Student CAD/ACS Study guide

CAD & Acute Coronary Syndrome

Impact of CAD on Health

CAD= profound effect on perfusion.

Perfusion depends on the hearts ability to generate enough cardiac output to distribute blood to all bod tissues.

CAD negatively affects cardiac function; impaired CO and decrease perfusion.

Defining Coronary Artery Disease (CAD)

Coronary artery disease is defined as a condition affecting the blood vessels due primarily to atherosclerosis. This condition initiates when adipose (fat) deposits accumulate in the arterial walls, leading to a progression termed atherosclerosis, often referred to colloquially as "hardening of the arteries." Over time, this accumulation leads to the stiffening and narrowing of the arterial walls, which hinders normal blood flow and can result in severe cardiac events.

• ARTHEROSCLEROSIS- major cause of CAD

  • Lipid deposits within intima of artery.

  • Endothelial injury and inflammation play a major role in development.

Key Terminology in CAD

• Atheromas: FATTY DEPOSITS- form in coronary arteries called CAD.

• ASHD (Arteriosclerotic Heart Disease): This encompasses heart diseases caused specifically by the hardening and narrowing of arteries.

• CVHD (Cardiovascular Heart Disease): A broader category that captures various heart-related complications arising from vascular problems.

• IHD (Ischemic Heart Disease): Refers to conditions caused by insufficient blood flow to the heart muscle, frequently resulting from CAD.

• CHD (Coronary Heart Disease): A subtype of heart disease that specifically stems from atherosclerotic changes in the coronary arteries.

Pathophysiology of CAD

Primary Etiology

• Collateral circulation

• Arterial anastomoses (connections) within coronary circulation.

• Contributing factors:

  • Inherited

  • Presence of chronic ischemia.

• Rapid onset of CAD or coronary spasm results in severe ischemia or infarction.

Development of Atherosclerotic Lesions

• Fatty Streaks: Earliest lesion; lipid flilled, smooth muscle cells, appears yellow.

  • Starts at age 20 and increases as aging.

  • Treatment to lower LDL may slow process.

• Atherosclerosis causes CAD due to fatty deposits narrowing the vessel making it harder for 02 to get where it needs to go.

• CAUSES/RF- SODDA

  • S- stress, stimulants, smoking, severe weather, sexual activity

  • O- obesity, (BMI over 25)

  • D- diabetes and hypertension (140/90)

  • D- Diet high in cholesterol

  • A- African American males and age over 50.

Complication of Plaque Lesions

• Complicated Lesions: Persistent inflammation may destabilize plaques, resulting in ulceration or rupture. Such destabilization can lead to acute thrombotic events, where platelets aggregate to form a thrombus that severely obstructs arterial diameter, exacerbating ischemic conditions in the heart.

Evaluating Risk Factors for CAD

Assessment Approaches

To determine an individual's risk of developing heart disease or stroke, healthcare providers generally conduct an assessment that combines both 10-year and lifetime risk evaluations. This multifactorial approach considers various demographic, lifestyle, and laboratory data.

• Treatment guidelines for treating high LDL are based on 10 year and life time risk score for having heart disease and stroke.

• Data considered: age, gender, race, tobacco use, diabetes, systolic BP, diastolic BP, use of BP drugs, total cholesterol level, and HDL level.

Major Risk Factors for CAD

• Demographics: Key demographic risk factors include variables such as age, gender, and ethnicity, all influencing the likelihood of CAD.

• Lifestyle Factors: Identified lifestyle contributions include tobacco use, diabetes presence, and blood pressure levels, which have a direct correlation with heart disease risk.

• Laboratory Values: Laboratory evaluations consisting of total cholesterol levels and HDL (high-density lipoprotein) concentrations provide critical insights into an individual's cardiovascular health.

Modifiable Risk Factors Commonly Associated with CAD

• High Serum Lipids:

  • Cholesterol: Total cholesterol levels exceeding 200 mg/dL are regarded as a potential risk factor warranting intervention.

  • HDL Level:GOOD An HDL level beneath 40 mg/dL signifies higher cardiovascular risk, while elevated levels are associated with protective benefits against lipid accumulation.

  • LDL Level:BAD LDL levels surpassing 130 mg/dL significantly increase risk, emphasizing the necessity for therapeutic lifestyle and pharmacological interventions.

• Hypertension:

  • Blood Pressure Classification: Recognized categories include:

    • Normal: Less than 120/80 mmHg.

    • Elevated: 120-129 systolic and less than 80 diastolic.

• Tobacco Use: The consumption of tobacco and nicotine has adverse effects that elevate heart rate and blood pressure, propelling the development of atherosclerosis.

• Physical Inactivity- lack of regular exercise.

  • Recommend: 30-60 minutes of brisk walking 5days/week.

• Obesity- BMI more than 30, increased LDL/triglycerides/HTN/insulin resistance.

Additional Contributing Modifiable Risk Factors

• Diabetes: This condition enhances CAD risk by 2 to 4 times due to metabolic derangements associated with insulin resistance and glucose intolerance.

• Metabolic Syndrome: Defined by a cluster of pathologies including central obesity, hypertension, dyslipidemia, and elevated fasting glucose levels, all contributing to increased cardiovascular risk.

Further Considerations on Risk Factors

• Psychological States: Personality traits aligning with type A characteristics are linked to heightened stress, anxiety, and depressive symptoms—factors that adversely affect endothelial health and increase injury propensity over time.

• Increased Homocysteine Levels: Elevated homocysteine plays a detrimental role on endothelial integrity, contributing to the formation of atherosclerotic plaques.

• Substance use- cocaine and meth= coronary artery spasm= chest pain and MI.

Non-Modifiable Risk Factors for CAD

Non-modifiable risk factors consist of inherent attributes like age, gender, race, family history, and genetic predispositions, which increase susceptibility to CAD, independent of lifestyle or behavioral modifications.

• AGE

• GENDER

• ETHNICITY

• FAMILY HISTORY

• GENETICS

Management Strategies for High-Risk Individuals

Prevention and Education Strategies

The emphasis should be on controlling modifiable risk factors, facilitating health education, and promoting lifestyle changes that optimize cardiovascular health.

Recommendations for Physical Activity

• FITT Framework for Exercise:

  • Frequency: Encourage engagement in physical activity several times per week.

  • Intensity: Aim for moderate levels of exertion during activities for cardiovascular benefits.

  • Type: Prioritize aerobic exercises complemented by elements of strength training for comprehensive fitness.

  • Time: Aim for a minimum of 30 minutes of daily exercise throughout the week.

Nutritional Therapy and Dietary Recommendations for CAD

Astute dietary modifications are advised, which advocate reduction in saturated fats and cholesterol, while promoting the intake of complex carbohydrates and dietary fiber, thereby fostering cardiovascular health.

