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Pt.2 PHRM/PHYS/NS > week 4: Perfusion - Coronary Artery Disease > Flashcards

week 4: Perfusion - Coronary Artery Disease Flashcards

1
Q

perfusion is the flow of the blood through arteries and capillaries delivering nutrients

A

true

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2
Q

cardiac circulation : review

top of the heart

bottom of the heart

A

broader base

bottom of the heart- apex, points down to the left

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3
Q

cardiac circulation : review

superior/inferior vena cava
pulmonary arteries
pulmonary veins

A

superior/inferior vena cava - return unoxygenated blood to the heart

pulmonary arteries - carries venous blood to the lungs

pulmonary veins- return freshly oxygenated blood to the left side of the heart

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4
Q

atrioventricular (AV) valves : what undergoes it

A

Tricuspid valve - right AV

Mitral valve- left AV

open during diastole ( ventricles fill with blood )

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5
Q

semilunar valves:
what undergoes it

A

pulmonic valve
aortic valve
open during systole

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6
Q

seminar valves :
pulmonic valve
aortic valve
open during systole
and describe it

A

pulmonic valve- right side

aortic valve - left side

open during systole ( blood ejected from the heart )

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7
Q

hemodynamics : review
SATA within the systemic circulation:
arteries supply tissues of the body with nutrient and oxygen rich blood

veins return blood to pulmonary circulation

LA/LV to aorta to body and back to RA/RV

A

all is true

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8
Q

hemodynamics review : pulmonary circulation

define what undergoes this

A

ra/rv pulmonary artery to lungs pulmonary veins to LA/LV

re-oxygenated and returned to systemic circulation

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9
Q

___ carries oxygenated blood ( give description on this )

A

arteries

carries oxygenated blood ( this is very bright red high pressure system ) –> the system that brings oxygen to tissues

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10
Q

this is carrying the deoxygenated blood which makes it a darker colour of blood

A

veins

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11
Q

Mechanical Properties : consists of what ?

A

this consists of mechanical and electrical

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12
Q

this is the amount of blood ejected by the left ventricle during each contraction

A

stroke volume

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13
Q

what is the hearts main goal ?

A

the hearts main goal is pump blood to other tissues maintaining perfusion

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14
Q

how well the heart can perfuse other tissues is measured through what ?

A

cardiac output

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15
Q

CO= HR x SV
3- 6 L/min in adult is this true or false.

A

this is true

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16
Q

what does preload and afterload influence?

A

this influences stoke volume and cardiac output

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17
Q

The heart will adjust to the needs of the body by increasing what ? ( for example : FIT workout or high incline workout this will be tough and because the body tissues need more perfusion the what is going to meet this demand ) ?

A

cardiac output

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18
Q

An increase volume and increase stretch and increase in SV is what law ?

A

frank starling law

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19
Q

Is this statement true or false.

The stimulation of our sympathetic nervous system will increase out heart rate and the stimulation of our Parasympathetic system will slow it down.

A

true

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20
Q

what are the five factors affecting cardiac output

A

cardiac contractility
heart rate
preload ( stretch )
afterload ( squeeze )
blood volume

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21
Q

Mechanical Properties “
preload and afterload quickly explain what they mean

A

preload - volume of blood in the ventricles at the end of diastole ( end diastolic pressure )

afterload - resistance left ventricle must overcome to circulate blood

increased in :
hypertension
vasocontriction

increase in afterload means increase in cardiac workload

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22
Q

electrical properties : what should we regulate ?

A

we should regulate heart rate and rhythm

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23
Q

electrical properties :cardiac muscle cells have the following properties

A

excitability
conductivity
contractility
refractoriness

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24
Q

when there is a decrease perfusion an area of the heart and cardiac heart cells dysrhythmias ( this calls for cardiac output and life threatening ). is this true or false?

A

true

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25
Q

What is SA ?

