 NRSG 311 9  Primary Hypertension: Etiology and Risk Factors Glucose Advancing Heavy alcohol Cigarette Elevated intolerance age consumption smoking serum lipids (DM) High dietary Gender Family history Obesity Ethnicity sodium intake Sedentary Socioeconomi Psychosocial lifestyle c status stress R. Stent Winter 2025 NRSG 311 10  Primary Hypertension: Pathophysiology Genes: Familial heritability is significant factor, likely arises from multiple genes Sodium and water retention: Excessive dietary intake of sodium strongly linked to HTN; when sodium intake restricted, BP often falls Altered RAAS: High plasma renin activity = increased conversion of angiotensinogen to angiotensin I  direct arteriolar constriction, promotes vascular hypertrophy, indices aldosterone secretion Stress and increased SNS activity: Physiological responses to stress normally protective, but when ongoing results in prolonged increase in SNS activity (vasoconstriction, increased HR, increased renin release) DM: Insulin resistance associated with endothelial dysfunction; hyperinsulinemia simulates SNS and RAAS activity, impairs nitric oxide-mediated vasodilation; pressor effects of insulin include vascular hypertrophy, increased renal sodium reabsorption Endothelial cell dysfunction: Vascular endothelial cells are source of multiple vasoactive substances; some people with HTN have reduced vasodilator response to nitric oxide; ET  pronounced and prolonged vasoconstriction Obesity: Complex, unclear relationship; likely linked to hormone abnormalities R. Stent Winter 2025 NRSG 311 11  Hypertension: Clinical Manifestations Lanthanic (silent) disease Frequently asymptomatic until severe and target-organ disease has occurred Symptoms of severe hypertension are related to effect on blood vessels in various organs/tissues or to increased workload of heart Fatigue Reduced activity tolerance Dizziness Palpitations Angina Dyspnea Extremely high BP: Headache, nosebleeds, and dizziness may occur R. Stent Winter 2025 NRSG 311 12  Older Adult with Primary Hypertension BP rises with age due to age-related BP measurement technique changes: May be wide auscultatory gap, failure to Loss of tissue elasticity: Increased collagen inflate cuff enough may result in false low and stiffness of myocardium reading Increased peripheral vascular resistance Older persons are sensitive to BP changes Decreased β-adrenergic receptor sensitivity Reducing SBP to 120-130 mmHg *Rate of rise more important than absolute value in determining need for emergency treatment Prompt recognition and management is essential Most common in patients with history of HTN who have failed to adhere to medication regimen or been unmedicated Rising BP thought to trigger endothelial damage and release of vasoconstrictor substances Vicious cycle of BP elevation Life-threatening damage to target organs Causes: Stroke, MI, encephalopathy, Illicit drug use (complicated by drug-induced seizures) Classified by degree of organ damage and rapidity with which BP must be lowered R. Stent Winter 2025 NRSG 311 22  Hypertensive Crisis: Clinical Manifestations Hypertensive encephalopathy: Sudden rise in BP Headache, nausea, vomiting, seizures, confusion, stupor, coma, blurred vision, transient blindness Renal insufficiency Range from minor impairment to complete renal shutdown Rapid cardiac decompensation (range from unstable angina to infarction and pulmonary edema) with associated chest pain and dyspnea Aortic dissection Excruciating chest and back pain, diaphoresis, loss of pulse in an extremity Neurological manifestations of hypertensive emergency Often similar presentation to stroke, without focal or lateralizing signs often seen with stroke R. Stent Winter 2025 NRSG 311 23  Hypertensive Crisis: Nursing and Interprofessional Management BP alone not major factor in deciding treatment Association between elevated BP + signs of new or progressive end-organ damage determines seriousness Necessitates: Hospitalization Parenteral administration of antihypertensive medications; oral agents may be administered in addition Critical care monitoring Initial treatment goal: decrease mean arterial pressure (MAP) 10-20% in first 1-2 hours, with further gradual reduction over the next 24 hours Lowering too far, too fast may decrease cerebral perfusion, precipitate stroke If aortic dissection, unstable angina, or signs of MI, must have SBP lowered to 100-120mmHg as quickly as possible Patient with severe