• Reduced saturated fats and cholesterol

• Increased complex carbs and fiber. (whole grains, fruits, veggies) Fiber=beans-legumes.

• Reduced red meat, egg yolks, and whole milk(these are saturated fats)

• Increased omega 3 fatty acids (salmon, tuna, and mackerel)

• Unsaturated fats (unsalted nuts-walnuts, peanuts, almonds) and avocado.

• Use fresh or frozen veggies and fruits over canned.

Lipid-Lowering Pharmaceutical Therapy

• Initial Statin Therapy Recommendations: Statins are commonly prescribed for patients diagnosed with CAD or exhibiting elevated levels of LDL, with an emphasis on reinforcing lifestyle changes and medication concordance is paramount.

• Drug Options for Lipid Management:

  • Statins: Statins inhibit hepatic cholesterol synthesis, contributing to lower LDL levels while also elevating protective HDL levels; however, regular monitoring is vital due to potential side effects.

    • Rosuvastatin (crestor)- most potent statin, serious adverse reactions are rare.

      • S/E- liver damage, myalgia(muscle ache or weakness without breakdown of skeletal muscle).

    • Simvastatin (Zocor)- increased risk for rhabdomyolysis when used with fibric acid derivatives (gemfibrozil), niacin, or erythromycin.

      • PTT times may increase in patients taking warfarin.

      • Dose should not exceed 40 mg daily.

      • Use caution in patients on amiodarone because is increases the risk of myopathy.

    • Atorvastatin (Lipitor), Fluvastatin (Lescol XL), lovastatin, pitavastatin, pravastatin.

      • S/E: rash, GI problems, increased liver enzymes, myopathy, rhabdomyolysis.

      • Well tolerated with few side effects, monitor liver enzymes and recheck them after any increase in dosage, assess CK-MM if s/s of myopathy(muscle aches, weakness).

  • Additional Drug Types:

    • Niacin: Reduces LDL and triglyceride by inhibiting synthesis, increased HDL.

      • S/E- flushing, pruritus, GI symptoms, orthostatic hypotension.

      • Teach patient: flushing may occur within 20 mins after taking drug and last 30-60 mins.

      • Premedicate with aspirin 30 mins before taking to reduce flushing.

      • Use of extended release niacin may decrease side effects.

      • Take with food.

    • Fibric Acid Derivatives: Reduces triglycerides, increased HDL.

      • Fenofibrate (Tricor), gemfibrozil (Lopid)

      • S/E: rashes, nausea, diarrhea, increased liver enzymes.

      • Increases bleeding with warfarin and effects of antihyperglycemic drugs(repaglinide).

      • USE CAUTION IN PATIENTS TAKING STATINS DUE TO R/F MYOPATHY.

• Drug therapy is life long.

• Concurrent diet changes, weight loss, and increased physical activity.

• Reassess after 6 weeks.

Therapeutic Classes for Lipoprotein Reduction

• Bile Acid Sequestrants: Increase conversion of cholesterol to bile acids; reduced total cholesterol and LDL.

  • Colesevelam (Welchol), colestipol (Colestid), cholestyramine (Prevalite).

    • S/E: GI side effects (constipation, bloating, indigestion), reduced absorption of other drugs, unpleasant quality of taste

    • Side effects lessen with time.

    • Interferes with absorption of digoxin, thiazide diuretics, warfarin, penicillin.

    • Take other drugs 1 hour before or 3-4 hours after this medication.

• PCSK9 Inhibitors: Block PCSK9 to lower LDL; given subcutaneously.

  • Alirocumab (Praluent), evolocumb (Repatha).

    • S/E: injection site reactions, muscle pain, limb pain, and fatigue.

    • Used with diet therapy and maximum statins.

Cholesterol Absorption Inhibitors

• Ezetimibe (Zetia): Decrease absorption of dietary and biliary cholesterol; combine with statin.

  • S/E= infrequent but may include headache and mild GI distress.

  • When used with a statin, further reduces LDL.

  • Avoid in patients with liver problems.

• Antiplatelet therapy- low dose aspirin (81mg)- contraindicated with risk of bleeding.

  • Clopidogrel (plavix)

Gerontologic Considerations CAD.

Older adults exhibit a higher incidence and risk associated with CAD, leading to the necessity for tailored long-term management strategies that address this population's unique needs and vulnerabilities.

• Increased incidence and mortality associated with CAD in older adults.

• Reduce risk and treat CAD

  • treat hypertension and increased lipids.

  • Smoking cessation, increased physical activity.

  • Most likely to change when hospitalized or have chest pain.

Chronic Stable Angina

Definition and Characterization

• Asymptomatic results in chronic stable chest pain (angina)

  • 02 demand greater than 02 supply results in myocardial ischemia.

  • Angina= clinical manifestation.

    • 1 or more arteries are blocked 70% or more in myocardial ischemia.

    • 50% or more for left main coronary artery.

• The most common reason for angina to develop is significant narrowing of 1 or more coronary arteries by atherosclerosis.

• Chronic stable angina refers to chest pain that occurs intermittently over a long period of time with a similar pattern of onset, duration, and intensity of symptoms.

  • Often provoked by stress, physical exertion, or emotional upset.

Characteristics of Symptoms

• S/E: pressure/heaviness/discomfort in chest, squeezing/heavy/tight/suffocating sensation. Dyspnea, fatigue.

• Duration of pain: usually only a few minutes.

• Subsides when precipitating factor resolved

  • Rest, calm down, sublingual nitroglycerin.

  • Usually does not change with position or breathing.

Pain Management Approaches

Management of anginal pain typically involves cessation of activity, use of nitroglycerin for rapid symptomatic relief, and close observation for any accompanying ECG changes that may suggest worsening ischemia.

• PQRST

  • P- precipitating events- what events or activities triggered the pain.

  • Q- quality of pain- what does the pain feel like (pressure, dull, tight)

  • R- region- location and radiation of pain.

  • S- severity of pain- 0-10 or faces

  • T- timing- when did it start, has it happened before.

Silent Ischemia

Definition

Silent ischemia refers to ischemic events occurring without overt symptoms, often diagnosed through the presence of characteristic changes on the ECG during clinical assessments.

• Ischemia that occurs in absence of any subjective symptoms.

• Associated with diabetic neuropathy.

• Confirmed by ECG changes. (ST depression and T wave inversion)

Precipitating Factors of Angina

• Circadian rhythm patterns- early morning.

• Consumption of a heavy meal- can increase workload of the heart.

• Physical exertion- increased HR, isometric excercise of the arms (raking, lifting heavy objects, snow shoveling.)

• Sexual activity- increases cardiac workload and sympathetic stimulation.

• Stimulants- cocaine/amphetamines- increase HR and BP= increases myocardial 02 demand. Stimulate vasoconstriction, may precipitate dysrhythmias.

• Strong emotions- stimulate the sympathetic nervous system, activating the stress response.

