1. Antianginal Agents

2. Coronary Ischemia: Supply and Demand Economics

3. Coronary Ischemia: Supply and Demand Economics

4. The Grip of Angina

5. Supply-Demand Mismatch

6. Myocardial Oxygen Demand
Heart Rate
Wall Stress
Contractility
Adapted from Runge et al, Netter’s Cardiology

7. Determinants of Myocardial Oxygen Supply

8. Determinants of Myocardial Oxygen Supply

9. Coronary Flow Reserve
Adapted from Maseri A, Ischemic Heart Disease, Churchill Livingstone, 1995

10. Angina Pectoris (Chest Pain)
When the supply of oxygen and nutrients in the blood is insufficient to meet the demands of the heart, the heart muscle aches.
The heart demands a large supply of oxygen to meet the demands placed on it.

11. Types of Angina
Chronic stable angina (also called classic or effort angina)
Unstable angina (also called preinfarction or crescendo angina)
Vasospastic angina (also called Prinzmetal’s or variant angina)

12. Angina Drug Therapy

13. Antianginal Agents
Nitrates
Beta blockers
Calcium channel blockers

14. Antianginal Agents: Therapeutic Objectives
Increase blood flow to ischemic heart muscle
and/or
Decrease myocardial oxygen demand

15. Antianginal Agents: Therapeutic Objectives
Minimize the frequency of attacks and decrease the duration and intensity of anginal pain
Improve the patient’s functional capacity with as few side effects as possible
Prevent or delay the worst possible outcome, MI

16. Nitric Oxide
Opie LH: Heart Physiology Lippincot Williams & Wilkins, 2004

17. Antianginal Agents: Nitrates
Available forms:
Sublingual Ointments
Buccal Transdermal patches
Chewable tablets Inhalable sprays
Capsules Intravenous solutions

18. Antianginal Agents: Nitrates
Cause vasodilation due to relaxation of smooth muscles
Potent dilating effect on coronary arteries
Used for prophylaxis and treatment of angina

19. Antianginal Agents: Nitrates
Nitroglycerin
Prototypical nitrate
Large first-pass effect with PO forms
Used for symptomatic treatment of ischemic heart conditions (angina)
IV form used for BP control in perioperative hypertension, treatment of CHF, ischemic pain, and pulmonary edema associated with acute MI

20. Antianginal Agents: Nitrates
isosorbide dinitrate (Isordil, Sorbitrate, Dilatrate SR)
isosorbide mononitrate (Imdur, Monoket, ISMO)
Used for:
Acute relief of angina
Prophylaxis in situations that may provoke angina
Long-term prophylaxis of angina

21. Antianginal Agents: Nitrates
Side Effects
Headache
Usually diminish in intensity and frequency with continued use
Tachycardia, postural hypotension
Tolerance may develop

22. Nitrate Tolerance
Occurs with chronic administration of long acting nitrates.
Efficacy of drug diminishes with chronic exposure (tachyphylaxis).
Tolerance readily reverses with nitrate free interval.

23. Antianginal Agents: Beta Blockers
atenolol (Tenormin)
metoprolol (Lopressor)
propranolol (Inderal)
nadolol (Corgard)

24. Adrenergic Receptors Beta1 Beta2 Alpha
SA node, AV node, His-Purkinje system
Myocardium
Juxtaglomerular apparatus
Adipocytes
Beta2
Peripheral and coronary vasculature
Bronchi
Peripheral Muscle
Uterine Muscle
Alpha
Peripheral circulation
Beta-1
Beta-2
Alpha
Adapted from Runge et al, Netter’s Cardiology

25. Antianginal Agents: Beta Blockers
Mechanism of Action
Decrease the HR, resulting in decreased myocardial oxygen demand and increased oxygen delivery to the heart
Decrease myocardial contractility, helping to conserve energy or decrease demand

26. Antianginal Agents: Beta Blockers
Therapeutic Uses
Antianginal
Antihypertensive
Cardioprotective effects, especially after MI

