cardiac disorder Flashcards
Age-Related Changes
Heart
Increased density of connective tissue and decreased elasticity
Number of pacemaker cells in the SA node decreases, as does the number of nerve fibers in the ventricles
Blood vessels
Changes in connective tissue and elastic fibers in arteries cause them to become stiffer.
Veins stretch and dilate, leading to venous stasis and sometimes impaired venous return
Creatine Kinase (CK, CK-MB)
this enzyme found in brain, heart (CK-MB) and skeletal muscle. Levels rise 4-6 hours after muscle cell damage, peak in 12-24 hours, and diminish in 2-3 day if no new injury to muscle cells. CK-MB after MI can more than 6 times the normal value
Troponin
protein involved in contraction of muscles. Two types (T and I) are specific to cardiac muscle and are released into circulation after a MI. Elevate in 3-6 hours, peak in 24, and circulate for up to 2 weeks
Myoglobin
less reliable as an indicator of MI, a protein found in cardiac and skeletal muscles released quickly after cell damage, rises in 2-3 hours after an MI
slow HR and increase force of myocardial contraction
Cardiac glycosides- lanoxin
treat acute anginal episodes mostly by vasodilation
Anti-anginals nitroglycern; calcuim channel blockers
in general they work by decrease HR, decrease automaticity or resistance to premature stimulation. Also used in chronic angina
Anti-dysrhythmics betablockers
work against the renin-angiotensin-aldosterone system to dilate arteries and decrease resistance to blood flow in arteries (dcrease afterload)
Angiotensin-converting enzyme inhibitors (ACE-Inhibitors)- Plavix, ASA
decrease fluid retention
Diuretics Lasix
prevent clot formation
Anti-coagulants Heparin Low-molecular-weight heparin (LMWH) Warfarin
decreased platelet aggregation, prolongs bleeding time
Anti-platelet Agents
(also called thrombolytics) “clot busters”
Fibrinolytic agents r-tPA
Abnormal thickening, hardening, loss of elasticity of arterial walls
Arteriosclerosis
Form of arteriosclerosis; inflammatory disease that begins with endothelial injury and progresses to the complicated lesion seen in advanced stages of the disease process
Atherosclerosis
naturally occurring, yellow streaking of coronary arteries and aorta, no symptomology, onset as early as age 10
progression of lesions
Fatty streak
builds over fatty streaks, protrudes our from wall of artery , other substances can adhere to and collect within plaque, white or grayish colored
Fibrous plaque
progression of lesions
develop as ulceration or rupture of plaque, platelets adhere and can trigger formation of a thrombus
progression of lesions
Complicated lesions-
Branches grow from existing arteries; provide increased blood flow
Collateral circulation
risk factors of coronary artery disease
Nonmodifiable
Age, gender, heredity, and race
Modifiable
Increased serum lipids, high blood pressure, cigarette smoking (nicotine), diabetes mellitus with elevated blood glucose, obesity, sedentary lifestyle
Other factors
Stress, sex hormones, birth control pills, excessive alcohol intake, high homocysteine levels
The most common symptom of CAD
Demand for oxygen by myocardial cells exceeds supply
angina pectoris
Occurs with exercise or activity and usually subsides with rest
Stable angina
Pain more severe, occurs at rest or with minimal exertion, is often not relieved by NTG or requires more frequent NTG administration, and is not predictable
Unstable angina
Caused by coronary artery spasm
may not be associated with CAD
Unpredictable and often occurs
at rest
Variant angina
medical treatment for angina pectoris
Initial therapy for patients
with angina
A Aspirin and antianginal therapy
B Beta-blocker and blood pressure
C Cigarette smoking and cholesterol
D Diet and diabetes
E Education and exercise