• Temperature extremes- increase the workload of the heart.

Types of Angina

• Prinzmetal's Angina: rare form of angina that often occurs at rest without increased physical demand. Hyperreactivity of the smooth muscle of a major coronary artery resulting in strong contraction (spasm) of the vessel.

  • Triggered by smoking, increased level of histamin, epinephrine, cocaine.

    • R/F- migraine headaches, Raynaud’s phenomenon, and heavy smoking.

    • S/S: pain may occur during rapid eye movement (REM) sleep when myocardial 02 consumption increases btwn midnight and early morning or at rest. Cyclic, short bursts of pain at the same time each day may occur.

    • Treatment- pain relieved by SL nitro or may disappear spontaneously. Exercise training may reduce episodes of angina.

      • Calcium channel blockers or nitrates.

• Microvascular Angina: Chest pain occurs in the absence of significant CAD or coronary spasm of a major coronary artery. Chest pain is related to myocardial ischemia from atherosclerosis or spasm of the small distal branch vessels of the coronary microcirculation. More common in women.

  • Often prolonged and brought on by physical exertion.

    • daily living activities- shopping, work, exertion.

  • Positive stress test.

  • Treatment- nitro (long and short)

• Unstable Angina- rupture of unstable plaque, exposing thrombogenic surface.

  • New onset angina

  • Occurs at rest or with minimal exertion.

  • Lasts more than 10 mins.

Nursing Responsibilities for Stable Angina

Interventions Focus

Nursing care should center on optimizing myocardial perfusion, leveraging medications that enhance cardiac output and ultimately improve patient outcomes.

• Assess patient for restlessness, ECG changes, high HR/RR/BP, clutching chest or bed linens.

• Position upright, apply oxygen.

• Assess: VS, heart, and breath sounds.

• Continuous ECG monitor, 12 lead ECG.

• Pain relief- NTG, IV opioid if needed.

• Obtain cardiac biomarkers

• Obtain chest xray

• provide support, reduce anxiety.

Acute Care for Angina Management

Essential Management Practices

Immediate management strategies encompass appropriate patient positioning, timely medication administration, and diligent monitoring of vital signs and ECG to recognize any acute deterioration in condition.

• A- antiplatelet/anticoagulant therapy, antianginal therapy, ACE inhibitor/angiotensin receptor blocker.

• B- beta blocker, BP control.

• C- cigarette smoking cessation, cholesterol management, calcium channel blockers, cardiac rehabilitation.

• D- diet, diabetes management, depression screening.

• E- education, exercise.

• F- flu vaccination.

Ambulatory Care Strategies for Angina

Patient Education

Patient education initiatives should revolve around recognizing angina symptoms accurately and implementing effective management strategies for associated cardiovascular risk factors.

• Diet low in salt and saturated fats.

• Maintain ideal body weight

• Physical activity

• Avoid triggers.

• Medications

  • Nitro- ortho static hypotension, monitor BP.

    • Warn patient- headache, dizziness, flushing may occur.

  • angiotensin-converting enzyme (ACE)

  • Beta Blocker

  • Calcium Channel Blockers

  • Aspirin

Drug Therapies for Angina Management

• Aspirin and Nitrates: These medications are frequently prescribed for short-term relief of anginal pain while helping to mitigate ischemic episodes.

• Long-Acting Nitrates: Used in chronic angina management with attention to potential side effects like headaches; patient counseling on these effects is essential. {Isosorbide dinitrate (Isordil) and isosorbide mononitrate (Imdur).

  • 10-14 hours nitrate free period everyday.

  • Reduce frequency of angina attacks and treat Prizmetal angina.

• Nitrates:

  • Keep SL NTG tablet in dark, airtight container.

  • Sit down before taking sort acting nitrates.

  • Teach patient not to combine NTG with drugs used for erectile dysfunction (Sildenfil) d/t severe hypotension risk.

  • Never cardiovert of defibrillate over NTG ointment or patch.

ACE Inhibitors and β-Blockers

These therapeutic classes are critical in reducing myocardial workload and preventing subsequent cardiac damage; emphasis on potential side effects is warranted for patient safety.

ACE- Lisinopril

• Take with chronic stable angina if ejection fraction of 40% or less, diabetes, hypertension, or CKD.

• Prevent or reverse ventricular remodeling in patients who have had an MI.

BETA - {carvedilol (Coreg), metoprolol (Toprol XL), bisoprolol (Zebeta)

• Relieve angina symptoms in patients with chronic stable angina. .

• Contraindicated in asthma, severe bradycardia, and acute decompensated HF.

• S/E: bradycardia, hypotension, wheezing, GI effects, weight gain, depression, fatigue, sexual problems.

Calcium Channel Blockers

These agents promote vasodilation and are key contributors to angina treatment regimens, requiring detailed education about possible adverse effects and the integration of newer formulations into patient care.

• Amlodipine, nifedipine (cause more vasodilation) and verapamil, diltiazem (decrease HR and contractility).

• If beta blockers are contraindicated, poorly tolerated, or do not control angina s/s then we use calcium channel blockers.

• S/E: fatigue, headache, dizziness, flushing, hypotension, and peripheral edema.

• Monitor if on digoxin, can increase levels.

• Verapamil can cause severe constipation in older adults.

Diagnostic Studies for Angina

Assessment Protocols

The clinical evaluation of angina typically employs a variety of diagnostic tools, including ECGs and serum cardiac biomarkers, to assess cardiac health and functionality.

• ECG / 12 lead

• Labs: cardiac biomarkers, lipid profile, CRP

• Chest xray- heart enlargement, aortic calcifications, pulmonary congestion.

• Echocardiogram- detect resting LV wall motion abnormalities.

Cardiac Catheterization Procedures

Purpose

The primary objective of cardiac catheterization is to ascertain the presence of CAD and evaluate for any potential occlusions within coronary arteries. It further facilitates both the diagnostic assessment and intervention when needed.

• Can identify and localize CAD.

• If coronary blockage- coronary revascularization with percutaneous coronary intervention.

Stent Placement

Stent placement involves understanding internal components and stresses the importance of correctly deploying stents following percutaneous coronary interventions (PCI) for optimal patient outcomes.

Post-Stent Care Requirements

Post-stent care necessitates administering medications aimed at preventing complications, with dual antiplatelet therapy recommended to mitigate thrombotic risk following implantation.

Nursing Management: Pre and Post PCI

Comprehensive Assessment

Thorough evaluation criteria established prior to and following catheter-based interventions are crucial for safeguarding patient safety and achieving successful outcomes.

Preprocedural:

• Assess for allergies- contrast??, assess renal function.

• Vitals, distal pulses/color

• NPO X 6-12 HRS

• Baseline labs- cardiac biomarkers, creatinine.

• Teach post procedure care.

Monitoring After Procedures

Continual observation for potential complications post-PCI must be coupled with patient education covering post-discharge care instructions, ensuring comprehensive understanding of self-management practices.

