Ischemic Heart Disease Overview

Ischemic Heart Disease (Coronary Artery Disease)

• Ischemic heart disease involves atherosclerotic plaques in coronary vessels, leading to reduced blood flow.
• The coronary vessels supply oxygen-rich blood to the myocardium, which is essential for heart muscle function.
• A significant decrease in oxygen delivery to the myocardium occurs primarily due to atherosclerosis.
• Atherosclerosis refers to fatty plaques that develop within the vessel walls, obstructing blood flow.
• Other less common causes of decreased oxygen supply to the myocardium exist but are not as prevalent as atherosclerosis.

Pathophysiology

• In healthy individuals, blood vessels deliver oxygen and nutrients while removing carbon dioxide and waste.
• During ischemic heart disease, plaques partially block blood flow, reducing oxygen delivery to the myocardium.
• Insufficient oxygen prevents ATP production, which is crucial for myocardial contraction and function.
• When oxygen is low, myocardial cells cannot effectively depolarize, leading to muscle failure.

Risk Factors for Atherosclerosis

• A mnemonic to remember key risk factors is "BAD HEART":
  • B: BMI ≥ 30 (obesity)
  • A: Age ≥ 65 (increased age)
• Additional risk factors may include hypertension, smoking, high cholesterol, and diabetes.
• Lifestyle changes and medical interventions are crucial for managing and mitigating these risk factors.### Risk Factors for Ischemic Heart Disease
• Non-modifiable risk factors include age and family history of coronary artery disease (CAD).
• Modifiable risk factors include obesity, diabetes, hypertension, and alcohol abuse.
• Diabetes is a significant risk factor for coronary artery disease.
• Hypertension is the most common risk factor for ischemic heart disease.
• Tobacco use increases endothelial injury and plaque formation.

Atherosclerosis and Ischemic Events

• Atherosclerosis is the leading cause of decreased oxygen supply to the myocardium.
• Other causes include emboli, vessel inflammation, and vasospasm (less common).
• High demand for oxygen (e.g., tachycardia, left ventricular hypertrophy) can lead to ischemic events if supply is inadequate.

Types of Angina

• Stable Angina

  • Substernal chest pain occurring during exertion, relieved by rest.
  • Usually associated with ≥70% occlusion of coronary arteries.
  • Leads to sub-endocardial ischemia but no cell death.

• Unstable Angina

  • Chest pain occurs at rest or with increasing severity.
  • Associated with unstable plaques and near-total occlusion (>90%).
  • Leads to significant ischemia and can progress to infarction.

Myocardial Infarction (MI) Types

• NSTEMI (Non-ST Elevation MI)

  • Caused by unstable plaque causing near-total occlusion but not complete.
  • Leads to irreversible tissue damage after ≥30 minutes of ischemia.
  • Chest pain can occur at rest with elevated troponins.

• STEMI (ST Elevation MI)

  • Complete occlusion (>100%) of a coronary artery.
  • Causes transmural infarction affecting the entire myocardium supplied by the affected artery.
  • Characterized by ST segment elevation on EKG and elevated troponins.

Complications of Myocardial Infarction

• Ventricular Arrhythmias

  • Increased risk of PVCs, V-tach, and V-fib within the first 24 hours post-MI.

• Cardiogenic Shock

  • Associated with left ventricular failure, leading to hypotension and poor organ perfusion.

• Rupture Syndromes

  • Potentially fatal complications within 1-3 days include:
    • Ventricular Septal Rupture: Causes new murmur and can lead to mixed oxygenation.
    • Free Wall Rupture: Blood enters the pericardial cavity, leading to cardiac tamponade.
    • Papillary Muscle Rupture: Leads to acute mitral regurgitation.

• Pericarditis

  • Inflammation of the pericardium typically occurs between 3-14 days post-MI.
  • Characterized by sharp chest pain and pericardial friction rub.

• Left Ventricular Aneurysm

  • Occurs from scar tissue formation between 14 days to 1 month post-MI, risk of rupture and thrombus formation.