A

normally sets the rhythm of the heart rate ( natural peacemaker of the heart )

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26
Q

true or false. Heart needs its own oxygen to supply in order to function. They get it from the coronary arteries

A

true

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27
Q

this is an artery that feeds the front side of the heart

A

LAD ( left anterior descending )

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28
Q

this is around the heart lateral and posterior circumflex artery , where there is a disease, it interrupts the blood flow and feeding , anything distal = interrupted

A

left main coronary artery

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29
Q

coronary circulation

coronary artery : explain the supplies that undergoes right coronary artery and what blockage in this area can cause…

A

supplies : R atrium, R ventricle & part of LV ( interior ) , SA node, AV node, Bundle of His

blockage in this area can cause : RV failure
bradycardia heart block

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30
Q

coronary circulation :
coronary artery : left anterior descending ( LAD )

what are the supplies and what blockage in this area can cause ?

A

supplies : anterior wall of LV
Heart valves

Blockage in this area can cause : LV failure, dysrhthimias. highest mortality rate

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31
Q

coronary circulation :

coronary artery : circumflex

what are the supplies and what blockage in this area can cause ?

A

Supplies :
L Atrium
Lateral & Posterior walls of LV
SA node (50%)

blockage can cuase : LV failure *Dysrhythmias

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32
Q

LAD has the worst outcomes, and impact the ventricle ( main powerhouse ) for the perfusion which leads into left sided heart failure , life threatening dysrhythmias

A

true

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33
Q

what are the two kinds of chlosterol?

A

low density lipoprotein (LDL)
high density lipoprotein (HDL)

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34
Q

select all that apply regarding chlosterol:
Water-insoluble fat, must be bound to lipoproteins in the plasma (HDL, LDL)

Used in plasma membranes and to build Vitamins and Hormones

A

truuu

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35
Q

what are lipids made up (3 different)

A

chlosterol, triglycerides, phospholipids

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36
Q

what does cholestrol lead to?

A

cholesterol - chylomicrons - vldl and hdl - vldl leads to ldl

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37
Q

what does triglycerides lead to?

A

triglycerides - fatty acids - saturated and unsaturated; unsaturated leads to monounsaturated - oleic acid and polyunsaturated - omega 3, omega 6, linoleum acid

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38
Q

what is an ldl?

A
  • majority of cholesterol in blood and most strongly associated with CAD risk
  • Causes of LDL thought to include diet high in lipids, saturated fatty acids, and cholesterol
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39
Q

what is an hdl?

A
  • reduces risk of CAD by removing cholesterol from LDL and stabilizing plaques
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40
Q

what is the goal in terms of cholesterol ?

A

reduce LDL’s and higher HDL’s

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41
Q

true or false regarding Hdl’s: It will actually reduce the risk of heart disease by removing cholesterol from the peripheral tissues and returning them back to the liver where it is disposed of,
which helps in stabilizing plaques.

A

true

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42
Q

what is the consequences of low perfusion?

A

myocardial ischemia - result increase oxygen demand or decrease o2 supply

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43
Q

true or false: When a person has narrowed coronary arteries, it reduces
supply of oxygen to the heart muscle. This leads to myocardial ischemia.

A

true

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44
Q

what are the clinical manifestations of CAD?

A

Stable angina pectoris (typical angina)
Silent ischemia (symptomless ischemia)
Unstable angina
Acute myocardial infarction (heart attack)
Heart failure

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45
Q

what is the first sign of CAD?

A

1st sign - ischemia, causes pain, managed by meds and rest, ALWAYS a warning sign that blood flow to heart muscle is reduced

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46
Q

what are the clinical manifestations of CAD - angina?

A

Angina Pectoris (chest pain)
* Angina is referred cardiac pain that results from ischemia
* Not everyone with ischemia develops angina (ex: silent ischemia)
* Various pain patterns (see below)
* May be described as pressure, aching, heaviness or squeezing
* Atypical symptoms: indigestion, aching jaw, fatigue, shortness of breath, dizziness, generalized anxiety, weakness, flu-like symptoms (often experienced by Women, Older adults)
* Adults over 80 may experience disorientation or acute confusion

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47
Q

what is atypical symptoms of angina?

