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Pathophysiology 1 > Jan 9 - Coronary Heart Disease Part 1 > Flashcards

Jan 9 - Coronary Heart Disease Part 1 Flashcards

1
Q

Which artery is most commonly affected by athersclerosis?

A

The left main coronary artery because it’s the most important because its on the left side, they push the blood for the whole body and transporting oxygenated blood

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2
Q

When are the coronary arteries perfused with blood?

A

Diastole because they fill during resting period

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3
Q

What factors that can affect oxygen supply?

A 
Oxygen content (hemoglobin)
Blood flow (athersclerosis, vasospasm, collateral supply)
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4
Q

What are factors that can affect oxygen demand?

A 
Heart rate (directly proportionate)
Blood pressure (directly proportionate)
Contractile force (how hard the heart is beating - squeeze)
Ventricular wall tension (how flexible the ventricles are - stretch; afterload, preload and wall thickness)
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5
Q

What is preload?

A

The amount of blood that is returned to the heart that causes the stretch in the ventricle

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6
Q

What is afterload? Why is it important?

A

Pressure exerted against the heart; the resistance of the arteries pushing back on the heart.

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7
Q

Why is preload and afterload important?

A

It’s important because if someone has damaged their heart, the preload and afterload are affected. Preload and afterload can be manipulated via drug intervention

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8
Q

What is ischemia?

A

Inadequate blood supply to a part of the body causing a shortage of oxygen/nutrients

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9
Q

What are the potential causes of ischemia?

A

The main cause is athersclerosis. Other causes include: coronary artery disease, blood clot/embolus/constriction of artery, hypovolemia (decrease in volume of blood plasma), cancer that is pinching something off, vasospasm

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10
Q

Describe the process leading to atherosclerosis

A
  1. Lipid accumulation (LDL - yellow particles)
  2. Macrophages, scavenger white blood cells “eat” the LDL and become foam cells
  3. Foam cells (bad) collect and form fatty streaks, fatty deposits attached to the endothelium (layer of cells that line the vessel walls)
  4. Smooth muscle cells and T-cells can produce cytokines, which induce inflammation
  5. Smooth muscle cells can also take up LDL and become part of the lesion (muscle cells get stuck within group of foam cells)
  6. Plaques form a fibrous cap - these caps can rupture and get stuck downstream vessels. They also trigger a response from platelets and fibrin (Ca2+ makes cap hard)
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11
Q

What is vasospasm?

A

Arteries have a “freak out” and open/close; closing restricts blood supply

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12
Q

Name the six ways coronary blood flow is regulated

A
  1. Autoregulation - dilation of downstream vessels
  2. Collateral blood flow - extra vessels
  3. Metabolic regulation
  4. Endothelial lining protection
  5. Artery compression during systole/diastole
  6. Perfusion pressure (or coronary blood flow)
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13
Q

How does autoregulation help regulate coronary blood flow?

A

It dilates downstream vessels (the artery past the blockage). Arteriolar dilation allows coronary blood flow for exertion

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14
Q

How does collateral blood flow help regulate coronary blood flow?

A

Connections between smaller arteries try to compensate for narrowings in the large arteries. These connections allow for better flow to ischemic areas

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15
Q

How does metabolic regulation help regulate coronary blood flow?

A 
Changes in O2 needs trigger metabolic mediators such as:
Adenosine (ATP/AMP) - vasodilation 
Nitric oxide - vasodilation
Prostaglandins
CO2
H+
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16
Q

Why is adenosine important?

A

The presence of adenosine provokes the realization that there’s a lack of blood flow. This facilitates energy transfer and there is a major vasodilation in the area

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17
Q

How does endothelial lining protection help regulate coronary blood flow?

A

It protects the artery wall by inhibiting thrombogenesis and promoting relaxation (makes the vessel bigger and prevents clotting). Once disrupted (i.e., athersclerotic plaque), inflammatory cytokines, platelet activating factor, vasoconstriction and thrombosis occur

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18
Q

How does artery compression during systole/diastole help regulate coronary blood flow?

A

During diastole (relaxed), the coronary arteries are perfused well (low pressure). During systole (contraction), the coronary arteries are squashed (high pressure) and perfused less

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19
Q

How does perfusion pressure (or coronary blood flow) help regulate coronary blood flow?

A

Measures the blood flow through the coronary arteries. It’s measured via the difference between aortic diastolic pressure (relaxation) and right atrial pressure at the same time point

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20
Q

Name some modifiable risk factors for coronary heart disease

A

Smoking, dyslipidemia, hypertension, obesity/sedentary lifestyle, stress, chronic kidney disease, illicit drugs

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21
Q

Name some non-modifiable risk factors for coronary heart disease

A

Male, age (>40 years), genetics/family history, ethnicity, environmental factors, diabetes

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22
Q

Does obesity directly correlate with heart disease?

A

No, but it increases the chances

23
Q

How is diabetes both a non-modifiable and modifiable risk factor

A

Type I diabetes: non-modifiable

Type II diabetes: kinda modifiable (can be due to poor diet or could be hereditary)

24
Q

How is a stable angina produced?

A

A stable atherosclerotic plaque impairs perfusion. The ischemia reduces production of ATP, decreases normal Na/K pump function, causes the loss of myocardial membrane pump integrity and increases the production of chemicals by myocytes and platelets. There is no washout of acidic/chemical substances (concentration of lactate increases, concentration of K+ decreases).

25
Q

What type of chemicals do myocytes produce (stable angina)?

A

Lactate, serotonin, bradykinin, histamine, reactive oxygen species and adenosine*

26
Q

What type of chemicals do platelets produce (stable angina)?