Diagnostic Approaches

• 12-Lead EKG

  • Critical for evaluating ST segment changes; pivotal in diagnosing STEMI and NSTEMI.
  • Anterior MI associated with changes in leads V1 to V4.
  • Lateral MI indicated by changes in leads I, aVL, V5, V6.
  • Inferior MI indicated by changes in leads II, III, aVF.

• Biomarkers

  • Troponins and CK-MB are essential in diagnosing myocardial infarction.
  • Troponin levels rise 12-24 hours after injury, while CK-MB normalizes faster.

Treatment

• Patients with ST elevation undergo immediate catheterization (cath lab).
• For NSTEMI, risk stratification is done using the TIMI score to determine need for catheterization.
• Medical management prescribed for low-risk patients.
• Pharmacological stress tests performed for patients unable to exercise, using dobutamine, adenosine, or dipyridamole.

Miscellaneous

• Familiarity with nuanced concepts such as coronary steel syndrome, epigastric presentation of inferior MIs, and atypical presentations in populations like diabetics and the elderly is crucial for effective patient assessment and management.
• Key to recognize that not all ischemic events present with typical angina symptoms, especially in high-risk groups.### EKG Interpretation
• Normal sinus rhythm identified through consistent rate and regular rhythm; upright P wave in lead II, inverted in aVR.
• ST segment analysis reveals:
  • Lead I: ST depression
  • Lead II, III, aVF: ST elevation indicates inferior wall involvement.
  • Reciprocal changes observed in lead I and aVL.
• Inferior ST elevation myocardial infarction (STEMI) suspected due to elevations in leads II, III, and aVF.
• Right coronary artery occlusion often leads to inferior STEMI and potential right ventricular infarction, necessitating right-sided chest leads (V1R, V2R, V3R, V4R).
• ST elevation in right-sided leads indicates right ventricular myocardial infarction.

Posterior and Inferior STEMI Consideration

• Subtle ST elevation in lead II and aVF, along with ST depression and T-wave inversion in leads V1 through V4.
• Importance of posterior chest leads (V7, V8, V9) to assess for posterior STEMI if initial chest leads show no clear elevation.
• Significant ST elevation identified in posterior leads suggests possible combined posterior and inferior wall involvement.

Treatment of Ischemic Heart Disease

• Focus on addressing plaque rupture and reducing thrombus formation.
• Key medications used in treatment:
  • Aspirin: Inhibits thromboxane A2 formation, reducing platelet aggregation.
  • P2Y12 Receptor Inhibitors: Such as Clopidogrel (Plavix) and Ticagrelor (Brilinta); block ADP binding to receptors, decreasing platelet aggregation and thrombus risk.
  • Heparin: Used in STEMI and unstable angina, enhances antithrombin III activity, which inhibits thrombin and factor X, reducing clot formation.
• Mechanism of action: Heparin binds to antithrombin III, enhancing its ability to inhibit necessary clotting factors.

Key Points on Elements of EKG Changes

• Inferior STEMI presence is confirmed by lead elevations.
• Need for vigilance on potential right ventricular infarctions with inferior STEMIs; utilize right-side leads for accurate assessment.
• Posterior chest leads are crucial for detection of subtler ST elevations and diagnosing posterior infarctions.

Ischemic Heart Disease Overview

• Ischemic heart disease results from atherosclerotic plaques in coronary arteries, leading to diminished blood flow to the heart muscle (myocardium).
• Coronary arteries are responsible for supplying oxygen-rich blood, essential for myocardial health and function.
• Atherosclerosis is characterized by the accumulation of fatty plaques within vessel walls, significantly obstructing blood flow and oxygen delivery.

Pathophysiology

• In individuals with healthy blood vessels, oxygen and nutrients are delivered, while waste products are removed.
• Atherosclerotic plaques limit blood flow, leading to reduced oxygen supply, which prevents ATP generation necessary for myocardial contractions.
• Lack of sufficient oxygen impairs myocardial cell depolarization, resulting in muscle dysfunction.

Risk Factors for Atherosclerosis

• Key mnemonic: "BAD HEART"
  • B: BMI ≥ 30 (obesity)
  • A: Age ≥ 65
• Other significant risk factors include hypertension, smoking, high cholesterol, and diabetes.
• Lifestyle adjustments and medical treatments are essential in managing atherosclerosis risk factors.

