Therapeutic Interventions for Angina Pectoris, Myocardial Infarction, and Cerebrovascular Accident

Question 1

Myocardial Ischemia

Answer 1

• condition in which the supply of oxygen to the myocardium does not meet the metabolic demands of the myocardium
• oxygen supply depends on: blood flow the myocardum - impacted by CAD, atherosclerosis, vasospasms and oxygenation of blood reaching myocardium - impacted by anemia, respiratory disease
• oxygen demand depends on sympathetic activity, physical activity

Question 2

CAD

Answer 2

• narrowing of coronary arteries, usually due to atherosclerotic plaques (fatty, fibrous material that reduces elasticity of arteries)
• reduces myocardial O2 supply
• responsible for both angina and myocardial infarction (MI)
• develops over a long period of time
• high fat diet, smoking, hypertension are all risk factors for developing atherosclerosis and CAD

Question 3

Angina

Answer 3

chest pain caused by dying cells because they are not receiving the oxygen they need.
chest pain, stable, unstable, or angina of effort

Question 4

Angina Pectoris: Types

Answer 4

• silent: myocardial ischemia occurs but no pain, asymptomatic; high risk for acute MI
• unstable - unpredicable, occurs at rest
• ## angina of effort - occurs when patient over-exerts during an activity, increasing oxygen demand

Question 5

Nutritional therapy

Answer 5

• avoid large meals, increase work load, reduced blood flow to coronary arteries
• lie down for 1-2 hours after large meal
• quit smoking as it causes vasoconstriction. and increases HR.
• limit sale and saturated fats. maintain ideal body weight
• limit or abstain from alcohol
• maintain glucose levels.

Question 6

Physiotherapy

Answer 6

• a regular program that conditions but does not over stress the heart
• walking on a flat surface 30 minutes a day 5 days a week is recommended
• nitro tablets may be used prophylactically before physical exertion or sexual intercourse

Question 7

Mental Health

Answer 7

• emotionally stressful situations ca precipitate an attack.
• counseling should be provided.

Question 8

Oxygen Therapy

Answer 8

• during an acute attack supplemental oxygen may be necessary. only if O2 sat is below 92%

Question 9

Goals of therapy in pharmacological management of Angina pectoris

Answer 9

• reduce the frequency and intensity of angina episodes
• increase exercise tolerance
• prevent other CAD complications including dysrhythmias, heart failure, MI

Question 10

Pharmacologic Approaches to angina

Answer 10

• increase oxygen supply - dilate coronary arteries to increase blood flow
• decrease oxygen demand - reduce preload, afterload, HR and contractility (beta blockers, diuretics, calcium channel blockers, ACE inhibitors)

Question 11

Organic Nitrates

Answer 11

terminate anginal episodes by dilating coronary arteries to increase O2 supply

Question 12

Beta-adrenergic blockers

Answer 12

• prevent anginal episodes by reducing cardiac workload and O2 demand (decrease contractility)

Question 13

Calcium channel blockers

Answer 13

• prevent anginal episodes by either reducing CO (decrease O2 demand) or dilating coronary arteries (increase O2 availability) or both

Question 14

Organic Nitrates (vasodilate blood vessel to heart)

1. indications
2. mechanism of action
3. adverse effects

Answer 14

1. preventing and terminating anginal episodes
2. donate nitric oxide, a potent vasodilator. relax venous muscle –> reduces preload and decreases O2 demand on myocardium. relax arterial muscle –> increases blood flow and O2 supply to myocardium
3. hypotension/dizziness/flushed/tachycardia

Question 15

Nitroglycerin

1. trade name
2. therapeutic effects and uses
3. mechanism of action
4. adverse effects
5. route
6. serious side effects

Answer 15

1. nitro-dur, minitran, nitrostat, trinipatch
2. acute angina. acute congestive heart failure. Acute pulmonary edema. Acute myocardial infarction. severe/emergency hypertension.
3. forms nitric oxide, a vasodilator. relaxes vascular smooth muscle of arteries - increases O2 supply, decreases afterload, and O2 demand. and veins (decreasing preload and O2 demand)
4. flushed, headache/orthostatic hypotension
5. sublingual, PO, IV, nitropatch
   6/. anaphylaxis, methemoglobinemia

