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Phys: Cardio > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

Where does the RCA originate?

A

Originates from ascending aorta at the right sinus of valsalva

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2
Q

Where does the Left Main CA originate from?

A

Originates from ascending aorta at the left sinus of valsalva

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3
Q

What are the branches of the LCA?

A

Left Circumflex Artery (CX)

Left Anterior Descending Artery (LAD)

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4
Q

What are the branches of the RCA?

A

Posterior Descending Artery (PDA)

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5
Q

When does the most flow to the LV occur?

A

Most coronary flow to LV occurs during diastole

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6
Q

When does most flow to the RV occur?

A

RV receives equal coronary flow in systole and diastole

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7
Q

How is flow to the coronary arteries regulated?

A
  1. Under local metabolic control in response to changes in O2 consumption
  2. Incr. cardiac activity, there is an incr. in O2 consumption
    A. as HR incr, myocardial O2 consumption/demand also increases
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8
Q

What does the LCA supply?

A
  1. Supplies anterior & left lateral portions of LV

2. Supplies LA & interventricular septum

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9
Q

What does the Right Coronary artery supply?

A
  1. Supplies most of right ventricle as well as posterior portion of LV in 80-90% individuals
  2. Supplies RA & portions of conducting system
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10
Q

What does the Great Cardiac vein drain?

A

Drains blood from region supplied by LAD

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11
Q

What does the middle cardiac vein drain?

A

Drains area supplied by PDA

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12
Q

What does the small cardiac vein drain?

A

Drains blood from posterior surfaces of RA & RV

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13
Q

How does blood from the cardiac veins return to the ra?

A

Via the coronary sinus

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14
Q

How is coronary blood flow controlled?

A
  1. When cardiac contraction increases, O2 consumption increases, & rate of coronary blood flow increases
  2. Sympathetic Nervous System
    Release of norepinephrine & epinephrine
    Increase heart rate
    Increase in contractility
    Increase heart metabolism
    Local blood flow provides regulatory mechanisms for dilating coronary vessels
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15
Q

What is the major controller of myocardial blood flow?

A

Myocardial oxygen consumption

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16
Q

what are examples of ischemic heart disease?

A
  1. Acute coronary ischemia
  2. Acute coronary occlusion
  3. Myocardial infarction
  4. Congestive heart failure
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17
Q

Define coronary ischemia?

A

Decreased blood flow through coronary artery secondary to atherosclerotic plaques

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18
Q

What is the pathophys of coronary ischemia

A
  1. LDL deposits below endothelium throughout arteries
  2. Fibrous tissue & calcium deposits intertwine within cholesterol deposits
  3. Net result is atherosclerotic plaque
  4. Decreases lumen of vessel, resulting in impaired blood flow to area
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19
Q

Where is the most common site for plaque development?

A

Most common site for plaque development is the first few centimeters of major coronary arteries

20
Q

Define acute coronary occlusion and its effects

A
  1. Atherosclerotic plaque leads to thrombus which occludes artery
  2. Local vasospasm of coronary artery
  3. Vasospasm sometimes can lead to secondary thrombus
21
Q

where are lipoproteins synthesized?

A

small intestine and liver

22
Q

WHat causes endothelial cell injury?

A

Smoking, elevated LDL, immune mechanisms, and mechanical stress asst w/ HTN share potential for causing endothelial injury which causes adhesion of monocytes and plts

23
Q

What does the migration of inflammatory cells to the endothelial cell injury site cause?

A
  1. Endothelial cells begin to express selective adhesion molecules that bind monocytes and other inflammatory cells that initiate the atherosclerotic lesions
  2. After adherence to endothelium, monocytes localize to initima, transform into macrophages, and engulf lipoproteins, largely LDL
24
Q

What are foam cells and why are they important in the formation of atherosclerosis?

A
  1. Activated macrophages oxidize LDL; they then ingest the oxidized LDL to form foam cells
  2. Foam cells release growth factors and cytokines that promote recruitment of smooth muscle cells and stimulate neointimal proliferation, continue to accumulate lipid, and support endothelial cell dysfunction
25
Q

What is the structure of plaque? How is it formed?

A
  1. Fibrous atheromatous cap formation w/ central core of lipid-laden foam cells and fatty debris
  2. exposes circulating platelets and coagulants to the underlying matrix, thereby initiating thrombosis, and triggering a cascade of events leading to a fibroproliferative lesion and luminal narrowing
26
Q

What are the steps in atherosclerosis?

A

I. Endothelial cell injury
II. Migration of Inflammatory cells
III. Lipid accumulation and Smooth muscle cell proliferation
IV. Plaque structure

27
Q

Define atherosclerotic plaques. What can plaques cause?

