CAD, ACS, and ADHF Notes

Coronary Artery Disease (CAD), Acute Coronary Syndrome (ACS), & Acute Decompensated Heart Failure (ADHF)

Objectives

• Explain the clinical manifestations, complications, diagnostic studies, and collaborative care of the patient with ACS, CAD, and ADHF.

• Evaluate commonly used drug therapy in treating patients with ACS, CAD, and ADHF.

• Prioritize key components to include in client education and nursing care of patients recovering from ACS and coronary revascularization procedures.

Cardiovascular Disease (CVD)

• Leading cause of death in the world.

  • Pt usually comes in due to crisis (ex. MI, hypertension)

• CVD includes several disorders of the heart and blood vessels.

• Coronary Artery Disease (CAD): asymptomatic or chronic stable angina (chest pain).

• Acute Coronary Syndrome (ACS): unstable angina (UA) or myocardial infarction (MI).

• Perfusion depends on cardiac output (CO).

Coronary Artery Disease (CAD) Review

Coronary Artery Disease

• A type of blood vessel disorder.

  • Elevations in blood pressure because of plaque building up in arteries

• C-reactive protein (CRP) may be increased.

  • Inflammatory marker

• Atherosclerosis: begins as soft deposits of fat that harden with age.

  • CRP also an inflammatory marker

• Lipid deposits within the innermost layer of the arterial wall (intima).

• Endothelial injury and inflammation affect the development of atherosclerosis.

• Damage to the endothelial lining due to: tobacco use, hyperlipidemia, hypertension, toxins, diabetes, inflammation, and infection.

• Due to high lipoprotein and homocysteine levels.

• Damage the inner lining of blood vessels.

• Promote plaque buildup.

• Change clotting mechanism = clots more likely to occur.

Developmental Stages of Atherosclerosis

• Fatty Streak (Stage 1):

  • Lipid-filled smooth muscle cells.

  • Yellow tinge appears, appears by age 20.

  • Treatments that lower LDL cholesterol may slow this process.

• Fibrous Plaque (Stage 2):

  • Progressive changes to endothelium.

  • Grayish/whitish appearance, appears by age 30 and increases with age.

  • Plaques can form on one side of the artery or in a circular fashion.

• Complicated Lesion (Stage 3):

  • Continued inflammation can result in plaque instability, ulceration, and rupture.

  • Platelets accumulate = thrombus = ↑ GP Iib/IIIa receptors to bind fibrinogen = enlarging thrombus.

  • Most dangerous stage and can lead to ACS.

Collateral Circulation

• Arterial anastomoses or connections exist within the coronary circulation (creates new pathways)

  • More common in older population as they’ve had more time to develop. An MI is more deadly in younger populations as they’ve had don’t have collateral circulation.

  • Ex. Think of a freeway that’s backed up → people go to the streets.

• Two Contributing Factors:

  • Angiogenesis: inherited predisposition to develop new blood vessels.

  • Presence of chronic ischemia (poor blood flow).

• Collateral Circulation has a chance to develop if blockage occurs slowly over a long time.

• Acute coronary occlusion = not enough time for collateral circulation to develop.

Risk Factors for CAD

• Non-Modifiable:

  • Age

  • Gender

  • Ethnicity

  • Family History

  • Genetics

• Major Modifiable:

  • High serum lipids

  • Hypertension

  • Tobacco Use

  • Physical Inactivity

  • Obesity

  • Diabetes

  • Metabolic Syndrome

• Contributing Modifiable:

  • Psychological state

  • Substance use

Interprofessional and Nursing Management: CAD

• Identify High-Risk Persons.

  • Obesity

  • Family Hx

  • Diabetes

  • Poor socioeconomic status (unhealthy diet)

  • Sedentary lifestyle

• Physical Activity.

  • At least 150 minutes of moderate intensity exercise every week.

  • 30 mins of brisk walking per day??

• Nutrition Therapy.

