Pharm, Cardiac Drugs

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Pharm, Cardiac Drugs
2011-11-02 08:53:23

Cardiac Drugs
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  1. Brings blood back to the Right side of the heart.
    • Vena Cava
    • -Cranial
    • -Caudal
  2. Flow of blood
    • Veins from body
    • Right Atrium
    • Tricuspid Valve
    • Right Ventricle
    • Pulmonic Valve
    • Lungs (via pulmonary artery)
    • Left Atrium (viathe pulmonary veins)
    • Bicuspid (Mitral) Valve
    • Left Ventricle
    • Aortic Valve
    • To the body/ heart
  3. allows heart muscle cells to fire spontainiously and independantly
  4. A group of cells in the Right Atrium that depolarizes faster than any other cells in the heart.
    • Sinoatrial Node (SA Node)
    • - heart's pacemaker sets HR
  5. Contraction of the atria on an EKG is seen as a...
    • P wave
  6. The wave of depolarization reaches the ventricles through a cluster of cells called:
    The Atrioventricular Node
  7. The PR Interval or P-QRS Interval is:
    • When the depolarization wave travles through the AV Node causing a delay between contractions of the atrium and Ventricles
    • Displayed on EKG as a flat line after the P wave
  8. Depolarization of the heart
    • SA Node fires
    • -Atrium contract
    • AV Node depolarizes
    • -PR interval (flat line)
    • Bundle of His depolarises
    • Purkinje fibers depolarize
    • -Ventricles contract
    • ventricular cells repolarize
  9. When the ventricles contract (depolarize) it is seen on an EKG as:
    QRS complex