elevation of BP but no target-organ damage may not require emergent therapy or hospitalization Sit 20-30 minutes, quiet environment Institute/adjust oral medications Encourage verbalizing fears, answer questions, eliminate excess noise Once hypertensive crisis resolved, important to determine cause to avoid future crises R. Stent Winter 2025 NRSG 311 24  Knowledge Check Which BP-regulating mechanism(s) can result in the development of hypertension if defective? (Select all that apply.) a) Release of norepinephrine b) Secretion of prostaglandins PGE2 and PGI2 c) Stimulation of the sympathetic nervous system d) Stimulation of the parasympathetic nervous system e) Activation of the renin–angiotensin–aldosterone system R. Stent Winter 2025 NRSG 311 25  Knowledge Check You are providing education to a client newly diagnosed with hypertension. Which ideas are important to include regarding controlling the condition? a) All clients with elevated BP will require medication b) It is not necessary to limit salt in the diet if taking a diuretic c) People with obesity must achieve optimal weight in order to lower BP d) Lifestyle modifications are indicated for all people with elevated BP R. Stent Winter 2025 NRSG 311 26  Knowledge Check What is a major consideration in the management of an older person with hypertension? a) Prevent pseudo-hypertension from converting to true hypertension b) Recognize that older people are less likely to adhere to medication therapy than younger adults c) Ensure that the client receives a larger initial dose of antihypertensive medications because of impaired absorption d) Use careful technique in assessing the BP of the client because of the possible presence of an auscultatory gap R. Stent Winter 2025 NRSG 311 27  Knowledge Check Mrs. Carter is newly diagnosed with hypertension. She has a blood pressure of 158/98mmHg after 12 months of exercise and diet modifications. What is the likely course of action recommended to Mrs. Carter? a) Medication may be required because the BP is still not within the normal range b) Continued monitoring of BP every 3-6 months is all that is necessary at this time c) Because lifestyle modifications were not effective, Mrs. Carter can discontinue these behaviour changes and medications will be used instead d) Mrs. Carter may have to make more vigorous changes in lifestyle if she wants to remain off antihypertensive medications R. Stent Winter 2025 NRSG 311 28  Knowledge Check Mr. Collings is admitted to the hospital in hypertensive emergency (BP 244/142mmHg) Sodium nitroprusside is started to treat the elevated BP. Which management strategy would be appropriate? Select all that apply a) Measure hourly urine output b) Decrease the MAP by 50% within the first hour c) Continuous BP monitoring with an intra arterial line d) Maintain bed rest and provide sedation to lower the BP e) Assess Mr. Collings for signs and symptoms of heart failure and changes in mental status R. Stent Winter 2025 NRSG 311 29  Atherosclerosis Major cause of coronary artery disease Progressive over many years Characterized by deposits of lipids within intima of artery By the time patient is symptomatic, atherosclerosis is advanced Fatty streaks Fibrous plaque Complicated lesion Risk factors: Nonmodifiable: age, sex, ethnicity Major modifiable: elevated serum levels, hypertension, tobacco use, activity levels, obesity Modifiable: diabetes mellitus, metabolic syndrome, psychological state, homocysteine, substance use R. Stent Winter 2025 NRSG 311 30  Atherosclerosis: Etiology and Pathophysiology Endothelium (inner lining of vessel wall) normally nonreactive to platelets, leukocytes, coagulation, fibrinolytic, complement factors Endothelium can be injured by tobacco use, hyperlipidemia, HTN, toxins, diabetes, hyperhomocysteinemia, or infection Injury causes local inflammatory response to occur C-Reactive Protein produced by liver, non-specific marker of inflammation that is increased in patients with CAD R. Stent Winter 2025 NRSG 311 31 FIG. 36.1 Pathogenesis of atherosclerosis.  