Cardiovascular Disorders II Flashcards
(38 cards)
Coronary Artery Disease (CAD)
aka Coronary Heart Disease (CHD) or Ischemic Heart Disease (IHD)
2nd leading cause of death in Canada
1 in 12 Canadian adults live with diagnosed heart disease
Left Main Coronary Artery (LMCA)
left side of heart muscle 2 branches a. left anterior descending (interventricular) - front and left side of heart b. circumflex - outer side and back of heart
Right Coronary Artery (RCA)
right side of heart muscle
right ventricle and atrium, SA and AV nodes
Pathophysiology of CAD
- decreased perfusion to myocardium due to occlusion of 1+ coronary arteries or branches
- inadequate blood supply to meet the myocardial oxygen demand
- myocardial ischemia
- myocardial death
Atherosclerosis
++ blood levels of lipids irritate or damage intima of arterial vessels
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fatty substances enter vessels after damaging the protective barrier, accumulate and form fatty streak
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smooth muscle cels move to intima to engulf fatty substance
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fibrous tissue formation and calcification
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atheroma grows, vessel wall becomes thick, fibrotic and calcified, lumen narrows
* impedes blood flow with risk for thrombosis
Collateral Circulation
with gradual occlusion of the larger vessels, the smaller collateral vessels increase in size and provide alternative channels for blood flow
CAD Risk Factors
Non-modifiable
a. age
b. sex (women, men have slightly higher risk at younger age)
c. family history (familial hypercholesterolemia, mutation on gene LDL receptors
Modifiable
a. serum lipid alterations (decreased HDL and increased LDL and triglycerides)
b. hypertension
c. smoking
d. diabetes mellitus (insulin resistance)
- endothelial damage
e. diet
f. obesity (lipid metabolism)
g. lack of physical activity
Cholesterol
serum lipid abnormality is responsible for atherogenesis
- it is what creates plaque
high triglyceride level with high HDL or low HDL increases risk for atherosclerosis
= lipid synthesized by the liver or ingested
= required for synthesis of certain hormones and bile salts
= insoluble in water, requires lipoprotein for transportation
Lipoproteins relevant to CAD
Very-low-density lipoproteins (VLDL)
- produced by liver and converted in blood stream to LDLs
- for delivery of TRIGLYCERIDES to non-hepatic tissue
Low-density lipoproteins (LDL)
- produced in liver as VLDL
- for delivery of mainly CHOLESTEROL to non-hepatic tissue
High-density lipoproteins (HDL)
- produced in liver and small intestine
- reverse cholesterol transport, helps to EXTRACT EXCESS CHOLESTEROL deposited in blood vessels back to liver for elimination
- antioxidant and anti-inflammatory functions
Metabolic Syndrome
specific risk factors markedly increase potential for heart disease
3 out of 5 conditions:
a. Waist circumference
Men > 102cm
Women > 88cm
b. Triglyceride levels
> 1.7 mmol/L
c. HDL cholesterol
Men < 1 mmol/L
Women < 1.3 mmol/L
d. BP
SBP > 130 mmHg
DBP > 85 mmHg
e. fasting glucose
> 5.6 mmol/L
Management of CAD
a. modify risk factors (control bp, diabetes, lifestyle, weight)
b. health promotion (identifying at risk, manage underlying condition)
c. nutrition therapy (complex carbohydrates, omega-3 fatty acids)
d. medications (cholesterol-lowering, anti-platelet agents)
Diagnostic tests of CAD
a. ECG detect myocardial ischemia b. Stress testing effects of exercise (stress) on heart c. Cardiac catheterization catheter through a peripheral artery into aorta and left heart under fluroscopic imaging d. Coronary angiography injection of contrast medium into coronary arteries to visualize lesions
Percutaneous Transluminal Coronary Angioplasty (PTCA)
blocked or narrowed portions of the artery are dilated with a catheter and inflated ballon to flatten plaque
may be followed by a mesh stent insertion to keep it open, may also prevent further plaque build up
Coronary Atherectomy
removal of plaques that form a blockage
- generally used BEFORE angioplasty balloon is inflated
- reduce blockage and force needed to inflate balloon
Coronary Bypass Grafting (CABG)
surgical intervention to bypass blockages between the aorta and the myocardium with grafting of vessels distal to the area of blockage
Myocardial Ischemia
occurs when blood flow to the heart muscle is obstructed by a partial or complete blockage of a coronary artery by a buildup of plaques
*myocardial O2 deficit greater than 20 mins = myocardial infarction
Stable angina (angina pectoris)
transient (<10 min) precordial discomfort or distressing sensation, typically provoked by exertion or stress, relieved by rest and the use of nitrates
result from: atherosclerosis
Unstable angina
anginal discomfort when resting or that awakens pt from sleep, caused by significant CAD
increased risk of progression to MI
result from: atherosclerosis with blood clot
Variant (prinzmetal) angina
chest discomfort with atypical characteristics, often occurs during rest, follows a cyclic or regular pattern of occurrence (same time each day)
result from: coronary artery spasm
Acute Coronary Syndromes (ACS)
sudden coronary obstruction caused by thrombus formation such that part of the heart muscle is unable to function properly
Three clinical manifestations:
a. unstable angina
b. ST Elevation Myocardial Infarction (STEMI)
c. Non-ST Elevation Myocardial Infarction (NSTEMI)
- less damage than STEMI
*sustained ischemia > myocardial infarction > myocardial inflammation and necrosis
Manifestations of Myocardial Ischemia
a. chest pain (may radiate to left arm, neck, jaw or shoulder blad)
- major subjective symptom, caused by decreased O2
b. shortness of breath
- left ventricular failure > pulmonary edema
c. diaphoresis, cool, clammy skin
- SNS stimulation
d. ++ HR and BP (initially)
- release of catecholamines
e. nausea and vomiting
- result of severe pain, vasovagal reflexes
f. fever (within first 24hr up to 1 week post)
- inflammatory process result from cell death
g. loss of consciousness
- inadequate cerebral perfusion
Myocardial Infarction (MI)
prolonged myocardial ischemia results in myocardial infarction MEDICAL EMERGENCY
occurs at the central zone of ischemic injury, zone of infarction
most MIs involve ventricles (especially left)
irreversible damage to the affected myocardium may result WITHIN 2-4 HRS without adequate perfusion, necrosis with subsequent scar formation or fibrosis
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permanent impairment of contraction ability
Classification of MI by extent
Transmural infarcts
= involve full thickness of ventricular wall, most commonly occur when there is obstruction of a single artery
Subendocardial infarcts
= involve the inner 1/3-1/2 of the ventricular wall, occurs more frequently in the presence of severely narrowed but still patent arteries
Intramural Infarcts
Subepicardial infarcts (outer wall)
Classification of MI by location
Anterior MI
= left anterior descending (LAD) artery occlusion, left ventricular failure (LVF)
Inferior MI
= right coronary artery (RCA) occlusion or circumflex occlusion
Septal MI
= left anterior descending (LAD) artery occlusion
Lateral MI
= circumflex occlusion