Risk Factors for Ischemic Heart Disease

• Non-modifiable factors include age and family history of coronary artery disease (CAD).
• Modifiable factors comprise obesity, diabetes, hypertension, and alcohol use.
• Diabetes plays a critical role in increasing the risk of coronary artery disease.
• Hypertension is frequently the most prevalent risk factor for ischemic heart disease.
• Tobacco use exacerbates endothelial damage, promoting plaque formation.

Atherosclerosis and Ischemic Events

• Atherosclerosis is the chief contributor to decreased myocardial oxygen supply.
• Other lesser causes include embolization, vessel inflammation, and vasospasm.
• Situations of high oxygen demand, like tachycardia or left ventricular hypertrophy, can trigger ischemic events if supply fails.

Types of Angina

• Stable Angina:
  • Substernal chest pain linked to physical exertion, relieved by rest; associated with at least 70% coronary occlusion.
• Unstable Angina:
  • Chest pain occurring at rest or progressively worsening; indicates unstable plaques with near-total occlusion (over 90%) and can lead to myocardial infarction.

Myocardial Infarction (MI) Types

• NSTEMI (Non-ST Elevation MI):
  • Results from unstable plaque causing significant blockage, leading to irreversible tissue damage after 30 minutes; characterized by elevated troponins.
• STEMI (ST Elevation MI):
  • Full occlusion of a coronary artery causing transmural infarction; marked by ST segment elevation on EKG and significant troponin rises.

Complications of Myocardial Infarction

• Ventricular Arrhythmias: Increased likelihood of PVCs and potentially life-threatening rhythms within 24 hours post-MI.
• Cardiogenic Shock: Results from left ventricular dysfunction, leading to lower blood pressure and inadequate organ perfusion.
• Rupture Syndromes:
  • Ventricular septal rupture, free wall rupture, and papillary muscle rupture pose dire risks shortly after MI.
• Pericarditis: Occurs 3-14 days post-MI causing sharp chest pain with a characteristic rub.
• Left Ventricular Aneurysm: Develops 2-4 weeks post-MI due to scar tissue, carrying risks for rupture and clot formation.

Diagnostic Approaches

• 12-Lead EKG: Vital for identifying ST segment changes; essential for diagnosing STEMI and NSTEMI.
• Biomarkers: Troponins and CK-MB are critical in MI diagnosis; troponins increase 12-24 hours after injury, while CK-MB levels return to baseline more quickly.

Treatment Strategies

• Immediate catheterization is imperative for patients with ST elevation.
• For NSTEMI, patient risk is assessed via the TIMI score to determine the need for catheterization.
• Medical management recommended for low-risk cases, while pharmacological stress tests may utilize dobutamine, adenosine, or dipyridamole.

EKG Interpretation

• Normal sinus rhythm is noted by regular rhythm and rate with specific P wave characteristics.
• ST segment changes are significant:
  • Lead II, III, aVF elevations imply inferior wall ischemia.
  • Reciprocal changes in leads I and aVL.

Posterior and Inferior STEMI Consideration

• Subtle changes in lead II and aVF with possible T-wave inversions in V1-V4 indicate posterior STEMI; use posterior leads (V7-V9) for assessment.

Treatment of Ischemic Heart Disease

• Emphasis on managing plaque rupture and thrombus formation.
• Medications:
  • Aspirin: Reduces platelet aggregation by inhibiting thromboxane A2.
  • P2Y12 Receptor Inhibitors: Clopidogrel and Ticagrelor inhibit ADP binding to receptors, minimizing thrombosis risk.
  • Heparin: Enhances antithrombin III activity, crucial for preventing clot formation in STEMI and unstable angina.

Key Points on EKG Changes

• Monitoring ST elevations in leads confirms inferior STEMI.
• Right ventricular infarctions can occur with inferior STEMIs; employ right-sided leads for comprehensive evaluations.
• Posterior chest leads provide critical insights into detecting subtler ST elevation and diagnosing posterior myocardial infarction.

