basic cardiac principle Flashcards

1
Q

What is the function of the circulatory system?

A
  • maintain’s blood flow supply to the body
  • delivers oxygen, nutrients and other needed substances to all of the body’s cells and removes the waste of metabolism
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2
Q

what is the interface between blood and the artery wall?

A

the endothelium

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3
Q

What are endothelial cells metabolic functions?

A
  • maintain vessel tone
  • hemostasis
  • angiogenesis
  • neutrophil chemotaxis
  • hormone secretion
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4
Q

What produces nitric oxide & endothelin?

A

endothelium

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5
Q

injury to endothelium causes _____________

A

dysfunction

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6
Q

What is the outermost part of the heart?

A

pericardium

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7
Q

What is the muscle layer of the heart called?

A

myocardium

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8
Q

What is the innermost layer of the heart?

A

endocardium

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9
Q

What are the four valves of the heart?

A

aortic
pulmonic
tricuspid
mitral (bicuspid)

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10
Q

What are the two atrioventricular valves?

A

tricuspid
bicupid(mitral)

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11
Q

Where are atrioventricular valves located?

A

located between the atrial & ventricular chambers on each side

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12
Q

What prevents backflow into the atria when the ventricles contract?

A

AV valves

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13
Q

What does the bicuspid (mitral) valve consist of?

A

two flaps or cusps of the endocardium

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14
Q

What does the tricuspid valve consist of?

A

three flaps

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15
Q

What are the two semilunar valves?

A

pulmonic
aortic

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16
Q

What guards the bases of the two large arteries leaving the ventricular chambers?

A

semilunar valves

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17
Q

How does blood move from deoxygenated to oxygenated in the heart?

A

superior & inferior vena cava, rt atrium, tricuspid valve, rt ventricle, pulmonic valve, pulmonary arteries, lungs, pulmonary veins, lt atrium, mitral valve, lt ventricle, aortic valve, aorta

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18
Q

Which term is used to describe the amount of stretch on the myocardium at the end of diastole?
A. afterload
B. cardiac index
C. cardiac output
D. preload

A

D. preload

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19
Q

What 2 factors are used to calculate cardiac output? SATA
A. heart rate
B. blood pressure
C. stroke volume
D. mean arterial pressure
E. systemic vascular resistance

A

A. heart rate
C. stroke volume

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20
Q

Which statement best describes cardiac after load?
a. the volume amount that fills the ventricles at the end of diastole
b. the volume of blood the ventricles must pump out of the heart
c. the amount of blood the left ventricle pumps with each heart beat
d. the pressure the venticles must work against to open the semilunar valves so blood can be pumped out of the heart

A

d. the pressure the venticles must work against to open the semilunar valves so blood can be pumped out of the heart

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21
Q

a pt with hypovolemic shock is given Iv fluids. IV fluids will help ______________ cardiac output by ____________
a. decrease; decreasing preload
b. increase; increasing preload
c. increase; decreasing afterload
d. decrease; increasing contractility

A

b. increase; increasing preload

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22
Q

Which of the following is the main difference between unstable and stable angina?
a. stability of the plaque
b. age of the pt
c. type of activity bringing on chest pain
d. pain has never had chest pain before

A

a. stability of the plaque

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23
Q

Which catergory of beta blockers inhibit both beta 1 and beta 2 receptors?
a. selective beta blockers
b. non-selective beta blockers

A

b. non-selective beta blockers

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24
Q

What is the heart the size of?

A

a fist

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25
Q

How much does a heart weigh?

A

about a pound

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26
Q

What occurs during systole?

A

the heart contracts and pumps out blood; high pressure causes AV valves to open and ejects blood out of the heart

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27
Q

What are the 5 characteristics of metabolic syndrome?

A
  • hypertension
  • obesity
  • abnormal cholesterol levels
  • chronic inflammation
  • insulin resistance
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28
Q

What two diseases does metabolic syndrome put someone at risk of?

A

heart disease
diabetes

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29
Q

What body shape puts someone at higher risk for metabolic disease?

A

apple shape

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30
Q

What happens in diastole?

A

the atria & ventricals relax allowing blood to flow into the heart; “filling phase”; 2/3 of the cardiac cycle

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31
Q

What is cardiac output?

A

the amount of blood the heart pumps per minute from the left ventricle

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32
Q

How is cardiac output measured?

A

heart rate x stroke volume

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33
Q

What is normal cardiac output?

A

4-8L per minute

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34
Q

What is stroke volume?

A

the amount of blood pumped by the ventricles with each heartbeat

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35
Q

Can stroke volume be measured?