Also known as: Arteriosclerotic heart disease (ASHD); cardiovascular heart disease (CVHD); ischemic heart disease (IHD); coronary heart Coronary Artery disease Disease (CAD) Common heart condition Involves atherosclerotic plaque formation in the vessel lumen Leads to impaired blood flow and oxygen delivery to myocardium Blood vessel disorder in general category of atherosclerosis Greek words: athere (fatty mush) and skleros (hard) Begins as soft deposits of fat, harden with age; often referred to as “hardening of the arteries” May affect heart’s arteries and produce pathological effects Reduced flow of oxygen and nutrients to myocardium Progressive, develops over many years Can be asymptomatic or develop chronic stable angina By the time symptoms occur, disease usually well advanced Identify people at risk, initiate therapeutic lifestyle changes and treatment strategies early More serious manifestations: Acute Coronary Syndrome (ACS) R. Stent Winter 2025 NRSG 311 32  Coronary Artery Disease: H yp Etiology alm ertensi o risk st doub n o o l ar t e f c o r o n e s ry d a isea ry se Mechanism: Shear stress: response-to-injury hypothesis of atherogenesis Results in endothelial dysfunction Causes impairment in synthesis and release of potent vasodilator nitric oxide Decreased nitric oxide level promotes development and acceleration of atherosclerosis and plaque formation = atherosclerosis Intimal layer exposed to activated white blood cells and platelets Growth factors released by vascular endothelium and platelets may induce smooth muscle proliferation within the lesion Arteriolar changes may account for high incidence of coronary artery disease and resulting conditions of angina and MI R. Stent Winter 2025 NRSG 311 33  Coronary Artery Disease: Risk Factors Modifiable: Non-Modifiable: Serum lipid (elevated triglyceride and LDL, decreased Increasing age HDL) Men higher risk than Blood pressure > 140/90 mmHg women until 65 Tobacco use Ethnicity (Black Physical inactivity populations are higher Obesity (especially consider waist circumference) risk) Other contributing factors: DM, elevated fasting blood Genetic predisposition glucose, psychosocial risk factors (e.g. stress, and family history depression), elevated homocysteine levels, substance use Contributing risk factors for women: early menarche or premature menopause, polycystic ovary disease, breast cancer, autoimmune disorders R. Stent Winter 2025 NRSG 311 34  Dyslipidemia Screening: Important Risk Factor for Development of Cardiovascular Disease Men over 40, women over 50 (or postmenopausal) should undergo lipid screening every 3-5 years Screen earlier: high-risk ethnic groups (people of South Asian decent, Indigenous peoples) Screen earlier: women with history of pregnancy- induced HTN First test: non-fasting blood sample for lipid and lipoprotein If triglyceride > 4.5 mmol/L, have fasting lipid levels tested R. Stent Winter 2025 NRSG 311 35 Coronary Artery Disease: Collaborative Management Nutritional therapy Decrease saturated fats and cholesterol Increase complex carbohydrates DASH, Mediterranean, Portfolio Diets Omega-3 fatty acids Medications Goal: restrict lipoprotein production (Statin medications) What are some complications or side effects of these medications? What labs must be monitored regularly with these medications? R. Stent Winter 2025 NRSG 311 36  Coronary Artery Disease: Health Promotion Prevent, modify, or slow down progression Identify people at high risk Early stages will likely be asymptomatic Risk screening: Health history (family history, symptoms, environmental factors, psychosocial factors, employment, etc.) Attitudes/beliefs about health and illness Health behaviours Current medications (names, dosages, adherence) R. Stent Winter 2025 NRSG 311 37 Coronary Artery Disease: Patient and Family Teaching Monitor BP, report when >140/90 mmHg (or as discussed with provider) Take prescribed medications as ordered Diet modifications: Mediterranean, DASH, or Portfolio patterns of eating Adjust total caloric intake to achieve/maintain ideal body weight Avoid crash or fad diets: not effective long-term Smoking reduction/cessation Weight reduction Regular exercise (30-60 min moderate intensity 4-7 days/week) Stress reduction, adequate rest and sleep Manage comorbidities (especially diabetes mellitus) Follow medication regimens, attend follow-up appointments, ongoing monitoring R. Stent Winter 2025 NRSG 311 38 Coronary Artery Disease: Chronic Stable Angina CAD is a progressive disease Individuals may be asymptomatic for years or may develop chronic, but stable, chest pain syndromes Angina is a clinical manifestation of reversible myocardial ischemia Chest pain that occurs intermittently over long period with same pattern of onset, duration, and intensity Demand for myocardial O2 exceeds ability of coronary arteries to supply