Ischemic Heart Disease Overview

• Ischemic heart disease results from atherosclerotic plaques in coronary arteries, leading to diminished blood flow to the heart muscle (myocardium).
• Coronary arteries are responsible for supplying oxygen-rich blood, essential for myocardial health and function.
• Atherosclerosis is characterized by the accumulation of fatty plaques within vessel walls, significantly obstructing blood flow and oxygen delivery.

Pathophysiology

• In individuals with healthy blood vessels, oxygen and nutrients are delivered, while waste products are removed.
• Atherosclerotic plaques limit blood flow, leading to reduced oxygen supply, which prevents ATP generation necessary for myocardial contractions.
• Lack of sufficient oxygen impairs myocardial cell depolarization, resulting in muscle dysfunction.

Risk Factors for Atherosclerosis

• Key mnemonic: "BAD HEART"
  • B: BMI ≥ 30 (obesity)
  • A: Age ≥ 65
• Other significant risk factors include hypertension, smoking, high cholesterol, and diabetes.
• Lifestyle adjustments and medical treatments are essential in managing atherosclerosis risk factors.

Risk Factors for Ischemic Heart Disease

• Non-modifiable factors include age and family history of coronary artery disease (CAD).
• Modifiable factors comprise obesity, diabetes, hypertension, and alcohol use.
• Diabetes plays a critical role in increasing the risk of coronary artery disease.
• Hypertension is frequently the most prevalent risk factor for ischemic heart disease.
• Tobacco use exacerbates endothelial damage, promoting plaque formation.

Atherosclerosis and Ischemic Events

• Atherosclerosis is the chief contributor to decreased myocardial oxygen supply.
• Other lesser causes include embolization, vessel inflammation, and vasospasm.
• Situations of high oxygen demand, like tachycardia or left ventricular hypertrophy, can trigger ischemic events if supply fails.

Types of Angina

• Stable Angina:
  • Substernal chest pain linked to physical exertion, relieved by rest; associated with at least 70% coronary occlusion.
• Unstable Angina:
  • Chest pain occurring at rest or progressively worsening; indicates unstable plaques with near-total occlusion (over 90%) and can lead to myocardial infarction.

Myocardial Infarction (MI) Types

• NSTEMI (Non-ST Elevation MI):
  • Results from unstable plaque causing significant blockage, leading to irreversible tissue damage after 30 minutes; characterized by elevated troponins.
• STEMI (ST Elevation MI):
  • Full occlusion of a coronary artery causing transmural infarction; marked by ST segment elevation on EKG and significant troponin rises.

Complications of Myocardial Infarction

• Ventricular Arrhythmias: Increased likelihood of PVCs and potentially life-threatening rhythms within 24 hours post-MI.
• Cardiogenic Shock: Results from left ventricular dysfunction, leading to lower blood pressure and inadequate organ perfusion.
• Rupture Syndromes:
  • Ventricular septal rupture, free wall rupture, and papillary muscle rupture pose dire risks shortly after MI.
• Pericarditis: Occurs 3-14 days post-MI causing sharp chest pain with a characteristic rub.
• Left Ventricular Aneurysm: Develops 2-4 weeks post-MI due to scar tissue, carrying risks for rupture and clot formation.

Diagnostic Approaches

• 12-Lead EKG: Vital for identifying ST segment changes; essential for diagnosing STEMI and NSTEMI.
• Biomarkers: Troponins and CK-MB are critical in MI diagnosis; troponins increase 12-24 hours after injury, while CK-MB levels return to baseline more quickly.

Treatment Strategies

• Immediate catheterization is imperative for patients with ST elevation.
• For NSTEMI, patient risk is assessed via the TIMI score to determine the need for catheterization.
• Medical management recommended for low-risk cases, while pharmacological stress tests may utilize dobutamine, adenosine, or dipyridamole.

EKG Interpretation

• Normal sinus rhythm is noted by regular rhythm and rate with specific P wave characteristics.
• ST segment changes are significant:
  • Lead II, III, aVF elevations imply inferior wall ischemia.
  • Reciprocal changes in leads I and aVL.

Posterior and Inferior STEMI Consideration

• Subtle changes in lead II and aVF with possible T-wave inversions in V1-V4 indicate posterior STEMI; use posterior leads (V7-V9) for assessment.

