Cardiac Part II Content Guide-Fall 2021 Assigned Reading: Please review green underlines in Chapters 33, 34 Chapter 35 content will be covered in Advanced Med-Surg Medications to Review in this Content Area: HMG-CoA Reductase Inhibitors (Statins) Niacin Fibric acid derivatives Bile acid sequestrants PCSK9 inhibitors Cholesterol absorption inhibitors (ex: Zetia) Aspirin Clopidogrel (Plavix) Nitrates (sublingual, nitro paste, metered sprays, long-acting nitrates) ACE inhibitors Angiotensin II receptor blockers Beta-blockers Calcium channel blockers Low-molecular weight heparin (ex: Lovenox) Heparin Warfarin Morphine Thrombolytic agents (ex: alteplase) Neprilysin-Angiotensin Receptor Blockers (ex: Entresto) Aldosterone antagonists Hydralazine/Isosorbide Dinitrate Combination (ex: Bidil) Digitalis Diuretics (ex: loop diuretics) Chapter 33: Coronary artery disease - Blood vessel disorder caused by atherosclerosis o Describe the pathophysiology of atherosclerosis. How does a plaque develop? What plays a key role in the development of atherosclerosis? Damaged endothelium Fatty streak and lipid core formation Fibrous plaque covers the lipid core Complicated lesion: plaque rupture with thrombus formation o What is collateral circulation? How can it be beneficial to the body? Arterial anastomoses (or connections) within coronary circulation help re-routing blood when there is blockage in the main vessels. Contributing factors: Inherited predisposition for angiogenesis Cardiac Part II Content Guide-Fall 2021 Presence of chronic ischemia (poor blood flow) Slowly developing blockages increase collateral circulation and allow adequate blood and oxygen to heart; except with increased workload (e.g. exercise) With rapid-onset CAD or coronary spasm, collateral circulation has not had time to develop results in severe ischemia or infarction o What are the risk factors for CAD? Which are modifiable vs. nonmodifiable? Modifiable: Serum lipids TCL >200 LDL>130 HDL <40 men and <50in women triglycerides>150 BP Diabetes: endothelium dysfunction Tobacco use Physical inactivity Obesity Contributing factors: psychosocial factors, high homocysteine levels, substance abuse Non-modifiable: Age Gender Ethnicity Genetic predisposition/family history of heart disease o What are nonpharmacologic therapies that may be used in patients with CAD? Diet: Reduced salt diet, reduced fat, increase carbs, increase veggies, reduced cholesterol Exercise, weight bearing Stop smoking Regular checkup for lipids levels, blood pressure, blood glucose Stress, anxiety referrals. For HTN: exercise, smoking cessation, reduce salt o What kinds of pharmacologic therapies may be used in patients with CAD? - SAT for lipids - For hypertension: diuretics, beta blockers, calcium channel blockers, ACE, ARB Chronic stable angina o What is chronic stable angina? Chronic and progressive: Predictable, treatable Chronic intermittent chest pain that occurs over a long period with similar pattern of onset, duration, and intensity of symptoms Cardiac Part II Content Guide-Fall 2021 Angina: low oxygen supply o How is it brought on? Physical exertion, stress, emotional upset o How long does it last? Expect this will only last a few minutes and should subside when precipitating factor is resolved (see Table 33.9) o How do we assess for the presence of it? PQRST: Precipitating events, Quality of pain, Region/location/radiation, Severity (scale), Timing of pain. o Initial treatment: Nitroglycerin 1 tab sublingual or 1-2 metered sprays sublingual Is s/s unchanged, repeat nitro every 5 min for max of 3 doses Call 911 if 2/2 unresolved after 3 doses Storage: keep nitro with them and replace every 6 months Can cause: Dizziness and headache caused by vasodilation due to opening the vessels and they need to be on fall risk because they might be orthostatic o What kinds of diagnostic studies may be done when a patient presents with chest pain? 12-lead EKG Lab studies: cardiac biomarker(troponin), lipid profile, CRP (non-specific indicator of inflammation) Chest X-ray- can show fluid or cardiac enlargement Echocardiogram Exercise Stress test Cardiac catheterization: to identify