A

indigestion, aching jaw, fatigue, shortness of breath, dizziness, generalized anxiety, weakness, flu-like symptoms (often experienced by Women, Older adults)

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48
Q

true or false: * Adults over 80 may experience disorientation or acute confusion

A

true

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49
Q

what does chronic stable angina mean?

A

Brought on by moderate to prolonged exertion
Pattern is predictable
Frequency, duration and intensity constant over months Only slight limitation of activity
Associated with a STABLE plaque
managed with nitrates

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50
Q

what is vasospastic angina?

A

Used to be called Prinzmetal or
variant angina
* Rare
* Angina due to vasospasm
* Triggers include cocaine, meds (migraine, chemo), magnesium deficiency, allergic reaction
very scary in young children

51
Q

what are some manifestations of ischemia in CAD?

A

every organ needs oxygen to function
1) Angina pectoris
“Chest squeeze”
2) Diastolic and Systolic Dysfunction
Failure of heart to relax and fill properly
Results in shortness of breath (dyspnea)
3) Electrical disturbances
ECG changes (ST depression)

52
Q

what does the heart layers consist of from inner to outer?

A

epicardium, visceral pericardium, pericardial space and parietal pericardium

53
Q

what are factors that determine collateral circulation?

A

genetic disposition
chronic ischemia

54
Q

anyone who doesn’t have this circulation or if they have any type of heart attack will turn into a lethal situation because they do not have those bypasses

A

collateral circulation

55
Q

These are bypasses that develop

A

collateral circulation

56
Q

vasospasm ( quick narrowing happening in thier artery ) closes artery which results in no blood that follows ( cocaine could be an example or certain drugs )

A

collateral circulation has been disrupted.( arterial occlusion is rapid )

57
Q

True or false. Chronic ischemia could extended the years of survival ?

A

true, they have years of reduced blood flow, that will have collateral develop, they have a better chance of survival because of this circulation

58
Q

true or false. Genetics ( somehow who has a history of hypercholesterol anemia ) doesn’t allow collateral to develop making them die in their early 20s.

A

true

59
Q

Coronary artery disease : what is it ?

A

reduction of blood flow to the heart muscle primary muscle.

60
Q

true or false. Plaque build up also affect large arteries as well

A

true

61
Q

Coronary after disease : name all the characteristics

A

most common form of heart disease

also called coronary heart disease, or ischemic heart disease

62
Q

what is the primary cause of CAD?

A

atherosclerosis

63
Q

Atherosclerosis: what is it ?

A

this is injury of the blood vessels that causes inflammation plaque in the arterial wall

64
Q

what is the definition of atherosclerosis ?

A

formation of fatty, fibrous plaque within the intima layer of the artery

65
Q

this progresses for years until the disease is detected, could appear in childhood non actual symptoms ( at this point significant of narrowing the artery begin to develop )

A

atherosclerosis

66
Q

true or false. Atherosclerosis is usually asymptomatic ?

A

true

67
Q

SATA : ATHEROSCLEOROSIS

> 75 % occlusion- signs of ischemia with exertion

90% occlusion - ischemia at rest

A

all

68
Q

role of endothelium : what is the tunica intima

A

tunica intima is the inner most layer made of endothelium

69
Q

endothelium have many funcitons such as what ?

A

serves a barrier from coming into contact in toxins allowing blood to flow without allowing to stick the vessel

70
Q

role of endothelium : define all of them

A

lines the blood vessels

separate the blood stream from the artery wall, preventing substances from the blood from moving into the blood vessel wall

atherosclerosis beings with a small injury to the endothelium lining

71
Q

atherosclerosis : The stages : how many stages are there ?`

A

4 stages

72
Q

how does atherosclerosis occur ? in the first stage

A

begins damage with the endothelial layer, tear in the lining breaks the barrier allowing LDL from the bloodstream to enter the intima layer to initiates an inflammatory process,

monocytes then move to the area and transform to macrophages adjust the ldl until become full and die

73
Q

Fatty streak stage 2 of atherosclerosis : what is occuring ?

