Therapeutic Interventions for Angina Pectoris, Myocardial Infarction, and Cerebrovascular Accident Flashcards
1
Q
Myocardial Ischemia
A
- 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
2
Q
CAD
A
- 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
3
Q
Angina
A
chest pain caused by dying cells because they are not receiving the oxygen they need.
chest pain, stable, unstable, or angina of effort
4
Q
Angina Pectoris: Types
A
- 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
5
Q
Nutritional therapy
A
- 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.
6
Q
Physiotherapy
A
- 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
7
Q
Mental Health
A
- emotionally stressful situations ca precipitate an attack.
- counseling should be provided.
8
Q
Oxygen Therapy
A
- during an acute attack supplemental oxygen may be necessary. only if O2 sat is below 92%
9
Q
Goals of therapy in pharmacological management of Angina pectoris
A
- reduce the frequency and intensity of angina episodes
- increase exercise tolerance
- prevent other CAD complications including dysrhythmias, heart failure, MI
10
Q
Pharmacologic Approaches to angina
A
- 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)
11
Q
Organic Nitrates
A
terminate anginal episodes by dilating coronary arteries to increase O2 supply
12
Q
Beta-adrenergic blockers
A
- prevent anginal episodes by reducing cardiac workload and O2 demand (decrease contractility)
13
Q
Calcium channel blockers
A
- prevent anginal episodes by either reducing CO (decrease O2 demand) or dilating coronary arteries (increase O2 availability) or both
14
Q
Organic Nitrates (vasodilate blood vessel to heart)
- indications
- mechanism of action
- adverse effects
A
- preventing and terminating anginal episodes
- 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
- hypotension/dizziness/flushed/tachycardia
15
Q
Nitroglycerin
- trade name
- therapeutic effects and uses
- mechanism of action
- adverse effects
- route
- serious side effects
A
- nitro-dur, minitran, nitrostat, trinipatch
- acute angina. acute congestive heart failure. Acute pulmonary edema. Acute myocardial infarction. severe/emergency hypertension.
- 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)
- flushed, headache/orthostatic hypotension
- sublingual, PO, IV, nitropatch
6/. anaphylaxis, methemoglobinemia
16
Q
Nitroglycerin use
A
- 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
17
Q
Nitro Patch
A
- 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
18
Q
Beta-blockers
- indications
- mechanism of action
- adverse effects
- interactions
A
relieve angina by decreasing the oxygen demands of the heart. Often considered first line drugs for chronic angina
- angina, hypertension, dysrhythmias, heart failure
- block beta1 receptors - reduces HR and contractility decreasing O2 demand. stabilizing conductivity of heart decreasing incidence of dysrhythmia. reduce incidence of MI.
- bradycardia/dysrhythmias/hypotension/fatigue/lethargy/depression/may exacerbate asthma/respiratory distress
- Exacerbates heart block with calcium channel blockers and/or cardiac glycosides
19
Q
Calcium Channel Blockers
A
relieve angina by dilating coronary vessels and reducing workload of the heart
20
Q
Calcium Channel Blockers
- indications
- mechanism
- adverse effects
- interactions
A
- vasospastic angina, stable angina, hypertension, atrial dysrhythmias
- relax arterial muscle (increases O2 supply. decreases afterload, decreasing O2 demand). some reduce heart rate and contractility which decreases O2 demand
- hypotension/exacerbates some dysrhythmias/exacerbates heart failure/peripheral edema
- promotes heart block when taken with beta1 blockers and/or cardiac glycosides
21
Q
Diltiazem
- therapeutic effects and uses
- mechanism of action
- adverse effects
A
- stable angina/atrial dysrhythmias/hypertension
- 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)
- bradycardia/hypotension/flushing, dizziness, headache/peripheral edema
22
Q
Myocardial Infarction
A
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
23
Q
Pathophysiology of Myocardial Infarction
A
- 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
24
Q
Treatment Goals of MI
A
- 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)
25
Q
Thrombolytics
- indication
- mechanism of action
- adverse effects
A
- MI, CVA
- 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.
- severe risk of bleeding - most effective if given within 4 hours of clot formation
