Myocardial Function and Heart Disease Quiz

Cardiac Anatomy & Physiology

• The heart wall has three layers: epicardium, myocardium, and endocardium.
• The myocardium is the thickest layer and responsible for contraction.
• Cardiomyocytes provide the contractile force.
• Coronary arteries and veins are located between the myocardial layers.
• The right coronary artery (RCA) supplies the backside of the left ventricle and the right side of the heart.
• The left coronary artery (LCA) supplies the left side of the heart.
• Coronary arteries supply blood to different areas of the heart.
• Occlusion of either the RCA or LCA can cause left ventricular damage.

Coronary Circulation

• The RCA feeds the backside of the LV and right side of the heart.
• The LCA feeds the left side of the heart.
• Coronary arteries supply blood to different areas of the heart.
• Occlusion of either the right or left coronary artery can cause LV damage.
• RCA occlusion damages the SA node, which affects the electric pulse to the LCA.

Collateral Circulation

• Collateral vessels form through arteriogenesis and angiogenesis.
• Collateral circulation helps supply blood to areas with decreased blood supply due to CAD.
• Collateral circulation develops alongside atherosclerosis.
• Symptoms of CAD do not appear until the disease is advanced.

Normal Electrocardiogram (ECG) & Cardiac Electrical Activity

• The ECG measures electrical activity of the heart.
• Depolarization and repolarization are represented in the ECG.
• Atrial depolarization is represented by a P wave.
• Ventricular depolarization is represented by a QRS complex.
• Ventricular repolarization is represented by a T wave.

Progression of Atherosclerosis

• Endothelial injury initiates atherosclerosis.
• Inflammation of the endothelium is a key aspect.
• Cytokines are released.
• Cellular proliferation occurs.
• Macrophages migrate.
• LDL oxidation occurs, forming foam cells with oxidative stress.
• Fatty streaks, fibrous plaques and complicated plaques develop.
• Result is partial or total occlusion of coronary arteries.

Atherosclerosis & Coronary Artery Disease (CAD)

• Atherosclerosis is the most common cause of CAD.
• CAD narrows or occludes coronary arteries.
• Dyslipidemia (abnormal lipoproteins) is strongly linked to CAD.
• Imbalance between coronary blood supply and myocardial demand can cause myocardial ischemia.
• Myocardial ischemia can cause irreversible infarction.

Modifiable Risk Factors for CAD

• Maintaining normal blood pressure is crucial.
• Smoking cessation is recommended.
• Limiting alcohol consumption, maintaining a healthy weight, and adhering to a nutritious diet are also beneficial.
• Regular exercise is an important factor in preventing CAD.

Nontraditional Risk Factors for CAD

• Markers of inflammation,ischemia, and thrombosis (like CRP).
• Adipokines (like adiponectin and leptin).
• Chronic kidney disease.
• Air pollution and ionizing radiation.
• Certain medications.
• Coronary artery calcification and carotid wall thickness.
• Microbiome
• Chronic kidney disease
• C-reactive protein

Pathophysiology Continuum of CAD

• CAD: transient ischemia, persistent ischemia, myocardial infarction (MI)
• Stable angina: predictable, intermittent chest pain, not at rest.
• Acute coronary syndrome (ACS): unpredictable, often at rest. Includes unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).
• Unstable angina: pain with increasing frequency, occurs during rest or minimal exertion.
• Myocardial infarction (MI): irreversible, sustained myocardial ischemia.

Stable Plaque Versus Unstable Plaque

• Stable plaques have a stable, fibrous cap, while unstable plaques have a large lipid core and a thin, vulnerable fibrous cap.
• Unstable plaques are more likely to rupture and cause thrombosis.

Pathophysiology of Acute Coronary Syndromes (ACSs)

• Plaque progression, disruption, and subsequent clot formation are common in ACS.
• Unstable angina (UA): transient episodes of thrombotic vessel occlusion.
• Myocardial infarction (MI): irreversible cardiac cellular death. (NSTEMI and STEMI)

Oxygen Supply & Demand

• Oxygen supply depends on blood flow to the myocardium, affected by CAD and atherosclerosis.
• Oxygen demand depends on sympathetic activity, physical activity, etc.

Cycle of Myocardial Ischemic Events

• Sudden events & heart failure can result from imbalances between coronary supply and myocardial demand.
• Dysrhythmias are caused by abnormal electrical impulses. Greater than 20 minutes of myocardial ischemia is likely a myocardial infarction (MI).

Pathogenesis of Unstable Plaque

• Shear forces, inflammation, apoptosis and macrophage-derived enzymes may increase inflammation.
• Increased inflammation can lead to the rupture of the fibrous cap, which initiates thrombosis

Evaluation and Treatment of Unstable Angina

• Evaluation: Serum biomarkers (troponin, CPK-MB) and ECG are important diagnostic tools.
• Treatment: Immediate hospitalization, administration of nitrates, antithrombotics, and anticoagulants.
• PCI is crucial if conditions do not improve.

Myocardial Infarction (MI)

• Irreversible damage to the heart muscle due to prolonged ischemia.
• Subendocardial MI results from transient or incomplete coronary occlusion.
• Transmural MI results from prolonged and/or complete occlusion.

