Coronary Artery Disease &Acute Coronary Syndrome Kelly Marchant

Learning Objectives  At The Completion of this presentation, the nursing student will be able to successfully  Describe Coronary Circulation  Apply the pathophysiology of atherosclerosis to development of CAD and ACS  Differentiate between Myocardial Injury, Ischemia, and Infarction  Evaluate physical symptoms, and patients at risk for development of ACS  Prioritize Nursing Assessments and Interventions for patients in ACS

Cardiac Circulation

Review Cardiac Circulation  Cardiac circulation provides blood for cardiac tissue  Occurs during systole  Left Coronary Artery (LAD, LCx)  Left Anterior Descending supplies anterior 2/3 of Intraventricular Septum, most of R & L Bundle Branches, the anterior and lateral wall of Left Ventricle  Left Circumflex artery supplies Left Atrial Wall, lateral and posterior wall of Left Ventricle  Right Coronary Artery  Supplies Right Atrial & Ventricular Walls, the AV Node, Bundle of His, and interior wall of Left Ventricle

Coronary Artery Disease  Type of blood vessel disease  Major cause is atherosclerosis “hardening of the arteries”  Progressive Disease that develops over many years  Leading cause of death in US (AHA, 2014)  17,000,000 patients  800,000 new heat attacks annually  320,000 recurrent attacks annually

Atherosclerosis  Most common cause of CAD  Deposits of fat in the intima of the artery that harden with age  Deposit of fat causes endothelial injury and inflammation  3 Stages  Fatty Streak  Fibrous Plaque (leads to instability, rupture, & plaque)  Complicated Lesion (platelets accumulate, thrombus formation, reduces circulation)  Collateral Circulation

Types of Plaques  STABLE  Plaque is fixed  Obstructs blood flow= stable angina  Collateral circulation  UNSTABLE  Plaque can rupture and cause platelet adhesion and thrombus formation (complicated lesion)  Unstable angina  Myocardial infarction

Pathophysiology of Plaque  FIG 34-1

3 Determinants of Plaque Vulnerability to Rupture  “Size of the lipid rich core and the stability of its fibrous cap”  “The presence of inflammation within the plaque”  “The lack of smooth muscle cells with impaired healing and plaque stabilization”

Coronary Thrombogenesis Secondary to Plaque Deterioration

Modifiable Risk Factors  Serum Lipids  Hypertension  Diabetes  Tobacco Use  Physical Inactivity  Obesity  Diabetes  Psychological state

Elevated Serum Lipid  Risk of CAD associated with  Total Cholesterol >200  Triglycerides > 150  LDL > 160  HDL <40 (men), <50 women

Hypertension  Increases risk of MI 10 fold in all populations  Defined as Blood Pressure > 140/90  >130/80 if patient has DM or CKD  Stress of HTN increases rate of atherosclerosis  development (shearing stress)  Salt intake (increased intravascular volume, increase SVR)  Treat with Beta Blockers, ACE Inhibitors, CCB

Tobacco Use  Risk of developing CAD is 2-6 times higher in those who smoke or use smokeless tobacco than non-users  CAD mortality drops to that of a nonsmoker within 12 months of quitting

Physical Inactivity & Obesity  Physical Inactivity  Exercise increase thrombolytic activity  May encourage collateral circulation formation  Obesity  Defined as BMI > 30kg/m2  Pear-shaped  Increased insulin resistance

Diabetes  Incidence of CAD 2-4 times more likely for patient with diabetes (even when well controlled)  Increased tendency for diabetics toward endothelial dysfunction  Diabetics have altered lipid metabolism, higher cholesterol and triglycerides

Psychological State  Framingham Heart Study “Type A”  Stressful State; Depression, Acute & Chronic Stress, Anxiety, Anger & Hostility, Lack of Support  Stressful State stimulates SNS, increased catacholamine levels lead to increased HR & myocardial O2 demand

Non Modifiable Risk Factors  Increased Age  Gender (more common in men until age 65)  Ethnicity (more common in whites than AA)  Genetic predisposition and family Hx

Identification & Management of HR Patients  Proper Identification of HR patients can prevent, modify, or slow progression of disease  Risk Screening Includes  Health Hx (DM, HTN, CHO) Family Hx  Cardiovascular Symptoms  Environmental Factors, diet, exercise, Smoking, ETOH, psychological stressors  Management  Lifestyle Modification, Diet & Exercise, smoking cessation  Lipid Lowering Agents  Antiplatelet therapy