heart with oxygen  myocardial ischemia Myocardial ischemia can be due to increased demand for O2 or decreased supply of O2 Symptoms or Manifestations: Unpleasant feeling: “constrictive”, “squeezing”, “heavy”, “choking”, or “suffocating” sensation Rarely sharp or stabbing, usually does not change with position or breathing Many people report indigestion or burning sensation in epigastric region Pain mostly substernal, may occur in neck or radiate to jaw, shoulders, down arms, between shoulder blades Anginal pain usually lasts 3-5 minutes, commonly subsides when precipitating factor is relieved Pain at rest is unusual R. Stent Winter 2025 NRSG 311 39  Assessment of Angina R. Stent Winter 2025 NRSG 311 40  Chronic Stable Angina: Interprofessional Management and Nursing Interventions Interprofessional Nursing interventions Management Treatment aim: Administer short-acting nitrates (first-line Decrease O2 demand, increase O2 therapy: dilate peripheral blood vessels, supply, or both coronary arteries, and collateral vessels) Reduce risk factors If symptoms unchanged or worse, repeat dose Medication therapy aim: q5 min to a total of 3 doses in 15 min Prevent MI and death If not effective after 3 doses, emergency Reduce symptoms services should be contacted **Do not mix nitrates with erectile dysfunction Nitrate therapy: enhance coronary products – may produce intractable blood flow hypotension and death** Antiplatelet and cholesterol- Long-acting nitrates or transdermal controlled- lowering medications release nitrates can reduce incidence of anginal attacks Other medications: See Table 36.11 R. Stent Winter 2025 NRSG 311 41  Prinzmetal’s Angina or Variant Angina Often occurs at rest Rare form of angina Usually in response to spasm of a major coronary artery When spasms occur: Patient experiences angina and transient ST segment elevation May be seen in patients Migraine headaches with history of: Raynaud’s phenomenon Pain may be relieved Moderate exercise by: May disappear spontaneously Not usually precipitated by Strong contraction of smooth muscle in coronary artery caused by increase increased physical in intracellular calcium demand: Treatment: Calcium channel blockers and/or nitrates used to control the angina R. Stent Winter 2025 NRSG 311 42 Acute Coronary Syndrome More serious manifestations of coronary artery disease Myocardial Unstable angina infarction R. Stent Winter 2025 NRSG 311 43  Acute Coronary Syndrome (ACS) Group of diseases in which blood flow to heart decreases Myocardial ischemia that is prolonged and not immediately reversed will develop into ACS Distinct diagnoses with related pathophysiology, prognosis, and interventions: Unstable angina Non-ST-segment elevation myocardial infarction (NSTEMI) ST-segment elevation myocardial infarction (STEMI) Associated with deterioration of once-stable atherosclerotic plaque Plaque ruptures, exposing intima to blood, stimulating platelet aggregation and local vasoconstriction with thrombus formation Unstable lesion may be partially occluded by a thrombus, manifesting as UA or NSTEMI Unstable lesion may be totally occluded by a thrombus, manifesting as STEMI R. Stent Winter 2025 NRSG 311 44  ACS: Unstable Angina (UA) Manifestations Chest pain that is new onset, occurs at rest, or has worsening pattern May develop after chronic stable angina or be first sign of CAD Patients with chronic stable angina can develop UA May experience significant change in pattern of angina Increasing frequency, easily provoked with no or minimal exertion, occurs at rest or during sleep Unpredictable, emergency situation Women often seek support faster than men Symptoms: Fatigue (most prominent symptom) SOB Indigestion Anxiety R. Stent Winter 2025 NRSG 311 45 R. Stent Winter 2025 NRSG 311 46  ACS: Myocardial Infarction (MI) Occurs as result of sustained ischemia, causing irreversible myocardial cell death 80-90% of MIs are due to development of thrombus, halts perfusion to myocardium distal to occlusion Cardiac cells can withstand ischemic conditions for approximately 20 minutes In 5-6 hours, entire thickness of heart muscle becomes necrosed Infarctions described based on location of damage Anterior, inferior, lateral, or posterior wall infarction Damage can occur in more than one location (e.g. Anterolateral MI) Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration is hallmark of MI Pain usually described as: Heaviness, pressure, tightness, burning, constriction, crushing