test 7 Flashcards
1
Q
What is Angina Pectoris?
A
- Sudden, severe, crushing chest pain
* can radiate to neck, jaw, back, shoulders, and arms
2
Q
Types of Angina
A
- Stable, effort-induced, classic, or typical angina
- Unstable angina
- Prinzmetal, variant, vasospastic, or rest angina
- Acute coronary syndrome
3
Q
Classic Angina
A
- Most common form
- Caused by a fixed coronary artery obstruction
- Usually due to atherosclerosis
- Pattern of pain remains stable
- Does not always present as pain
* More common in women, DM, and elderly
4
Q
Classic Angina pain relieved by
A
- rest or nitroglycerin
5
Q
Unstable Angina
A
- Chest pain occurs with increased frequency, duration, and intensity
* Result of less effort - Rest angina lasting longer than 20 min.
- Increasing (crescendo) angina
- Sudden onset of shortness of breath
- Pain not relieved by rest or nitroglyce
6
Q
Rest Angina
A
- Pain occurs at rest due to coronary artery spasm
- Pain is unrelated to exertion
- Treated with calcium channel blockers and nitroglycerin
7
Q
Acute Coronary Syndrome
A
- Rupture of an atherosclerotic plaque
- Disruption of an atherosclerotic lesion
* Inflammatory cells and platelets are activated
* Thrombus forms and propagates
* Vasoconstriction occurs - Necrosis of cardiac muscle
- Increase in serum levels of biomarkers
* Troponins
* Creatine kinase (CK) - Present as ST elevation, MI, or unstable angina
8
Q
Angina Drug Strategies (2)
A
1. Increase O2 delivery
•Increasing coronary flow
2. Decrease O2 demand
• Altering determinates of myocardial oxygen
consumption
• Wall stress
• Heart rate
• Contractility
9
Q
β-blockers
A
- Decrease oxygen demand by blocking β1 receptors
- Decrease in HR, contractility, and BP
- Reduce the frequency of angina attacks
- Increase exercise duration and tolerance
- Recommended at initial antianginal therapy
* Not for vasospastic angina - Reduce the risk of MI and death
* Prior MI - Improve mortality in patients with HTN and HF
10
Q
β-blockers: Adverse Effects
A
- Bradycardia
- Hypotension
- Fatigue
- Insomnia
- Sexual dysfunction
- Alter lipid panel
* Decrease HDL
* Increase triglycerides
11
Q
Calcium Channel Blockers
A
- Cardiac ischemia leads to membrane depolarization, increasing calcium flow into the cells
- Leads to activation of ATP-consuming enzymes which depletes energy stores worsening ischemia
- Block the inward movement of calcium into the cell
- Causes relaxation of smooth muscle and a decrease in contractility in cardiac muscle
- Decrease afterload which decreases myocardial oxygen demand
- Dilate the coronary arteries which increases myocardial oxygen delivery
12
Q
Diphenylalkylamines: Verapamil
A
- Effects cardiac and vascular smooth muscle
* More selective for cardiac muscle - Slows AV conduction
- Decreases HR, contractility, and BP
- Negative inotropic effects
13
Q
Benzothiazepines: Diltiazem
A
- Non-selective
- Slows AV conduction
- Coronary artery vasodilator
* Relieves coronary artery spasm - Negative ionotropic effects
14
Q
Dihydropyridines: Amlodipine, Felodipine, Nifedipine
A
- Greater affinity for vascular smooth muscle calcium channels
- Minimal effect on cardiac conduction
- Do not use in patients with CAD
* Increase mortality after an MI
15
Q
Summary of what Dihydropyridines do
A
- Produce arterial dilation
- Reduces PVR
- Reduces BP
- Reduces myocardial oxygen demand
