Cardiac Medications Used To Treat Angina Pectoris


I. Types of Angina

a. Stable Angina

b. Unstable Angina

c. Prinzmetal Angina

After all is said and done, angina pectoris is due to an imbalance between the work being demanded of the heart and the amount of perfusion the heart has moment to moment.

 Example : If the person has just eaten a large meal, the body diverts a great deal of blood to the digestive system in order to digest the meal. This takes away blood volume from other organs, including the heart. Why, then, would a large meal place a burden on the heart ?

Answer : Eating causes an increase in the heart rate just due to the thermogenic effects of food and the shunting of blood to the digestive tract. The increased heart rate represents an increased work burden on the heart. In hearts that are already sick (CAD) the increased heart rate, shortened diastolic rest phase and the increase in MVO2 can be enough stress in a sick heart to bring on angina.

 Example : If a person is under a great deal of emotional stress, like being involved in a bank holdup, a plane crash or a fire, the adrenal medulla will release large quantities of epinephrine and some norepinephrine. Epinephrine has the effect of causing the heart rate to increase, the blood vessels will constrict and the force of the heart's contraction will increase. Why, then, would stress be able to trigger angina ?

Answer : Epinephrine has the ability to vasoconstrict blood vessels throughout the body. It is also a potent hormone that drives up the heart rate (increases heart chronotrophy) and increases the strength of contraction (increases heart inotrophy). Anytime you increase the work of the heart by driving up the heart rate and strength of each contraction, you increase the myocardial oxygen demand (MVO2). In a sick heart, these stressors can bring on angina because the heart has reached its anginal threshold.

 Example : If a person has a great deal of physical work that they have to perform, like shoveling snow in the winter time, the upper extremities will have to do a great deal of pushing, lifting and throwing. When people perform a lot of lifting and throwing, they will frequently Valsalva and hold their breath. Why would shoveling snow in the cold weather bring on an episode of angina pectoris ?

Answer : Whenever a person performs a Valsalva maneuver, the blood return to the heart is inhibited thus reducing filling volumes and ejection fractions. Also, the Valsalva deranges blood pressure and thus represents a derangement of vascular pressures - an important concept to remember when you recall that the heart receives its perfusion during diastole and depends on good ejection fractions and intravascular pressures for adequate perfusion. Additionally, upper extremity work (snow shoveling) represents a significantly higher work burden because the upper extremities generally have a lower absolute VO2max capability and upper extremity muscle mass is smaller. Therefore for any absolute work burden, the actual cost of performing the work will be higher for the upper extremities versus a lower burden for the lower extremities.

Upper extremity work also causes the heart rate to be higher than when the same absolute work load is performed by the lower extremities. Therefore, anytime you increase heart rate and therefore increase MVO2 for the heart, you place it at risk for angina if CAD is present.

 Example : If a person smokes a cigarette, we know that it causes the blood vessels to constrict because tobacco has a great deal of nicotine - a powerful vasoconstrictor. Why would a chronic smoker be more likely to suffer from angina than a non-smoker ?

Answer : Nicotine is a powerful vasoconstrictor and therefore inhibits perfusion to any organ system. Plastic surgeons do not like to perform re-attachments or flaps or skin grafts on smokers until they have stopped smoking for 2-4 weeks. Plastic surgeons correctly maintain that the blood supply to an extremity of to a flap or skin graft is jeapordized if the patient smokes. Additionally, it is well known that atherosclerotic processes are acclerated in smokers. The burdens of decreased perfusion due to nicotine and the decreased perfusion due to atherosclerotic plugging of the coronary vessels creates the poor perfusion conditions that lead to angina pectoris and eventually to a myocardial infarction.

 A. Stable Angina

Onset due to :

a. exercise

b. emotional stress or tension

c. eating a large meal

 With stable angina, there is a definite perfusion-to-work-demand ratio that is stable, known and when that level is exceeded, angina is felt. Stable angina is always alleviated by rest or by decreasing the work intensity below the anginal threshold.


Treatment Philosophy :

a. Increase Perfusion To The Heart

b. Decrease Afterload On The Heart

c. Decrease End-Diastolic Filling Pressures

d. Decrease Myocardial Wall Tensions


B. Unstable Angina

Onset due to :

a. advancing atherosclerosis

b. sudden closure of small vessels within the heart muscle

c. friable vessel walls that fissure, crack and bleed forming thrombi

 Treatment Philosophy :

a. Maximally Dilate The Coronaries

b. Try To Reduce Atherosclerotic Obstruction

c. Stress Management


C. Prinzmetal Angina (Atypical Angina)

Onset due to :

a. Vasospastic Disorder

b. Not Related To Atherosclerotic Disease

c. Not Necessarily Relieved By Rest

 Treatment Strategies :

a. Reduce the effects of the catecholamines on the heart

b. Reduce emotional stress

c. Rule out Pheochromocytoma

Calcium Channel Blockers

Members :

Verapamil (Calan, Isoptin)

Nifedipine (Procardia)

Diltiazem (Cardizem)

Bepridil (Bepadin, Vascor)

Felodipine (Plendil)

Isradipine (Dynacirc)


 Mechanisms of Action:

1. Systemic vasodilatation and a reduction in blood pressure.

2. Reduction of pre-load & after-load.

3. Reduces the work of the heart w/ a reduction in MVO2 demand

4. Reduces cardiac contractile strength


Side Effects : Headaches, flushing, peripheral edema, dizziness, swelling in the feet and legs, nausea, syncope, hypotension, tachycardia, bradycardia.