Myocardial Ischemia  Occurs when demand for myocardial oxygen exceeds coronary arteries’ ability to supply oxygen to the heart  Angina clinical term for reversible chest pain  For ischemia secondary to atherosclerosis to occur >75% of vessel must be occluded  Myocardial cell hypoxia occurs within 10 seconds of coronary occlusion  Delay in depolarization and repolarization of cardiac cells  In ischemic conditions, cardiac cells are viable for 20 minutes

Ischemia Algorithm

Types of Angina Table 34-9  Chronic Stable Angina; CAD  Episodic pain, last 5-15 minutes, provoked by exertion, relieved by rest or NTG  Prinzmetal’s Angina; Coronary Vasospasm,  Occurs at rest, triggered by smoking or other substance (histamine, epi)  Microvascular Angina; Microvascular Ds affecting distal branches of CA  More common in women, triggered by everyday activities, may respond to NTG  Unstable Angina; Rupture of Plaque  New onset CP, occurs with minimal exertion, does not respond to NTG

Myocardial Injury  When Ischemia is prolonged anoxic cardiac cells sustain injury  Hypoxia prevents generation or conduction of electrical impulses (EKG Changes), leads to inability to contract  Ability to recover to normal function is related to the length and degree of injury

Myocardial Infarction  Occurs because of severe sustained ischemia  Persistent hypoxia secondary to increased supply, and decreased demand  80-90% of acute MI caused by thrombus, No Blood Flow distal to thrombus  No electrical current  Cell Death is Irreversible, necrosis and scarring  Described by location of damage

Acute Coronary Syndromes  Term used to describe cases of acute, prolonged ischemia that is not immediately reversible  Medical Emergency  Includes  Unstable Angina  Non ST Elevation Myocardial Infarction (NSTEMI)  ST Elevation Myocardial Infarction (STEMI)  ST segment elevation on EKG, patients have complete coronary occlusion on angiography

EKG Changes  EKG Changes Occur with ACS  T wave inversion  ST segment elevation  Abnormal Q wave  Changes vary with duration, location, and extent of ischemia

Location of Infarction  Septal MI; LAD  Anterior MI; LAD  Anteroseptal MI; LAD  Anterolateral MI; LAD or L Cx  Inferior MI; RCA or L Cx

Acute Septal MI 12 Lead

Anterior MI 12 LEAD EKG

Acute Anterior MI 12 LEAD  Sinus Rhythm 60, with sinus arrhythmia  St Segment Elevation V1-V4  Interpretation; Acute Anterior MI

Acute Inferior MI 12 LEAD  Sinus Rhythm 88  ST Segment Elevations V2-V4  Interpretation Inferior MI

Acute Anterolateral MI 12 LEAD  Sinus Rhythm 80  QRS 0.10  St Segment Elevation I, aVL, V2-V6,  ST Segment Depression II, III, aVF  Interpretation Acute Anterolateral MI

Acute Interior MI 12 Lead  Sinus Tacchycardia 115 with unifocal PVCs  ST Segment Elevation II, III, aVF,  ST Segment Depression I, aVL  Interpretation Acute Inferior MI

Acute Coronary Syndrome Gender Differences Men  Average age of onset Men 64.5  Present with Acute MI more frequently as first manifestation of CAD  Develop greater collateral circulation Women  Average age of onset 70.4  Risk of MI quadruples post menopause  Do not present with classic symptoms  Increased rate of “silent MI”  Increased rates of fatal MI

ACS Gender

Gerontologic Considerations  Incidence of CAD increased in older adults, and is leading cause of death  Risk factor reduction efforts are effective but frequently nor prescribed  Aggressive Risk Factor Management antidyslipemic, antihypertensives, planned pprogram of physical activity,  Most likely to consider lifestyle changes  When hospitalized  When symptomatic

Nursing Care & Considerations

Expected Signs & Symptoms  Pain  Palpitations  Dyspnea  Cough  Wheezing  Anorexia  Nausea  Vomiting

Location of CP

Chronic Stable Angina  Education  Lifestyle Modification  Nitroglycerine  Short acting, Sublingual  Long Acting Isosorbide Dinitrate  Statins  Beta Blockers, ACE Inhibitors, CCB

Clinical Manifestations of MI  Result of sustained ischemia  Causes irreversible myocardial necrosis  Necrosis of entire thickness of myocardium occurs after 4 hours, can take up to 12 hours  Degree of altered cardiac function related to location, duration, and size of the infarct  Contractile function of heart is disrupted in areas of myocardial necrosis  Most MIs involve Left Ventricle