Treatment of Ischemic Heart Disease

• Emphasis on managing plaque rupture and thrombus formation.
• Medications:
  • Aspirin: Reduces platelet aggregation by inhibiting thromboxane A2.
  • P2Y12 Receptor Inhibitors: Clopidogrel and Ticagrelor inhibit ADP binding to receptors, minimizing thrombosis risk.
  • Heparin: Enhances antithrombin III activity, crucial for preventing clot formation in STEMI and unstable angina.

Key Points on EKG Changes

• Monitoring ST elevations in leads confirms inferior STEMI.
• Right ventricular infarctions can occur with inferior STEMIs; employ right-sided leads for comprehensive evaluations.
• Posterior chest leads provide critical insights into detecting subtler ST elevation and diagnosing posterior myocardial infarction.

Ischemic Heart Disease Overview

• Ischemic heart disease results from atherosclerotic plaques in coronary arteries, leading to diminished blood flow to the heart muscle (myocardium).
• Coronary arteries are responsible for supplying oxygen-rich blood, essential for myocardial health and function.
• Atherosclerosis is characterized by the accumulation of fatty plaques within vessel walls, significantly obstructing blood flow and oxygen delivery.

Pathophysiology

• In individuals with healthy blood vessels, oxygen and nutrients are delivered, while waste products are removed.
• Atherosclerotic plaques limit blood flow, leading to reduced oxygen supply, which prevents ATP generation necessary for myocardial contractions.
• Lack of sufficient oxygen impairs myocardial cell depolarization, resulting in muscle dysfunction.

Risk Factors for Atherosclerosis

• Key mnemonic: "BAD HEART"
  • B: BMI ≥ 30 (obesity)
  • A: Age ≥ 65
• Other significant risk factors include hypertension, smoking, high cholesterol, and diabetes.
• Lifestyle adjustments and medical treatments are essential in managing atherosclerosis risk factors.

Risk Factors for Ischemic Heart Disease

• Non-modifiable factors include age and family history of coronary artery disease (CAD).
• Modifiable factors comprise obesity, diabetes, hypertension, and alcohol use.
• Diabetes plays a critical role in increasing the risk of coronary artery disease.
• Hypertension is frequently the most prevalent risk factor for ischemic heart disease.
• Tobacco use exacerbates endothelial damage, promoting plaque formation.

Atherosclerosis and Ischemic Events

• Atherosclerosis is the chief contributor to decreased myocardial oxygen supply.
• Other lesser causes include embolization, vessel inflammation, and vasospasm.
• Situations of high oxygen demand, like tachycardia or left ventricular hypertrophy, can trigger ischemic events if supply fails.

Types of Angina

• Stable Angina:
  • Substernal chest pain linked to physical exertion, relieved by rest; associated with at least 70% coronary occlusion.
• Unstable Angina:
  • Chest pain occurring at rest or progressively worsening; indicates unstable plaques with near-total occlusion (over 90%) and can lead to myocardial infarction.

Myocardial Infarction (MI) Types

• NSTEMI (Non-ST Elevation MI):
  • Results from unstable plaque causing significant blockage, leading to irreversible tissue damage after 30 minutes; characterized by elevated troponins.
• STEMI (ST Elevation MI):
  • Full occlusion of a coronary artery causing transmural infarction; marked by ST segment elevation on EKG and significant troponin rises.

Complications of Myocardial Infarction

• Ventricular Arrhythmias: Increased likelihood of PVCs and potentially life-threatening rhythms within 24 hours post-MI.
• Cardiogenic Shock: Results from left ventricular dysfunction, leading to lower blood pressure and inadequate organ perfusion.
• Rupture Syndromes:
  • Ventricular septal rupture, free wall rupture, and papillary muscle rupture pose dire risks shortly after MI.
• Pericarditis: Occurs 3-14 days post-MI causing sharp chest pain with a characteristic rub.
• Left Ventricular Aneurysm: Develops 2-4 weeks post-MI due to scar tissue, carrying risks for rupture and clot formation.