R. Stent Winter 2025 NRSG 311 47 ACS: Clinical Manifestations of MI Clinical Complications: Manifestations: Pain Dysrhythmias SNS stimulation Heart failure Cardiovascular Cardiogenic shock manifestations Papillary muscle Nausea and vomiting dysfunction Fever Ventricular aneurysm Pericarditis Dressler’s syndrome R. Stent Winter 2025 NRSG 311 48  ACS: Unstable Angina (UA) and Myocardial Infarction (MI) Diagnostic Studies Electrocardiogram Serum cardiac markers Coronary angiography (ECG): Primary tool to rule or confirm Cardiac enzymes and troponins Can be used to evaluate UA or MI based on changes in After MI, released into blood in large extent of disease, determine QRS complex, ST segment, quantities from necrotic heart muscle most appropriate therapeutic and T wave Increase in serum markers occurring modality Important to distinguish after cellular death: Important in PCI may be performed at this between UA, STEMI, and diagnosis of MI time if appropriate NSTEMI for diagnosis and Can indicate whether cardiac damage is Only way to confirm diagnosis treatment present and approximate extent of of Prinzmetal’s angina When possible, compare with damage previous ECG recordings Creatinine kinase (CK): levels rise ECG may be normal or approximately 3-12 hrs after MI, peak in nondiagnostic at first; serial 24 hrs; return to normal within 2-3 days ECGs are to be obtained as Cardiac-specific troponin: levels increase ECG may change within hours 3-12 hrs after onset of MI, peak 24-48 Cardiac rhythms will be hrs, return to baseline over 5-14 days; covered in NRSG 415 highly specific and sensitive indicators of MI Myoglobin: one of first serum cardiac markers to rise after MI, but lacks cardiac specificity and rapidly excretes R. Stent Winter 2025 in urine, limited NRSG diagnostic 311 value 49  ACS: Myocardial Infarction Interprofessional Care 1. Emergent percutaneous coronary intervention:  First line treatment with confirmed ECG changes  Goal: open affected artery within 90 min, cardiac catheterization to locate blockage(s), stents may be placed 2. Fibrinolytic therapy Goal: reduce pain  Soon as possible: ideally 2-3 hours, no longer than 12 hours and improve  Via IV (have multiple sites available)  See Table 36.13 for contraindications of Fibrinolytic therapy coronary blood 3. Medication therapy flow  IV nitroglycerin and morphine  B-Adrenergic blockers and ACE Inhibitors Most often occurs in ER,  Antidysrhythmic medications requires rapid diagnosis  Cholesterol lowering medications to preserve cardiac  Stool softeners muscle 4. Nutritional therapy  NPO aside from sips of water in the beginning 5. Coronary surgical revascularization  E.g. coronary artery bypass graft surgery (CABG) R. Stent Winter 2025 NRSG 311 50 Chronic Stable Angina and Acute Coronary Syndrome: Diagnostics and Medication Therapy Diagnostic Studies: Medications (Table 36.11): Detailed health history Antiplatelet Agents (ASA) Physical examination Clopidogrel (Plavix) Chest x-ray (cardiac enlargement, aortic calcifications, Nitrates pulmonary congestion) 12-lead ECG (compare with earlier tracing when B-Adrenergic Blockers possible) Calcium Channel Blockers Labs (e.g. lipid profile) ACE Inhibitors Echocardiography Heparins Exercise stress test Opioids (Morphine) Coronary angiography Fibrinolytic Therapy Holter monitor (Alteplase) R. Stent Winter 2025 NRSG 311 51  Chronic Stable Angina and Acute Coronary Syndrome: Nursing Management Overall goals: Pain relief, preservation of myocardium, immediate and Percutaneous coronary appropriate treatment of ischemia, effective coping with illness-associated anxiety, participation in rehabilitation plan, intervention (PCI) reduction of risk factors Catheter equipped with inflatable The following nursing measures should be balloon tip inserted into narrowed instituted for patient experiencing angina: coronary artery, balloon inflated 1. Administer supplemental oxygen Major nursing responsibilities 2. Measure of vital signs for care of the patient following 3. 