Objective Symptoms  Vital Signs  Rate and Rhythm changes, tacchypnea, BP changes  Apperance of Skin  Cold, sweaty, clammy, cyanotic  Cardiovascular Signs  Distant Heart Sounds, S3 S4, edema  Respiratory signs  Rales, rhonchi, wheezing, dyspnea

Lab Values  Myoglobin  Elevation indicates skeletal OR cardiac muscle injury  CK-MB  More specific to cardiac muscle injury  May be useful in re-infarction  Troponin  Gold Standard for Cardiac Injury  Distinguishes cardiac from skeletal muscle injury  Remains elevated for 5-14 days  Takes 30 minutes to appear in serum

Cardiac Biomarkers Elevation

Management of ACS  Prompt Response  All chest pain assumed cardiac until ruled out  Goal is Repurfusion  Fibrinolytic Administration  Antiplatelets (ASA, Clopidogrel)  Anticoagulants (Heparin, lovenox)  Thrombolytic Agents, (tPA) Converts plasmin into plasminogen, dissolves the fibrin binding platelets

Nursing Interventions  Maintain Airway  Administer O2 via NC  Obtain 12 Lead EKG  Insert two PIV  Medicate for Pain (Morphine, NTG)  Continuous ECG monitoring  Obtain Lab Studies  Portable Chest Xray  Frequent VS; document response to treatments  Provide Reassurance  Advanced Directives

Complications of MI  Dysrhythmias  Heart Failure  Cardiogenic Shock  Papillary Muscle Dysfunction  Rare, has high mortality rate  Control Dysrhythmias, IABP& vasoactive drugs to support contractility  Ventricular Aneurysm; infacrted Myocardial wall bulges during contraction  HF, dysrhythmia, angina  Thrombus formation, increased risk of stroke  Pericarditis; inflammation of visceral or parietal myocardium  Occurs 2-3 days post MI  CP aggrivated by DP, cough  EKG shows diffuse ST elevation  Tx NSAIDS, corticosteroids  Dressler Syndrome; pericarditis with effusion and fever, develops 4-6 wk post MI  Ag/Ab rection to necrotic myocardium  Pericardial pain, fever, friction rub, pericardial effusion, arthralgia  Tx, ST corticosteroids

Percutaneous Transluminal Coronary Angioplasty PTCA  Insertion of Balloon-tipped Catheter into occluded CA  Followed by inflation of Balloon  Fractures plaque and dilates arterial lumen  Can be done with or without stent

Balloon Angioplasty

Coronary Artery Stenting

Surgical Revascularization  CABG  OPCAB  MIDCAB  Can be with or without IABP

Reperfusion Therapy  Emergent PCI, Thrombolytic Therapy, or Surgical Interventions  Assess Time & Risk  Assess Intervention

“Fibrinolynic Therapy”  AKA Thrombolytic Therapy  Especially Important in facilities without interventional cardiac catheterization lab  Breaks up fibrin meshwork in clots  Gal of administration is 30 minutes from arrival to ED  Review Contraindications (Table 34-14)  Active internal bleeding, HX cerebral aneurysm or AV malformation, known intracranial neoplasm, HX cerebral hemorrhage, ischemic stoke in last 3 months, suspected aortic dissection

Pharmacology in Acute MI  IV Nitroglycerine  Morphine Sulfate  Beta Blockers  ACE Inhibitors  Antidysrhythmics  Cholesterol Lowering Agents  Stool Softeners

Patient Teaching Table  Signs & Symptoms of an MI, and what to do if they occur  When & How to seek help (EMS)  A&P of Heart  Cause & Effect of Atherosclerosis  ID and Plans to reduce Risk Factors  Rationale for Tests & Tx  Recovery & Rehabilitation Plan  Resumption of ADLs (work, physical & sexual activity)

Sudden Cardiac Death  Unexpected death resulting from a variety of cardiac causes  Sudden disruption in cardiac functioning and abrupt loss of CO and cerebral blood flow  Estimated 382,800 deaths annually  56% occur outside hospital  Of patients that survive SCD approximately 80% sustain neurological impairment  Majority of SCD caused by acute ventricular dysrhythmias

References  Lewis et al., (2014). Medical Surgical Nursing; assessment and Management of Clinical Problems, Chapter 34  McCance et al., (2010). Pathophysiology; The Basis for Disease in Adults and Children, Chapter 30  American heart Association ures-only