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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
Cause of ischemia
Mechanical, biochemical and electrical disturbances --> decreased myocardial oxygen tension --> inadequate perfusion
26
Effects of ischemia
``` Regional disturbance of ventricular contractility Segmental hypokinesia Segmental akinesia Segmental dyskinesia Reduced myocardial pump function ```
27
So the heart cannot function properly:
Dramatic decreased BP | Hyperperfusion in the brain (loss of consciousness)
28
Transient left ventricle failure
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
29
Transient ischemia leads to
Angina pectoris
30
Prolong ischemia leads to
Acute MI (necrosis; irreversible damage)
31
What is happening when you have ischemia?
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
32
EKG in ischemia
Helps to determine if it is ischemia or MI Acute vs chronic Extent (entire thickness or partial) Location
33
Partial Ischemia
Probelms with repolarization | ST depression
34
Entire thickness ischemia
ST elevation
35
Ischemia Arrhythmias
Electrical instability which may lead to isolated ventricular premature beats or even ventricular tachycardia or fibrillation
36
Sudden death from IHD caused by
Ischemia-induced ventricular tachyarrhythmias
37
Asymptomatic
No clinical manifestations despite exercise induced EKG changes, coronary artery plaques and scars secondary to MI
38
Symptoms
Chest discomfort due to angina pectoris or acute MI
39
Progressive IHD
Symptoms are currently more often or occur after exercise so they decrease their exercise but the symptoms keep coming
40
Acute Coronary Syndromes (ACS)
``` Acute MI with STEMI and Q wave Unstable angina, non-ST elevation NSTEMI, no Q wave Sudden cardiac death Prinzmetal's Variant Angina ```
41
P wave
Reflects the initial stimulation of impulses from atria to ventricle
42
QRS =
Depolarization of ventricles
43
ST
``` Depression = ischemia Elevation = IHD, MI or angina ```
44
Q wave
Represents the normal left to right depolarization
45
IHD + Atherosclerosis
Narrowing of the lumen, decreased blood flow --> ischemia is prevalent
46
IHD + Plug
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
Partial occlusion represents
Unstable angina pectoris or NSTEMI
48
Thormbus healing represents
Chronic coronary artery disease or stable angina pectoris
49
Complete occlusion =
STEMI
50
Partial occlusion =
NSTEMI or unstable angina
51
Stable Angina Pectoris
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
Stable Angina Pectoris Clinical Manifestations
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
Symptoms of MI other than angina
Dyspnea Nausea Fatigue Faintness
54
Indication of UA
Angina occuring with less exertion than in the past Occuring at rest Awakening the patient from sleep
55
Intermittent claudication Stroke TIA - things to ask
FH of premature IHD DM, hyperlipidemia, HTN Smoking RF for atherosclerosis
56
Physical Exam
Search for evidence of atherosclerotic disease at other sites Xanthomas Ophtalmologic examination of HTN Anemia, thyroid disease (lipid abnormalities) Cardiac enlargment Systolic murmur
57
Carotid arterial bruits
Noise at the carotid artery bc of decreased flow
58
Lab Exams
``` Urine for DM Cholesterol A1c Creatinine Hct Thyroid Xray Protein C EKG Stress test ```
59
Define NSTEMI/UA
Angina pectoris or equivalent ischemic discomfort with at least one of three features
60
Features is NSTEMI/UA
Occurs at rest for 10 minutes or more Sever and new onset Occurs with a crescendo pattern
61
NSTEMI/UA Pathophysiology
Athersclertic plaque rupture or erosin with a nonocclusive thrombus Progressive mechanical obstruction Secondary to increased myocardial oxygen demand or decreased supply
62
NSTEMI/UA Manifestations
Severe chest pain Dyspnea and epigastric discomfort Pale cool skin, sinus tachycardia, third or fourth hear sound, hypotension
63
NSTEMI/UA Biomarkers
CKMB and troponin: elevation = NSTEMI | Troponin elevation = CHF, myocarditits, PE or false positives
64
Why are CKMB and troponin increases seen?
Myocardial destruction releases them
65
STEMI
Myocardial cell death due to prolong and severe ischemia | - Complete occlusion by thrombus
66
STEMI Pathophysiology
Thrombotic occlusion previously affected by atherosclerosis Thrombus develops rapidly Plaque ruptures
67
Plaques prone to disruption:
Rick lipid core and thin fibrous cap | Increased amount of inflammatory cells
68
Extent of damage
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
STEMI RF
Multiple coronary RF UA Hypercoagulability Collagen vascular disease (autoimmune disorder) Cocaine abuse Intracardiac thrombi (sluggish blood flow) Coronary emboli
70
STEMI Clinical manifestations
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
STEMI Physical Findings
``` Substernal chest pain >30 minutes + diaphoresis Tachycardia/HTN (anterior MI) Bradycardia/HypOTN (inferior MI) Pericardial friction rub Fever Systolic pressure decline ```
72
STEMI EKG
ST elevation | Q wave present
73
STEMI Biomarkers
Troponin Troponin-1 CK CKMB
74
MI is
the most common form of IHD | Deaht of cardiac muscle due to prolong severe ischemia
75
STEMI =
Transmural infarction Entire thickness ST elevation
76
NSTEMI =
Subendocardial infarction Partial thickness ST depression
77
If a patient dies within 24 hours...
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
Day 3-4 after MI
Inflammatory changes are prominent | Lack of nuclei can be seen
79
Day 7-10 after MI
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
Day 10-weeks after MI
Repair process leads to scar tissue made of collagen
81
Reperfusion
Restore circulation to the tissue | - Not always a good thing!
82
Reperfusion can lead to:
Arrhythmias, hemorrhage, prolong ischemic function
83
Preconditioning is
preparing the tissue for repetitive ischemia to occur
84
If ischemia is longer and reperfusion occurs after 2-4 hours,
the tissue will be nectrotic but some of it can be healthy after time
85
Complications of MI + mortality
30% mortality rate now down to 7% mortality rate if patient receiving therapy timely
86
Arrhythmias are the:
Most common cause of pre-hospital death
87
Papillary muscle dysfunction leads to
Mitral regurgitation
88
Cardiac tamponade
Accumulation of blood in the pericardium
89
Cerebrovascular Disease
Dealing with changes in the nervous tissue in the brain due to vascular changes such as thrombosis, embolism, hemorrhage
90
Thrombosis, embolism, hemorrhage are all related to
atherosclerosis and HTN
91
Thrombosis and embolism
Decreased blood supply to the CNS leading to ischemia (infarction), hypoxia and tissue damage
92
Hemorrhage
Rupture of blood vessel walls
93
Global cerebral ischemia
Affects the entire brain Leads to systemic issues Can cause: cardiac arrest, shock, sever hypotension
94
Focal cerebral ischemia
One area of the brain | Caused by: embolic occlusion, thrombotic occlusion, vasculitis, atherosclerosis
95
Mild cases of ischemia
Post-ischemic confusional state followed by complete recovery
96
Sever cases of ischemia
Death or vegetative state
97
Hemorrhagic:
Emboli
98
Nonhemorrhagic:
Thrombosis

Cardio Exam 2 (10 decks)

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