A

after the first stage , foam cells create fatty streaks, which is the earliest lesions of atherosclerosis ( this is asymptomatic atp, around age of 15 -> lumpy and more turbulent flow

74
Q

Fibrous plaque ( stage 3 of atherosclerosis )

more prominenet ( age 30)

A

fibrous plaque stage platelets and ldls are released

platelets derived growth factor which stimulates smooth muscle vibration and thickening of arterial wall

collagen and elastic is released creating collagen cap or fibrous cap over the lipid pool this change causes hardening and thickening of the artery and taking up space and impairing blood flow

75
Q

true or false. Complicated lesion is the worst scenario amongst all the stages of atherosclerosis. Define why

A

true , this is the most scary as the fibrous grows, this can become damage,
and become unstable.

It can rupture fibrous plaque and once this is ruptured it exposes the artery in our wall , platelets will rush creating a thrombus and if this is not remove –> lead to cell death

76
Q

What trigger the inflammatory process?

A

when it cause injury to he endothelium
such as HTN
tobacco use , hyperlipidemia, diabetes, homocysteinemia, viruses and toxins

77
Q

triggers Inflammatory to the endothelial cell layer of the artery can be physical or chemical

A

yes true

78
Q

describe why hypertension and tobacco use can be trigger the inflammatory process ?

A

HTN = cause physical damage of the turbulent flow

Tobacco use - nicotine causes the release of epi, catecholamines, this causes vasconstric. which causes the heart BP to be elevated –> endothelial injury this also increases LDL

79
Q

explain why hyperlipidemia and diabetes can trigger inflammatory process

A

hyperlipidema - high levels of LDL, causes damage to the vessel wall ( chemical injury )

diabetes - causes arterial damage

80
Q

explain why homocysteinemia and viruses and toxins can trigger inflammatory process

A

Homocysteinemia - this results from inherited metabolic defect , which leads to very high levels of homocysteine ( high levels is toxic to endothelium )

viruses and toxins- leads to damage ( injury to endothelium

81
Q

CAD : What are the risk factors ?
what are non modifiable and modifiable

A

non modifiable - increasing age
male > female
family history

modifiable - elevated serum lipid levels
HTN
Tobacco use
physical inactivity
obesity
psychological risk factors

82
Q

true or false. People who are born female until the age around is ‘protected from cardio disease’ explain why ?

A

true, because they have estrogen, and estrogen is cardio protective ( it has an anti-inflammatory blood vessels )

83
Q

true or false. The older you are, the higher the risk ( which comes down to plaques ) build up over time as we age and it becomes higher )

A

true

84
Q

hyperlipidemia and adipose tissue does causes insulin resistance ,one of the most crucial things is to manage blood sugars. true or false.

A

true

85
Q

Physical inactivity is associated with what?

A

associated with high blood pressure and cholesterol

86
Q

what is the other risk factors that can lead to cad

A

dm
elevated homocysteine levels

87
Q

clinical manifestations of angina?

A

Angina Pectoris (chest pain)

  • Angina is referred cardiac pain that results from ischemia
  • Not everyone with ischemia develops angina (ex: silent ischemia)
  • Various pain patterns (see below)
  • May be described as pressure, aching, heaviness or squeezing
  • Atypical symptoms: indigestion, aching jaw, fatigue, shortness of breath, dizziness, generalized anxiety, weakness, flu-like symptoms (often experienced by Women, Older adults)
  • Adults over 80 may experience disorientation or acute confusion
88
Q

what is acute coronary syndrome?