12-lead ECG PCI involves: Monitor for signs of recurrent angina 4. Prompt pain relief (nitrate followed by opioid analgesic prn) Frequent assessment of vital signs 5. Auscultation of heart sounds Evaluate groin site for signs of bleeding 6. Comfortable positioning Maintain bed rest per institutional R. Stent Winter 2025 NRSG 311 policy 52  Chronic stable angina and Acute Coronary Syndrome Patient Teaching Begins with emergency nurse and progresses through staff nurse to community health nurse Careful assessment of learning needs helps set goals and objectives that are realistic and patient-centred Physical activity is necessary for optimal physiological functioning and psychological well-being Sexual counseling for cardiac patients and their partners should be provided “Living Well with Heart Disease” on Heart and Stroke Website Assess psychological adjustment of patient and family to diagnosis and treatment regimen, threat to identity or self-esteem, changes in roles R. Stent Winter 2025 NRSG 311 53  ACS: Sudden Cardiac Death Abrupt disruption in cardiac function, producing abrupt loss of cardiac output and cerebral blood flow Death usually occurs within 1 hour of onset of acute symptoms (e.g. angina, palpitations) Majority of cases caused by acute ventricular dysrhythmias (e.g. ventricular tachycardia, ventricular fibrillation) Patients who survive are at risk for recurrent SCD due to continued electrical instability of myocardium that caused initial event Risk factors: Male, family history of premature atherosclerosis, tobacco use, diabetes mellitus, hypercholesterolemia, hypertension, and cardiomyopathy Most SCD patients have lethal ventricular dysrhythmia Require 24-hour Holter monitoring or other type of event recorder, exercise stress testing, signal-averaged ECG, and electrophysiological study (EPS) Most common approach to preventing recurrence and improving survival: implantable cardioverter-defibrillator (ICD) R. Stent Winter 2025 NRSG 311 54 Emergency Management: Chest Pain Etiology Assessment Interventions Ongoing Findings Monitoring Cardiovascular Pain, epigastric pain ABC Vital signs, LOC, cardiac Respiratory Cold, clammy skin, Vitals rhythm, O2 saturation Chest trauma diaphoresis Oxygen Response to Nausea and vomiting medications Gastrointestinal IV access Irregular HR Provide emotional Other Pain support Dyspnea, crackles, Medications are ordered wheezes Explain all interventions Continuous ECG Weakness Anticipate need for monitoring intubation Anxiety, feeling of Obtain labs impending doom Prepare for CPR R. Stent Winter 2025 NRSG 311 55 Left Ventricular Hypertrophy (LVH) Sustained high BP increases cardiac workload Produces LVH Risk doubles with associated obesity Initially an adaptive or compensatory mechanism, strengthens cardiac contraction and increases CO Increased contractility increases myocardial work and oxygen consumption When heart can no longer meet demands for myocardial oxygen, heart failure develops Progressive LVH, especially in association with coronary artery disease, is associated with development of heart failure R. Stent Winter 2025 NRSG 311 56  Heart Failure (HF) Abnormal clinical syndrome involving impaired cardiac pumping and/or filling Common complication of chronically elevated BP and MI Compensatory mechanisms are activated to maintain adequate CO Can have abrupt onset or be insidious process resulting from slow, progressive changes Heart’s compensatory adaptations are overwhelmed, heart can no longer pump enough blood to meet metabolic needs of body Pumping action diminished, contractility depressed, SV and CO decreased Not all patients will have pulmonary congestion or volume overload; depending on severity and extent of injury, may have initial subtle signs: Mild dyspnea, restlessness, agitation, slight tachycardia Other signs: pulmonary congestion on chest radiograph; S3 or S4 heart sounds on auscultation; crackles on auscultation of breath sounds; jugular vein distension (right-sided heart failure) Characterized by ventricular dysfunction, reduced exercise tolerance, diminished quality of life, and shortened life expectancy Classified as being accompanied by either reduced ejection fraction (systolic) or preserved ejection fraction (diastolic) To maintain balance in HF, several counter-regulatory processes are activated, including production of hormones from the heart muscle to promote venous and arterial vasodilation R. Stent Winter 2025 NRSG 311 57  Types of Heart Failure Usually manifested by biventricular failure As result of pathological conditions, one side may fail first, while other side continues to function normally for a time Because of prolonged strain, functioning side eventually fails, resulting in biventricular failure. Most common form of initial HF is left-sided failure Resulting from left ventricular dysfunction Blood backs up into left atrium and pulmonary