  • Increase 9:03***LISTEN TO LECTURE

• Lipid-Lowering Drug Therapy.

• Complete lipid profile every 5 years beginning age 20; Middle-aged adults every 1-2 years.

• Antiplatelet Therapy.

• ↑ Lipoprotein Removal

  • Bile Acid Sequestrants

  • Proprotein Convertase Subtilisin/kexin 9 inhibitors

• ↓ Cholesterol Absorption

  • Ezetimibe (Zetia)

• Restrict Lipoprotein Production

  • HMG-CoA reductase inhibitors (Statins)

  • Niacin (water-soluble B vitamin)

  • Fibric Acid Derivatives (Gemfibrozil)

  • ATP-citrate lyase Inhibitor (Bempedoic Acid)

Angina

• Chest pain due to myocardial ischemia. Artery >70% stenosed or >50% in L main coronary artery.

• Chronic Stable Angina: due to chronic CAD over a long period of time.

  • Provoked by physical exertion, stress, emotional upset, sexual activity, stimulants.

  • Pain usually lasts for only a few minutes and does not change with position or breathing.

  • Treatment: rest, calming down, sublingual nitroglycerin, drug therapy, ↓ O2 demand & ↑ O2 supply.

• Unstable Angina: new-onset pain that may increase in frequency, duration, or severity.

  • Occurs at rest or with exertion and lasts more than 10 minutes.

  • Unpredictable.

  • Incomplete occupation of vessel

  • Rupture of unstable plaque = thrombus formation = MI

• Silent Angina: ischemia with the absence of any symptoms.

  • Diabetes due to neuropathy affecting the nerves that innervate the cardiovascular system.

  • Women: fatigue, SOB, epigastric pain, anxiety, nausea.

Interprofessional and Nursing Care: Angina

• Drug Therapy: Nitrates (every 5 mins), ACE inhibitors, ARBs, β-adrenergic blockers, Calcium Channel blockers, Lipid-lowering drugs.

• Goal: ↓ O2 demand & ↑ O2 supply to heart and rest of body.

• Nursing Care:

  • Pain relief (morphine helps with pulmonary congestion)

  • Immediate and appropriate treatment

  • Preservation of heart muscle if MI suspected

    • Oxygenate (perfuse the issue to prevent cell and muscle death)

  • Effective coping with illness-associated anxiety

  • Participation in a rehabilitation plan

  • Reduction of risk factors

• Patient Education

  • Identify risk factors for CAD

  • Reduce modifiable risk factors

  • Precipitating factors for angina

  • Medications

  • Diet

  • Physical Exercise

Acute Coronary Syndrome (ACS)

Acute Coronary Syndrome (ACS) - Medical Emergency !!

• Chest pain from ischemia is prolonged and not immediately reversible

• Coronary artery disease

• Chronic stable angina

• Acute coronary syndrome

  • Unstable angina

  • Non-ST-segment-elevation MI

  • ST-segment-elevation MI (STEMI)

Acute Coronary Syndrome (ACS) - UA

• Unstable Angina (UA): chest pain at rest, new onset, worsening symptoms, unpredictable, usually lasts >10 mins

• Chronic angina/CAD that can lead to myocardial infarction

• Rupture of unstable plaque = thrombus formation

• Incomplete occlusion of vessel

Acute Coronary Syndrome (ACS) - MI

• Myocardial Infarction: abrupt stoppage of blood flow through a coronary artery with thrombus d/t platelet aggregation

  • Will have ischemia

  • Pt will present with cold and clammy skin that has a gray-ish in appearance

• Non-ST-elevation Myocardial Infarction (NSTEMI)

  • Incomplete occlusion of vessel

  • NOT emergent. Cardiac cath in 12-72 hrs. No thrombolytics.

