Pharmacology Exam II Notes Review Part 1

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  1. sinoatrial node
    pacemaker; beta 1 receptors
  2. ECG wave tracing; P wave
    atrial depolarization
  3. ECG wave tracing; QRS
    ventricular depolarization
  4. ECG wave tracing; T
    ventricular repolarization
  5. Sodium is responsible for
    initial depolarization
  6. Calcium is responsible for
    sustained contraction
  7. Potassium is responsible for
  8. Atrial flutter
    200-300 bmp; rapid regular beat of atrial depolarization
  9. Atrial fibrilation
    no p-shape; random, rapid, and uncoordinated depolarization
  10. Ventricular depolarization
    repetitive, rapid, randomized excitation of ventricles
  11. Average blood pressure
    120/80 mmHg
  12. High BP
    greater than 140 systolic or 90 in diastolic
  13. Diastolic
    the pressure your left ventricle has to overcome to push blood out
  14. Why is diastolic extremely important?
    because the higher the value is the more your hear has to work out to push blood out and it will eventually start failing
  15. Normal Heart Rate
    70 bpm
  16. Angina characteristics
    inadequate oxygen to heart; increase heart rate and coronary vessels are constricted
  17. What is the first treatment used to treat angina?
  18. Nitroglycerin is converted to
    nitric oxide (NO) which is a potent vasodilator
  19. Nitrates
    general class name of Nitroglycerin
  20. Nitroglycerin
    sublingual (under tongue) works in 1-3 minutes and only lasts for 30 minutes. Mainly used for emergency situations
  21. Nitro ointment
    onset is 15 minutes and has a duration of 4-8 hours; work as beta blockers
  22. Beta blockers
    decrease heart rate and decrease force of contraction which overall decreases cardiac work which takes care of the increase of heart rate
  23. Calcium blockers
    • can be used to help coronary vessel constriction
    • decreases constriction in vasculature
    • decreases force of contraction which will therefore decrease heart rate
    • SA node = decrease in heart rate
    • AV node = decrease conduction velocity
    • SA and AV node decrease cardiac output
  24. Calcium channel blocker drugs
    • Verapamil- affects mainly heart, usually to decrease heart rate; little effect on vasculature
    • Amolodipine (Norvase) - vasculature
    • Diltilazem -¬† middle heart vessels to decrease cardiac output
  25. Combine Beta and Calcium channel blockers?
    No, because this would cause hypotension which would put patient at risk
  26. Anti-arrhythmic drug classes
    • Normal electrical impulse impaired
    • SA -> AV = bundle of His (parkinje fibers)
    • ectopic foci = alternative pacemaker
  27. Class I Anti-arrhythmic Drug
    • Sodium channel blockers
    • slows conduction velocity
    • prolongs refractory period
  28. Quinidine
    • Sodium channel blocker for arrthymia
    • decreases inotropic activity in heart
    • decreases electrical impulses through the heart
    • one major side effect of pushing the T and P wave further apart (beats are further and could end in cardiac arrest)
  29. 3 Classes of Drugs to treat angina
    • Nitrates
    • B-blockers
    • Calcium Blockers
  30. More than one p-wave in ekg
    it shows your heart is contracting to fast to disperse blood
  31. No p or t wave
    no blood in ventricles and no blood is getting shut out. This is the worst type of arhythmia
  32. Class I drugs
    Quinidine and Procainamide are two drugs that act as sodium blockers
  33. Class II
    • Beta blockers
    • decrease conduction velocity
    • decrease cardiac work
    • decrease heart rate
    • decrease force of contraction
  34. Class II drugs
    propranolol (B1 and B2), atenolol (B1 specific), and sotalol
  35. Class III Anti-arrhythmic
    • Potassium channel blockers
    • extend period of repolarization
  36. Class III drugs
    Bretylium (prolongs action potential) and Sotalol (Potassium channel and Beta blockers)
  37. Class IV Anti-arrhythmic drugs
    Calcium channel blockers
  38. Class IV drugs
    Verapamil (decreases cardiac work)
  39. Congestive heart failure (CHF)
    • swollen ankles and extremities
    • worst type is when left ventricle is affected
  40. 4 main consequences of CHF:
    • 1) backup of fluid in vessels and lungs (leads to hypertension b/c of more pressure and heart works harder)
    • 2) physiological compensation: increases sympathetic activity
    • 3) compensation mechanisms fail: decrease in cardiac output, hypoxia -> fatigue
    • 4) death - no drugs to prevent; only prolong
  41. CHF etiology
    • Atheroschlerosis (myocardial weakness)
    • Ahrrythmias/valvular defects (pumping restrictions)
    • Hypertension (increased after load; the work the heart has to do to pump blood out to the rest of the body)
  42. Myocardial weakness leads to
  43. Atheroschlerosis leads to
    plaque buildup in blood vessels that block the way for blood flow which limits oxygen which will give you necrotic cells, this then leads to a decreased pumping capacity, ventricles become stiff (b/c heart becomes more muscular to try and pump more blood) and fluid backs up
  44. CHF is a
    long process that takes years to develop
  45. Hypertension
    chronically high BP; provides resistance which heart has to overcome to change in pressure to pump blood out -> hypertrophic -> decrease in cardiac output -> increase in fluid volume -> increase in pulmonary congestion
Card Set:
Pharmacology Exam II Notes Review Part 1
2013-10-07 23:44:11
notes pharmacology exam two

notes for pharm unt
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