where the coronary artery is Diagnostic vs. interventional cath: o Diagnostic used to diagnose o Interventional cath used to do something (stenting, etc) Nursing role pre-procedure o Contrast dye allergies and shellfish o Baseline assessment: clotting labs (PT, INR), pulses, sensation, edema, color, temp, baseline cardiac. o Kidney fx: creatinine, BUN Nursing role post-procedure o Bleeding/hematoma at the cath site Cardiac Part II Content Guide-Fall 2021 o Compare with baseline assessment: neurovascular o Q15 minute checks o Monitor chest pain and EKG o Monitor ECG, lipidemia, antiplatelets, o Check of infection o How do we as the nurse manage a patient with chronic stable angina in acute care? o What is the nursing role pre-procedure and post-procedure for a patient undergoing a cardiac catheterization? What is the difference between diagnostic and interventional cardiac cath? What types of stents may we use? What types of drugs may be used after stent placement? o What patient education should you as the nurse provide for a patient with stable angina? How should we encourage patients to manage this at home? Medication’s information Signs and symptoms of complications, infection o Why may a patient have a CABG vs. having a PCI? CABG: coronary arterial bypass graft Arterial or venous grafts placed from aorta/branch to heart muscle distal to blockage Requires sternotomy (opening of chest cavity) and cardiopulmonary bypass (CPB) Potential complications o Inflammation o Bleeding o Anemia o Infection (surgery site, leg or harvest site) o Dysrhythmias o Wound infections: from harvest site that was used for graft Nursing care focus o Wound care o Pain management o VTE prevention: SCD, early ambulation o Respiratory complication prevention o What type of post-op complications could occur after CABG surgery? What type of nursing care can you provide to assess for or mitigate these risks? o What kind of drug therapy do you anticipate your patient with stable angina may be on? Be familiar with how each of these drugs work to help your patient. Encourage patients to rest, take nitroglycerin Nitroglycerin administration Nitroglycerin storage Cardiac Part II Content Guide-Fall 2021 Nitroglycerin patient education Progression of chronic stable angina: unusual changes need to let the HCP to examine progression. Storage in purse, something on you but avoid direct body contact (avoid body heat) Nitro patient education: headache, flushing, dizziness, orthostatic hypotension (due to vasodilation), tingling sensation Acute care of chronic stable angina: Sit up right for better O2, O2 supplementation VS, heart sounds, breath sounds, continuous EKG, 12-lead EKG. (12-lead ECG gives more views of the heart) Pain management: first with NGT; IV opioid if needed Cardiac biomarkers: troponin and CKMB CXR Support, reduce anxiety Patient education for CAD/angina Focus on risk factor modification; provide education about CAD, angina, precipitating factors for angina, medications to treat angina Precipitating factors and how to avoid or control them (Table 33.9) Information about how to reduce risk factors (Table 33.2) Diet: heart healthy diet Physical activity: 30-60 min for 5 days/week. Medications: aspirin, Statin, niacin, diuretics, Ace inhibitor, arbs, beta blocker, nitroglycerin Psychological support What is silent ischemia? What is it associated with? What is the relationship between chronic stable angina and acute coronary syndrome? o ACS is caused by a deterioration of a once-stable atherosclerotic plaque and includes How does unstable angina differ from chronic stable angina? o Chest pain new in onset; occurs at rest; or with increase in frequency, duration, or with less effort than chronic stable pattern o Pain typically lasts > 10 minutes o Unpredictable; needs immediate treatment What types of EKG changes will you see with a STEMI? What about a NSTEMI? What are the pathophysiologic differences between these two types of myocardial infarctions? o NSTEMI (partial occlusion of coronary artery) Will have positive cardiac biomarkers Thrombolytic therapy not indicated for NSTEMI Cardiac Part II Content Guide-Fall 