A
  1. Narrowing of the vessel and production of ischemia
  2. Sudden vessel obstruction due to plaque hemorrhage or rupture
  3. Thrombosis and formation of emboli resulting from damage to the vessel endothelium
  4. Aneurysm formation due to weakening of the vessel wall
28
Q

Define collateral circulation. How is blood flow different in collateral circulation?

A
  1. If one artery is blocked, capillary circulation continues due to anastomosis or collateral blood flow
  2. When blood flow is occluded, small anastomosis dilate within seconds
  3. However, blood flow through these collaterals usually less than half of cardiac requirements
  4. Collateral flow doubles by second or third day
  5. Collaterals are able to achieve normal coronary circulation within one month
29
Q

How can collateral circulation lead to CHF?

A

With extensive atherosclerosis, collateral vessels will sometimes develop plaque; when this happens, the heart muscle’s pumping ability is severely impaired, leading to CHF

30
Q

Define the pathophys of an MI

A
  1. Occurs when coronary artery is occluded to the point of no blood flow
  2. Soon after the infarction, small amounts collateral blood seeps into infarcted area
  3. Due to decreased oxygen, dilation of local vessels occurs
  4. Within few hours of minimal/no blood supply, cardiac muscle cells die
31
Q

Define the pathophys of subendocardial infarction

A
  1. Subendocardial plexus is located immediately beneath endocardium
  2. Sometimes, subendocardial layer becomes infarcted without involvement of epicardial arteries
  3. Any condition that compromises blood flow to heart usually causes damage to subendocardial layer first; damage then spreads outward toward epicardium
32
Q

What conditions can cause death after an MI?

A
  1. Decreased cardiac output
  2. Pulmonary edema
  3. Ventricular fibrillation from hypokalemia
  4. Heart rupture
33
Q

Define decreased cardiac output and why it leads to death

A
  1. Pumping ability of heart greatly compromised when portions of heart muscle are damaged/necrotic
  2. Systolic Stretch
    A. When normal portions of ventricle contract, the ischemic muscle is forced outward by the pressure within ventricle
    B. Results in hypokinetic wall
  3. Can lead to cardiogenic shock
34
Q

Define pulmonary edema and its pathophys

A
  1. Due to decreased cardiac output, blood begins to back up in venous system
  2. In addition, decreased cardiac output leads to decreased renal perfusion
  3. Renal-angiotensin-aldosterone system is activated
  4. Leads to fluid retention, Na retention
  5. Fluid overload leads to pulmonary edema
35
Q

When does pulmonary edema occur after an MI?

A

A few days

36
Q

When is V fib most likely to occur after an MI?

A
  1. Two periods when V A. Fib likely to occur:
    Within first 10 minutes of infarct
    B. One hour to several hours after infarction
37
Q

What is the etiology of V fib after an MI?

A
  1. Acute loss of blood supply to myocardium leads to rapid loss of K from muscle cells
  2. Ischemic muscle cannot completely repolarize
  3. Sympathetic stimulation increases irritability of heart
  4. Cardiac muscle weakness causes LV to dilate, leading to abnormal conduction pathways
38
Q

How does ventricular rupture occur after an MI?

A
  1. Occurs with increasing systolic stretch
  2. Results from excessively thin ventricle secondary to infarct
  3. When rupture occurs, leads to excessive blood into pericardial space, leading to cardiac tamponade
39
Q

How does the heart recover from an acute MI?

A
  1. Shortly after coronary occlusion, muscle fibers in center of ischemic area die
  2. Necrotic area expands circumferentially due to lack of O2
  3. Collateral circulation supplies outer rim surrounding dead fibers so that area recovers
  4. Normal areas of heart hypertrophy to compensate for dead musculature
40
Q

Define angina and its etiology

A
  1. Substernal chest pain/pressure sometimes radiating to L neck, L jaw, L shoulder, L arm, L face
  2. Occurs as a result of decreased O2 supply to heart
41
Q

Where is referred cardiac pain located?

A

Pain of heart attack may be initially felt over chest wall & down left arm

42
Q

Why is cardiac pain referred?

A

Sensory information from heart is relayed to exact same level of spinal cord as sensory information from spinal nerves
Brain cannot immediately distinguish the true source of painful stimulus & initially interprets the pain as originating in T1-T5 dermatomes rather than from the heart muscle

43
Q

What disease is asst. with aortic aneurysms?

A
  1. Atherosclerosis is most common disease associated with aortic aneurysms
  2. HTN is a risk factor
44
Q

What is the pathophys of aneurysms?

A
  1. Plaque weakens aortic wall leading to dilation of vessel
    A. Degenerative changes create focal weakness in muscular layer of aorta
    B. Allows tunica intima/media to stretch outward
45
Q

What is the most common location of aneurysms?

A
  1. Aortic aneurysms often occur in abdominal area (75%)

2. Thoracoabdominal aneurysms account for 25% aortic aneurysms

Phys: Cardio (6 decks)

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