Complications:

• abrupt closure from coronary artery dissection or rupture.

• Vascular injury at the artery access site.

• acute MI from acute stent thrombosis or from plaque dislodging and blocking the vessel distal to the ordinal blockage.

• stent embolization

• coronary spasm

• dye allergy

• renal problems

• bleeding -retroperitoneal bleeding)

• infection

• stroke

• emergency CABG.

Monitoring

• ECG d/t increased r/f dysrhythmias.

• assess cathetar site for bleeding, neurovascular assessment.

• Monitor for s/s of chest pain or other discomfort.

• Antianginals and antiplatelet.

• Bedrest as needed.

• Discharge drugs (aspirin, clopidogrel, lipid lowering drugs.

Assistive personal

• Take vitals and report to RN.

• Report any pain.

• Help with oral hygiene and hydration, meals, toileting.

• Record I&Os

Coronary Surgical Revascularization

CABG Indications

Coronary artery bypass grafting (CABG) is strategically indicated in instances where medical management fails to alleviate symptoms or improve quality of life effectively.

CABG Surgical Methods

The traditional surgical approach entails the placement of grafts following sternotomy while utilizing cardiopulmonary bypass (CPB). In recent years, advancements in minimally invasive techniques explore smaller incision strategies, linking to improved patient outcomes and faster recovery.

Advanced Surgical Techniques

Innovative techniques such as Totally Endoscopic Coronary Artery Bypass (TECAB) and Transmyocardial Laser Revascularization are evolving to cater to specific anatomical variations and patient requirements.

Postoperative Care Following CABG

Providing detailed insights into intensive care unit (ICU) monitoring parameters essential for successful postoperative management are outlined to ensure optimal recovery and mitigate complication risks.

• Hemodynamic monitoring, arterial line continuous BP monitoring.

• pleural/Chest drain

• mechanical ventilation

• Urinary catheter to monitor urine output.

• NG tube for gastric decompression.

Teaching:

• Wound care

• mange pain/ prevent venous thromboembolism.

  • early ambulation, sequential compression devices.

• Respiratory complications

  • incentive spirometry, splinting during coughing, deep breathing exercises.

Common Postoperative Complications

Recognizing and managing potential complications that may arise after CABG surgery, such as bleeding, infection, or graft failure, is crucial for facilitating positive recovery trajectories.

• Systemic inflammation.

• Bleeding/anemia from damage to RBC and platelets.

• Fluid and electrolyte imbalances.

• Hypothermia and infections. (warming blankets, monitor drain sites)

• FOCUS ON BLEEDING!!

• Postop dysrhythmias (atrial fibrillation).

• BETA BLOCKERS ASAP after surgery to delay AF and control HF, start anticoagulation.

• Posttoperative cognitive dysfunction: can manifest days to weeks after surgery.

  • S/S: impaired memory, concentration, language comprehension, and social integration. Depression and anxiety are common.

Ongoing Management of Complications

Management strategies focus on effective pain control, prevention of venous thromboembolism (VTE), and addressing respiratory concerns during the critical recovery phase following surgical interventions.

Alternative Therapies for Angina Management

Enhanced External Counterpulsation (EECP)

This novel therapy explores mechanisms, applications, and contraindications that may serve as effective treatment modalities for patients dealing with angina symptoms.

Acute Coronary Syndrome Overview

Definition and Types

Acute coronary syndrome (ACS) is characterized by episodes of prolonged ischemia, presenting differently based on individual circumstances and underlying causes, necessitating unique management approaches tailored to each scenario.

• When chest pain from ischemia is prolonged and not immediately reversible, acute coronary syndrome may develop. ST elevations on the 12 lead ECG likely indicate a STEMI. Whereas patients with unstable angina and non ST elevation may or may not have ST segment depression or T wave inversion. WE MUST EVALUTE SERUM CARDIAC BIOMARKERS.

• ACS occurs when previously stable atherosclerotic plaque ruptures. releasing the lipid core into the vessel.

Relationship Between CAD and ACS

Understanding the distinctions between chronic stable angina and acute coronary syndrome is vital for providing clarity in clinical presentation and subsequent management strategies.

Clinical Presentation in ACS

Key focus is directed toward recognizing classic chest pain presentations accompanied by specific ECG changes that indicate the occurrence of a myocardial infarction (MI).

Cellular Response to Acute Coronary Ischemia

Examining the cellular consequences of total occlusion elucidates the pathophysiological responses occurring during acute coronary events, reinforcing the importance of timely intervention.

Etiology of ACS

Mechanisms of Plaque Deterioration

This section highlights various mechanisms leading to plaque instability, which culminates in acute coronary syndrome episodes, including unstable angina (UA) or non-ST elevation myocardial infarction (NSTEMI).

Characteristics of Unstable Angina

Unstable angina is chest pain that is new in onset, occurs at rest, or occurs with increasing frequency, duration, or less effort than the patients chronic stable angina patter. The pain usually lasts 10 mins or more.

• Unpredictable and must be treated immediately.

• S/E: chest pain that progressed rapidly in the past few hours. ST depression and or T wave inversion.

Myocardial Infarction Details

Causes

Myocardial infarction (MI) occurs because of an abrupt stoppage of blood flow through a coronary artery with a thrombus caused by platelet aggregation. This causes irreversible myocardial cell death (necrosis) in the heart muscle beyond the blockage.

• STEMI is an emergency. To limit the infarct size, the artery must be opened within 90 MINUTES of presentation to restore blood and 02 to the heart muscle.

  • 1st line of treatment is PCI (cath lab). 2nd Thrombolytic therapy.

• Hypokinesis (worsening myocardial contractility)

• Akinesis (absent myocardial contractility)

Treatment Approaches for STEMI and NSTEMI

Period of urgent treatment following indications tailored towards clinical presentations of STEMI versus NSTEMI highlights the importance of timely medical interventions aimed at preserving heart function.

Evolution of Myocardial Infarction

The progressive stages of tissue damage in MI correlating with specific time frames elucidate the consequential areas affected throughout this pathological process.

Atherosclerosis=plaque rupture= MI

Clinical Manifestations of Myocardial Infarction

Detailed descriptions of the hallmark pain and other clinical presentations typical during myocardial infarctions emphasize the complexities and urgency of these acute events.

• S/E: Pain- persistent and unlike any other pain, heavy/pressure/tight/burning/crushing feeling. (Neck/lower jaw/arms), weakness, nausea, indigestion, SOB, fatigue.

  • diaphoresis, increased HR and BP, vasoconstriction of peripheral blood vessels, ashen/clammy/cool skin.

• Diabetics s/s may be different due to cardiac neuropathy (SOB usually).

• Older adults- may have mental status change, SOB, pulmonary edema, dizziness, dysrhythmia.