What Causes Cellular Injury in MI?

• Inadequate O2 and nutrients deplete energy reserves in minutes.
• Anaerobic metabolism produces lactic acid, leading to cellular acidosis.

Cellular Death in MI

• After about 20 minutes, irreversible hypoxic injury causes cellular death and tissue necrosis.
• Enzymes like troponin are released into the bloodstream, enabling diagnosis of MI.

Structural and Functional Changes in Acute MI

• Myocardial stunning: temporary loss of contractile function.
• Hibernating myocytes: adapt to prolonged ischemia through metabolic adaptation for survival.
• Myocardial remodeling occurs in the myocardium after MI.
• Infarcted myocardium is surrounded by a zone of hypoxic injury.

Diagnostic Tools for MI

• ECG: Changes can indicate location, extent (partial/subendocardial, vs entire wall thickness/transmural).
• Serum Biomarkers (Cardiac troponin, CPK-MB, LDH) indicate MI or cardiac damage.

Cardiac Specific Serum Biomarkers

• Cardiac biomarkers are released when myocardial cells die.
• Troponin and CPK-MB are commonly checked as serum biomarkers of myocardial cells damage.

Non-Cardiac Specific Serum Biomarkers

• Lactate dehydrogenase (LDH): an enzyme found in many body tissues, including the heart.
• Myoglobin: present in cardiac and skeletal muscles; quickly released when myocardial damage occurs.

Additional Labs in MI

• Leukocytosis: an elevation in white blood cell count.
• Elevated CRP: indicates inflammation
• Hyperglycemia: evident during early phase after AMI.

Symptoms/Assessment of MI

• Sudden severe chest pain that can radiate, often described as heavy or crushing.
• Pain can be located in the neck, jaw, shoulder, or left arm.

Atypical Symptoms of MI

• Atypical symptoms differ from the typical chest pain in some cases, such as in women or people with diabetes.
• Severe chest pain is not always present.
• Hypotension can accompany severe myocardial damage.

Treatments for MI

• Bed rest: Reduce cardiac workload
• Morphine: pain relief, vasodilator, reduce cardiac workload
• Stools softeners: reduce exerting activities/increasing cardiac workload
• Non-pharmacological (PCI or CABG)

Coronary Artery Disease (CAD)

• CAD is a process that occurs over a long time, often involves buildup of plaque in the walls of coronary arteries.
• Plaques are composed of lipids, cholesterol, inflammatory cells, and connective tissue.
• Plaques can rupture creating thrombi.
• Thrombi can block blood flow.

Relationship between CAD, ACS, and Heart Failure (HF)

• CAD can lead to the development of ACS and/or HF
• Risk factors, like diabetes, HTN, smoking, and obesity, play a role in all three conditions.
• Understanding how they are related is crucial for risk assessment, prevention, and treatment of all three diseases.

Pharmacotherapy for CAD, ACS, HF

• Drugs like aspirin, beta blockers, and ACE inhibitors are commonly used to treat or prevent CAD/ACS/HF.
• Nitroglycerin is used for chest pain (angina) treatment.
• Anticoagulants/antithrombotics are used to prevent blood clot formation.
• Pharmacotherapy for CAD, ACS, and HF is designed to reduce cardiac workload, and/or improve oxygen supply, and reduce afterload and preload.

Pharmacotherapy: Coagulation Modifiers

• Antiplatelets (aspirin, clopidogrel) reduce platelet aggregation.
• Anticoagulants (heparin, warfarin) prevent clot formation.
• Thrombolytics (tPA) dissolve existing clots.
• Administration and monitoring for adverse effects are crucial when using these medication types.

Pharmacotherapy Classifications and Uses

• Many medications and classes of medications are used to treat these conditions
• Opioids: pain relief
• Calcium channel blockers for vessel dilation
• ẞ₁-adrenergic receptor blockers slow heart rate
• ACE inhibitors reduce afterload
• Mineralocorticoid receptor antagonists improve sodium and water excretion
• Loop diuretics: treat edema
• Thiazide diuretics: treat hypertension
• Cardiac glycosides: treat heart failure
• Antidysrhythmics: maintain a normal heart rhythm

Antidotes for specific classes of anticoagulants

• protamine sulfate for heparin
• Vitamin K for warfarin

Nursing Implications for specific classes of drugs

• Monitor vital signs and look for signs of adverse effects

Pathophysiology of Heart Failure

• Heart failure involves a condition when the heart cannot pump enough blood to meet the body's needs.
• There are two main types of heart failure (systolic and diastolic).
• Systolic HF involves a problem with the contraction of the heart.
• Diastolic HF involves a problem with the relaxation phase of the heart.
• Pathophysiology of heart failure describes the disease processes leading to the various problems.
• Compensatory mechanisms are activated to address the reduced output, but they ultimately lead to more damage.

Assessment & Monitoring for HF

• Physical examination for signs of fluid overload (edema, JVD)
• Auscultation for murmurs or abnormal sounds
• ECG
• Chest X-ray (CXR)
• Echocardiography (important for EF and ejection fraction)
• Serum troponin (and CPK-MB) to monitor for myocardial injury
• Serum BNP for assessment of fluid volume status
• Complete blood count (CBC) to rule out anemia or infection