2021 Non ST elevation (depression or emergence) Treatment within 12-72 hrs. o STEMI (total occlusion of coronary artery) Considered an emergency; artery must be opened quickly ST elevation MI PCI within 90 min, within 30 min if thrombolytic. Prefer PCI. What are the clinical manifestations of an MI? What should be included in your nursing assessment? What diagnostic studies may we use? o Manifestations: Pain: chest pain not relieved by rest, position change, and nitroglycerin. Tightness, pressure, brushing, etc. Can be atypical symptoms like tiredness, dysrhythmia, change in consciousness (esp. in women, older adults, diabetes) Sympathetic nervous system stimulation: from catecholamine release. Ashy clammy cool skin, sweating Cardiovascular: reduced BP, decrease renal perfusion, blood back up in lungs cause crackles, abnormal heart sounds. Nausea/vomiting Fever o Nursing assessment: o Diagnostic studies: What does emergency management of a patient with ACS look like? What kind of drugs may be used in management of ACS? o 12-lead EKG; continuous EKG monitoring o Position patient upright unless contraindicated o Give oxygen per nasal cannula to keep O2 saturations greater than 93% o Obtain IV access for drug administration o Give SL NTG o Give aspirin if not already given before arrival to ED o Give high-dose statin o Draw/monitor serum cardiac biomarkers o Other drugs that may be given after emergency timeframe Beta-blocker ACE inhibitor or ARB Stool softener (avoid vagal stimulation) What are some considerations for thrombolytic therapy? When is it indicated? When is it contraindicated? What are our major complications with this therapy? o Indication: STEMI – back up treatment to break up clots when the hospital doesn’t have the means to do PCI or Cath labs. o Contraindications: active internal bleeding, suspected aortic dissection o Prior to administration: invasive procedure before, IVs before, Cardiac Part II Content Guide-Fall 2021 o During administration: try monitor VS, rhythm, cerebral bleeding (neuro assess), heart sounds, o After reperfusion: ST segment return to baseline -normal sinus rhythm. o Major concerns/complications: reocclusion (chest pain, ECG changes), internal bleeding (hypotension, pallor, changes in mental status) How long does it take to heal after an MI? o 10 to 14 days after MI, scar tissue is still weak Heart muscle vulnerable to stress Monitor patient carefully as activity level increases o By 6 weeks after MI, scar tissue has replaced necrotic tissue Area is said to be healed, but less compliant May be clinically manifested in abnormal wall motion on echocardiogram, LV dysfunction, dysrhythmias, or HF o Ventricular remodeling Normal myocardium will hypertrophy and dilate to compensate for infarcted muscle What are the major complications post MI? How will you assess for/treat these complications? What patient education should you provide someone recovering from ACS? When can they get back to usual activities? Are there any safety considerations r/t activity that you should warn them about? o Psychosocial Response to ACS and Patient Teaching o May see various psychosocial responses to ACS Ex: anger anxiety, denial, depression, etc. Assess support systems o Provide appropriate patient teaching Assess health literacy and learning needs Consider timing of teaching Ex: patient likely doesn’t want to learn about atherosclerosis right after their MI. They may want to know about when they can get out of the ICU, when they can go back to work, will this happen again, etc. Chapter 34: What are major causes and risk factors for heart failure? o Causes Conditions that directly damage the heart: heart attack, HTN, CAD Conditions that increase the workload of the heart: anemia, sleep dyspnea, infection o Risk Factors: HTN (modi), CAD, diabetes, metabolic syndrome, tobacco use Cardiac Part II Content Guide-Fall 2021 What are the different classifications of heart failure? o Left vs. right Right: blood backs up in venous system ascites, edema, renal megalo, o HFrEF (EF=ejection fraction below 40%) vs. HFpEF (normal EF) HFrEF: reduce ejected fraction, also called systolic, SBP: <40 