Quiz 2

• Atherosclerosis


  Narrowing of an artery by plaque from endothelial dysfunction, dyslipidemia, inflammation, or plaque rupture
• Atherosclerosis


  • Causes progressive hardening and narrowing of the arteries
  • The plaques are formed of lipid and thrombus
• Atherosis


  Fat build up, the first detectable lesion is the fatty streak
• Irritants such as smoke inhalation

  Causes damage to the endothelium which allows waste products in the blood to collect in the subendothelium
• Macrophages


  • Released to control plaque build up, but then inflammatory process continues and macrophages become lipid laden
• Sclerosis


  Hardening of the vessel walls, reduces blood vessel compliance
• Coronary artery thrombus


  Occurs due to the rupture or erosion of an existing artery plaque, will completely occlude blood flow
• Mechanism of atherosclerosis


  1. Insult

  2. Infiltration

  3. Aggregation

  4. Proliferation
• Collateral circulation is when atherosclerosis develops slowly, collateral circulation develops to meet the hearts needs
• Coronary artery disease (CAD)


  Obstruction that limits coronary blood flow but does not inhibit heart muscle function, caused by atherosclerosis

  
• CAD diagnosis


  • Diagnosed by cardiac catheterization at the wrist or groin, not felt until >70% occluded, symptoms include SOB and angina
• CAD treatment options


  • CABG
  • PTCA
  • Medications
  • Lifestyle
  • Exercise
• Angina pectoris


  Caused by an imbalance in supply and demand of myocardial oxygen, a discomfort felt anywhere above the waist, common in chest, neck, and jaw, described as a dull ache, tightness, burning, indigestion
• Stable angina


  • Classic or exertional angina, occurs with physical or emotional stress, disappears with rest or nitroglycerin sublingually
• Unstable angina


  • Accelerating in frequency or severity, may occur at rest, requires quick recognition and referral to treatment
• Pre-infarction angina


  • Classified as unstable angina, occurs at rest, worsens with activity, can wake someone up, lasts longer than 15 minutes, "elephant sitting on my chest", abrupt increase in intensity and frequency of symptoms, MEDICAL EMERGENCY
• Post-infarction angina


  • Occurs after an MI, takes place because residual ischemia triggers an episode of angina
• Variant angina (Prinzmetal angina)

  Produced from a vasospasm of the coronary arteries in a sense of occlusive disease, pain at rest, due to emotional upset or inspiration of cold air, responds to nitroglycerin, long term tx = calcium channel blockers
• Myocardial infarction (MI)


  Development of ischemia with resultant necrosis of myocardial tissue, 80-90% of MIs result from coronary thrombus, symptoms start at 70-80% blockage
• MI symptoms


  • Chest discomfort
  • SOB
  • Discomfort in upper body
• Creatine kinase (CK)


  Three isoenzymes: CK-MB = myocardial injury, CK-MM = skeletal muscle injury, CK-BB = brain tissue injury
• Troponins


  GOLD STANDARD for MI diagnosis, Tnl inhibits the interaction between actin and myosin, TnT binds troponin to tropomyosin, increased cardiac muscle damage releases troponin into the bloodstream
• Normal lab values


  • Troponin I normal = <0.1
  • Troponin T normal = <0.4
  • CK-MB normal = <5%
  • CK normal = 30-170
• Other MI diagnostic tests

  • EKG to determine acute MI or past MI
  • Coronary angiography can show blockage or thrombus
  • Echocardiogram shows reduced EF can be indicative of cardiac muscle dysfunction

  
• Acute coronary syndrome


  Used to describe unstable angina or an acute myocardial infarction, significant rise/drop in troponins plus one of the following: proof of sx of ischemia, ECG changes, new cardiac muscle damage

  
• STEMI


  • ST elevation + pathological q-wave, happens as a result of a complete blockage in coronary artery, transmural - full thickness

  
• NSTEMI


  • Due to partially blocked artery, reduced blood flow, AKA nontransmural - does not affect the full thickness of the myocardium, no pathological q-wave on ECG, troponins are elevated but no ST elevation

  
• Complications of an MI

  • Impaired contractility
  • Tissue necrosis
  • Electrical instability
  • Pericardial inflammation
  • Renal dysfunction
  • Cardiogenic shock
  • Stroke
• Risk of re-infarction is increased in women, HTN, elevated cholesterol
• Cardiomyopathy


  A disease in which the contraction and relaxation of myocardial muscle fibers are impaired, can be primary (pathological process in the heart muscle) or secondary (systemic disease)

  
• Types of cardiomyopathy


  • Dilated
  • Hypertrophic
  • Restrictive
• Dilated cardiomyopathy


  • The ventricles are enlarged and thin walls, less effective pump and fluid backs up into the ventricles, produces an ineffective systolic pump, slowed ventricular emptying and low EF
• Chain of events for dilated cardiomyopathy


  1. Weakened heart begins to dilate and is unable to pump blood effectively

  2. The chambers of the heart respond to stretching more to accommodate more blood and increase the strength of contraction

  3. The heart is stretched out and is weak

  4. Heart failure

  
• Symptoms of dilated cardiomyopathy

  • SO, fatigue, LE edema, jugular venous distention, abdominal swelling
• Causes of dilated cardiomyopathy

  • CAD, genetics, alcohol use, HTN, diabetes, infection
• Hypertrophic cardiomyopathy


  • Causes diastolic dysfunction and impairs the ability to fill the ventricles, high risk of sudden cardiac death, tx with ICD placement, susceptibility is genetic, rapid ventricular emptying and high EF
• Symptoms of hypertrophic cardiomyopathy

  • fatigue, SOB, arrhythmias, dizzy, lightheaded, syncope
• Causes of hypertrophic cardiomyopathy

  • Genetics, HTN, aging
• Restrictive cardiomyopathy


  • The chambers of the heart are stiff, diastolic dysfunction, rapid ventricular emptying and high EF, caused by other health conditions, scarring, chemo, excess iron

  
• Takotsubo cardiomyopathy


  Temporary and reversible weakening of the heart caused by physical or emotional stress