Diagnostic Approaches

• 12-Lead EKG: Vital for identifying ST segment changes; essential for diagnosing STEMI and NSTEMI.
• Biomarkers: Troponins and CK-MB are critical in MI diagnosis; troponins increase 12-24 hours after injury, while CK-MB levels return to baseline more quickly.

Treatment Strategies

• Immediate catheterization is imperative for patients with ST elevation.
• For NSTEMI, patient risk is assessed via the TIMI score to determine the need for catheterization.
• Medical management recommended for low-risk cases, while pharmacological stress tests may utilize dobutamine, adenosine, or dipyridamole.

EKG Interpretation

• Normal sinus rhythm is noted by regular rhythm and rate with specific P wave characteristics.
• ST segment changes are significant:
  • Lead II, III, aVF elevations imply inferior wall ischemia.
  • Reciprocal changes in leads I and aVL.

Posterior and Inferior STEMI Consideration

• Subtle changes in lead II and aVF with possible T-wave inversions in V1-V4 indicate posterior STEMI; use posterior leads (V7-V9) for assessment.

Treatment of Ischemic Heart Disease

• Emphasis on managing plaque rupture and thrombus formation.
• Medications:
  • Aspirin: Reduces platelet aggregation by inhibiting thromboxane A2.
  • P2Y12 Receptor Inhibitors: Clopidogrel and Ticagrelor inhibit ADP binding to receptors, minimizing thrombosis risk.
  • Heparin: Enhances antithrombin III activity, crucial for preventing clot formation in STEMI and unstable angina.

Key Points on EKG Changes

• Monitoring ST elevations in leads confirms inferior STEMI.
• Right ventricular infarctions can occur with inferior STEMIs; employ right-sided leads for comprehensive evaluations.
• Posterior chest leads provide critical insights into detecting subtler ST elevation and diagnosing posterior myocardial infarction.

Ischemic Heart Disease Overview

• Caused primarily by atherosclerotic plaques in coronary vessels, limiting oxygenated blood supply to the myocardium.
• Reduced blood flow due to atherosclerosis leads to decreased oxygen delivery and can impair cardiac function.

Atherosclerosis

• Involves fatty plaque development within vessel walls, obstructing blood flow and causing oxygen deficiency.
• Insufficient oxygen results in reduced ATP production, leading to potential heart failure.

Risk Factors for Atherosclerosis

• Mnemonic: BAD HEART
  • B: Obesity (BMI ≥ 30)
  • A: Age (≥ 65 years)
• Other unidentified factors contribute, but obesity and age are significant.

Physiological Consequences

• Coronary artery blockage decreases oxygen and waste removal from myocardial cells.
• Insufficient oxygen negatively impacts heart muscle contraction and overall function.

Key Risk Factors for Ischemic Heart Disease

• Non-modifiable: Age and family history of CAD.
• Modifiable: Obesity, diabetes, hypertension, smoking, alcohol use.
• Diabetes and hypertension significantly increase ischemic heart disease risk.
• Hyperlipidemia (increased LDL, decreased HDL) enhances atherosclerosis risk.

Ischemia and Oxygen Supply

• Atherosclerosis is the primary cause of decreased oxygen supply, leading to ischemia.
• Less common causes include emboli, vessel inflammation, and vasospasm.
• Increased myocardial oxygen demand from conditions like tachycardia worsens ischemic states.

Angina Types

• Stable Angina: Chest pain during exertion, resolves with rest (≥70% occlusion).
• Unstable Angina: Chest pain at rest due to unstable plaques, severe occlusion (≥90%).
• NSTEMI: Myocardial damage from prolonged ischemia (≥30 minutes), chest pain at rest.
• STEMI: Complete occlusion causes severe chest pain, regardless of activity.

Acute Coronary Syndrome (ACS)

• Comprises unstable angina, NSTEMI, and STEMI, indicating severe ischemia.
• Stable angina can progress to ACS due to plaque rupture and thrombus formation.

Clinical Features of Ischemic Heart Disease

• OPQRST approach for chest pain assessment:
  • Onset: Duration varies; stable (5-10 mins) vs. unstable (longer).
  • Palliative/Provocative: Symptoms improve with rest in stable angina.
  • Quality: Described as tight, squeezing, or crushing pain.
  • Radiation: Pain may radiate to arm, jaw, or abdomen (notably inferior STEMI).
  • Severity: Generally constant in nature.