27. Antianginal Agents: Beta Blockers
Side Effects
Body System Effects
Cardiovascular bradycardia, hypotension second- or third-degree heart block heart failure
Metabolic Altered glucose and lipid metabolism

28. Antianginal Agents: Beta Blockers
Side Effects
Body System Effects
CNS dizziness, fatigue, mental depression, lethargy, drowsiness, unusual dreams
Other impotence wheezing, dyspnea

29. Antianginal Agents: Calcium Channel Blockers
verapamil (Calan)
diltiazem (Cardizem)
nifedipine (Procardia)

30. Role of Calcium Channels in Myocardial Contraction
Opie LH, Heart Physiology, Williams Lippincott and Williams 2004

31. Role of Calcium Channel in Vascular Smooth Muscle Function
Opie LH, Heart Physiology, Williams Lippincott and Williams 2004

32. Antianginal Agents: Calcium Channel Blockers
Mechanism of Action
Cause peripheral arterial vasodilation
Reduce myocardial contractility (negative inotropic action)
Result: decreased myocardial oxygen demand

33. Antianginal Agents: Calcium Channel Blockers
Therapeutic Uses
First-line agents for treatment of angina, hypertension, and supraventricular tachycardia
Short-term management of atrial fibrillation and flutter
Several other uses

34. Antianginal Agents: Calcium Channel Blockers
Side Effects
Very acceptable side effect and safety profile
May cause hypotension, palpitations, tachycardia or bradycardia, constipation, nausea, dyspnea

35. Treatment of Ischemic Heart Disease

36. Antianginal Agents: Nursing Implications
Before administering, perform a complete health history to determine presence of conditions that may be contraindications for use or call for cautious use.
Obtain baseline VS, including respiratory patterns and rate.
Assess for drug interactions.

37. Antianginal Agents: Nursing Implications
Patients should not take any medications, including OTC medications, without checking with the physician.
Patients should report blurred vision, persistent headache, dry mouth, dizziness, edema, fainting episodes, weight gain of 2 pounds in 1 day or 5 or more pounds in 1 week, pulse rates under 60, and any dyspnea.

38. Antianginal Agents: Nursing Implications
Alcohol consumption and hot baths or spending time in jacuzzis, hot tubs, or saunas will result in vasodilation, hypotension, and the possibility of fainting.
Teach patients to change positions slowly to avoid postural BP changes.
Encourage patients to keep a record of their anginal attacks, including precipitating factors, number of pills taken, and therapeutic effects.

39. Antianginal Agents: Nitroglycerin
Nursing Implications
Instruct patients in proper technique and guidelines for taking sublingual NTG for anginal pain.
Instruct patients never to chew or swallow the SL form.
Instruct patients that a burning sensation felt with SL forms indicates that the drug is still potent.

40. Antianginal Agents: Nitroglycerin
Nursing Implications
Patients are taught to take up to three tablets every 5 minutes. If no relief from chest pain is obtained after three tablets, they should seek medical assistance.
Absorption nitroglycerin ointments best over a nonfatty and nonhairy portion of skin. The upper torso is the preferred site of application. The nurse should wear gloves when applying to prevent transdermal absorption by the applier. The ointment is measured as one straight line on the nitroglycerin patch and is gently spread over paper and applied, but not rubbed, into the skin.

41. Antianginal Agents: Nitroglycerin
Nursing Implications
Instruct patients to keep a fresh supply of NTG on hand; potency is lost in about 3 months after the bottle has been opened.
Medications should be stored in an airtight, dark glass bottle with a metal cap and no cotton filler to preserve potency.

42. Antianginal Agents: Nitroglycerin
Nursing Implications
Instruct patients in the proper application of nitrate topical ointments and transdermal forms, including site rotation and removal of old medication.
To reduce tolerance, the patient may be instructed to remove topical forms at bedtime, and apply new doses in the morning, allowing for a nitrate-free period.

43. Antianginal Agents: Nitroglycerin
Nursing Implications
Instruct patients to take prn nitrates at the first hint of anginal pain.
If experiencing chest pain, the patient taking SL NTG should be lying down to prevent or decrease dizziness and fainting that may occur due to hypotension.
Monitor VS frequently during acute exacerbations of angina and during IV administration.

