Coronary Artery Disease Flashcards
Arteriosclerosis vs. Atherosclerosis
ARTERIOsclerosis: narrowing of artery
ATHEROsclerosis: narrowing d/t plaque build up;
–when this narrowing occurs in coronary arteries = CAD/CHD/ or heart disease
–when this narrowing occurs in peripheral vessels =
peripheral artery disease (PAD)
Patho of atherosclerosis
lipoproteins and fibrous tissue accumulate in arterial wall d/t injury/inflamm. or endothelial cells in arterial wall
- -monocytes & lipids enter injured vessel»_space;
- -smooth muscle builds w/i vessel wall»_space;
- -fatty accumulations (streaks) develop»_space;
- -plaque enlarges and vessel narrows»_space;
- -blood flow decreases»_space;
- -plaque may RUPTURE and form THROMBUS, which could obstruct blood flow
CAD non-modifiable risk factors:
p. 1108
~age
- -men >/= 45
- -women >/= 55
~gender (men dx earlier than women)
~family hx of CAD (males dx before 55, female before 65)
~ Race (AA higher risk)
CAD modifiable risk factors:
p. 1108
- hyperlipidemia (tx @ > 200)
- high LDL & low HDL
- smoking (vasoconstricts)
- HTN
- DM (have small vessels)
- stress
- kidney disease
- Obesity / physical inactivity
- atherogenic diet
- oral contraceptives/HRT
** METABOLIC SYNDROME **
what is metabolic syndrome?
p. 1110
a group of metabolic risk factors that create a HIGH RISK CAD
- –3 underlying causes: —
1) overweight/obesity
2) physical inactivity
3) genetic factors
RISK FACTORS:
- -large waistline
- -high triglyceride level
- -low HDL level
- -HTN
- -elevated fasting blood glucose
Preventing CAD
1) prevent occurrence of CAD
2) early detection & stopping progression of CAD
FOUR MAJOR AREAS:
- ->control cholesterol
- –fasting lipid profile q6wks after acute event
- ->stop smoking
- –nicotine replacement has same risks as tobacco
- –bupropion (zyban) –antidepressant
- ->manage HTN (repeatedly > 140/90)
- –HTN damages vessels»_space;causes inflamm & incr. atherosclerosis
- ->control DM
- –hyperglycemia fosters abnormal lipid levels, increased platelet aggregation, & altered RBC function»_space;> leads to THROMBUS formation
Diet: SATURATED FATS (BAD)
biggest dietary cause of LDL
found in animal products --butter --milk --cheese --cream --fatty meats also found in coconut & palm oils
Diet: UNSATURATED FATS (GOOD)
help lower cholesterol if used to REPLACE SATURATED FATS; BUT they have a lot of calories (so limit them)
A) MONOunsaturated fats
—nuts, avocados, olive oil, canola oil
B) POLYunsaturated fats
- –fish, safflower, sunflower, corn, soybean
- -best = omega 3 fatty acids in fish and flaxseeds
Diet: COMPLEX CARBOHYDRATES (GOOD)
provide vitamins, minerals, and FIBER!!
- breads
- legumes
- rice
- pasta
- starchy vegetables
Diet: SIMPLE CARBOHYDRATES (BAD)
broken down QUICKLY to be used as energy but lack vitamins, minerals, and fiber (empty calories)
–fruits, milk, milk products, cake, candy, refined sugars
Diet: PROTEIN
choose these low fat products:
- -LEAN MEATS
- -POULTRY w/o SKIN
- -FISH
- -DRIED BEANS
- -low-fat / fat-free dairy
Physical Activity
regular, moderate exercise REDUCES TRIGLYCERIDES & INCREASES HDL
- -** 30 min/day 5 - 6 days/week
- -5 min warm up and cool down
- -STOP IF any CP, unusual SOB, lightheadedness, or nausea (classic s/s of MI), or jaw pain
angina vs. ACS vs. MI
angina = ISCHEMIA (CP)
ACS = INJURY
MI = DEATH (cell)
Angina pectoris
“angina”
ischemic pain d/t precipitating factors (physical activity, stress/emotion, big meal, or exposure to cold)
causing INCREASED MYOCARDIAL O2 DEMAND, which results in INSUFFICIENT CORONARY BLOOD FLOW
ELDERLY MAY HAVE SILENT ISCHEMIA
DIABETICS MAY NOT HAVE PAIN D/T NEUROPATHY
Tx: sublingual NITROGLYCERIN (q5min x 3) to vasodilate arteries and improve perfusion