A

no

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36
Q

What three factors impact stroke volume?

A
  • preload
  • afterload
  • contractility
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37
Q

What does preload refer to?

A

the stretching of muscle fibers in the ventricles to the greatest of their ability

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38
Q

The bigger the stretch the more ________ you have, therefore the more ______ you have in the left ventricle.

A

preload; blood

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39
Q

The biggest stretch is the blood in the ventricle at the ____ of diastole; when the ________ valve is still closed.

A

end; mitral

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40
Q

What is starling’s law?

A

the more the heart muscles stretch during diastole the more forcefully it will contract during systole

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41
Q

during ______, the more blood I get in, the more blood I get out.

A

preload

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42
Q

What 4 things does preload help with?

A
  • accommodating greater blood volume
  • increasing sacromere length
  • increasing sensitivity of Ca++
  • encouraging strong contractions
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43
Q

When you have more preload you are increasing ______ _______

A

cardiac output

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44
Q

What are the 8 things that can increase preload?

A
  • increased central venous pressure
  • reduced heart rate
  • valvular regurgitation
  • increased aortic pressure
  • ventricular systolic heart failure
  • increased circulating volume
  • mitral insufficiency
  • aortic insufficiency
45
Q

What are the 7 ways preload can be decreased?

A
  • decreased central venous pressure
  • increased heart rate
  • decreased circulating volume
    bleeding
    third spacing
  • mittral stenosis
  • vasodilator use (nitro)
  • atrial fib
  • cardiac tamponade
46
Q

What is contractility?

A

ability of the myocardium to contract normally (squeezing of the ventricles)

47
Q

What does increased contractility cause?

A

an increase in stroke volume

48
Q

What is contractility influenced by?

49
Q

What is positive inotropy?

A

increased force of contraction; decreased preload & afterload

50
Q

What is negative inotropy?

A

decreased force of contraction

51
Q

If the stretch during preload is not strong, there is not as strong of a ____________

A

contraction

52
Q

Are there medications that can moderate the force of contraction?

A

yes there are meds to increase or decrease force of contraction

53
Q

What is afterload?

A

refers to the amount of resistance the heart must pump against when ejecting blood

54
Q

to eject blood out of the ventricles the ___ valves must be pushed open

55
Q

What is the example used for afterload?

A

overcoming the kink in the hose

56
Q

In what condition is heart contractility not great and the heart has to work harder to open up the valves?

A

heart failure

57
Q

What happens when afterload is low?

A

ventricles do not have to exert much effect to get the blood out of the heart; easy workload

58
Q

What happens when afterload is high?

A

increased due to increased systemic vascular resistance; think HTN; vasoconstriction

59
Q

What is ejection fraction?

A

how much blood the left ventricle pumps out with each contraction

60
Q

How is ejection fraction measured?

A

stroke volume/ preload; expressed in a %

61
Q

What is the normal & abnormal measurement for ejection fracture?

A

normal - 55 to 70%
abnormal - below 40%

62
Q

What does an abnormal ejection fraction tell us?

A

the heart is not putting out a lot of oxygenated blood to the rest of the body

63
Q

What happens in the heart during sympathetic nervous system response?

A
  • HR & BP increase
  • preload decreasd & afterload increased to get blood oxygenated more quickly
  • epinephrine & norepinephrine are secreted to increase blood flow
  • heart increased output & vasodilation occurs to oxygenate tissues more quickly
64
Q

What are beta 1 receptors responsible for?

A

signaling sympathetic nervous system

65
Q

Beta 1 is involved in response of what organ?

66
Q

When beta 1 is activated what 4 things occur?

A
  • increase force of contraction
  • increased rate of contraction (HR)
  • increased HR & contractility will increase stroke volume & cardiac output
67
Q

What can happen when there is too much activation of beta 1 receptors?

A

abnormal arythmia

68
Q

What happens when we block the activation of beta 1 receptors (use beta blockers)?

A

HR & force of contractions decrease

69
Q

What does beta 2 do?

A

act as a vasodilator
- play a role in glucose metabolism
- more involved in resp & GI systems

70
Q

What is the RAAS?

A

a hormone signaling system that regulates blood volume, BP, fluid & electrolytes, and systemic vascular resistance

71
Q

What are the three main substances involves in RAAS?

A

renin (enzyme)
aldosterone (hormone)
angiotensin II (hormone)

72
Q

What do renin, aldosterone & angiotensin II help regulate and how?

A

BP by increasing sodium absorption, water reabsorption, & vascular tone(how much vasoconstriction)

73
Q

What do kidneys play a role in?