A

Serotonin, thromboxane A2 and 5-hydroxytryptamine

27
Q

How do these chemicals affect the area in which they are produced?

A

They stimulate chemoreceptors and mechanoreceptors innervated by unmyelinated nerve cells within the cardiac muscle fibres and around the coronary vessel. These nerve fibres travel along the sympathetic afferent pathways from the heart and enter the sympathetic ganglia in the lower cervical and upper thoracic spine (C7-T4). Impulses are transmitted to the thalamus and activate corresponding area of the cerebral cortex. The cortex transmits this pain in a very characteristic pattern to the dermatomes that supply the afferent nerves to the same segments of the spinal cord (the same patient will have the same distribution of pain from one angina attack to the next)

28
Q

What is the primary mediator of angina?

A

Most likely adenosine via the stimulation of A1 adenosine receptor

29
Q

Name six symptoms of stable angina

A

Pain, radiation of pain, shortness of breath, bradycardia, tachycardia, nausea/vomiting

30
Q

What is pain with regards to stable angina? Why does pain occur in stable angina?

A

The squeezing, pressure, burning, tightness “fist-like” in the chest. It’s due to the buildup of chemicals. It resolves with rest and short duration (2-5 minutes). It’s triggered by activity (cold, stress, physical activity)

31
Q

What is radiation of pain with regards to stable angina? Why does radiation of pain occur?

A

Pain radiates to the arms, shoulders, neck, jaw, back, throat, teeth, upper abdomen. Sympathetic afferent fibres in atrium and ventricle refer to upper thoracic dorsal roots = pain referral

32
Q

What causes shortness of breath during a stable angina?

A

Systolic and diastolic dysfunction of heart

33
Q

What is bradycardia? What causes bradycardia?

A

Slow heart rate (<60 bpm) caused by impaired blood supply to the AV node

34
Q

What is tachycardia? What causes it?

A

Fast heart rate >100 bpm. It’s caused by stress/panic and release of catecholamines

35
Q

What causing nausea/vomiting during stable angina?

A

Vagus nerve stimulation (anterior blockage)

36
Q

What should a patient do if they experience an angina attack?

A

Sit down for a couple minutes. If it does not get better, it is because they are experiencing acute coronary symptoms

37
Q

What are the three diagnostic tests for angina?

A

Electrocardiogram
Stress test
Angiogram

38
Q

What an electrocardiogram?

A

Graph of what the heart is doing.
The p-wave: atria contraction
Straight line: isoelectric point (anything above or below demonstrates electrical activity in the heart)
Q-R-S complex: ventricles contracting (hidden - atria repolarizing)
T-wave: ventricles repolarizing
All waves together represents one heart beat (normal heart rate 70 bpm)

39
Q

What is something abnormal that could occur in an ECG?

A

ST segment elevation/depression, T wave inversion -> signs of ischemia

40
Q

What is a stress test?

A

Aka ETT
Patient runs on a treadmill for 20 minutes running as fast as you can and they monitor your heart (looking for signs of ischemia during exertion)

41
Q

What is an angiogram?

A

Picture of blood vessels (feed catheter through, inject dye and find areas of ischemia)

42
Q

What ways of managing chronic stable angina?

A
  1. Lifestyle changes (smoking, exercise, weight reduction, diet)
  2. Manage comorbidities (diabets, hypertension)
  3. Antiplatelet therapy (aspirin, clopidogrel if allergic)
  4. Cholesterol-lowering therapy
  5. Anti-anginal medications
43
Q

How do nitrates work as anti-anginal medications?

A

They dilate the arteries/veins to reduce myocardial oxygen demand (decreased wall tension) leading to decreased preload. Vasodilation reduces preload (dilating the periphery causes more blood to be driven away from the heart and the return to the heart is less, creating less stress on the heart). It improves flow in the arteries

44
Q

How de beta-blockers work as anti-anginal medications

A

They reduce cardiac oxygen demand by decreasing heart rate, contractility and blood pressure; this is the first line of prevention against MI/cardiac death. Beta-blockers (beta-1 specific) block beta receptors in the heart

45
Q

Where are all the different beta receptors found?

A

Beta-1 receptors are in the heart

Beta-2 receptors are in the lungs and blood vessels

46
Q

What do calcium channel blockers affect?

A

Oxygen supply and oxygen demand

47
Q

How do calcium channel blockers affect oxygen supply?

A

They dilate coronary arteries improving blood flow, prevent vasospasm and decrease coronary vascular resistance

48
Q

How do calcium channel blockers affect oxygen demand?

A

They reduce conduction velocity through SA and AV nodes, decrease blood pressure (arterial dilation), decrease contractility

49
Q

Name the two types of calcium channel blockers and give some examples of drugs of each type

A

Dihydropyridine calcium channel blockers (amlodipine, felodipine, nifedipine)
Non-dihydropyridine calcium channel blockers (diltiazem, verapamil)

50
Q

How do non-dihydropyridine calcium channel blockers work?

A

They act similar to beta-blockers (reduce heart rate, blood pressure, contractile force, ventricular wall tension)

51
Q

How do dihydropyridine calcium channel blockers work?

A

They deal with blood flow, prescribed for patients with vasospasm (calms down the arteries)

52
Q

How do lipid-lowering medications work as anti-anginal medications?

A

They decrease LDL and prevent destabilization of atherosclerotic plaques (help prevent plaques from forming, or prevent current plaques from getting bigger)

53
Q

How do anti-platelet medications work as anti-anginal medications?

A

They prevent platelet aggregation if disruption of atherosclerotic plaque occurs, which reduces death and heart attacks (approx 30% decrease). They also improve blood flow

Pathophysiology 1 (11 decks)

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