• ST-elevation Myocardial Infarction (STEMI)

  • Complete occlusion of vessel

  • Emergency - Door to balloon < 90 mins or Door to drug < 30 mins

Clinical Manifestations

• Chest pain

  • Heavy, pressure, tight, burning, constricted, or crushing pain in the substernal or epigastric area. May radiate to neck, lower jaw, arms, or back.

  • Atypical: “discomfort”, weakness, nausea, indigestion, SOB, fatigue

  • Older adult: mental status change, SOB, pulmonary edema, dizziness, dysrhythmia

• Sympathetic Nervous System Stimulation

  • ↑ HR and BP initially, vasoconstriction of peripheral blood vessels, diaphoresis, clammy/ashen/cool to touch skin

    • Due to catecholamine release (epinephrine and norepinephrine release as compensation)***

• Cardiovascular

  • ↓ HR and BP d/t ↓ cardiac output = ↓ renal perfusion & urine output

  • LV dysfunction = Crackles, S3 and S4 heart sounds

  • RV dysfunction = JVD, hepatic engorgement, peripheral edema

• Nausea and Vomiting

  • LISTEN TO LECTURE 20:17****

• Fever

Healing Process - MI

• Cell death = inflammatory process

• Within 24 hours leukocytes infiltrate the area, dead heart cells release enzymes, lipolysis, and glycogenolysis occurs

• Necrotic muscle wall thins by day 4 d/t neutrophils and macrophages

• New scar tissue forming, but still weak after 10-14 days

• 6 weeks after MI, scar tissue has replaced necrotic tissue → Considered healed at this point.

  • Ø Risk for life-threatening dysrhythmias = sudden cardiac death (SCD)

  • Ø Ventricular remodeling: myocardium hypertrophies and dilates → NOT GOOD.

    • The healthy heart tissue that remains has to compensate for the ischemic muscles.

    • Thick heart muscles cannot pump out blood effectively (hypertrophy) → HF

    • Dilated/thin heart muscles cannot pump to blood effectively → HF

      • Harder force of contraction (increased inotrope)

Diagnostics and Intervention Studies

• 12 Lead ECG -NOT TESTED ON EACH LEAD

  • Each lead looks at heart at a different angle.

    • Provides information on which coronary artery is involved

    • ST depression and/or T wave inversion facing ischemia/infarction

    • Ischemic changes seen in UA or NSTEMI

    • STEMI

      • ST elevation in the leads facing the infarcted wall

      • ST segment elevation of 1mm or greater in 2 contiguous leads or 2mm or more in V2 and V3

    • Pathologic Q waves → tells us if there’s some type of damage to heart (ex. CMP, late HF)

      • If the patient does not seek immediate treatment

      • Deep Q wave or Q wave ≥ 1/3 of R wave height

    • Always compare to previous ECGs if possible!

Diagnostics and Intervention Studies

Diagnostics and Intervention Studies (Tested on textbook values)

• Serum Cardiac Biomarkers:

  • UA: negative

  • NSTEMI: positive

• Echocardiogram:

  • Hypokinesis: worsening myocardial contractility

  • Akinesis: absent myocardial contractility

Diagnostics and Intervention Studies

• Cardiac Catheterization: Gold standard test for increasing angina symptoms to identify and localize CAD and for MI

  • A catheter is inserted into the coronary arteries to do several tests

    • Visual blockages (diagnostic)

    • Open blockages (interventional)

• Coronary Angiogram/Angiography (CTA):

  • Inject contrast dye to assess blood flow

Interprofessional Care

• Coronary Revascularization with Percutaneous Coronary Intervention (PCI)

  • Balloon Angioplasty/Intracoronary Stents:

    • Catheter with a deflated balloon tip is inserted into the blocked artery and then inflated. This pushes the plaque against the artery wall and a stent is usually placed. (Insertions site often the groin).

    • Bare metal stent (BMS)

    • Drug-eluting stent (DEC): coated with a drug to reduce overgrowth of the intimal lining

    • DAPT (aspirin + clopidogrel) used until intimal lining grows over stent. Minimum of 12 months. Aspirin continues forever with a stent.