• women- nausea/vomiting, pain in back, fatigue, pain in shoulder or jaw.

Cardiovascular Changes During MI

This section outlines hemodynamic changes occurring during myocardial infarctions, including potential complications directly related to heart function.

• BP and HR high at first, later BP drops, decreased renal perfusion and urine output

• Crackers may persist several hours, possibly LV dysfunction.

• Right ventricular dysfunction: S/E: jugular venous distention, hepatic engorgement, peripheral edema.

Gastrointestinal Symptoms Associated with MI

Recognition of gastrointestinal manifestations, such as vomiting and transient fever, post-MI exemplifies the systemic effects typically observed following acute cardiac events.

• Nausea, vomiting (r/t vasovagal reflexes)

Other s/s

• Fever- may increase to 100.4 within 24-48 hours. R/T systemic inflammatory process.

Healing Process Subsequent to Myocardial Infarction

Stages of the healing and cellular regeneration phases following myocardial infarction highlight critical insights into the recovery process and associated clinical considerations for ongoing patient care.

10-14 Days Post-MI Monitoring

Accentuates the need for diligent monitoring during early scar formation and evaluations of exercise tolerance as patients progress through their recovery.

Formation of Scar Tissue

Describes long-term implications of myocardial healing through the scar formation process and the remodeling effect on cardiac function and health outcomes over time.

Complications Occurring Post-MI

Risks of Dysrhythmias

This section elucidates the prevalence of arrhythmias following MI and outlines effective management strategies to address these complications.

• Ventricular tachycardia and ventricular fibrillation are the most common cause of death in patients in the prehospital period.

• Bradycardias can develop when key areas of the conduction system are destroyed.

• Electrolyte imbalances= potassium!!

Presentation of Heart Failure

Focus on manifestations specific to left-sided and right-sided heart failure resulting from myocardial infarction reveals the complexity of post-MI recovery and management strategies.

• Left sided HF: mild dyspnea, restlessness, agitation, slight tachycardia, pulmonary congestion, S3 heart sound, crackles on auscultation of the lungs, paroxysmal nocturnal dyspnea, and orthopnea.

• Right sided HF: jugular vein distention, hepatic congestion, abdominal distention, lower extremity edema.

Management of Cardiogenic Shock

Cardiogenic shock occurs when 02 and nutrients supplies to the tissues are inadequate because of severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, or right ventricular infarction.

• TX: control dysrhythmias, mechanical circulatory devices, extracorporeal membrane oxygenation (ECMO), and support of contractility with vasoactive drugs (dobutamine).

• Goals: maximize 02 delivery, reduce 02 demand, prevent complications (Acute kidney injury)

Structural Complications: Papillary Muscle and Ventricular Dysfunction

Discusses how myocardial infarction can lead to significant structural changes, including mitral valve dysfunction, necessitating surgical evaluation and potential intervention in severe cases.

• Rare and life threatening complication, causes acute and massive mitral valve regurgitation with no time for the heart to compensate.

• S/E: dyspnea, pulmonary edema, and decreased CO result from the backup of blood in the left atrium.

• Treatment: afterload reduction with nitroprusside (Nipride) and/or IABP therapy and immediate surgery with mitral valve repair or replacement.

Urgency of Septal Ruptures

Addresses the pressing need for surgical interventions following septal ruptures that may occur post-myocardial infarction, emphasizing the critical nature of timely treatment.

• A new loud systolic murmur heard in patients with acute MI may signal ventricular septal wall rupture. This requires prompt evaluation and diagnostic imaging to confirm the presence of the rupture, as delays can significantly increase morbidity and mortality rates.

Pericarditis and Its Implications

Explores symptoms and appropriate treatment strategies for managing post-MI pericarditis, which requires ongoing attention to patient care during recovery.

• Acute pericarditis- an inflammation of the visceral and/or parietal pericardium, may occur 2-3 days after an acute MI.

• S/E: mild to severe chest pain that increases with inspiration, coughing, and movement of the upper body. Sitting in a forward position often relieves the pain, fever, hypotension, narrow pulse pressure.

• Assess for presence of a friction rub over the pericardium./ MID to lower left sternal border.

• ECG changes: ST elevations, Inflammation of the pericardium.

• TX: high doses of aspirin, nonsteroidal anti-inflammatory drugs and corticosteroids are avoided first 4 weeks after MI.

Dressler's Syndrome

Investigation into Dressler's syndrome, a form of chronic inflammation following myocardial infarction, emphasizes the need for targeted management strategies to alleviate symptoms and improve patient outcomes.

• Dressler syndrome is pericarditis and fever that develop 1-8 weeks after MI. Cause is unclear, may be an autoimmune reaction to the necrotic heart muscle.

• S/E: chest pain, fever, malaise, arthralgia, pericardial friction rub.

• Labs: high white blood cell count and sedimentation rate.

• TX: high dose aspirin

Diagnostic Studies for Acute Coronary Syndrome

Importance of Health Assessment

Emphasizes the significance of a thorough health history and ECG evaluations in confirming a diagnosis of acute coronary syndrome, guiding effective treatment strategies.

• HX of pain, risk factors, healthy history.

• Unstable angina vs MI (STEMI vs NSTEMI)

• 12 lead ECG

• serum cardiac biomarkers

Serum Cardiac Biomarkers Characterization

Identifies the critical importance of serum cardiac biomarkers—including troponins and their timelines—regarding assessing the severity and occurrence of myocardial infarction events.

• Proteins released into the blood from necrotic heart muscle after an MI.

• UA= negative biomarkers.

• NSTEMI= positive biomarkers

• Troponin and CK levels

Timing Considerations for Catheterization

Presents detailed timelines and strategies for determining interventions in both STEMI and NSTEMI contexts, including recommended treatment approaches.

Emergency Management Strategies in ACS

Essential Response Protocols

Details the necessary emergency response protocols for clinical interventions required during the onset of acute coronary syndrome, emphasizing collaborative care delivery.

• Vitals, 12 lead ECG, upright position, 02 nasal cannula, IV access, give SL NTG, morphine, high dose statin (atorvastatin) Baseline labs.

• ST elevation= directly taken to cardiac catheterization.

• ST depression and/or T wave inversion= admit to ICU or telemetry unit for ongoing care.

• UA and NSTEMI start on heparin or GP IIB/IIIA inhibitors (epitifibate) before cath or at the time of PCI.

Differential Findings in ECG and Subsequent Management

Differentiation between STEMI and NSTEMI based on ECG findings serves to inform subsequent management decisions and therapeutic interventions.

Glycoprotein IIb/IIIa Inhibitors

Discusses the timing and effectiveness of glycoprotein receptor inhibitors during the acute treatment phases of acute coronary syndromes, offering insight into management protocols.

Acute Care Management in Hospital Settings

Highlights the necessity for intense monitoring and supportive measures during early acute coronary events, underscoring the commitment to patient safety and quality of care.