Complications After Myocardial Infarction

• Ventricular Arrhythmias: Risk of PVCs, VT, VF leading to sudden cardiac death within 24 hours post-MI.
• Cardiogenic Shock: Low perfusion due to left ventricular failure following significant MI.
• Rupture Syndromes (1-3 days post-MI):
  • Ventricular Septal Defect: Murmur due to interventricular septum rupture.
  • Free Wall Rupture: Leads to cardiac tamponade from blood in pericardial space.
  • Papillary Muscle Rupture: Causes mitral regurgitation murmur.

Long-Term Complications

• Pericarditis: Post-MI inflammation causing positional sharp chest pain.
• Left Ventricular Aneurysm: Risk of thrombus formation due to blood stasis.

Diagnosis of Ischemic Heart Disease

• 12-lead EKG: Essential for initial assessment, revealing signs based on ischemic type.
• Biomarkers:
  • Troponin levels indicate myocardial damage.
  • CK-MB useful for reinfarction assessments.
• Coronary Angiography: Definitive test for diagnosing and treating occlusions.

Stress Testing

• Assesses flow-limiting stenosis in suspected stable angina.
• Exercise or Pharmacological Testing: Increases myocardial oxygen demand, can induce ischemic events.

Management of Ischemic Heart Disease

• Understanding angina types, features, complications, and diagnostics is key for effective treatment.

EKG Interpretation

• Normal sinus rhythm confirmed by regular P waves and QRS complexes.
• Lead 1 shows ST segment depression; Leads 2, 3, and AVF show ST segment elevation indicating MI.
• Reciprocal ST changes suggest inferior STEMI in patients with ST elevation in inferior leads.

Right Ventricular Infarction

• Use right-sided chest leads (V1R-V4R) to assess RV involvement; significant ST elevations indicate RVMI with inferior STEMI correlation.

Posterior and Inferior STEMI

• Leads 2, 3, and AVF can show subtle ST elevations indicating inferior wall involvement.
• Precordial leads may show T-wave inversions and ST depressions suggesting posterior infarction.

Treatment of Ischemic Heart Disease

• Aims to reduce plaque formation and thrombus risk on ruptured plaques.
• Anti-platelet Agents:
  • Aspirin reduces platelet aggregation by inhibiting thromboxane A2.
  • P2Y12 inhibitors block ADP receptors, further decreasing aggregation.
• Heparin: Increases antithrombin III effectiveness, decreasing thrombin activity in vulnerable patients.

Key Notes on Drug Mechanisms

• Aspirin and P2Y12 inhibitors prevent thrombus formation during myocardial infarctions.
• Heparin enhances antithrombin III function to inhibit thrombin and clot formation.

Ischemic Heart Disease Overview

• Caused primarily by atherosclerotic plaques in coronary vessels, limiting oxygenated blood supply to the myocardium.
• Reduced blood flow due to atherosclerosis leads to decreased oxygen delivery and can impair cardiac function.

Atherosclerosis

• Involves fatty plaque development within vessel walls, obstructing blood flow and causing oxygen deficiency.
• Insufficient oxygen results in reduced ATP production, leading to potential heart failure.

Risk Factors for Atherosclerosis

• Mnemonic: BAD HEART
  • B: Obesity (BMI ≥ 30)
  • A: Age (≥ 65 years)
• Other unidentified factors contribute, but obesity and age are significant.

Physiological Consequences

• Coronary artery blockage decreases oxygen and waste removal from myocardial cells.
• Insufficient oxygen negatively impacts heart muscle contraction and overall function.

Key Risk Factors for Ischemic Heart Disease

• Non-modifiable: Age and family history of CAD.
• Modifiable: Obesity, diabetes, hypertension, smoking, alcohol use.
• Diabetes and hypertension significantly increase ischemic heart disease risk.
• Hyperlipidemia (increased LDL, decreased HDL) enhances atherosclerosis risk.