Medical Uses :

1. Hypertension

2. Prevent a person from going back into tachydysrythmias

3. To treat all types of angina pectoris



Members :

Nitroglycerin (Nitro-Bid, Nitrostat, Nitro-Dur)

Isosorbide Dinitrate (Iso-Bid)

Erythrityl Tetranitrate (Cardilate)

Pentaerythritol Tetranitrate (Peritrate)

Amyl Nitrite

Nitroglycerin Patches


Mechanisms of Action :


The nitrates basically cause vasodilation. How ?

 They do this by activating guanylate cyclase which cleaves GTP (guanosine triphosphate) into cGMP. cGMP (a second messenger) activates a protein kinase which dephosphorylates myosin in smooth muscle. If myosin has no phosphate group to activate it, myosin cannot connect to actin and cause muscle contraction. Hence, since myosin is essentially inactivated, then there is a permissive vasodilation or relaxation of vessel tone. The net effect is as follows :

1. Dilatation of arterial and venous smooth muscle with a reduction of peripheral resistance.

2. Pre-load and after-load is reduced.

3. Lower myocardial oxygen demand due to less work against peripheral resistance.

4. Pulmonary artery pressure is reduced.


Side Effects : Orthostatic Hypotension, Headaches, Dizziness, Vertigo, Flushing, Sweating


Medical Uses : To treat angina quickly.


The Nitroglycerin Paradigm : With the onset of angina, sit down and take one tablet under the tongue (sublingual) and wait 3-5 minutes. If the angina has not subsided, take another tablet sublingually and wait 3-5 minutes. If the angina has not subsided, take a third tablet of nitroglycerin and call 911 for help.

Beta Blockers

Members :

Propranolol (Inderal) NS

Atenolol (Tenorman) Beta-1 Nadolol (Corgard) NS Beta

Metoprolol (Lopressor) Beta-1 Penbutolol (Levatol) NS Beta

Acebutolol (Sectral) Beta-1 Sotalol (Betapace) NS Beta

Betaxolol (Kerlone) Beta-1 Pindolol (Visken) NS Beta

Bisoprolol (Zebeta) Beta-1 Timolol (Blocarden) NS Beta

Esmolol (Brevibloc) Beta-1 Carteolol (Cartrol) NS Beta

Labetolol (Normodyne) Alpha-1, NS Beta

Note : NS means non-selective

Mechanisms of Action :

1. Beta blockers inhibit the release of norepinephrine and thus allow permissive vasodilation.

2. Beta blockers inhibit the release of renin. Renin converts angiotensin to angiotensin I. Angiotensin I is made into angiotensin II - a very potent vasoconstrictor. The net result is that the peripheral resistance is lowered. Also, fluid retention is inhibited.

3. Beta blockers slow the electrical conduction velocity in the heart - slows heart rate and also drops the inotrophy of the heart - the force of contraction.

4. Beta blockers also slow the heart rate by blocking the receptors that bind with the catecholamines - hormones that stimulate the heart to beat faster. Sympathetic drive on the heart is thus reduced.

5. Beta blockers drop the rate-pressure product (the double product = HR x Systolic BP)

6. Beta blockers lower the MVO2 of the heart.

7. After-load on the heart is reduced because of lowered peripheral resistance - i.e. - vasodilatation.

8. Perfusion is improved through the coronaries because of vasodilation and prolonged diastole.

9. The heart can experience a greater ejection fraction due to prolonged diastolic filling time.


Side Effects : Fatigue, hypotension, bradycardia, skin rashes, increased airway resistance and bronchoconstriction (blockade of beta-2 receptors thus inhibiting bronchodilation - beta blockers should be only cautiously given to patients with COPD), hypoglycemia (blockade of beta-2 receptors in liver thus preventing glycogenolysis - this becomes a problem for diabetics).

 Medical Uses :

1. Beta blockers are used to prevent/suppress supraventricular tachydysrythmias such as :

a. premature atrial contractions (PACs)

b. supraventricular tachycardia (SVT)

c. junctional premature beats (JPBs)

d. atrial flutter

e. atrial fibrillation


2. Beta blockers are used to suppress the re-occurrence of ventricular dysrythmias such as :

a. premature ventricular contractions (PVCs)

b. ventricular tachycardia (V-tach)

c. ventricular fibrillation (V-fib)


3. Beta blockers are used to treat hypertension.

4. Beta blockers are used to chronically treat angina.

5. Beta blockers are used to treat patients with panic attacks.

6. Beta blockers are prescribed for the treatment of migraine headaches.

7. Beta blockers are prescribed for patients with tachycardia due to hyperthyroidism.

8. Beta blockers are prescribed for patients with pheochromocytoma and who cannot undergo surgery for that condition.


 General Clinical Considerations For All Of These Cardiac Medications For Physical Therapists To Remember :

1. Know your patient's medications

2. Know what the patient's medications are doing in this individual

3. Guard the patient against falling due to hypotension or syncope as a result of these meds

4. Do not exercise the patients on these meds in the heat - hot weather also causes vasodilation

5. Rehab activities that increase MVO2 should be carefully evaluated

6. Remember that Beta-Blockade absolutely suppresses heart rate effecting ex. prescription

7. Make sure the patient brings their medications with them to the clinic (Nitroglycerin, etc.)

8. Know whether the medications the patient is on are PRN or scheduled meds


Email : Questions Or Comments To Me At Work

Email : Questions Or Comments To Me At Home