Heparin Therapy Application

Critical consideration of heparin therapy in the management of unstable angina, NSTEMI, and MI within acute care scenarios is an essential strategy for reducing thrombotic events.

PCI as Primary Treatment Option

Outlines the timing and essential clinical goals for utilizing percutaneous coronary interventions (PCI) to effectively reopen obstructed arteries during acute presentations, prioritizing quick restoration of blood flow.

Advantages and Risks of PCI

Comparison of the advantages associated with PCI relative to CABG, while also identifying potential complications that may arise from the procedure encourage informed patient decision-making.

Thrombolytic Therapy Discussion

This section details indications for administering thrombolytic therapy, including the optimal timing necessary for achieving the best outcomes in the management of acute coronary events.

• Give thrombolytic within 30 mins of the patients arrival to the ED.

Criteria for Administering Thrombolytics

Outlines contraindications and essential assessments that are required prior to administering thrombolytics to ensure patient safety and therapeutic efficacy.

• All thrombolytics (Tenecteplase, alteplase) are given IV.

• Complication: major or minor bleeding. s/e: drop in BP, increase in HR, sudden change in the patients mental status, blood in urine or stool.

Monitoring Strategies During Thrombolysis

Key measures to be observed during the administration of thrombolytics are essential for averting negative outcomes and guaranteeing effective reperfusion.

Evaluating Reperfusion Outcomes

Identifying the distinctions between successful and unsuccessful outcomes following reperfusion efforts post-thrombolytic therapy provides critical insights for patient management strategies, guiding decision-making in ongoing care.

Comprehensive Overview of Drug Therapy in ACS

Multimodal Pharmacological Strategies

Explores the necessity for multimodal pharmacological strategies integral to the effective management of patients diagnosed with acute coronary syndrome, enhancing overall therapeutic effectiveness.

Further Pharmaceutical Considerations

Investigates the role of specific medication types in the comprehensive management of acute coronary syndrome and their contributions to patient outcomes.

• IV nitro- SL until IV. S/E: hypotension, monitor BP, IV fluid bolus.

• Morphine- vasodilator and relieves chest pain. Monitor BP and RR.

• Beta blockers- reduce HR.BP, and contractility. Reduce the risk of reinfarction and HF.

• Angiotensin- converting enzyme inhibitors and angiotensin receptor blockers.

  • ACE started within 24 hours if BP is stable and no contraindications.

  • ARBS if patient cannot tolerated ACE (angioedema, cough)

• Antidysrhythmic

• Lipid lowering drugs- Lipid panel, ACS and CAD should receive lipid lowering drugs indefinitely.

• Aldosterone antagonists- spironolactone, eplerenone- decrease mortality after a Stemi.

• Stool softeners- prevent straining and the Valsalva maneuver.

Nutritional Therapy Post-ACS

Prescribing initial dietary interventions post-ACS events emphasizes prioritizing low salt, fat, and cholesterol intake as vital components of recovery protocols.

• NPO until stable

• Low salt, low saturated fat, low cholestrol.

Comprehensive Nursing Assessment Strategies in ACS

Effective Data Collection Techniques

Comprehensive assessment strategies include both subjective and objective data collection, crucial for the formulation of an effective nursing plan of care tailored for individual patient needs.

Nursing Management Strategies During ACS

Focus on Pain Management and Monitoring

Focus on key areas such as pain management strategies, monitoring techniques, and comfort strategies tailored specifically for patients experiencing acute coronary syndrome.

Addressing Psychological Factors in Recovery

Supporting Emotional Responses

Understanding and supporting patients’ emotional responses to acute coronary syndrome is vital for promoting overall recovery and bolstering emotional resilience throughout the healing process.

Promoting Safe Increases in Physical Activity

Consideration of Gender Differences

Suggests carefully considered strategies for increasing physical activity levels following acute coronary syndrome, exhibiting sensitivity to gender differences and patient preferences.

Goals of Comprehensive Cardiac Rehabilitation

Holistic Rehabilitation Objectives

Outlines the multifaceted goals of cardiac rehabilitation focused on improving recovery, enhancing cardiovascular function, and ultimately elevating quality of life indicators, demonstrating the scope of rehabilitative care.

Guidance on Resuming Sexual Activity Post-MI

Communication and Comfort Considerations

Provides clear guidelines to patients regarding the safe resumption of sexual activity following a myocardial infarction, underscoring the importance of open communication and patient comfort in the process.

Sudden Cardiac Death (SCD) Overview

Definition and Exploration of Etiology

Sudden cardiac death is defined while delving into its etiology and the underlying risk factors contributing to its occurrence, providing a comprehensive framework for understanding this critical phenomenon.

• A sudden disruption in heart function from a life threatening dysthymia causes an abrupt loss of CO and cerebral blood flow.

• CAD is the main cause of SCD

Clinical Manifestations Indicative of SCD

Identifying Early Signs

Describes the early manifestations of sudden cardiac death and how they correlate with preceding myocardial infarction events, offering a basis for recognition and intervention.

Interprofessional Management Strategies for SCD

Importance of Collaborative Care

Highlights essential diagnostic considerations and effective treatment modalities that emphasize the necessity of an interprofessional approach to managing acute cardiac events and emergencies.

Preventative Strategies to Mitigate Recurrence of SCD

Comprehensive Intervention Outline

Overview of comprehensive interventions aimed at preventing SCD recurrence, which include the placement of implantable cardioverter-defibrillators (ICDs) and educational initiatives focused on CPR and emergency response measures.

Psychosocial Impacts of Sudden Cardiac Death

Addressing Patient Challenges

Addresses the various psychosocial challenges faced by patients recovering from sudden cardiac events to highlight supportive strategies that assist them in their emotional and psychological well-being during recovery.

Coronary Artery Disease

CAD - coronary arteries deliver a continuous supply of blood to the heart muscles. In CAD it will start to develop fatty plaques (restrict blood flow to the heart).

Fatty plaques are caused by Atherosclerosis, which is the buildup of fats, cholesterol, and other substances in and on the artery walls.

• Plaque buildup=rupture=thrombosis formation= R/F- MI, HF, HTN

• R/F= smoking, obesity, hyperlipidemia, sedimentary lifestyle, diabetes, family history.

• S/S: early stages= asymptomatic, chest pain with activity/fatigue/SOB (relieved with rest)

  • Progressing- more intense chest pain- nitro ins’t working, fatigue (NEEDS TX)

• Stable vs unstable angina

• Diagnostics

  • Lipoprotein {LDL(BAD), HDL(GOOD), total cholesterol, triglycerides}

  • EKG- ST or T wave issues

    • ST depression=ischemia

    • ST elevation= injury

  • Holter monitor: Continuous monitoring of heart rhythm to detect arrhythmias over a 24-hour period.