Interprofessional Care

• Coronary Revascularization with Coronary Artery Bypass Graft Surgery (CABG)

  • Place one or more arterial/venous grafts to provide blood distal to blocked coronary artery. Uses saphenous vein, radial artery, or internal mammary artery.

  • Recommended if patient:

    • Does not respond well to medical management

    • Left main coronary artery or 3-vessel disease

    • Not candidates for PCI

    • Continue to have chest pain after PCI

    • Patients with DM, LV dysfunction, and/or CKD

Interprofessional Care

• Thrombolytic Therapy (tenecteplase, alteplase)

  • STEMI cases in agencies without cath lab

  • Limits infarction size by dissolving thrombus in the coronary artery

  • Administer within 3o mins

  • Inclusion criteria:

    • Chest pain < 12 hrs with 12-lead ECG findings of a STEMI

    • No absolute contraindications (active internal bleeding, hx of intracranial hemorrhage, etc.)

• Drug Therapy

  • ACS = Antiplatelet, IV nitro, high-dose atorvastatin

  • Morphine, β-adrenergic blockers, ACE inhibitors/ARBs, antidysrhythmics, lipid-lowering, aldosterone antagonists, stool softeners

• Nutrition Therapy

  • NPO until stable

Nursing Management

• Immediate goals: pain relief, quick and appropriate treatment, and preservation of heart muscle

• Monitor vital signs, continuous ECG monitoring, 12-lead ECG, and draw serum cardiac biomarkers, bed rest/limit activity for 12-24 hours, administer nitro, morphine and oxygen therapy for chest pain, notify HCP of ANY changes (neuro status, etc), emotional support, patient education

  • Heparin—UA and NSTEMI

  • DAPT—NSTEMI and UA with stent

  • Aspirin—UA

  • Cardiac Catheterization—UA and NSTEMI

  • Medical management: PCI or CABG

  • Reperfusion therapy—STEMI

    • Emergent PCI

    • Thrombolytic therapy

• Physical Activity: MET, limit isometric activities and continue isotonic activities, monitor HR

• Cardiac Rehabilitation: restoration of a person to an optimal state of function in 6 areas.

• Sexual Activity: resume when able to tolerate exercise ≥3-5 w/o chest pain or SOB

Nursing Management

• Pre-procedure: assess allergies, baseline assessment and vitals, NPO 6-12 hours, lab values, patient education

• Cardiac Catheterization and PCI:

  • Post-procedure: assessment, monitor ECG, administer medications, monitor for complications, patient education

• CABG:

  • Post-procedure: ICU (24-48 hours), hemodynamic monitoring, arterial line, chest tubes, ECG monitoring, ET tube to vent, urinary catheter, NG tube. Assess fluid status, replace blood/electrolytes, restore temperature, medications, sensory/motor function, pain management

Complications

• Dysrhythmias: Ventricular tachycardia (VT), Ventricular fibrillation (VF), Heart Blocks

• Heart Failure: Ventricle’s pumping action is reduced

• Cardiogenic Shock: occurs when O_2 and nutrients to the tissues are inadequate

  • Goal: ↑ O2 delivery, ↓ O2 demand, and prevent complications

• Papillary Muscle Dysfunction/Rupture: occurs if infarct near muscle that attaches to the mitral valve

  • New systolic murmur = indication of mitral valve regurgitation

• Left Ventricular Aneurysm: infarcted heart muscle wall thins and bulges out during contraction

• Ventricular Septal Wall Rupture/ Left Ventricular Free Wall Rupture: new loud systolic murmur

• Pericarditis: inflammation of the visceral and/or parietal pericardium

• Dressler Syndrome: pericarditis and fever 1-8 weeks after MI

Sudden Cardiac Death

• Sudden Cardiac Death (SCD): abrupt, unexpected death resulting from a variety of cardiac issues without 1 hour of symptom onset

