Ischemic Heart Disease Flashcards

1
Q

Ischemic Heart Disease

Define Ischemic Heart Disease

A

imbalance between myocardial oxygen supply and demand

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2
Q

Ischemic Heart Disease

What does ischemic heart disease cause?

A

results in myocardial hypoxia and accumulation of metabolic waste products

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3
Q

Ischemic Heart Disease

What is the primary cause of ischemic heart disease?

A

narrowing of coronary artery as a result of athersclerotic plaque

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4
Q

Ischemic Heart Disease

What are “ischemic syndromes?”

A

manifestations of ischemic heart disease

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5
Q

Myocardial Oxygen Supply

What two things determine myocardial oxygen supply?

A
  • O2 carrying capacity
  • Coronary blood flow
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6
Q

Myocardial Oxygen Supply

What are the 2 factors effecting oxygen carrying capacity?

A
  • blood oxygen saturation level (SaO2%)
  • hemoglobin (Hg) content
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7
Q

Myocardial Oxygen Supply

What are considered normal levels of blood oxygen saturation level?

A

usually 97 - 100%

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8
Q

Myocardial Oxygen Supply

What are considered normal Hg content for men and women?

A

Men: 12 -15.5 mg/dl
Women: 13.5 -17.5 mg/dl

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9
Q

Myocardial Oxygen Supply

Key Point

A

oxygen carrying capacity is usuallt constant unless anemia or obstructive lung disease is present

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10
Q

Myocardial Oxygen Supply

What does coronary blood flow depend on?

A
  • perfusion pressure
  • vascular resistance
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11
Q

Myocardial Oxygen Supply

What is Darcy’s Law?

A

Q = (P1 - P2) / R

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12
Q

Myocardial Oxygen Supply

How is perfusion pressure (P) related flow?

A

P is directly related to flow (Q)

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13
Q

Myocardial Oxygen Supply

How is vascular resistance related to flow?

A

R is inversely proportional to flow (Q)

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14
Q

Myocardial Oxygen Supply

It is important to know that coronary blood flow occurs mainly during what portion of the heart cycle?

A

diastole (left coronary)

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15
Q

Myocardial Oxygen Supply

How can perfusion pressure (P) be estimated?

A

by diastolic pressure in aorta

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16
Q

Myocardial Oxygen Supply: Perfusion Pressure

The left main coronary blood flow is zero in early systole due to what?

A

extravascular myocardial compression of small coronary microvessels

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17
Q

Myocardial Oxygen Supply: Perfusion Pressure

Left coronary artery flow returns to diastolic level in systole but flow is maximum when?

A

during diastole

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18
Q

Myocardial Oxygen Supply: Perfusion Pressure

When does right coronary artery flow increases and why?

A
  • during both systole and diastole
  • this is due to less compression in right ventricle during systole
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19
Q

Myocardial Oxygen Supply: Perfusion Pressure

What is the typical aortic flow pressure? How is the accomplished?

A
  • fairly constant flow between diastolic pressure of 60 - 150 mmHg
  • this is done by autoregulation
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20
Q

Myocardial Oxygen Supply: Perfusion Pressure

Does P or R have greater contribution to flow alterations?

A

R is the major factoer that controls changes in coronary flow

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21
Q

Myocardial Oxygen Supply: Perfusion Pressure

Conditions that decrease aortic diastolic BP to less the 60 mmHg can cause what?

A

reduced coronary artery perfusion in left and right coronary artery; this increases risk of ischemia
- common issue in elderly

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22
Q

Myocardial Oxygen Supply

What is important to know about myocardial oxygen extraction?

A

it is almost maximal (75%) at rest

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23
Q

Myocardial Oxygen Supply

What is important to know about myocardium in regards to increased O2 requirement?

A

the demand must be met primarily by increased coronary blood flow (CBF)

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24
Q

Myocardial Oxygen Supply

What is the resting coronary blood flow and oxygen extraction?

A
  • about 250 ml/min
  • 70 - 80% in the heart
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25
Q

Myocardial Oxygen Supply

How does myocardial extraction differ from other parts of the body?

A
  • it is much higher
  • compared to about 25% in skeletal muscle
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26
Q

Myocardial Oxygen Supply

How is increased O2 consumption dealt with in the heart?

A

mainly be reducing vascular resistance

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27
Q

Myocardial Oxygen Supply: Vascular Resistance

Describe Poiseulle’s Law, Darcy’s Law, and the equation for resistance.

A

look them up

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28
Q

Myocardial Oxygen Supply: Vascular Resistance

What does it mean if:
1. flow (Q) through a tube is directly proportional to pressure gradient (delta P) and radius (r) of a vessel
2. Q is inversely proportional to resistance (R)

A
  • R is indirectly proportional to r^4
  • R is directly proportional to length (l) and viscosity of blood
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29
Q

Vascular Resistance and atherosclerotic

3 Key Points

A
  • small resistance arterioles distal to plaque dilate (increase radius), which increases flow (Q) to tissue, in order to compensate for proximal stenosis and reduced flow
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30
Q

Maximal CBF is compromised when lesion damage is what?

