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Cardio Exam 2 > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

Define IHD

A

Condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium

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2
Q

IHD typically occurs when

A

there is an imbalance between myocardial oxygen supply and demand

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3
Q

Most common cause of IHD is

A

atherosclerotic disease of an epicardial coronary artery or arteries sufficient enough to cause a decrease in blood flow and perfusion

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4
Q

Symptoms of IHD

A

may not appear until someone exerts themselves

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5
Q

What RF are associated with the emergence of IHD

A

Genetics
High fat and energy-rich diet
Smoking
Sedentary lifestyle

Obesity
Insulin resistance
T2DM

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6
Q

Myocardial oxygen demand =

A

Oxygen delivery

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7
Q

Oxygen problems

A

No oxygen = ischemia

Anemia = less oxygen carrying capacity

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8
Q

Define Hypoxia

A

Lack of oxygen

Exacerbates effects of atherosclerosis

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9
Q

Example of Hypoxia

A

Anemia
Cyanotic heart disease (abnormal connection between left and right heart –> lack of blood)
Advanced lung disease (problems with oxygenating the blood)

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10
Q

MVO2 Demaind

A 
Heart rate
Myocardial contractility
Myocardial wall tension (stress)
BP
Inotropic status
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11
Q

Satisfactory level of oxygen-carrying capacity determined by:

A

Inspired level of oxygen
Pulmonary function
Hgb concentration and function

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12
Q

Coronary Blood Flow & 3 arteries where 75% of total resistance occurs

A

Blood flows through the coronary arteries, majority during diastole

  1. Large epicardial arteries (R1)
  2. Prearteriolar vessels (R2)
  3. Arteriolar and intramyocardial capillary vessels (R3)
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13
Q

Major determinants of coronary resistance is

A 
Prearteriolar vessels (R2)
Arteriolar and intramyocardial capillary vessels (R3)
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14
Q

Metabolic regulation

A

Exercise
Emotional stress (coronary vascular resistance)
Muscles –> aerobic –> lactic acid –> decrease pH –> affects size of blood vessels

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15
Q

Auto regulation

A

Coronary blood flow is maintained on the same level, independently on physiologic alterations in BP
Protective mechanisms

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16
Q

Where would the most myocardium be affected?

A

Left coronary artery atherosclerosis

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17
Q

Rupture of atherosclerotic plug

A

Fibrosis cap breaks which leads to tissue factor that is normally separate from the blood to be exposed
TF initiates coagulation leadign to a thrombus which leads to narrowing of blood vessels, complete occlusion, or resolve

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18
Q

Spasm of a atherosclerotic plug

A

Sudden contraction of the coronary arteries –> Prinzmetal’s angina

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19
Q

Define Emboli

A

Blockage of the blood vessels and related to a thrombosis

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20
Q

Where does coronary atherosclerosis occur?

A

Sites of increased turbulence in coronary flow

Branch points in the epicardial arteries

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21
Q

Coronary atherosclerosis RF

A 
High LDL
Low HDL
Smoking
HTN
DM
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22
Q

50% Stenosis

A

Limited ability to increase blood flow in the response to an increased demand

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23
Q

80% stenosis

A

Blood flow at rest may be reduced

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24
Q

Stenosis that are hazardous?

A

Left main coronary artery or proximal left anterior descending coronary artery

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25
Q

Cause of ischemia

A

Mechanical, biochemical and electrical disturbances –> decreased myocardial oxygen tension –> inadequate perfusion

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26
Q

Effects of ischemia

A 
Regional disturbance of ventricular contractility
Segmental hypokinesia
Segmental akinesia
Segmental dyskinesia
Reduced myocardial pump function
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27
Q

So the heart cannot function properly:

A

Dramatic decreased BP

Hyperperfusion in the brain (loss of consciousness)

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28
Q

Transient left ventricle failure

A

Heart is pumping blood to the aorta but the blood is coming back to the atrium –> Left sided heart failure –> see problems in the pulmonary circulation

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29
Q

Transient ischemia leads to

A

Angina pectoris

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30
Q

Prolong ischemia leads to

A

Acute MI (necrosis; irreversible damage)

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31
Q

What is happening when you have ischemia?