A

Prolonged myocardial ischemia and not immediately reversible
➢Associated with unstable plaque which ruptures (thrombus forms)
➢Typically coronary artery is >90% occluded
➢Patients with ACS need immediate hospitalization

89
Q

what is this? Prolonged myocardial ischemia and not immediately reversible
➢Associated with unstable plaque which ruptures (thrombus forms)

A

acute coronary syndrome

90
Q

true or false regarding acute coronary syndrome: If it becomes too unstable, it can rupture. When a fibrous plaque ruptures or breaks off, it exposes the arteries, inner wall and platelets will rush to the site creating a thrombus. If this thrombus is not removed, it will lead to occlusion and cell death

A

true

91
Q

ACS: unstable angina (USA)

A

Chest pain that is new, occurs at rest, or is worsening, usually lasts 15-20 minutes (pattern change)
* Often not responsive to rest or medication (nitro spray)
* Most commonly related to rupture of stable atherosclerotic plaque and partial occlusion by thrombus (clot may dissolve or could progress to infarction)

92
Q

what is this: unstable plague that fully includes an artery

A

STEMI

93
Q

what is this describing: Most commonly related to rupture of stable atherosclerotic plaque and partial occlusion by thrombus (clot may dissolve or could progress to infarction)
person could be sleeping or resting

A

ACS - unstable angina

94
Q

what is acute coronary syndrome: MI? what are the two kinds

A

Plaque rupture and thrombus formation
* Cardiac cells can tolerate ischemia for 20 minutes before cell death begins
Necrosis begins on the endocardial surface (inside) and progresses to the pericardial surface (outside)

STEMI - full thickness infarction of ventricle
* NSTEMI - partial thickness infarction ventricle

95
Q

Prolonged ischemia leads to irreversible
dysfunction: what does this referred to ?

A

acute coronary syndrome: myocardial infarction

96
Q

what is this referring to? 100% occlusion EMERGENCY!!

A

STEMI

97
Q

what does this refer to: The sub endocardial surface will begin to die. Then it will progress out to the entire
thickness of the heart muscle. It takes about 6 h to progress across the entire
thickness of the ventricle wall.

A

acute coronary syndrome: myocardial infarction

98
Q

what are the manifestations of myocardial infarction?

A

chest pain: Severe, immobilizing, radiating to left arm (or other patterns)
* Usually in morning, at rest, last longer then 20 minutes, dyspnea: * See resp assessment

Atypical symptoms: weakness, fatigue,
anxious, dizziness
Older patients: sudden onset confusion, more likely to have atypical symptoms

99
Q

what are the manifestations of the skin, CVS, resp, GI, other in terms of myocardial infarction?

A

Chest Pain
* Severe, immobilizing, radiating to left arm (or other patterns)
* Usually in morning, at rest, last longer then 20 minutes
Dyspnea
* See resp assessment
Atypical symptoms: weakness, fatigue,
anxious, dizziness
Older patients: sudden onset confusion, more likely to have atypical symptoms
Skin:
* ashen, cool, and diaphoretic (SNS) CVS:
* Initially ↑HR and ↑ BP but with ↓ CO then ↓BP
* Dysrhythmias Respiratory:
* Dyspnea, ↑ RR, crackles, O2sats
* Nausea and vomiting (common in Inferior MI/Pain)
* Fever up to 389 could last for a week (inflammation caused by myocardial cell death)

100
Q

serum cardiac enzymes : describe what this contributes

A

Release of cardiac-specific enzymes when muscles die and release their contents

  • Detection of serum cardiac enzymes help with diagnosis
101
Q

what is important when it comes to diagnosing an MRI because they tell us there is a cardiac damage ?

A

serum cardiac enzymes

102
Q

true or false. Unstable angina patient will not have a change in troponin levels but may present with ST changes on ECG, troponin will be elevated and in both STEMI and NONSTEMI

A

true

103
Q

what is troponin? what is this one specific for ?