veins, causing pulmonary congestion and edema Primary cause of right-sided failure is left-sided failure Right-sided heart failure causes backward blood flow to right atrium and venous circulation Venous congestion in systemic circulation results in peripheral edema, hepatomegaly, splenomegaly, vascular congestion of gastro-intestinal tract, and jugular venous distension. R. Stent Winter 2025 NRSG 311 58 R. Stent Winter 2025 NRSG 311 59  Acute Decompensated Heart Failure: Clinical Manifestations ADHF typically manifests as pulmonary edema Clinical manifestations of pulmonary edema are distinct Most affected patients are anxious, pale, and possibly cyanotic Skin is clammy and cold from vasoconstriction caused by stimulation of SNS Patient has severe dyspnea, evidenced by use of accessory muscles of respiration, a respiratory rate greater than 30 breaths per minute, and orthopnea May be wheezing and coughing with production of frothy, blood-tinged sputum, auscultation of lungs may reveal crackles, wheezes, and rhonchi throughout R. Stent Winter 2025 NRSG 311 60  Chronic Heart Failure: Clinical Manifestations Crushing intense C: pain Depend on patient’s age, underlying type and extent of heart Radiates to arm, disease, and which ventricle is failing to pump effectively R: back, etc. Common symptoms include: Unrelieved by rest Fatigue U: or nitro Dyspnea (including paroxysmal nocturnal dyspnea, occurs when patient is asleep, caused by reabsorption of fluid from dependent body areas when S: Sweating patient is lying flat) Tachycardia H: Hard to breath Edema Increased HR and Nocturia I: BP Skin changes Nausea and Behavior changes N: Vomiting Chest pain Going to be Weight changes G: scared (anxiety) R. Stent Winter 2025 NRSG 311 61  Heart Failure Complications: Diagnostic Studies: Primary goal: determine underlying etiology Pleural effusion Physical examination Dysrhythmias Chest radiograph (signs of enlarged heart) Left ventricular Electrocardiogram (ECG) (electrical changes indicative of thrombus formation LVH) Laboratory data (cardiac enzymes, b-type natriuretic protein Hepatomegaly [BNP], serum chemistries, liver function studies, thyroid function studies, complete blood count) Renal failure Hemodynamic assessment Echocardiogram Stress testing R. Stent Winter 2025 NRSG 311 62  Medication Management of Chronic Heart Failure General therapeutic objectives for Medications: drug management of chronic HF Diuretics are used in HF to mobilize include: edematous fluid, reduce pulmonary venous 1. Identification of the type of HF and pressure, and reduce preload. underlying causes ACE inhibitors 2. Correction of sodium and water retention and volume overload, Angiotensin II receptor blockers 3. Reduction of cardiac workload β-adrenergic blockers 4. Improvement of myocardial Mineralocorticoid receptor antagonists (e.g. contractility Spironolactone) 5. Control of precipitating and Positive inotropic agents (Vasodilator drugs complicating factors and Nitrates) R. Stent Winter 2025 NRSG 311 63  Nursing and Collaborative Management of Heart Failure Goal of therapy for both ADHF and pulmonary edema: Improve ventricular function by decreasing intravascular volume, decreasing venous return (preload), decreasing afterload, improving gas exchange and oxygenation, and increasing CO Treatment strategies should include the following: Decreasing intravascular volume with use of diuretics or ultrafiltration Decreasing venous return (preload) to reduce amount of volume returned to LV during diastole. Decreasing afterload (resistance against which LV must pump) improves CO and decreases pulmonary congestion Gas exchange is improved by administration of IV morphine sulphate and supplemental oxygen. Inotropic therapy and hemodynamic monitoring may be needed in patients who do not respond to conventional pharmacotherapy (e.g., diuretics, vasodilators, morphine sulphate). Reduction of anxiety is facilitated by sedative action of morphine administered intravenously; when morphine is used, patient must be watched closely for respiratory R. Stent Winter 2025 NRSG 311 64 depression.  