A

Less energy production
Lactic acid production
Time: If the ischemia si very short, you might not have a MI but it is last 2-4 hours you will have cell death and MI
More time = more damage

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32
Q

EKG in ischemia

A

Helps to determine if it is ischemia or MI
Acute vs chronic
Extent (entire thickness or partial)
Location

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33
Q

Partial Ischemia

A

Probelms with repolarization

ST depression

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34
Q

Entire thickness ischemia

A

ST elevation

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35
Q

Ischemia Arrhythmias

A

Electrical instability which may lead to isolated ventricular premature beats or even ventricular tachycardia or fibrillation

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36
Q

Sudden death from IHD caused by

A

Ischemia-induced ventricular tachyarrhythmias

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37
Q

Asymptomatic

A

No clinical manifestations despite exercise induced EKG changes, coronary artery plaques and scars secondary to MI

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38
Q

Symptoms

A

Chest discomfort due to angina pectoris or acute MI

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39
Q

Progressive IHD

A

Symptoms are currently more often or occur after exercise so they decrease their exercise but the symptoms keep coming

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40
Q

Acute Coronary Syndromes (ACS)

A 
Acute MI with STEMI and Q wave
Unstable angina, non-ST elevation
NSTEMI, no Q wave
Sudden cardiac death
Prinzmetal's Variant Angina
41
Q

P wave

A

Reflects the initial stimulation of impulses from atria to ventricle

42
Q

QRS =

A

Depolarization of ventricles

43
Q

ST

A 
Depression = ischemia
Elevation = IHD, MI or angina
44
Q

Q wave

A

Represents the normal left to right depolarization

45
Q

IHD + Atherosclerosis

A

Narrowing of the lumen, decreased blood flow –> ischemia is prevalent

46
Q

IHD + Plug

A

Starts with platelet aggregation (adhere to endothelial)
Clot can lead to fully developed thrombus
Thrombus healing can lead to more narrowing or thrombus continues to grow and occludes the vessel –> MI

47
Q

Partial occlusion represents

A

Unstable angina pectoris or NSTEMI

48
Q

Thormbus healing represents

A

Chronic coronary artery disease or stable angina pectoris

49
Q

Complete occlusion =

A

STEMI

50
Q

Partial occlusion =

A

NSTEMI or unstable angina

51
Q

Stable Angina Pectoris

A

Male over 50 Women over 60
Chest discomfort
Typically places a hand over the sternum
Crescendo (loud and fast)-decrescendo (2-5 min)
Can radiate to either shoulder and to both arms

52
Q

Stable Angina Pectoris Clinical Manifestations

A

Arises in the back, root of the neck, jaw, teeth, epigastrium
Typically caused by exertion or emotions
Symptoms are relieved by rest or sublingual nitroglycerin

53
Q

Symptoms of MI other than angina

A

Dyspnea
Nausea
Fatigue
Faintness

54
Q

Indication of UA

A

Angina occuring with less exertion than in the past
Occuring at rest
Awakening the patient from sleep

55
Q

Intermittent claudication
Stroke
TIA
- things to ask

A

FH of premature IHD
DM, hyperlipidemia, HTN
Smoking
RF for atherosclerosis

56
Q

Physical Exam

A

Search for evidence of atherosclerotic disease at other sites
Xanthomas
Ophtalmologic examination of HTN
Anemia, thyroid disease (lipid abnormalities)
Cardiac enlargment
Systolic murmur

57
Q

Carotid arterial bruits

A

Noise at the carotid artery bc of decreased flow

58
Q

Lab Exams

A 
Urine for DM
Cholesterol
A1c
Creatinine
Hct
Thyroid
Xray
Protein C
EKG
Stress test
59
Q

Define NSTEMI/UA

A

Angina pectoris or equivalent ischemic discomfort with at least one of three features

60
Q

Features is NSTEMI/UA

A

Occurs at rest for 10 minutes or more
Sever and new onset
Occurs with a crescendo pattern

61
Q

NSTEMI/UA Pathophysiology

A

Athersclertic plaque rupture or erosin with a nonocclusive thrombus
Progressive mechanical obstruction
Secondary to increased myocardial oxygen demand or decreased supply

62
Q

NSTEMI/UA Manifestations

A

Severe chest pain
Dyspnea and epigastric discomfort
Pale cool skin, sinus tachycardia, third or fourth hear sound, hypotension

63
Q

NSTEMI/UA Biomarkers

A

CKMB and troponin: elevation = NSTEMI

Troponin elevation = CHF, myocarditits, PE or false positives

64
Q

Why are CKMB and troponin increases seen?