A

cardiac output; account for 20% of cardiac output

74
Q

What do the kidneys do in response to low BP?

A

release renin

75
Q

How is angiotensin converted into angiotensin I?

76
Q

How does angiotensin I become angiotensin II?

A

angiotensin I goes to the lungs where angiotensin converting enzymes (ACE) converts angiotensin I to angiotensin II

77
Q

What does Angiotensin II cause?

A

vasoconstriction causing an increase in BP
- causes adrenal glad to release aldosterone & pituitary gland to release ADH

78
Q

What is the role of aldosterone & ADH in the RAAS system?

A

causes sodium retention and fluid retention causing BP & blood volume to increase

79
Q

What do aldosterone & angiotension II stimulate?

A

sympathetic nervous system

80
Q

What is a big issue with angiotensin II?

A

it sheds our blood vessels

81
Q

What happens when RAAS is constantly activated?

A

leads to shredding of blood vessels & the development of atherosclerosis; Causes the heart to lose the ability to expand & contract normally due to remodeling

82
Q

What happens in the heart when angiotensin II is activated?

A

increased preload & afterload

83
Q

What prevents angiotensin I from becoming angiotensin II?

A

ACE inhibitors

84
Q

What can inappropriate RAAS activation cause?

A

endothelial dysfunction
vascular remodeling
elevated BP
artherosclerosis
plaque
impaired adipogenesis
glucose intolerence

85
Q

What is insulin resistance?

A

When cells fail to make effective use of insulin

86
Q

What happens to glucose levels in those with insulin resistance?

A

blood sugar increases; insulin is not able to reduce blood sugar; pt remains hyperglycemic

87
Q

where is insulin secreted from?

A

beta cells in the pancreas

88
Q

Should insulin be in circulation?

A

no; we want it in the cell; if it is in circulation this means it is not being used by the cells

89
Q

What can insulin resistance cause?

A
  • increased catecholamine
  • stimulates sodium reabsorption (increases BP)
  • endothelial dysfunction
  • RAAS & SNS dysfunction
  • increase smooth muscle proliferation which leads to hypertrophy & targeted organ damage
90
Q

What improves high BP related to insulin sensitivity?

A

meds that improve insulin sensitivity; ACEI

91
Q

What do you need to make nitric oxide?

92
Q

What role does insulin play in the vascular system?

A

plays a role in vascular protection; increases endothelial cell production of nitric oxide

93
Q

What puts someone in a state of low-grade chronic inflammation?

94
Q

What 4 things can a low-grade chronic inflammatory state cause?

A

CVD (increased thrombosis)
type 2 diabetes
hypertension
hyperlipidemia

95
Q

What can target organ damage increase the risk of?

A

dementia; decreased circulation meaning decreased O2 to the brain

96
Q

What target organ damage is caused by HTN?

A

brain damage (may cause stroke)
renal damage
retinopathy
PAD
left ventricular hypertrophy
atherosclerotic cardiovascular disease

97
Q

What are the risk factors that lead to endothelial dysfunction and therefore atherogenesis?

A

HTN
genetic susceptibility
hyperlipidemia
diabetes
physical inactivity
obesity
smoking
stress
aging

98
Q

How are FOAM cells formed?

A

macrophages ingest deposited cholesterol from LDLs; making “plaque”

99
Q

What does the build up of plaque lead to?

A

hypertrophy

100
Q

What does LDL do?

A

deposits cholesterol

101
Q

What happens when plaque ruptures?

A

a blood clot forms at the site & the muscle in that area of the blocked artery starts to die

102
Q

What causes things like CVD, PVD, & cerebral issues?

A

inadequate tissue perfusion; disruption of supply & demand

103
Q

What are the symptoms of inadequate tissue perfusion?

A

coronary issues
- stable angina
- unstable angina
peripheral disease
- claudication
cerebral
- TIA
- CVA

104
Q

What is present in stable angina?

A

a significant fixed lesion?

105
Q

What is present in unstable angina?

A

unstable plaque that could break off causing clotting and an acute MI; AKA acute coronay syndrome (ACS)

106
Q

What are the three main reperfusion strategies when an MI has occurred?

A
  • pharmacologic agents (fibrinolytic therapy)
  • percutaneous coronary intervention
  • CABG
107
Q

What are the types of PCIs that can be performed?

A
  • percutaneous transluminal coronary angioplasty (PTCA)
  • stents
  • artherectomy
  • thrombectomy
108
Q

What is a CABG?

A

Coronary Artery bypass graft; a healthy blood vessel is attached to the aorta to bypass a blockage

109
Q

What is a stent?

A

a small device that is put into a vein or artery to keep it open