Nursing Management of Heart Failure Overall goals for patient with HF include: 1. Decrease in peripheral edema 2. Decrease in shortness of breath 3. Increase in exercise tolerance 4. Adherence to drug regimen 5. No complications related to HF Patients with HF should be counselled to quit smoking and obtain yearly vaccinations against the flu Preventive care should focus on slowing progression of the disease R. Stent Winter 2025 NRSG 311 65  Knowledge Check A nurse is teaching a client about coronary artery disease. Which changes occur in this disorder? Select all that apply. a) Diffuse involvement of plaque formation in coronary veins b) Abnormal levels of cholesterol, especially low-density lipoproteins c) Accumulation of lipid plaques or calcification within the coronary arteries d) Development of angina due to a decreased blood supply to the heart muscle e) Chronic vasoconstriction of coronary arteries leading to permanent vasospasm R. Stent Winter 2025 NRSG 311 66  Knowledge Check A hospitalized client with angina tells the nurse that she is having chest pain. What are the nurse’s priorities? a) Perform vital signs and obtain an ECG b) Administer sublingual nitroglycerin and intravenous morphine c) Call the physician d) Inform the cardiac catheterization lab and interventional cardiologist R. Stent Winter 2025 NRSG 311 67  Knowledge Check What does the clinical spectrum of ACS include? a) Unstable angina and STEMI b) Unstable angina and NSTEMI c) Stable angina and sudden cardiac death d) Unstable angina, STEMI, and NSTEMI R. Stent Winter 2025 NRSG 311 68  Knowledge Check In a client recovering from an MI, in which period is the heart most vulnerable to stress? a) 3 weeks after the infarction b) 4 to 6 weeks after the infarction c) 10 to 14 days after the infarction d) When healing is complete, at 6 to 8 weeks R. Stent Winter 2025 NRSG 311 69  Knowledge Check A client is admitted to the ED with chest pain of 2 hours’ duration, ECG findings consistent with an acute MI, and occasional ventricular dysrhythmias. What pharmacological therapy would you expect the client to be managed with initially? a) Diuretics b) Nitroglycerin spray c) β-Adrenergic blockers d) Thrombolytic therapy with tissue plasminogen activator R. Stent Winter 2025 NRSG 311 70  Knowledge Check Five days after an MI, a client is restless and apprehensive. How can the nurse assist the client? a) By providing all care and doing everything for the client b) By structuring the environment and the routine so the client can rest c) By allowing the client to participate in planning and carrying out activities d) By encouraging the family to provide for the client’s physical care and give emotional support R. Stent Winter 2025 NRSG 311 71  Knowledge Check What is the most common pathological finding in individuals experiencing sudden cardiac death? a) Cardiomyopathies b) Mitral valve disease c) Atherosclerotic heart disease d) Left ventricular hypertrophy R. Stent Winter 2025 NRSG 311 72 Case Study Mr. Lee is a 62 year old male who presents to the emergency department with chest pain, radiating to the left arm, and shortness of breath. His chest pain began two hours ago while gardening. He describes it as a heavy, pressure-like sensation rated 8/10, and is accompanied by nausea and diaphoresis. He denies any recent trauma. Mr. Lee was diagnosed with hypertension 10 years ago, and it is not well-controlled. He also has a history of type 2 diabetes mellitus and dyslipidemia. He smokes 1 pack of cigarettes a day for 40 years and lives a fairly sedentary lifestyle. His father died at 68 from a myocardial infarct. His mother is alive and has a history of hypertension and stroke. Mr. Lee is a retired office worker, lives with his wife, and has a high-fat, high-sodium diet. He has three adult children. What are Mr. Lee’s modifiable risk factors? What are his non-modifiable risk factors? R. Stent Winter 2025 NRSG 311 73 Mr. Lee’s Case Study - Continued Upon assessment, you find: BP 180/110 mmHg, HR 110 bpm, RR 24/min, SpO2 91% RA, Troponin levels: Elevated Cholesterol Panel: LDL 4.8 mmol/L, HDL 0.9 mmol/L, Triglycerides 2.4 mmol/L What immediate actions would you take based on Mr. Lee’s presentation? R. Stent Winter 2025 NRSG 311 74 Mr. Lee’s Case Study - Continued Once Mr. Lee’s condition stabilizes, what patient education will need to be provided? What considerations need to be taken into account? R. Stent Winter 2025 NRSG 311 75 Kahoot! https://create.kahoot.it/details/222384f1-7c07-46cc- 9532-a4519d095426 9/4/20XX Presentation Title 76  Tyerman, J., & Cobbett, S. L. (Eds.). (2023). Lewis’s medical- surgical nursing in Canada: Assessment and management of clinical problems (5th ed.). Elsevier. Reference Chapter 35 Hypertension p. 773-793 Chapter 36 Coronary artery disease p. 796-825