A

Myocardial destruction releases them

65
Q

STEMI

A

Myocardial cell death due to prolong and severe ischemia

- Complete occlusion by thrombus

66
Q

STEMI Pathophysiology

A

Thrombotic occlusion previously affected by atherosclerosis
Thrombus develops rapidly
Plaque ruptures

67
Q

Plaques prone to disruption:

A

Rick lipid core and thin fibrous cap

Increased amount of inflammatory cells

68
Q

Extent of damage

A

Territory supplied by affected vessel
Extent of occlusion
Duration of occlusion
Quantity of blood supplied to affected tissue
Demand for oxygen of the myocardium whose blood supply is limited
Endogenous factors that can produce early spontaneous lysis of the occlusive thrombus

69
Q

STEMI RF

A

Multiple coronary RF
UA
Hypercoagulability
Collagen vascular disease (autoimmune disorder)
Cocaine abuse
Intracardiac thrombi (sluggish blood flow)
Coronary emboli

70
Q

STEMI Clinical manifestations

A

Pain is deep and visceral (heavy, squeezing, crushing)
Occurs at rest, more sever and last longer that AP
Anxiety, N/V
Make sure its not something else

71
Q

STEMI Physical Findings

A 
Substernal chest pain >30 minutes + diaphoresis
Tachycardia/HTN (anterior MI)
Bradycardia/HypOTN (inferior MI)
Pericardial friction rub
Fever
Systolic pressure decline
72
Q

STEMI EKG

A

ST elevation

Q wave present

73
Q

STEMI Biomarkers

A

Troponin
Troponin-1
CK
CKMB

74
Q

MI is

A

the most common form of IHD

Deaht of cardiac muscle due to prolong severe ischemia

75
Q

STEMI =

A

Transmural infarction
Entire thickness
ST elevation

76
Q

NSTEMI =

A

Subendocardial infarction
Partial thickness
ST depression

77
Q

If a patient dies within 24 hours…

A

It is hard to determine if there is tissue necrosis or not because all that occurs is a change in the myocyte shape but not a loss of nuclei

78
Q

Day 3-4 after MI

A

Inflammatory changes are prominent

Lack of nuclei can be seen

79
Q

Day 7-10 after MI

A

Macrophages are coming into the damaged tissue and removing necrotic tissue
new blood vessels are being formed
Elevated fibroblast can be see
Tissue is called Granulation tissue

80
Q

Day 10-weeks after MI

A

Repair process leads to scar tissue made of collagen

81
Q

Reperfusion

A

Restore circulation to the tissue

- Not always a good thing!

82
Q

Reperfusion can lead to:

A

Arrhythmias, hemorrhage, prolong ischemic function

83
Q

Preconditioning is

A

preparing the tissue for repetitive ischemia to occur

84
Q

If ischemia is longer and reperfusion occurs after 2-4 hours,

A

the tissue will be nectrotic but some of it can be healthy after time

85
Q

Complications of MI + mortality

A

30% mortality rate now down to 7% mortality rate if patient receiving therapy timely

86
Q

Arrhythmias are the:

A

Most common cause of pre-hospital death

87
Q

Papillary muscle dysfunction leads to

A

Mitral regurgitation

88
Q

Cardiac tamponade

A

Accumulation of blood in the pericardium

89
Q

Cerebrovascular Disease

A

Dealing with changes in the nervous tissue in the brain due to vascular changes such as thrombosis, embolism, hemorrhage

90
Q

Thrombosis, embolism, hemorrhage are all related to

A

atherosclerosis and HTN

91
Q

Thrombosis and embolism

A

Decreased blood supply to the CNS leading to ischemia (infarction), hypoxia and tissue damage

92
Q

Hemorrhage

A

Rupture of blood vessel walls

93
Q

Global cerebral ischemia

A

Affects the entire brain
Leads to systemic issues
Can cause: cardiac arrest, shock, sever hypotension

94
Q

Focal cerebral ischemia

A

One area of the brain

Caused by: embolic occlusion, thrombotic occlusion, vasculitis, atherosclerosis

95
Q

Mild cases of ischemia

A

Post-ischemic confusional state followed by complete recovery

96
Q

Sever cases of ischemia

A

Death or vegetative state

97
Q

Hemorrhagic:

A

Emboli

98
Q

Nonhemorrhagic:

A

Thrombosis

Cardio Exam 2 (10 decks)

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