A

greater than 60 - 70%

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31
Q

What effect does 60 - 70% lesion have on resting CBF?

A

no effect

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32
Q

When does resting CBF become compromised?

A

when the lesion is greater than 90%

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33
Q

Myocardial Oxygen Supply: Vascular Resistance

CBF is regulated by autoregulation of local vascular resistance via:

A
  • Metabolic factors
  • Endothelial factors
  • Neural factors
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34
Q

Myocardial Oxygen Supply: Vascular Resistance

Examples of metabolic factors and what they do?

A

adenosine: dilation
hypoxia: dilation

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35
Q

Myocardial Oxygen Supply: Vascular Resistance

Examples of endothelial factors and what they do?

A
  • NO, prostacyclin, EDHF: dilation
  • Endothelin-1: constriction
  • Angiotensin II: constriction
36
Q

Myocardial Oxygen Supply: Vascular Resistance

Examples of neural factors and what they do?

A

sympathetic nerve and circulation NE/Epi:
- alpha-1 adrenergic activation: constriction from sympathetics
- beta-2 adrenergic activation: dilation from Epi

37
Q

Myocardial Oxygen Demand

What 3 physiological factors create myocardial oxygen demand?

A
  • wall stress
  • heart rate
  • contractility
38
Q

Myocardial Oxygen Demand

Define Myocardial Oxygen Demand.

A

indicates metabolic rate or oxygen consumptoin of myocardium (MVO2)

39
Q

Myocardial Oxygen Demand: Wall Stress

Define wall stress

A

tangential force activation on the LV myocardial fibers tending to pull them apart

wall stress = (P * r) / h

40
Q

Myocardial Oxygen Demand: Wall Stress

What happens to wall stress, if P or r increases?

A

it increases; examples:

  • hyoertension or aortic stenosis increase LV P and increases wall stress
  • conditions (aortic regurg; heart failure) that augment LV chamber size via excess LV filling will increase wall stress
41
Q

Myocardial Oxygen Demand: Wall Stress

What may happen to h when P increases to maintain wall stress?

A

it increases, example:
- LV hypertrophies in response to chronic high BP to decrease wall stress

42
Q

Myocardial Oxygen Demand: Heart Rate

When does the number of contraction increase?

A

during exertion

43
Q

Myocardial Oxygen Demand: Heart Rate

What two things does increased contraction of the heart lead to?

A
  • increase in ATP per minute consumed
  • increased MVO2
44
Q

Myocardial Oxygen Demand: Heart Rate

Conversely, a decrease in HR can be caused by what? What will become reduced?

A
  • beta-blocker medication
  • MVO2
45
Q

Myocardial Oxygen Demand: LV myocardial contractility

What are three ways an increase in MVO2 can be caused?

A
  • increase in circulating norepinephrine
  • direct sympathetic nerve stimulation on LV myocardium
  • positive iontropic drugs will increase MVO2
46
Q

Myocardial Oxygen Demand: LV myocardial contractility

What can cause a decrease in MVO2?

A

beta-blockers or Ca+2 channel blockers

47
Q

Ischemic ‘Syndromes’

What are 5 types of ischemic syndromes?

A
  1. angina pectoris
  2. stable vs. unstable angina
  3. variant angina
  4. silent ischemia
  5. myocardial infarction
48
Q

Ischemic ‘Syndromes’: Angina Pectoris

What can the pain of angina pectoris be described as?

A

strangling in the chest

49
Q

Ischemic ‘Syndromes’: Angina Pectoris

Where do people typically feel discomfort?

A

substernal chest area from ischemia

50
Q

Ischemic ‘Syndromes’: Angina Pectoris

What are nociceptors in myocardial tissue stimulated by?

A

ischemic metabolites send afferent signals to brain

51
Q

Ischemic ‘Syndromes’: Angina Pectoris

Where else can someone feel pain radiate in their body?

A
  • left shoulder/arm
  • epigastric
  • neck/jaw
  • upper back
    (known as referred pain)
52
Q

Ischemic ‘Syndromes’: Angina Pectoris

What are precipitating causes?

A

physical exertion, emotional stress; relieved by rest

53
Q

Ischemic ‘Syndromes’: Angina Pectoris

Key Point

A

Angina results from imbalance between myocardial oxygen suppply and demand (MVO2)

54
Q

Ischemic ‘Syndromes’: Angina Pectoris

Quality of symptoms?

A

usually described as pressure, tightness, burning, squeezing
- last 5-10 minutes

55
Q

Ischemic ‘Syndromes’: Angina Pectoris

What could a time frame of longer than 10 minutes signify?

A

may be the start of myocardial infarction

56
Q

Ischemic ‘Syndromes’: Angina Pectoris

What are NOT symptom qualities?

A

sharp and stabbing pain
- change of pain with inspiration/expiration
- change of pain with palpating chest wall

57
Q

Ischemic ‘Syndromes’: Angina Pectoris

What are common associated symptoms?