  • Stress test: A clinical test that evaluates the heart's performance under physical exertion or stress, helping to identify ischemic changes that may not be evident at rest.

    • Nuclear stress test- tracer injected during activity.

  • Heart catheterization: A procedure used to diagnose and treat certain heart conditions by inserting a catheter into the coronary arteries and inject dye to assess blood flow and identify blockages.

    • ANY ALLERGIES (SHELLFISH/IODINE), npo

    • PCI- if they found a blockage they can inflate a balloon in clogged artery and open up the artery with a stent.

  • Atherectomy- remove plaque from artery.

  • CABG- open heart surgery if needed.

• Nursing intervention: Education!!!

  • Prevent progression of disease, lifestyle changes, exercise, medications, smoking cessation.

  • Discuss treatments.

  • Monitor BP/heart rate.

  • Monitor lipid profiles.

  • Medications:

    • Antiplatelets- prevent platelets from forming and growing.

      • Aspirin- watch GI bleeding

      • Plavix- bleeding risk, not for patient with new stent placement?

        • S/E- TTP clotting disorder- small clots in vital blood vessels. neuro changes, renal failure, fever, bruising, low platelets, anemia.

    • Nitrates

      • Nitroglycerin- dilates BV to allow more blood to heart.

        • Sublingual, take when chest pain starts, repeat every 5 minutes for no more then 3 doses.

        • If chest pain is not relieved, go to ER!!

        • NOT FOR PATIENTS ON PHOSPHODIETERASES INHIBITORS (VIAGRA”) as this combination can lead to severe hypotension.

    • Cholesterol medications:

      • Statins- lipitor, crestor, zocor = decrease LDL and total cholesterol levels, thereby reducing the risk of cardiovascular events.

        • Continue to excerize and diet.

        • S/E- muscle pain/weakness - CALL PCP AND SWITCH MEDICATION.

        • CPK levels- can increase- which causes muscle pain.

        • Liver function monitor

    • Beta blockers (metoprolol,

      • Less episodes of chest pain.

      • Monitor in diabetic patients, can block s/s of hypoglycemia.

      • NOT for asthma or COPD patients.

      • NO grapefruit juice.

    • ACE inibitors (Lisinopril

      • Vasodilation= lower BP= decrease workload on heart.

      • May develop dry cough.

Myocardial Infarction= sudden blockage of blood flow into the heart.

NSTEMI VS STEMI

• Atherosclerosis= plaque buildup/fatty deposits= ruptures= thrombosis which occludes blood flow to the heart.

  • S/E: Pain- persistent and unlike any other pain, heavy/pressure/tight/burning/crushing feeling. (Neck/lower jaw/arms), weakness, nausea, indigestion, SOB, fatigue.

    • diaphoresis, increased HR and BP, vasoconstriction of peripheral blood vessels, ashen/clammy/cool skin, decreased renal perfusion=decreased urine output, crackles (LV dysf), jugular vein distention, hepatic engorgement, peripheral edema (RV dysf), abnormal heart sounds (S3 or S4, new murmur)

  • Diabetics s/s may be different due to cardiac neuropathy (SOB usually).

  • Older adults- may have mental status change, SOB, pulmonary edema, dizziness, dysrhythmia.

  • women- nausea/vomiting, pain in back, fatigue, pain in shoulder or jaw.

• Diagnostics:

  • Labs- elevated cardiac enzymes

  • EKG- ST elevation or depression, T wave inversion, abnormal Q wave.

  • Cardiac cath

  • STEMI OR NSTEMI= echocardiogram- hypokinesis or akinesis of necrotic areas.

    • LV dysfunction depends on area of heart and size of infarction.

• Medications- ALL IV IN EMERGENCY SITUATIONS

  • Aspirin

  • Plavix

  • Thrombolytics (TPA)

  • anticoagulants

  • anti hypertensive agents (BETA BLOCKERS, ACE)

  • Statins

  • MONITOR FOR HYPOTENSION!!!

• Surgical

  • PCI- open up coronary arteries- MUST BE PERFORMED WITHIN 12-72 HOURS OF ONSET OF S/S FOR NSTEMI.

    • Cath with balloon threaded through blood vessel to the blockage to compress plaque and improve blood flow, often accompanied by the placement of a stent to keep the artery open and restore blood flow.

    • Post op- monitor for bleeding, check perfusion to extremity distal from insertion site.

    • Monitor for complications

      • artery dissection

      • reclusion of artery

  • CABG- bypasses 1 or more of patient’s coronary arteries due to blockage of ischemia.

    • Usually, saphenous vein but can also you grafted artery.

      • NO BP ON ARM IF GRAFT WAS TAKEN FROM IT!

    • Nursing care: monitor blood pressure, temp (post op hypothermia)= use warming measures. LOC, fluid and electrolytes, cardiac rhythm, pain levels, neurovascular status, donor site.

      • Monitor bleeding/chest tube site

        • They are on Herpin

          • Over 150cc per hour notify MD.

          • Complications: cardiac tamponade (

          • Sternal precautions- use pillow, dont lift arms above head.

      • Systemic infection

      • Wound care: monitor all sites!

      • Pain management- non pharm vs pharm

      • Prevent VTE- early ambulation, compression.

      • Respiratory complications

        • Incentive spirometer

        • Deep breath and cough

  • Atherectomy- remove plaque

• Nursing care

  • 02-

  • monitor for cardiogenic shock (hypotension, tachycardia, tachypnea, weak pulses) and heart failure

  • cardiac rehabilitation (outpatient)

  • Monitor activity level.

Complications Occurring Post-MI

Risks of Dysrhythmias

This section elucidates the prevalence of arrhythmias following MI and outlines effective management strategies to address these complications.

• Ventricular tachycardia and ventricular fibrillation are the most common cause of death in patients in the prehospital period.

• Bradycardias can develop when key areas of the conduction system are destroyed.

• Electrolyte imbalances= potassium!!

Presentation of Heart Failure

Focus on manifestations specific to left-sided and right-sided heart failure resulting from myocardial infarction reveals the complexity of post-MI recovery and management strategies.

-Left sided heart failure leads to right sided heart failure.

• Left sided HF: mild dyspnea, restlessness, agitation, slight tachycardia, pulmonary congestion, S3 heart sound, crackles on auscultation of the lungs, paroxysmal nocturnal dyspnea, and orthopnea.

• Right sided HF: jugular vein distention, hepatic congestion, abdominal distention, lower extremity edema.

Management of Cardiogenic Shock

Cardiogenic shock occurs when 02 and nutrients supplies to the tissues are inadequate because of severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, or right ventricular infarction.

• TX: control dysrhythmias, mechanical circulatory devices, extracorporeal membrane oxygenation (ECMO), and support of contractility with vasoactive drugs (dobutamine).

