Pathophysiology Study Guide pg 21-40
● Etiology of Coronary Heart Disease
○ Known risk factors: atherosclerosis, possible microcirculation abnormalities
○ Atherosclerosis causes narrowing of the arterial lumen (the passageway that blood flows
through) that can lead to cardiac ischemia (inadequate blood supply) through
■ thrombus formation.
■ coronary vasospasm. → aka prinzmetal angina when the arteries going into a spasm
■ endothelial cell dysfunction.
● Atherosclerosis can lead to these three things which can then cause ischemia
● Mechanisms of Coronary Atherosclerosis
○ Lipids are transported via apoproteins.
■ HDL’s actually clean up plaquing in the arteries, they take them back to the liver to
go bye bye THE GOOD FATS
■ LDL’s are sticky, stick to artery walls, irritate walls causing immune reaction leading
to atherosclerosis
■ LDL sticks to endothelial and irritates it. Send an alarm “we need help.” Macrophages are
sent to try to phagocyte the LDLs. The LDL’s start to oxidate and become hard. Recruit
smooth muscle cells. WBC’s come in and form a cap. → Makes a Plaque
○ Vulnerable plaques may rupture or become eroded, which stimulates clot formation on
the plaque.
■ Unstable plaques have
● large lipid core.
● thin cap.
● high shear stress.
■ Stable plaques have
● more collagen and fibrin.
● stable cap won't break free
Atherosclerosis (Risk factor for CHD)
● Three types of atherosclerosis:
○ Fatty Streaks – In children. Usually by age 20 they are
stagnant or start to regress. Not harmful.
○ Fibrous Atheromatous plaques – accumulation of lipids, growth of vascular smooth muscle, and
scar tissue. These lesions may continue to grow until they occlude the vessel or make it prone to
thrombosis formations.
○ Complicated lesion - A fibrous plaque but with hemorrhage. → Scar tissue, Hemorrhage, and
formation of thrombus due to the slow turbulent flow of blood around the lesion.
Angina (A symptom of CHD)
● A partial blockage of the Coronary arteries. The result of arteriosclerosis.
● When blood flow is needed the arteries are unable to provide it.
● Lack of blood means lack of oxygen to the heart muscle.
● Symptoms:
,Pathophysiology Study Guide pg 21-40
○ Pressure, Heaviness, Tightening, Squeezing or aching across the chest, particularly behind
the breastbone
,Pathophysiology Study Guide pg 21-40
● Treatment:
○ Nitroglycerin
■ A vasodilator, dilates arteries
○ Beta Blockers (Beta blockers relieve angina by inhibiting the effect of adrenaline on the heart.
Decreases the heart rate, lowers the blood pressure, and reduces the pumping force of the heart
muscle)
○ Calcium channel blockers (relieve angina by lowering blood pressure, and reducing the pumping
force of the heart muscle)
○ Angioplasty - procedure to restore flow
○ Coronary artery bypass
surgery. Acute Coronary Syndrome
● Occlusion → A obstruction, blood can’t go through and all the cells beyond blockage suffer
● Infarction → injury or death of tissue (as of the heart or lungs) resulting from inadequate blood supply
especially as a result of obstruction
● After 18 to 24 hours: area of infarction becomes pale
● 5 to 7 days: turns yellowish and soft
● At 1 to 2 weeks: necrotic tissue progressively degraded and cleared away; infarcted myocardium
weakened and susceptible to rupture
○ The Weak spot of dying muscle can break and blood can burst through and kill you
● By 6 weeks: necrotic tissue replaced by tough fibrous scar tissue
○ Scar Tissue is tough so the heart won’t be able to contract and therefore heart won’t be able
to pump as well as it should
● Lasts more than 15 minutes and is not relieved by rest or nitroglycerin
● Asymptomatic MI: silent MI (MI = Myocardial Infarction aka heart attack)
○ Left anterior descending coronary artery
○ Feeds muscles on left ventricle that push blood to the rest of the body
○ The most typical cause of heart attacks
● Women, the elderly, and patients with diabetic neuropathies
○ Atypical symptoms, including fatigue, nausea, back pain, and abdominal discomfort
● ECG changes
○ ST-segment elevation, large Q waves, and inverted T
waves Valvular Problems
● Stenosis: failure of the valve to open completely results in extra pressure work for the heart
● Regurgitation (insufficiency): inability of a valve to close completely results in extra volume work
for the heart. Blood flows backward
● Mitral Stenosis
○ Puts a strain on the heart, will lead to hypertrophy
● Mitral Valve Prolapse
○ Displacement (ballooning) of the mitral valve
○ Typically asymptomatic
, Pathophysiology Study Guide pg 21-40
Chapter 19 - Heart failure and Dysrhythmias: Common Sequelae of Cardiac Diseases
Heart Failure
● Etiology of Coronary Heart Disease
○ Known risk factors: atherosclerosis, possible microcirculation abnormalities
○ Atherosclerosis causes narrowing of the arterial lumen (the passageway that blood flows
through) that can lead to cardiac ischemia (inadequate blood supply) through
■ thrombus formation.
