Coronary Artery Disease Flashcards
What is coronary artery disease?
Disease of coronary arteries that supply the heart.
Can be asymptomatic or develop into stable angina
Unstable angina + MI = more serious manifestations of CAD (acute coronary syndrome)
What is the major cause of CAD?
ATHEROSCLEROSIS
- deposition of lipids within the intima of the artery
- C-reactive protein (CRP) is released by the liver and is increased during system inflammation AND unstable plaques and oxidation of LDLs
Steps of atherosclerosis
1) Damaged endothelium
- d/t hypertension, smoking, hyperlipidemia, hyperhomocysteinemia, diabetes, infection, toxins
2) Fatty streak
- lipids accumulate and migrate into SMCs
3) Fibrous plaque
- collagen covers the fatty streak
- vessel lumen is narrowed, reducing blood flow
- fissures can develop
4) Complicated lesion
- plaque rupture
- thrombus formation
- further narrowing or total occlusion of vessel
Stable Angina vs unstable angina
STABLE
- occlusion that is reversible w/ rest + use of nitroglycerin
- onset, pattern, and duration is predictable and same each time
UNSTABLE
- unstable plaque and lesion that intermittently occludes and opens
- may lead to a complete MI
- irreversible cell death and necrosis
- different type and quality of pain than that of stable angina
What is collateral circulation?
Arterial anastomoses or connections
- the body’s way of compensating when an artery becomes occluded due to atherosclerosis or CAD
- grwoth of connections increases in the presence of chronic ischemia
Is there collateral circulation in rapid onsets of CAD?
NO
When CAD has a rapid onset, or coronary spasm occurs, there may not be enough time for collateral circulation development
Diminished arterial blood flow ==> more severe ischemia ==> infarction
2 types of angina
Angina is the clinical manifestation of reversible ischemia
CHRONIC STABLE
- chest pain that occurs intermittently over a period w/ the same pattern of onset, duration, and intensity of symptoms
- constrictive, squeezing, heavy, choking, suffocating sensations
- pain is brief (3-5 mins) and goes away w/ rest
- precipitated by physical demand
PRINZMETAL ANGINA
- chest pain that occurs at rest randomly
- spasms of a major coronary artery
What should you do when a pt complains about chest pain?
1) take vitals
2) administer O2
3) 12 lead ECG
4) Administer nitrates and baby aspirin
- nitroglycerin spay
5) listen to heart sounds
S3 - transient - related to hyperdynamic state
- lots of fluid - makes a swishing sound against ventricle walls
- usually the first symptom of congestive heart failure
S4 - pathological sound
- usually there all the time
- resistance to ventricular filling bc they are stiff and noncompliant
Goals
Goals
- Pain relief
- Preservation of myocardium
- Immediate and appropriate treatment
- Effective coping w/ illness-associated anxiety
- Participation in a rehabilitation plan
- Reduction of risk factors
- Health promotion
○ Therapeutic lifestyle changes to reduce cardiac risk factors
How to diagnose CAD
ECG BLOOD WORK - cardiac markers (myoglobin, CK-MB, Troponin I) - CK-MB and troponin I are specific to cardiac muscle cells; are released when cells are dying - lipid profile to assess risk factors - CBC - chemistry -pt/INR CXR 2D ECHO CARDIAC ANGIOGRAM
Goal of drug therapy in CAD
Increase O2 supply
Decrease O2 demand
What meds are given to pts w/ CAD
ASPIRIN
- inhibit COX1 + COX2 (to prevent the production of thromboxane A2, a platelet activator)
- administer as soon as acute coronary syndrome is suspected
PLAVIX
- inhibit platelet aggregation
- alternative for pts who cannot use aspirin
- decrease risk of blockage
NITRATES - promotes peripheral vasodilation - decreases preload and afterload promote coronary artery vasodilation - reduces myocardial O2 consumption
BETA BLOCKERS ** preferred**
- inhibit symNS stimulation of heart
- reduce HR and contractility
- decrease afterload
- reduces workload and O2 demands
CA2+ CHANNEL BLOCKERS
- prevent Ca2+ entry into myocytes and vascular SMCs
- promote coronary and peripheral vasodilation
- reduce HR + contractility
- reduce workload + O2 demand
ACEi
- prevent conversion of angiotensin I –> angiotensin II
- decrease endothelial dysFN
- useful in treating heart failure, tachycardia, MI, hypertension, diabetes, CKD
non-modifiable risk factors for CAD
age gender: risk is > men ethnicity: caucasian family Hx genetic predisposition
Modifiable risk factors for CAD
- elevated serum lipids: blood cholesterol, LDL > HDL
- HTN: BP > 140/90
- tobacco use
- physical inactivity
- obesity: higher LDLs + HTN
- diabetes: incidence is 2-4X higher
- metabolic syndrome
- psychological states: type A personalities (greater stress, suppress anger)
- homocysteine level: breakdown of methionine that occurs when the inner lining of BVs becomes damaged
- substance use
What does health promotion involve for CAD?
ID high-risk individuals management for high-risk pts physical activity health education in schools nutritional therapy - lower LDLs, increase HDLs - diet high in complex carbs + fiber - omega 3 FAs reduce risks associated w/ CAD - pts w/ CAD are encouraged to take EPA and DHA supplements