• Goals: maximize 02 delivery, reduce 02 demand, prevent complications (Acute kidney injury)

Structural Complications: Papillary Muscle and Ventricular Dysfunction

Discusses how myocardial infarction can lead to significant structural changes, including mitral valve dysfunction, necessitating surgical evaluation and potential intervention in severe cases.

• Rare and life-threatening complication, causes acute and massive mitral valve regurgitation with no time for the heart to compensate.

• S/E: dyspnea, pulmonary edema, and decreased CO result from the backup of blood in the left atrium.

• Treatment: afterload reduction with nitroprusside (Nipride) and/or IABP therapy and immediate surgery with mitral valve repair or replacement.

Left Ventricular aneurysm= myocardial wall is thin, bulges out during contraction= may rupture and hide thrombi.

• Leads to HF, dysrhythmias, and angina

Urgency of Septal Ruptures - Ventral septal wall rupture!

Addresses the pressing need for surgical interventions following septal ruptures that may occur post-myocardial infarction, emphasizing the critical nature of timely treatment.

• A new loud systolic murmur heard in patients with acute MI may signal ventricular septal wall rupture. This requires prompt evaluation and diagnostic imaging to confirm the presence of the rupture, as delays can significantly increase morbidity and mortality rates.

Pericarditis and Its Implications

Explores symptoms and appropriate treatment strategies for managing post-MI pericarditis, which requires ongoing attention to patient care during recovery.

• Acute pericarditis- an inflammation of the visceral and/or parietal pericardium, may occur 2-3 days after an acute MI.

• S/E: mild to severe chest pain that increases with inspiration, coughing, and movement of the upper body. Sitting in a forward position often relieves the pain, fever, hypotension, narrow pulse pressure.

• Assess for presence of a friction rub over the pericardium./ MID to lower left sternal border.

• ECG changes: ST elevations, Inflammation of the pericardium.

• TX: high doses of aspirin, nonsteroidal anti-inflammatory drugs and corticosteroids are avoided first 4 weeks after MI.

Dressler's Syndrome

Investigation into Dressler's syndrome, a form of chronic inflammation following myocardial infarction, emphasizes the need for targeted management strategies to alleviate symptoms and improve patient outcomes.

• Dressler syndrome is pericarditis and fever that develop 1-8 weeks after MI. Cause is unclear, may be an autoimmune reaction to the necrotic heart muscle.

• S/E: chest pain, fever, malaise, arthralgia, pericardial friction rub.

• Labs: high white blood cell count and sedimentation rate.

• TX: high dose aspirin

Chronic Stable Angina

Acute Coronary Syndrome- total coronary occlusion=cellular response to 02 and glucose deprivation. TIME=HEART.

Acute Coronary Syndrome-

-TOTAL coronary occlusion= cellular response to 02 and glucose deprivation. TIME=HEART

-Deterioration of once stable plaque leads to ruptures= partial occlusion of coronary artery (UA or NSTEMI) vs total occlusion (STEMI)

-S/S

• S/S= chest pain(new onset, occurs at rest lasts more than 10 mins), ST elevations on 12 lead=stemi (3 or more), unpredictable- NEEDS TX NOW

• UA or NSTEMI= may or may not have ST depression or T wave inversion.

  • IF not, evaluate serum biomarkers

-Health History- Emphasizes the significance of a thorough health history and ECG evaluations in confirming a diagnosis of acute coronary syndrome, guiding effective treatment strategies.

• HX of pain, risk factors, healthy history.

• Unstable angina vs MI (STEMI vs NSTEMI)

• 12 lead ECG

• serum cardiac biomarkers

Serum Cardiac Biomarkers Characterization

Identifies the critical importance of serum cardiac biomarkers—including troponins and their timelines—regarding assessing the severity and occurrence of myocardial infarction events.

• Proteins released into the blood from necrotic heart muscle after an MI.

• UA= negative biomarkers.

• NSTEMI= positive biomarkers

• Troponin and CK levels

• TROPONIN IS BEST INDICATOR!

Essential Response Protocols

Details the necessary emergency response protocols for clinical interventions required during the onset of acute coronary syndrome, emphasizing collaborative care delivery.

• Vitals, 12 lead ECG, upright position, 02 nasal cannula, IV access, give SL NTG, morphine, high dose statin (atorvastatin) Baseline labs.

• ST elevation= directly taken to cardiac catheterization.

• ST depression and/or T wave inversion= admit to ICU or telemetry unit for ongoing care.

• UA and NSTEMI start on heparin or GP IIB/IIIA inhibitors (epitifibate) before cath or at the time of PCI.

Monitoring Strategies During Thrombolysis

Key measures to be observed during the administration of thrombolytics are essential for averting negative outcomes and guaranteeing effective reperfusion.

These include:

• Continuous cardiac monitoring for arrhythmias

• 2-3 LIVES FOR IV THERAPY

• Monitor heart rhythm, VS, pulse ox, assess heart, lungs, neuro status.

• Assessing vital signs frequently to detect hypotension or other hemodynamic changes

• Monitoring for signs of bleeding, particularly at puncture sites and within the gastrointestinal system

• Performing neurological assessments to identify any changes that may indicate a stroke or other complications.

Evaluating Reperfusion Outcomes

Identifying the distinctions between successful and unsuccessful outcomes following reperfusion efforts post-thrombolytic therapy provides critical insights for patient management strategies, guiding decision-making in ongoing care.

Comprehensive Overview of Drug Therapy in ACS

Multimodal Pharmacological Strategies

Explores the necessity for multimodal pharmacological strategies integral to the effective management of patients diagnosed with acute coronary syndrome, enhancing overall therapeutic effectiveness.

Further Pharmaceutical Considerations

Investigates the role of specific medication types in the comprehensive management of acute coronary syndrome and their contributions to patient outcomes.

• IV nitro- SL until IV. S/E: hypotension, monitor BP, IV fluid bolus.

• Morphine- vasodilator and relieves chest pain. Monitor BP and RR.

• Oxygen therapy!

• Beta blockers- reduce HR.BP, and contractility. Reduce the risk of reinfarction and HF.

• Angiotensin- converting enzyme inhibitors and angiotensin receptor blockers.

  • ACE started within 24 hours if BP is stable and no contraindications.

  • ARBS if patient cannot tolerated ACE (angioedema, cough)

• Antidysrhythmic

• Lipid lowering drugs- Lipid panel, ACS and CAD should receive lipid lowering drugs indefinitely.

• Aldosterone antagonists- spironolactone, eplerenone- decrease mortality after a Stemi.

• Stool softeners- prevent straining and the Valsalva maneuver.

Nutritional Therapy Post-ACS

Prescribing initial dietary interventions post-ACS events emphasizes prioritizing low salt, fat, and cholesterol intake as vital components of recovery protocols.

• NPO until stable

• Low salt, low saturated fat, low cholestrol.

-Nursing management

• Physical activity, FITT formula

• Cardiac rehab

3 OR MORE PVC RUNS= VTACH