–s/efx: HA, VISON CHANGES, & DECR. BP
3 types of angina
1) STABLE *GOAL!!! to maintain coronary blood flow
- -most common & predictable (r/t activity & stressors)
- -relieved w/ REST & NITRATES
2) Prinzmetal / Variant
- -atypical; occurs unpredictably (unrelated to activity)
- -caused by coronary artery spasm
3) UN-STABLE (headed to ACS)
- -increases in frequency, severity, & duration
- -UNPREDICTABLE
- -occurs w/ DECR. level of activity / stress
- -may occur at rest
- -AT RISK FOR MI
Acute Coronary Syndrome (ACS)
“unstable angina”
blood flow is acutely reduced but not fully occluded
- -myocardial cells are INJURED by the acute ischemia
- -precipitated by plaque rupture, CA spasm, vessel obstruction by plaque, inflamm. of CA
- **different from ANGINA b/c:
- CP lasts longer (10 - 20 min)
- may occur @ rest
- pain is more severe (indicates INJURY…not ischemia)
other manifestations:
- -dyspnea
- -diaphoresis / cool skin / pallor
- -tachycardia
- -hypotension
- -nausea / lightheaded
Acute Myocardial Infarction
“MI”
blood flow to a portion of cardiac muscle is COMPLETELY BLOCKED»_space; prolonged tissue ischemia & irreversible cell damage = INFARCTION / blockage
(CELL DEATH)…MUSCLE DOES NOT REGENERATE
- -SUDDEN ONSET ; unrelated to exercise or rest
- -SUBSTERNAL PAIN @ REST
- may RADIATE (back/neck/jaw/arm/shoulder)
- -pain = “crushing, pressure, squeezing, heavy”
- -LAST > 20 MINS
- -NOT relieved by nitroglycerin
MI manifestations
- dyspnea & SOB
- -tachycardia / tachypnea
- syncope (decreased BP)
- N/V (** very indicative of MI **)
- extreme weakness
- diaphoresis
- -cool, mottled skin / diminished peripheral pulses
- -palpitations / dysrhythmias
- denial / impending doom
- incr. HR (b/c of myocardial O2 demand)
- -CP is substernal/precordial (across chest)
- -s/s of L-SIDED HF (dyspnea, fatigue, weak, crackles)
- -decr. LOC
MI Complications:
DYSRHYTHMIAS
p. 1112
–infarcted tissue effects electrical conduction»_space; incr. risk for dysrhythmias
–PVCs MOST COMMON; may lead to VT or VF w/i 1h
–heart block or bradyarrhytmias
MI Complications:
PUMP FAILURE & CARDIOGENIC SHOCK
HF –> CHF –> SHOCK
MI reduces contractility & ventricle wall compliance, LEADING TO PUMP FAILURE (HF)
–anterior MI = L-sided HF
(dyspnea, fatigue, weak, crackles)
–inferior MI = R-sided HF
(neck vein distention, peripheral edema)
Cardiogenic shock = IMPAIRED TISSUE PERFUSION d/t pump failure (LOW C.O.)
–occurs when myocardial mass decr. by > 40%
– * heart is UNABLE TO PUMP ENOUGH BLOOD to meet needs of body & maintain organ function; also have IMPAIRED CORONARY ARTERY PERFUSION
MI Complications:
STRUCTURAL DEFECTS
necrotic muscle is REPLACED BY SCAR TISSUE
(thinner than ventricular muscle mass)
can result in:
- -ventricular aneurysm (out-pouching of vent. wall)
- -rupture of interventricular septum/papillary muscle
- -myocardial rupture
MI Complications:
PERICARDITIS
tissue necrosis prompts INFLAMMATORY RESPONSE
usually d/t VIRAL INFECTION
pericarditis = inflamm. of pericardial tissue around <3
–causes CP that is sharp / stabbing / aching
–pain is aggravated by movement or deep breathing
–may hear pericardial friction rub on auscultation
MI treatment Goals
1) RELIEVE CP
2) reduce infarction (damage)–“time is muscle”
3) maintain cardiovascular stability
4) decrease workload (dobutamine; metoprolol)
5) prevent complications
R E P E R F U S I O N:
–PCTA (percutaneous transluminal coronary angioplasty)»_space; cath. w/ balloon that goes through groin; inflate the balloon to push plaque aside and re-establish blood flow
–CABG (coronary artery bypass graft)
Immediate MI treatment
"MONA" Morphine (d.o.c. for acute MI) Oxygen (oxygenate circulating volume) Nitroglycerine Aspirin (ASA)--give 325mg of chewable aspirin