44. Antianginal Agents: Nitroglycerin
Nursing Implications
IV forms of NTG must be contained in glass IV bottles and must be given with infusion pumps.
Discard parenteral solution that is blue, green, or dark red.
Follow specific manufacturer’s instructions for IV administration. Use special IV tubing provided or non-PVC tubing.

45. Antianginal Agents: Calcium Channel Blockers
Nursing Implications
Blood levels should be monitored to ensure they are therapeutic.
Oral CCBs should be taken before meals and as ordered.
Patients should be encouraged to limit caffeine intake.

46. Antianginal Agents: Beta Blockers
Nursing Implications
Patients taking beta blockers should monitor pulse rate daily and report any rate lower than 60 beats per minute.
Dizziness or fainting should also be reported.
Constipation is a common problem. Instruct patients to take in adequate fluids and eat high-fiber foods.

47. Antianginal Agents: Beta Blockers
Nursing Implications
These medications should never be abruptly discontinued due to risk of rebound hypertensive crisis.
Inform patients that these medications are for long-term prevention of angina, not for immediate relief.

48. Antianginal Agents: Nursing Implications
Monitor for adverse reactions
Allergic reactions, headache, light-headedness, hypotension, dizziness
Monitor for therapeutic effects
Relief of angina, decreased BP, or both

49. Antidysrhythmic Agents

50. Antidysrhythmics Dysrhythmia Antidysrhythmics
Any deviation from the normal rhythm of the heart
Antidysrhythmics
Drugs used for the treatment and prevention of disturbances in cardiac rhythm

51. Cardiac Cell
Inside the cardiac cell, there exists a net negative charge relative to the outside of the cell.

52. Resting Membrane Potential: RMP
This difference in the electronegative charge.
Results from an uneven distribution of ions (sodium, potassium, calcium) across the cell membrane.
An energy-requiring pump is needed to maintain this uneven distribution of ions.
Sodium-potassium ATPase pump

53. Heart and Conduction System

54. Resting Membrane Potential of a Cardiac Cell

55. Abnormal Heart Rhythms
Arrhythmia
BPM
tachycardia
bradycardia
<60
atrial flutter
atrial fibrilation
>350
prem. atrial cont.
variable
prem. vent. cont.
vent. fibrilation

56. Premature Ventricular Contraction

57. Action Potential
A change in the distribution of ions causes cardiac cells to become excited.
The movement of ions across the cardiac cell’s membrane results in the propagation of an electrical impulse.
This electrical impulse leads to contraction of the myocardial muscle.

58. Action Potential Four Phases
The SA node and the Purkinje cells each have separate action potentials.

59. Action Potentials: Phases (SA Node)

60. Action Potentials: Purkinje Fiber

61. Action Potentials: Intervals

62. Abnormal Heart Rhythms
Caused by:
ischemia, infarction, alteration of body chemicals
Symptoms:
palpitations, syncope, lightheadedness, visual disturbances, pallor, cyanosis, weakness, sweating, chest pain, hypotension

63. Pharmaceutical Treatment
Aimed at preventing life-threatening conditions by restoring normal rhythm
Acts on the myocardium where the impulses are conducted
Some drugs influence heart rate, others influence movement of ions (Na and Ca)

64. Vaughan Williams Classification
System commonly used to classify antidysrhythmic drugs

65. Vaughan Williams Classification
Class Ia
Class Ib
Class Ic
Class II
Class III
Class IV
Other

66. Vaughan Williams Classification
Membrane-stabilizing agents
Fast sodium channel blockers
Divided into Ia, Ib, and Ic agents, according to effects

67. Vaughan Williams Classification
moricizine
General Class I agent
Has characteristics of all three subclasses
Used for symptomatic ventricular and life-threatening dysrhythmias

68. Vaughan Williams Classification
Class Ia
quinidine, procainamide, disopyramide
Block sodium channels
Delay repolarization
Increase the APD
Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, Wolff-Parkinson-White syndrome

