Lecture 6: CV Pathophysiology IV Flashcards
(44 cards)
What factors influence myocardial oxygen delivery?
- O2 carrying capacity of blood
- coronary blood flow
- coronary perfusion pressure
- coronary vascular resistance
- metabolic factors (adenosine, lactate, H+, CO2 - vasodilators)
- endothelial factors (NO and prostacyclin vasodilator, endothelin-1 constricts)
- neural factors (SNS leads to vasodilation because of increased O2 demand, PNS has no effect)
- atherosclerosis
What influences myocardial oxygen demand?
- HR
- cardiac contractility
- ventricular wall stress (enlarged ventricles need more O2; Law of Laplace)
What are the sex differences for CAD?
- leading cause of death for both
- more common in women
- estrogen has an anti-inflammatory effect but not if its synthetic
- men have more localized plaques –> easier to visualize and treat but more symptomatic
- women are more likely to have extensive plaques that minimize obstruction to blood flow
chest pain; too brief to cause cell death
angina pectoralis
irreversible necrosis of cardiac muscle cells
MI
What can be used to treat after an episode of angina?
- lifestyle changes
- vasodilators
- anti-coagulants
- beta-blockers
- statins
- PCI (angioplasty and stenting)
- coronary bypass surgery
insufficient blood flow (but not death)
ischemia
What is the difference in anterior and posterior wall MIs?
anterior - association with SNS; increased HR, contractility, and BP
posterior - association with vagus nerve; decreased HR an BP
What is angina typically preceded by?
increase in O2 demand (exercise, stress, sympathetic nerve activation)
What is stable angina?
when atherosclerotic coronary vessels reduce blood flow to critical levels
What is unstable angina?
when a clot causes ischemia but breaks down before necrosis occurs
How do you distinguish an MI from unstable angina?
enzymes tests that show enzymes released from dead myocardial cells
What events lead to coronary thrombosis?
- exposure of sub endothelial collagen (injury)
- turbulent flow contributes to clotting
- hemorrhage narrows vessel
- dysfunction of endothelium (low NO and prostacyclin levels)
Describe the symptoms of ischemia in men vs. women.
men - angina before and during MI
women - fatigue, sleep disturbances, and indigestion prior to an MI and SOB, weakness, fatigue, cold sweat, nausea during an MI
What changes occur on a molecular level during an MI?
- less ATP produced slows ion pumps leading the cell death
- lactic acid accumulates –> lower pH (results in functional changes in myocardium)
- rising K+ levels can cause arrhythmias
- rising Ca+ levels activate lipase that lead to cell death
- inflammation and myocardial edema
What changes occur on a molecular level after an MI?
-dead cells are cleared by macrophages and replaced by fibrotic scar tissue within 7 weeks
What changes occur on a functional level after an MI?
- decreased contractility/CO
- “stunned” or “hibernating” cells may region function
- ventricular remodeling (dilation of ventricle increases CO)
- ultimately will lead to heart failure though
What does a non-STEMI on an ECG indicate?
- partial occlusion or transient total occlusion of a vessel
- mild ischemia
- associated with high risk of MI but lower risk of death
What does a STEMI on an ECG indicate?
- total occlusion of a blood vessel
- greater risk of death
What are the serum markers for MI and what do they indicate?
creatine kinase - found in heart cells, indicative of damage
myoglobin - early indication of MI but less specific (found in other muscle)
troponin T and troponin I - cardiac specific
lactate dehydrogenase - peaks 3-5 days post MI
What can be used to treat an MI acutely?
- PCI (angioplasty and stenting)
- aspirin or heparin
- anti-ischemic therapy to decrease O2 demand including nitrates (veNOdilation), beta-blockers (decrease HR), calcium channel blockers (decrease HR and contractility)
What are potential causes of arrhythmia related to MI?
- damage to conduction pathway
- pH and ion permeability changes
- autonomic stimulation (PNS or SNS)
When does congestive heart failure occur and what are the consequences?
- develops when >40% of LV is damaged
- severely decreased CO and hypotension
- leads to further ischemic damage
- decreased SV leads to LV hypertrophy, which increased O2 demand
- mortality is >70%
What are some treatments for CHF?
- ionotropic agents (increase contractility and CO)
- arterial vasodilators (decrease afterload)
- intraaortic balloon pump (helps perfuse coronary and peripheral tissues
