341 exam 2

• Classic Stable Angina (Exertional Angina or Angina of Effort)

  Myocardial oxygen demand increases during exercise but oxygen supply doesn't increase proportionally
• Increase of oxygen demand in the face of fixed oxygen supply

  Leads to ischemia
• To correct the imbalance of oxygen demand and supply

  1. Decrease oxygen demand

  2. Increase oxygen supply
• Chronic stable angina (Chronic CAD)

  Results from imbalance of oxygen demand and supply
• Treatment of chronic stable angina

  Focuses on re establishing balance between oxygen demand and oxygen supply
• Acute coronary syndrome (ACS)


  Often caused by plaque rupture and thrombus formation which leads to sudden reduction of coronary blood flow
• Unstable angina


  Myocardial ischemia at rest
• Acute myocardial infarction (AMI)


  If prolonged ischemia
• Treatment of ACS


  • Thrombolytic agents
  • Antiplatelets
• Variant angina; Prinzmetal's angina

  Occurs in the absence of increased myocardial oxygen demand, don't need atherosclerosis to have this pain, occurs due to intense vasospasm in coronary arteries
• Treatment of variant angina

  • Vasodilators
• Determinants of Myocardial Oxygen Demand or Consumption (MVO2)

  • Wall stress (most important determinant)
  • Heart rate
  • Cardiac contractility
• Wall stress


  A function of preload and afterload
• Preload


  The amount of blood going back to the heart; how much volume you have in heart at the end of diastole
• Afterload


  Resistance to left ventricle ejection
• Cardiac Output (CO)


  Volume of blood pumped out (ejected) by heart each min
• Stroke Volume (SV)


  The volume of blood pumped out of ventricle in a single beat
• Coronary perfusion pressure (CPP)

  CPP = aortic diastolic pressure - LDVP
• Diastolic filling time


  The time the heart spends in diastole
• Increase preload


  Decrease CPP
• Increase CPP


  Increase O2 supply
• Hypotension


  Can reduce O2 supply
• Increase diastolic filling time

  Increase O2 supply
• Bradycardia


  Increase diastolic filling time
• Tachycardia


  Decreases diastolic filling time
• Determinants of Vascular Tone

  Control of sm. Muscle contraction & site of action of drugs
• Contraction of muscle cell

  1. Voltage gated Ca channel allows Ca into the cell

  2. Ca binds with calmodulin to make complex

  3. Complex activates myosin light chain kinase (MLCK)

  4. MLCK phosphorylates myosin light chain

  5. Phosphorylated myosin light chain it interacts within actin and cause contraction
• Drugs that can cause dilation

  • NO/Nitrates
  • CCB
  • Beta 2 agonist
  • K channel openers
• NO/Nitrates


  Increase cGMP, cGMP dephosphorylates myosin light chain and prevents interaction with myosin light chain and actin
• CCB


  Block Ca channel, Ca can't come in so no contraction
• Beta 2 agonist


  Activates AC and increase cAMP, cAMP inactivates MLCK
• K channel openers


  Opens K channel causes hyperpolarization, sends negative effect on Ca channel and closes Ca channel
• Atherosclerosis: Thickening & hardening of arteries; Endothelial cell injury, LDL & monocytes infiltration, macrophages, foam cells, & fatty streaks formation & transformation to plaques
• Classic stable angina or chronic CAD


  Results from an imbalance between MVO2 & Supplies due to atherosclerosis, treatment focuses on reestablishing this balance, by reduction of MVO2 or inc. O2 supply
• Acute Coronary Syndromes (ACS)


  Most often caused by atherosclerotic plaque ruptures & thrombus formation → leads to sudden reductions in coronary blood flow (CBF) → causes myocardial ischemia at rest
• Acute myocardial infarction (AMI)


  If ischemia is prolonged enough to cause myocardial necrosis
• Treatment of ACS


  • Reestablishing CBF by mainly using thrombolytic agents & antiplatelets, Vasodilators are also useful
• Variant angina


  Occurs in the absence of increased MVO2, atherosclerotic plaques are absent, & ischemia caused mainly by intensive vasospasm
• Treatment of variant angina

  • Vasodilators
• Determinants of MVO2


  • Cardiac contractility
  • Heart rate
  • Wall stress