A

sympathetic response
- tachycardia, diaphoresis, dyspnea, fatigue, nausea

58
Q

Ischemic ‘Syndromes’: Stable vs Unstable Angina

Define stable angina.

A

chronic pattern of angina has 3 features:
- exacerbated during physical exertion or emotion
- relieved with rest within 3-5 minutes or with sublingual nitroglycerin
- ST segment depression or T wave inversion on ECG

59
Q

Ischemic ‘Syndromes’: Stable vs Unstable Angina

Define unstable angina

A
  • pattern of increased “frequency or duration of anginal episodes” or “anginal symptoms at rest
  • indicates progression of disease and likely from partial thrombosis
  • high risk for progressing to myocardial infarction
60
Q

Ischemic ‘Syndromes’: Variant angina

What other name is this known as?

A

prinzmetal’s angina

61
Q

Ischemic ‘Syndromes’: Variant angina

How is the pain caused?

A

anginal discomfort comes from coronary vasospasm

62
Q

Ischemic ‘Syndromes’: Variant angina

What is the result of a coronary vasospasm?

A

decreased myocardial oxygens supply because of constriction (rather than increased MVO2)

63
Q

Ischemic ‘Syndromes’: Variant angina

When can this occur?

A

at rest or due to physical exertion

64
Q

Ischemic ‘Syndromes’: Variant angina

What groups of people experience this more commonly?

A

females and smokers

65
Q

Ischemic ‘Syndromes’: Variant angina

What is the estimated mechanism?

A

a result in part from impaired nitric oxide release or other dilators from endothelium, but cause is unknown

66
Q

Myocardial Ischemia on ECG

Subendocardial ischemias can be determined by what two things on an ECG?

A
  • T wave inversion
  • ST segment depression
67
Q

Myocardial Ischemia on ECG

Describe a subendocardial ischemia T wave inversion.

A
  • usually appears within seconds of onset of ischemia
  • due to delat in repolarization
68
Q

Myocardial Ischemia on ECG

Describe a subendocardial ischemia ST segment depression.

A
  • usually from severe subendocardial ischemia
  • leads to delayed repolarization in subendocardium
  • sometimes associated with inverted T wavs (but not always)
69
Q

Myocardial Ischemia on ECG

Define an ST segment depression.

A

depression of ST segment in mm below PQ segment (baseline)
- 0.08 msec (two small boxes) after the J point

70
Q

Myocardial Ischemia on ECG

3 Key ST segment characteristics used for determination.

A
  1. magnitude: in mm (severity of ischemia)
  2. distribution: # of leads
  3. slope of ST depression is significant
71
Q

Myocardial Ischemia on ECG

Describe what differing ST segment slopes mean.

A
  • downsloping = severe ischemia
  • horizontal = moderate ischemia
  • upsloping = non-diagnostic of ischemia
72
Q

Ischemic ‘Syndromes’: Silent Ischemia

Define Silent ischemia.

A

myocardial ischemia without symptoms of angina

73
Q

Ischemic ‘Syndromes’: Silent Ischemia

How does it present on an ECG?

A
  • may show up as ST segment depression or T wave inversion on ECG
  • difficult to diagnose without ECG
74
Q

Ischemic ‘Syndromes’: Silent Ischemia

What is the cause?

A

unknown

75
Q

Ischemic ‘Syndromes’: Silent Ischemia

Who experiences this more commonly?

A
  • patients with diabetes because of impaired pain sensation from peripheral neuropathy
  • women or has an unusual presentation then typical chest discomfort
76
Q

Pharmacological Treatment of Angina

What is the goal?

A

to prevent symptoms

76
Q

Ischemic ‘Syndromes’: Myocardial Infarctions

MI

A

discussed in next leture

77
Q

Pharmacological Treatment of Angina

What do nitrates do?

A

vaso and venodilator
- decrease MVO2 demand
- increase MVO2 supply

78
Q

Pharmacological Treatment of Angina

How do nitrates decrease MVO2 demand?

A

reduce preload via venodilation:
- decrease venous return back to heart
- decrease LV flling (decrease wall stress)

79
Q

Pharmacological Treatment of Angina

How do nitrates increase MVO2 supply?

A
  • increase coronary blood flow via vasodilation
  • decrease coronary vasospasm
80
Q

Pharmacological Treatment of Angina

What do beta-blockers do?

A

block cardiac beta-1 adrenergic receptors
- decrease MVO2 demand

81
Q

Pharmacological Treatment of Angina

How do beta-blockers decrease MVO2 demand?

A

decrease HR and contractility (decrease wall stress)

82
Q

Pharmacological Treatment of Angina

What do calcium channel blockers do?

A

blocks cardiac and VSMC L-type Ca2+ channels
- decrease MVO2 demand
- increase MVO2 supply

83
Q

Pharmacological Treatment of Angina

How do calcium channels blockers decrease MVO2 demand?

A
  • decrease preload, contractility, HR
84
Q

Pharmacological Treatment of Angina

How do calcium channel blockers increase MVO2 supply?

A
  • increase coronary blood flow via vasodilation
  • decrease coronary vasospasm