A

troponin is a myocardial muscle protein that is release with injury to cardiac muscle , it peaks and remains elevated for a long time and

this one is specific rises 3 to 12 hours after onset of an MI and peaks at 24 to 48 hours and return to normal in 5 to 14 days

104
Q

what cardiac enzymes do we usually look at ?

A

ck and troponin this is the most reliable

105
Q

this is the third major cardiac enzyme and it’s released within a few hours but its not specific to the heart and baseline

A

myoglobin

106
Q

_____ rises 3 to 12 hours after onset there’s a delay in peak time 24 hours and then return to normal within 2 to 3 days

A

creatine cardiac enzyme

107
Q

Myocardial Infarction: The Healing
Process define how the body heals

A

inflammation is body’s response to cell death

Neutrophils and macrophages remove all necrotic tissue in 2-3 days
(wall is thin and unstable)

  • Collateral circulation may limit area of injury
  • Over 2-3 months, scar tissue has replaced necrotic tissue (cannot contract)
  • Necrotic zone identified by EKG changes (Q wave)
  • Healthy myocardium hypertrophies and dilates as compensation (remodeling) and this can lead to heart failure
108
Q

select all that applies within the myocardial infraction: healing process
* Necrotic zone identified by EKG changes (Q wave)
* Healthy myocardium hypertrophies and dilates as compensation (remodeling) and this can lead to heart failure

A

all true

109
Q

what is a framingham risk score

A

this calculates the risk for MI in the next 10 years

110
Q

After endothelial injury this will start accumulating in the tunica intima, damaging often associated with lots of fats and diabetes type 2

A

LDL

111
Q

if a person has narrowed coronary arteries, it reduces the heart supplies which lead to what ?

A

myocardial ischemia

112
Q

explain what stable angina again

A

causes pain that is predictable and manageable with rest or medication, sometimes lifestyle modi can help but for some it will continue to plaque and lead to clot and lead to MI

113
Q

what’s the cause of angina ?

A

caused by imbalance by coronary arteries to supply oxygen to the heart muscle and the heart muscle demand for oxyegn

114
Q

silent ischemia usually occurs to what type of people ?

A

diabetic and people who had previous MI

115
Q

what is the common presentation of pain in angina ?

A

central chest pain that radiates to the neck shoulder and the jaw pain going to the right arm and epigastric area

could also present as an intrascapular pain ( between the shoulder blades )

116
Q

True or false. Chronic stable angina is reversible ?

A

true

117
Q

this is brought by an increase of physical activity , increases myocardial oxygen demand. No chest pain at rest but with any type of physical activity this will occur it is predictable.

A

chronic stable angina

118
Q

true or false. Chronic stable angina is managed with nitrates.

A

true

119
Q

What stage would chronic stable angina be in ?

A

fibrous stage, because at rest they are getting enough oxygenated blood but the ischemia is brought on by increase oxyegn demand, and exercising reduces that supply

it is still stable and no clot at this point

120
Q

why is vasospastic not connected to atherosclerosis or CAD

A

its not because its ultimately connected to interrupting the perfusion so it could lead to MI

121
Q

this is when there is a rupture of an unstable plaque, the clot creates a quick severe reduction of blood flow, meaning there is no oxygen being supplied and if ischemia is prolonged this causes damage to myocardium tissue and lead to necrosis

A

myocardial infraction

122
Q

this is undiagnosed or untreated angina

A

myocardial infraction

123
Q

what is abnormal Q
St elevation
T wave inversion

A
  1. area of cell death
  2. area of injury but not necrotic
  3. oxygen deprived tissue
124
Q

Diagnostic Tests for CAD: coronary angiography

name what angiogram ad angioplasty

A

angiogram
- cather inserted in radial or femoral artery threaded to heart and contrast injected directly into coronary arteries

  • done under xray using contrast dye
  • identify blockages and collateral circulation

angioplasty
- same as angiogram, can open obstructed arteries by inflating ballon +/ - stent

Pt.2 PHRM/PHYS/NS (14 decks)

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