Diastolic = HFpEF o AHA/ACCF vs. NYHA What compensatory mechanisms does the body use? What are some beneficial counterregulatory mechanisms that help the body maintain fluid balance? o Compensatory Mechanisms: the way the body helps to give the body more cardiac output or the way the boyd reacts to low cardiac output which sometimes might not be a good way sometimes RAAS System Promotes sodium/water retention with a goal of augmenting preload to maintain cardiac output Preload – volume, afterload - resistant. Sympathetic nervous system Baroreceptors sense low arterial pressure catecholamines released stimulation of β-adrenergic receptors which increases HR and contractility Ventricular dilation Enlargement of the heart chambers that occurs when pressure in left ventricle is elevated over time Initially effective (Frank-Starling Law); eventually this mechanism becomes inadequate and CO decreases Ventricular hypertrophy/remodeling Adaptive increase in muscle mass and heart wall thickness Initially effective; over time leads to poor contractility, increased O2 needs, poor coronary artery circulation, and risk for dysrhythmias o Beneficial Counterregulatory Mechanisms: helps us decrease extra fluid on broad Natriuretic peptides Released in response to increased blood volume and ventricular wall stretching causes diuresis, vasodilation, lowered BP and counteracts effects of SNS and RAAS Nitric oxide and prostaglandin Released from vascular endothelium in response to compensatory mechanisms relax smooth muscle which results in vasodilation and decreased afterload What are the clinical manifestations of heart failure? Cardiac Part II Content Guide-Fall 2021 o o o o o o o o o o o o o o Fatigue Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Cough Tachycardia Palpitations Edema; hepatomegaly, pulmonary edema, Decreased UOP Skin changes: poor clammy, ashy skin Neurologic manifestations: dizzy, LOC, Sleep problems Chest pain Weight changes What is the difference between acute decompensated heart failure and chronic heart failure? o Sudden increase in HF symptoms and decrease in functional status o Clinical Manifestations: dyspnea, orthopnea, coughing, anxiety, cyanosis, increase resp accessory muscle used, (basically signs of pulmonary edema), pink frothy sputum o Nursing Assessment/Monitoring Vital signs O2 sats: less spo2 due to fluid backing up into the lungs Weight Mentation EKG: to check for a-fib and dysrhythmia: irregular HB Symptoms of volume overload: edema, JVD, crackles, hypoxia Decreased perfusion: hypotension, decreased UOP, cool extremities, altered mentation, dysrhythmias, worsening renal or liver function What are the major complications of heart failure? o Pleural effusion (look for dyspnea, cough, chest pain) o Dysrhythmias watch for clots o Hepatomegaly o Cardiorenal syndrome o Anemia when our kidneys aren’t perfusioning well then, the kidneys can’t create arthopoitin which is need to create RBC What are our goals in treating heart failure? What will you as the nurse do to manage this condition? What drugs may we give? What drugs may be given in chronic heart failure vs. acute decompensated heart failure? o Symptom relief o Optimizing volume status and cardiac output Cardiac Part II Content Guide-Fall 2021 o o o o o o Supporting oxygenation and end organ perfusion Identifying and addressing causes of heart failure Avoiding complications Teaching related to exacerbations Improve quality of life Effective discharge planning What diagnostic studies may we use when looking at heart failure? What should we teach our patients with heart failure about nutrition? What should be included in the nursing assessment of a patient with heart failure? What patient teaching should be included in a patient with heart failure? Post-Class Work: Required: o Cardiac Part II Readiness Assessment due by October 3 at 9pm o Cardiac Part II DB Questions due by 1159pm tonight o Cardiac Part II Learning Assessment due Thursday at 1159pm Recommended for additional application practice: o Case Study on Myocardial Infarction on page 731 in your textbook o Case Study on Heart Failure on page 751 in your textbook