Question 16

Nitroglycerin use

Answer 16

• if your client is having chest pain there is a typical protocol for Nitro which is - immediately give a spray, assess pain in 5 minutes, if it is not resolved, give a second spray and call doctor if second spray does not help. can give a third if the patient is not hypotensive.
• call ECG
• stay at bedside
• call physician and ask for lab values
• call a code if patient becomes unresponsive

Question 17

Nitro Patch

Answer 17

• prevent angina
• upper right or left arm, chest, or back
• new one q12h
• do not put over body hair
• write date, time on patch and location

Question 18

Beta-blockers

1. indications
2. mechanism of action
3. adverse effects
4. interactions

Answer 18

relieve angina by decreasing the oxygen demands of the heart. Often considered first line drugs for chronic angina

1. angina, hypertension, dysrhythmias, heart failure
2. block beta1 receptors - reduces HR and contractility decreasing O2 demand. stabilizing conductivity of heart decreasing incidence of dysrhythmia. reduce incidence of MI.
3. bradycardia/dysrhythmias/hypotension/fatigue/lethargy/depression/may exacerbate asthma/respiratory distress
4. Exacerbates heart block with calcium channel blockers and/or cardiac glycosides

Question 19

Calcium Channel Blockers

Answer 19

relieve angina by dilating coronary vessels and reducing workload of the heart

Question 20

Calcium Channel Blockers

1. indications
2. mechanism
3. adverse effects
4. interactions

Answer 20

1. vasospastic angina, stable angina, hypertension, atrial dysrhythmias
2. relax arterial muscle (increases O2 supply. decreases afterload, decreasing O2 demand). some reduce heart rate and contractility which decreases O2 demand
3. hypotension/exacerbates some dysrhythmias/exacerbates heart failure/peripheral edema
4. promotes heart block when taken with beta1 blockers and/or cardiac glycosides

Question 21

Diltiazem

1. therapeutic effects and uses
2. mechanism of action
3. adverse effects

Answer 21

1. stable angina/atrial dysrhythmias/hypertension
2. blocks cardiac calcium channels (decreases HR and force of contraction, decreasing O2 demand of myocardium) blocks vascular smooth muscle channels (increases O2 supply in coronary arteries, decreases O2 demand by decreases afterload)
3. bradycardia/hypotension/flushing, dizziness, headache/peripheral edema

Question 22

Myocardial Infarction

Answer 22

BP starts high when the body goes into fight or flight and the sympathetic nervous system is engaged.
Then it will get low.
Increased resp rate for a bunch of reasons – increase oxygenation, stress, pain
Give an antiplatelet agent once it has been determined that it is an MI
An analgesics
Given them an urgent dose of a thrombolytic

Question 23

Pathophysiology of Myocardial Infarction

Answer 23

• due to advanced CAD leading to severe narrowing of coronary arteries
• plaque can block narrowed arteries (stimulating clot formation) depriving region of myocardium of oxygen
• cardiac output drops
• if artery is occluded long enough, permanent myocardial damage occurs

Question 24

Treatment Goals of MI

Answer 24

• restore blood supply to myocardium (thrombolytics, organic nitrates)
• reduce myocardial oxygen demand (beta blockers)
• control MI - associated dysrhythmias (beta blockers, calcium channel blockers)
• reduce post-MI mortality (ASA - antiplatelet agent - ACE inhibitors)
• manage severe MI pain and anxiety (analgesics)

Question 25

Thrombolytics

1. indication
2. mechanism of action
3. adverse effects

Answer 25

1. MI, CVA
2. stimulates formation of plasmin, an enzyme that breaks down fibrin, causing active clots to dissolve breaks down fibrin, causing active clots to dissolve. coronary artery opens allowing perfusion of myocardium.
3. severe risk of bleeding - most effective if given within 4 hours of clot formation