■ coronary vasospasm. → aka prinzmetal angina when the arteries going into a spasm
■ endothelial cell dysfunction.
● Atherosclerosis can lead to these three things which can then cause ischemia
● Mechanisms of Coronary Atherosclerosis
○ Lipids are transported via apoproteins.
■ HDL’s actually clean up plaquing in the arteries, they take them back to the liver to
go bye bye THE GOOD FATS
■ LDL’s are sticky, stick to artery walls, irritate walls causing immune reaction leading
to atherosclerosis
■ LDL sticks to endothelial and irritates it. Send an alarm “we need help.” Macrophages are
sent to try to phagocyte the LDLs. The LDL’s start to oxidate and become hard. Recruit
smooth muscle cells. WBC’s come in and form a cap. → Makes a Plaque
○ Vulnerable plaques may rupture or become eroded, which stimulates clot formation on
the plaque.
■ Unstable plaques have
● large lipid core.
● thin cap.
● high shear stress.
■ Stable plaques have
● more collagen and fibrin.
● stable cap won't break free
Atherosclerosis (Risk factor for CHD)
● Three types of atherosclerosis:
○ Fatty Streaks – In children. Usually by age 20 they are
stagnant or start to regress. Not harmful.
○ Fibrous Atheromatous plaques – accumulation of lipids, growth of vascular smooth muscle, and
scar tissue. These lesions may continue to grow until they occlude the vessel or make it prone to
thrombosis formations.
○ Complicated lesion - A fibrous plaque but with hemorrhage. → Scar tissue, Hemorrhage, and
formation of thrombus due to the slow turbulent flow of blood around the lesion.
Angina (A symptom of CHD)
● A partial blockage of the Coronary arteries. The result of arteriosclerosis.
● When blood flow is needed the arteries are unable to provide it.
● Lack of blood means lack of oxygen to the heart muscle.
● Symptoms:
,Pathophysiology Study Guide pg 21-40
○ Pressure, Heaviness, Tightening, Squeezing or aching across the chest, particularly behind
the breastbone
,Pathophysiology Study Guide pg 21-40
● Treatment:
○ Nitroglycerin
■ A vasodilator, dilates arteries
○ Beta Blockers (Beta blockers relieve angina by inhibiting the effect of adrenaline on the heart.
Decreases the heart rate, lowers the blood pressure, and reduces the pumping force of the heart
muscle)
○ Calcium channel blockers (relieve angina by lowering blood pressure, and reducing the pumping
force of the heart muscle)
○ Angioplasty - procedure to restore flow
○ Coronary artery bypass
surgery. Acute Coronary Syndrome
● Occlusion → A obstruction, blood can’t go through and all the cells beyond blockage suffer
● Infarction → injury or death of tissue (as of the heart or lungs) resulting from inadequate blood supply
especially as a result of obstruction
● After 18 to 24 hours: area of infarction becomes pale
● 5 to 7 days: turns yellowish and soft
● At 1 to 2 weeks: necrotic tissue progressively degraded and cleared away; infarcted myocardium
weakened and susceptible to rupture
○ The Weak spot of dying muscle can break and blood can burst through and kill you
● By 6 weeks: necrotic tissue replaced by tough fibrous scar tissue
○ Scar Tissue is tough so the heart won’t be able to contract and therefore heart won’t be able
to pump as well as it should
● Lasts more than 15 minutes and is not relieved by rest or nitroglycerin
● Asymptomatic MI: silent MI (MI = Myocardial Infarction aka heart attack)
○ Left anterior descending coronary artery
○ Feeds muscles on left ventricle that push blood to the rest of the body
○ The most typical cause of heart attacks
● Women, the elderly, and patients with diabetic neuropathies
○ Atypical symptoms, including fatigue, nausea, back pain, and abdominal discomfort
● ECG changes
○ ST-segment elevation, large Q waves, and inverted T
waves Valvular Problems
● Stenosis: failure of the valve to open completely results in extra pressure work for the heart
● Regurgitation (insufficiency): inability of a valve to close completely results in extra volume work
for the heart. Blood flows backward
● Mitral Stenosis
○ Puts a strain on the heart, will lead to hypertrophy
● Mitral Valve Prolapse
○ Displacement (ballooning) of the mitral valve
○ Typically asymptomatic
, Pathophysiology Study Guide pg 21-40
Chapter 19 - Heart failure and Dysrhythmias: Common Sequelae of Cardiac Diseases
Heart Failure