  10. When the ventricles repolarize (reset for the next fire) it is seen on an EKG as a:
    T wave

  11. Absolute Refractory Period
    When the Na+ channels are already open and the Na+ is rushing in the channels cannot open again, the cell cannot fire again despite the magnitude of the stimulus (during phase 0)
  12. Relative Refractory Period
    When the cell begins to repolarize a strong stimulus may cause the channels to reopen causing a weak fire (during phases 2 & 3)
  13. Rapid uncoordinated contractions
    Flutter or Fibrillation of the atria or ventricles.
  14. Sympathetic Nervous System causes:
    • Increased HR & force of contraction
    • Elevated BP
    • Constriction of peripheral blood vessels
    • Decreases perfusion of nonessential organs and tissues
    • Decreases activity of the GI tract
    • Dialates the bronchioles
  15. Neuro transmitters of the SNS
    • Epinephrine (adrenaline)
    • Norepinephrine
    • Bind to adrenergic receptors
  16. Adrenergic agonists
    Mimic the effects of epinephrine and norepinephrine by binding to the adrenergic receptors
  17. Adrenergic Antagonists
    Bind to the adrenergic receptors not to produce an effect, but to block the neurotransmitters from binding and stop their effects.
  18. Alpha 1 Adrenergic Receptor
    Causes vasoconstriction in skin and intestinal tract.
  19. Alpha 2 Adrenergic Receptor
    Located on the ends of adrenergic neurons and help regulate the release of norepinephrine
  20. Beta 1 Adrenergic Receptors
    • Located in the heart
    • Increase the HR, contraction strength, & speed of depolarization wave.
    • Tachycardia
  21. Beta 2 Adrenergic Receptors
    • Located in smooth m. surrounding blood vessels surrounding the heart, skeletal m., arteriols, and terminal bronchioles in the lungs.
    • Vasodilates
  22. Parasympathetic Nervous System
    • Slows the HR
    • Increases blood flow to intestinal tract
    • Decreases the diameter of the bronchioles
    • little effect on peripheral blood flow
  23. Acetylcholine
    • Main neuro transmitter of the PNS
    • Binds w/ choloinergic receptors
  24. Muscarinic receptors
    • Usually found on neurons associated w/ the PNS
    • Produce PNS effects: slowed HR, increased blood flow to intestines, pin-point pupils
  25. Nicotinic cholinergic receptors
    • found in both PNS and SNS and produce effects of both
    • found at neuromuscular junction
  26. Arrhythmia
    Any abnormal pattern of electrical activity in the heart.
  27. Ectopis Focus (foci pl.)
    • An area of myocardium (heart m.) or conduction system depolarizing out of sequence or faster than the SA node disrupting the normal electrical pattern.
    • Often areas of damaged cells allowing more Na+ leakage than normal (lower threshold).
  28. Premature Ventricular Contraction (PVC)
    • a single, large, bizzar wave on an EKG indicating an ectopic focus
    • Single intermittent PCVs on an EKG may not significantly affect the heart's ability to pump and sometimes occur in animals under general anesthesia
    • Paroxysm - short series of multiple PCVs
    • Ventricular flutter - longer series of PCVs
    • Ventricular Fibrillation - severe conduction disterbance causing ventricles to quiver.
  29. Short series of Premature Ventricular Contractions (PCVs)
  30. Longer series of Premature Ventricular Contractions (PCVs)
    Ventricular Flutter
  31. Severe conduction disterbance causing the ventricles to quiver
    Ventricular Fibrillation
  32. Antiarrhythmic Drugs
    Used to control ectopic foci or reverse conduction abnormalities of the heart
  33. Lidocaine, quinidine, and procainamide work by:
    decreasing the rate of Na+ influx into the cell resulting in a slower automaticity and allows the SA node to once again determine the HR
  34. Lidocaine
    • Only avalible in injectible form
    • Preferred method IV bolus of infusion
    • Preferred drug for canine PCVs and ventricular arrythmias and animals under anesthesia.
    • Not good for Atrial arrthmias
    • Cats more sensitive to side effects.
    • Slwo Na+ influx into the cell slowing the automaticity
  35. Lidocaine CNS effects
    • Light Toxicosis - sedation, ataxia, and drowsiness
    • Larger overdoses - excitement and sezures
    • Do NOT confuse w/ lidocaine packaged w/ epinephrine
    • Switch to Mexiletine for long term use
  36. Procainamide & Quinidine
    • Slows Na+ influx into cell slowing the automaticity and refractory periods
    • Control both Ventricular Ectopic Foci and atrial flutter or fibrillation (supraventricular tachycardia)
    • Most commonly administered PO allowing for long term maintenance
    • Quinidine frequently causes V/D and anorexia.
    • Procainamide has fewer GI problems
  37. Atrial flutter and fibrillation
    Depolarization wave is altered in its movement enough to allow the wave to encounter some of the myocardia that have completed their refractory phase causing them to depolarize again and the wave continues on.
  38. Quinidine's Paradoxic Ventricular Tachycardis Effect
    • Increased HR due to an antivagal effect.
    • - decreases effect of Vagus Nerve on AV node
    • - Vagus nerve slows impulses through the AV node
    • - antivagal effect allows AV node impulses to move faster speeding up ventricular contractions and increased overall HR
  39. Digoxin Toxicity from Quinidine
    • Drugs may be Carefully used together
    • Digoxin increases the strength of heart contractions
    • Quinidine displaces digoxin from it's binding sites and decreases its elimination doubling the plasma concentration
    • Digoxin doses should be decreased by 1/2
  40. Procainamide tablets
    • 2 forms standard tablet, sustained release
    • standard usually given QID
    • sustained release usually given TID
    • Owners must check stool for intact sustained release tablets
  41. Beta antagonists = Beta blockers
    • block the beta SNS response
    • help prevent the generation of ectopic foci in Dz heart
    • Allows parasympathetic dominance slowing conduction through the heart (i.e., SA and AV nodes)
    • present on EKG as slowed HR and a prolonged interval between the P wave and QRS complex (1st degree AV block)
    • 2nd degree AV block is when the conduction through the AV node is long enough to cause the wave to die out and there is no ventricular contraction
    • AV block or bradycardia caused by beta blockers can be treated w/ parasympathetic antagonists (i.e., atropine) but lowerning the beta blocker dose is better
  42. Upregulation
    • seen over time where the heart compensates by creating more beta 1 receptors and the patient appears to become tolarent to the drugs
    • because of this patients must be slowly taken off medications to allow for downregulation
    • Rate of withdrawl can be adjusted based on resting HR
  43. 2nd degree AV block
  44. Propranolol
    • Beta 1 antagonist
    • Blocks stimulation of beta 1 receptors by the catecholamines (i.e., epinephrine, norepinephrine, dobutamine)
    • Reduces tachycardia in stress response
    • Slows HR
    • Used to decrease rapid HR associated w/ hyperthyroidism in cats
    • Blocks beta receptors on SA and AV nodes, slows depolarization wave
    • Reduces chance of ventricular ectopic foci developing and producing cardiac arrythmias
    • Not very selective of beta 1 or beta 2
  45. Negative Inotropic Drugs
    • Drugs that decrease the contraction strength of the heart
    • Use w/ caution in animals w/ myocardial failure, may not allow the heart to beat with enough force to keep it alive
  46. Ca++ Channel Blocker Antiarrythmic Drugs
    • Block Ca channels of the myocardium
    • Decrease conduction of depolarization waves
    • Decrease automaticity of parts of the conduction system
    • May also reduce strength of contraction and cardiac output (negative inotropic effect), so use w/ caution in animals w/ congestive heart failure
    • Verapamil and diltiazam
  47. Diltiazam in cats
    • Cats w/ hypertonic cardiomyopathy, ventricular wall thickened & stiff and cannot contract efficiantly
    • Decreases thickness of left ventricle wall
    • Increases dilation of coronary blood vessels and decreases arrythmias
    • some cats become asymptomatic
  48. Positive Inotropic Drugs
    • increase contraction strength in weakened hearts
    • Directly or indirectly make more Ca more avalible or increasin the affinity between Ca and contractile proteins
    • Catecholamines (norepinephrine, epinephrine, dobutamine) are naturally occuring positive inotropic agents
    • Adrenergic/ Sympathomimetic drugs
    • Stimulate beta1 receptors
    • Relitively short acting due to downregulation
  49. Downregulation
    • Heart reduces # of beta1 (catecholamine) receptors
    • cause adrenergic drugs to lose their effects hrs to days after Tx initiation
  50. Digoxin
    • Drug of choice for producing long-term positive inotropic effect
    • Makes more Ca avalible indirectly by inhibiting the cells Na-K-ATPase pump
    • Increased Na in the cells increase the risk of spontanios depolarization and development of ectopic foci
    • Slows SA node HR and delays conduction through the AV node (1st degree AV block)
    • Used therapeutically to control supraventricular tachycardia caused by atrial fibrillation
    • Cardiac Glycoside, poison found in nature, digoxin origionaly durived from foxglove.
    • Sm therapeutic range
    • Early signs of digoxin toxicity include D/V, anorexia
    • As toxisity worsens RH will slow (SA node effect), PR interval will increase (1st degree AV block), then 2nd degree AV block will occure (P wave w/o QRS complex)