Ischemia and Oxygen Supply

• Atherosclerosis is the primary cause of decreased oxygen supply, leading to ischemia.
• Less common causes include emboli, vessel inflammation, and vasospasm.
• Increased myocardial oxygen demand from conditions like tachycardia worsens ischemic states.

Angina Types

• Stable Angina: Chest pain during exertion, resolves with rest (≥70% occlusion).
• Unstable Angina: Chest pain at rest due to unstable plaques, severe occlusion (≥90%).
• NSTEMI: Myocardial damage from prolonged ischemia (≥30 minutes), chest pain at rest.
• STEMI: Complete occlusion causes severe chest pain, regardless of activity.

Acute Coronary Syndrome (ACS)

• Comprises unstable angina, NSTEMI, and STEMI, indicating severe ischemia.
• Stable angina can progress to ACS due to plaque rupture and thrombus formation.

Clinical Features of Ischemic Heart Disease

• OPQRST approach for chest pain assessment:
  • Onset: Duration varies; stable (5-10 mins) vs. unstable (longer).
  • Palliative/Provocative: Symptoms improve with rest in stable angina.
  • Quality: Described as tight, squeezing, or crushing pain.
  • Radiation: Pain may radiate to arm, jaw, or abdomen (notably inferior STEMI).
  • Severity: Generally constant in nature.

Complications After Myocardial Infarction

• Ventricular Arrhythmias: Risk of PVCs, VT, VF leading to sudden cardiac death within 24 hours post-MI.
• Cardiogenic Shock: Low perfusion due to left ventricular failure following significant MI.
• Rupture Syndromes (1-3 days post-MI):
  • Ventricular Septal Defect: Murmur due to interventricular septum rupture.
  • Free Wall Rupture: Leads to cardiac tamponade from blood in pericardial space.
  • Papillary Muscle Rupture: Causes mitral regurgitation murmur.

Long-Term Complications

• Pericarditis: Post-MI inflammation causing positional sharp chest pain.
• Left Ventricular Aneurysm: Risk of thrombus formation due to blood stasis.

Diagnosis of Ischemic Heart Disease

• 12-lead EKG: Essential for initial assessment, revealing signs based on ischemic type.
• Biomarkers:
  • Troponin levels indicate myocardial damage.
  • CK-MB useful for reinfarction assessments.
• Coronary Angiography: Definitive test for diagnosing and treating occlusions.

Stress Testing

• Assesses flow-limiting stenosis in suspected stable angina.
• Exercise or Pharmacological Testing: Increases myocardial oxygen demand, can induce ischemic events.

Management of Ischemic Heart Disease

• Understanding angina types, features, complications, and diagnostics is key for effective treatment.

EKG Interpretation

• Normal sinus rhythm confirmed by regular P waves and QRS complexes.
• Lead 1 shows ST segment depression; Leads 2, 3, and AVF show ST segment elevation indicating MI.
• Reciprocal ST changes suggest inferior STEMI in patients with ST elevation in inferior leads.

Right Ventricular Infarction

• Use right-sided chest leads (V1R-V4R) to assess RV involvement; significant ST elevations indicate RVMI with inferior STEMI correlation.

Posterior and Inferior STEMI

• Leads 2, 3, and AVF can show subtle ST elevations indicating inferior wall involvement.
• Precordial leads may show T-wave inversions and ST depressions suggesting posterior infarction.

Treatment of Ischemic Heart Disease

• Aims to reduce plaque formation and thrombus risk on ruptured plaques.
• Anti-platelet Agents:
  • Aspirin reduces platelet aggregation by inhibiting thromboxane A2.
  • P2Y12 inhibitors block ADP receptors, further decreasing aggregation.
• Heparin: Increases antithrombin III effectiveness, decreasing thrombin activity in vulnerable patients.

Key Notes on Drug Mechanisms

• Aspirin and P2Y12 inhibitors prevent thrombus formation during myocardial infarctions.
• Heparin enhances antithrombin III function to inhibit thrombin and clot formation.

This quiz covers the essential aspects of ischemic heart disease, focusing on the role of atherosclerosis in obstructing blood flow to the myocardium. Understand how reduced oxygen delivery impacts myocardial function and the pathophysiology involved in this condition.