• Most common cause is acute ventricular dysrhythmias (VT or VF) with or without MI = loss of CO and cerebral blood flow

• Have a history of LV dysfunction (EF <35%), and/or structural heart disease (hypertrophic cardiomyopathy)

• Clinical Manifestations: angina, palpitations, dizziness/lightheadedness

• Use of an implantable cardioverter-defibrillator (ICD) to prevent event

• Rapid CPR, defibrillation, and use of an automatic external defibrillator (AED) for witnessed arrest cases

Acute Decompensated Heart Failure

Heart Failure Brief Overview

• Inability to provide sufficient blood to meet the oxygen demands of tissues and organs

• Primarily caused by HTN and CAD

• Left-sided HF

  • HFrEF

  • HFpEF

• Right-sided HF

• Biventricular

Preload and Afterload Brief Review

• Preload

  • Used to assess systemic fluid status of patient

  • Indirect estimate of left atrial pressure (LAP)

  • Right Heart Preload:

    • CVP

    • Normal: 2 – 8 mmHg

  • Left Heart Preload:

    • PAWP (LAP)

    • Normal: 6 – 12 mmHg

• Afterload

  • Right Ventricle Afterload is PVR.

    • Normal PVR: < 250 dynes-sec/cm^5

  • Left Ventricle Afterload is SVR.

    • Normal SVR: 800 – 1200 dynes- sec/cm^5

Summary of Effects of Preload & Afterload on Ventricular Function

• Increased Preload

  • Stroke Volume

  • Ventricular Work

  • Myocardial O_2 Needs

• Decreased Preload

  • Stroke Volume

  • Ventricular Work

  • Myocardial O_2 Needs

• Increased Afterload

  • Ventricular Work

  • Myocardial O_2 Needs

  • Stroke Volume

• Decreased Afterload

  • Ventricular Work

  • Myocardial O_2 Needs

  • Stroke Volume

Contractility

• The force & velocity with which ventricular ejection occurs is reflected by the stroke work index (SWI)

• SWI is the amount of work the ventricle performs with each heartbeat

• Right Heart Contractility is RVSWI (Right Ventricular Stroke Work Index)

  • Normal 7 – 12 g/m^2/beat

• Left Heart Contractility is LVSWI (Left Ventricular Stroke Work Index)

  • Normal 40 – 80 g/m^2$$/beat

New York Heart Association Classifications of Heart Failure

• I – No limitation of activity. Ordinary physical activity does not cause symptoms of HF

• II – Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF

• III – Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity results in symptoms of HF.

• IV – Inability to carry out any physical activity without discomfort. Symptoms may be present at rest.

ADHF Clinical Manifestations

• Sudden increase in symptoms of HF with a decrease in functional status.

• Pulmonary congestion

• Volume overload

• Interstital edema

• Tachypnea

• Pulmonary edema

ADHF: Interprofessional Care

• History and Physical Assessment

  • Determine underlying cause

• Chest X-Ray

• 12 lead ECG

• Hemodynamic Monitoring

• Echocardiogram

• Endomyocardial biopsy in certain patients

• Nuclear Studies

• Cardiac Cath

• Labwork

  • Serum chemistry

  • Cardiac Biomarkers

  • BNP / NT-proBNP

  • LFTs

  • Renal Function

  • Thyroid function

  • CBC

  • Lipid profile

  • UA

ADHF: Medications

• Positive Inotropes:

  • Dopamine

  • Dobutamine

• PDE inhibitors:

  • Milrinone

• Vasodilators:

  • Nitroprusside

ADHF: Nursing Management

• Positioning – High Fowler’s

• NIPPV or intubation

• Circulatory Assist Devices – IABP, ECMO, LVAD

• Continuous vital sign monitoring

• Urine output

  • Perfusion assessment (I&Os)

• Continuous ECG

• Hemodynamic monitoring – BP, PAWP, CO

• Cardioversion

• Ultrafiltration