69. Vaughan Williams Classification
Class Ib
tocainide, mexiletine, phenytoin, lidocaine
Block sodium channels
Accelerate repolarization
Decrease the APD
Used for ventricular dysrhythmias only (premature ventricular contractions, ventricular tachycardia, ventricular fibrillation)

70. Vaughan Williams Classification
Class Ic
encainide, flecainide, propafenone
Block sodium channels (more pronounced effect)
Little effect on APD or repolarization
Used for severe ventricular dysrhythmias
May be used in atrial fibrillation/flutter

71. Vaughan Williams Classification
Class II
Beta blockers: atenolol, esmolol, petaprolol, propranolol
Reduce or block sympathetic nervous system stimulation, thus reducing transmission of impulses in the heart’s conduction system
Depress phase 4 depolarization
General myocardial depressants for both supraventricular and ventricular dysrhythmias

72. Vaughan Williams Classification
Class III amiodarone, bretylium, sotalol, ibutilide
Increase APD
Prolong repolarization in phase 3
Used for dysrhythmias that are difficult to treat
Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter—resistant to other drugs
Sustained ventricular tachycardia
Ibutilide is specifically indicated only for treatment of recent-onset atrial fibrillation and flutter.
Patients taking amiodarone must have baseline and serial pulmonary function tests in order to monitor for potential pulmonary toxicity.

73. Vaughan Williams Classification
Class IV
verapamil, diltiazem
Calcium channel blockers
Depress phase 4 depolarization
Used for paroxysmal supraventricular tachycardia; rate control for atrial fibrillation and flutter

74. Vaughan Williams Classification
Other Antidysrhythmics
digoxin, adenosine
Have properties of several classes and are not placed into one particular class

75. Antidysrhythmics Digoxin Cardiac glycoside
Inhibits the sodium-potassium ATPase pump
Positive inotrope—improves the strength of cardiac contraction
Allows more calcium to be available for contraction
Used for CHF and atrial dysrhythmias
Monitor potassium levels, drug levels, and for toxicity

76. Antidysrhythmics adenosine (Adenocard)
Slows conduction through the AV node
Used to convert paroxysmal supraventricular tachycardia to sinus rhythm
Very short half-life
Only administered as fast IV push
May cause asystole for a few seconds
Other side effects minimal

77. Antidysrhythmics: Side Effects
ALL antidysrhythmics can cause dysrhythmias!!
Hypersensitivity reactions
Nausea
Vomiting
Diarrhea
Dizziness
Blurred vision
Headache

78. Antidysrhythmics: Nursing Implications
Obtain a thorough drug and medical history.
Measure baseline BP, P, and cardiac rhythm.
Measure serum potassium levels before initiating therapy.

79. Antidysrhythmics: Nursing Implications
Assess for conditions that may be contraindications for use of specific agents.
Assess for potential drug interactions.
Instruct patients regarding dosing schedules and side effects to report to physician.

80. Antidysrhythmics: Nursing Implications
During therapy, monitor cardiac rhythm, heart rate, BP, general well-being, skin color, temperature, heart and breath sounds.
Assess plasma drug levels as indicated.
Monitor for toxic effects.

81. Antidysrhythmics: Nursing Implications
Instruct patients to take medications as scheduled and not to skip doses or double up for missed doses.
Patients who miss a dose should contact their physician for instructions if a dose is missed.
Instruct patients not to crush or chew any oral sustained-release preparations.

82. Antidysrhythmics: Nursing Implications
For class I agents, monitor ECG for QT intervals prolonged more than 50%.
IV infusions should be administered with an IV pump.

83. Antidysrhythmics: Nursing Implications
Patients taking propranolol, digoxin, and other agents should be taught how to take their own radial pulse for 1 full minute, and to notify their physician if the pulse is less than 60 beats/minute before taking the next dose of medication.

84. Antidysrhythmics: Nursing Implications
Monitor for therapeutic response:
Decreased BP in hypertensive patients
Decreased edema
Regular pulse rate or
Pulse rate without major irregularities, or
Improved regularity of rhythm