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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
How much does a heart weigh?
about a pound
26
What occurs during systole?
the heart contracts and pumps out blood; high pressure causes AV valves to open and ejects blood out of the heart
27
What are the 5 characteristics of metabolic syndrome?
- hypertension - obesity - abnormal cholesterol levels - chronic inflammation - insulin resistance
28
What two diseases does metabolic syndrome put someone at risk of?
heart disease diabetes
29
What body shape puts someone at higher risk for metabolic disease?
apple shape
30
What happens in diastole?
the atria & ventricals relax allowing blood to flow into the heart; "filling phase"; 2/3 of the cardiac cycle
31
What is cardiac output?
the amount of blood the heart pumps per minute from the left ventricle
32
How is cardiac output measured?
heart rate x stroke volume
33
What is normal cardiac output?
4-8L per minute
34
What is stroke volume?
the amount of blood pumped by the ventricles with each heartbeat
35
Can stroke volume be measured?
no
36
What three factors impact stroke volume?
- preload - afterload - contractility
37
What does preload refer to?
the stretching of muscle fibers in the ventricles to the greatest of their ability
38
The bigger the stretch the more ________ you have, therefore the more ______ you have in the left ventricle.
preload; blood
39
The biggest stretch is the blood in the ventricle at the ____ of diastole; when the ________ valve is still closed.
end; mitral
40
What is starling's law?
the more the heart muscles stretch during diastole the more forcefully it will contract during systole
41
during ______, the more blood I get in, the more blood I get out.
preload
42
What 4 things does preload help with?
- accommodating greater blood volume - increasing sacromere length - increasing sensitivity of Ca++ - encouraging strong contractions
43
When you have more preload you are increasing ______ _______
cardiac output
44
What are the 8 things that can increase preload?
- increased central venous pressure - reduced heart rate - valvular regurgitation - increased aortic pressure - ventricular systolic heart failure - increased circulating volume - mitral insufficiency - aortic insufficiency
45
What are the 7 ways preload can be decreased?
- decreased central venous pressure - increased heart rate - decreased circulating volume bleeding third spacing - mittral stenosis - vasodilator use (nitro) - atrial fib - cardiac tamponade
46
What is contractility?
ability of the myocardium to contract normally (squeezing of the ventricles)
47
What does increased contractility cause?
an increase in stroke volume
48
What is contractility influenced by?
preload
49
What is positive inotropy?
increased force of contraction; decreased preload & afterload
50
What is negative inotropy?
decreased force of contraction
51
If the stretch during preload is not strong, there is not as strong of a ____________
contraction
52
Are there medications that can moderate the force of contraction?
yes there are meds to increase or decrease force of contraction
53
What is afterload?
refers to the amount of resistance the heart must pump against when ejecting blood
54
to eject blood out of the ventricles the ___ valves must be pushed open
AV valves
55
What is the example used for afterload?
overcoming the kink in the hose
56
In what condition is heart contractility not great and the heart has to work harder to open up the valves?
heart failure
57
What happens when afterload is low?
ventricles do not have to exert much effect to get the blood out of the heart; easy workload
58
What happens when afterload is high?
increased due to increased systemic vascular resistance; think HTN; vasoconstriction
59
What is ejection fraction?
how much blood the left ventricle pumps out with each contraction
60
How is ejection fraction measured?
stroke volume/ preload; expressed in a %
61
What is the normal & abnormal measurement for ejection fracture?
normal - 55 to 70% abnormal - below 40%
62
What does an abnormal ejection fraction tell us?
the heart is not putting out a lot of oxygenated blood to the rest of the body
63
What happens in the heart during sympathetic nervous system response?
- 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
What are beta 1 receptors responsible for?
signaling sympathetic nervous system
65
Beta 1 is involved in response of what organ?
the heart
66
When beta 1 is activated what 4 things occur?
- increase force of contraction - increased rate of contraction (HR) - increased HR & contractility will increase stroke volume & cardiac output
67
What can happen when there is too much activation of beta 1 receptors?
abnormal arythmia
68
What happens when we block the activation of beta 1 receptors (use beta blockers)?
HR & force of contractions decrease
69
What does beta 2 do?
act as a vasodilator - play a role in glucose metabolism - more involved in resp & GI systems
70
What is the RAAS?
a hormone signaling system that regulates blood volume, BP, fluid & electrolytes, and systemic vascular resistance
71
What are the three main substances involves in RAAS?
renin (enzyme) aldosterone (hormone) angiotensin II (hormone)
72
What do renin, aldosterone & angiotensin II help regulate and how?
BP by increasing sodium absorption, water reabsorption, & vascular tone(how much vasoconstriction)
73
What do kidneys play a role in?
cardiac output; account for 20% of cardiac output
74
What do the kidneys do in response to low BP?
release renin
75
How is angiotensin converted into angiotensin I?
via renin
76
How does angiotensin I become angiotensin II?
angiotensin I goes to the lungs where angiotensin converting enzymes (ACE) converts angiotensin I to angiotensin II
77
What does Angiotensin II cause?
vasoconstriction causing an increase in BP - causes adrenal glad to release aldosterone & pituitary gland to release ADH
78
What is the role of aldosterone & ADH in the RAAS system?
causes sodium retention and fluid retention causing BP & blood volume to increase
79
What do aldosterone & angiotension II stimulate?
sympathetic nervous system
80
What is a big issue with angiotensin II?
it sheds our blood vessels
81
What happens when RAAS is constantly activated?
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
What happens in the heart when angiotensin II is activated?
increased preload & afterload
83
What prevents angiotensin I from becoming angiotensin II?
ACE inhibitors
84
What can inappropriate RAAS activation cause?
endothelial dysfunction vascular remodeling elevated BP artherosclerosis plaque impaired adipogenesis glucose intolerence
85
What is insulin resistance?
When cells fail to make effective use of insulin
86
What happens to glucose levels in those with insulin resistance?
blood sugar increases; insulin is not able to reduce blood sugar; pt remains hyperglycemic
87
where is insulin secreted from?
beta cells in the pancreas
88
Should insulin be in circulation?
no; we want it in the cell; if it is in circulation this means it is not being used by the cells
89
What can insulin resistance cause?
- increased catecholamine - stimulates sodium reabsorption (increases BP) - endothelial dysfunction - RAAS & SNS dysfunction - increase smooth muscle proliferation which leads to hypertrophy & targeted organ damage
90
What improves high BP related to insulin sensitivity?
meds that improve insulin sensitivity; ACEI
91
What do you need to make nitric oxide?
insulin
92
What role does insulin play in the vascular system?
plays a role in vascular protection; increases endothelial cell production of nitric oxide
93
What puts someone in a state of low-grade chronic inflammation?
obesity
94
What 4 things can a low-grade chronic inflammatory state cause?
CVD (increased thrombosis) type 2 diabetes hypertension hyperlipidemia
95
What can target organ damage increase the risk of?
dementia; decreased circulation meaning decreased O2 to the brain
96
What target organ damage is caused by HTN?
brain damage (may cause stroke) renal damage retinopathy PAD left ventricular hypertrophy atherosclerotic cardiovascular disease
97
What are the risk factors that lead to endothelial dysfunction and therefore atherogenesis?
HTN genetic susceptibility hyperlipidemia diabetes physical inactivity obesity smoking stress aging
98
How are FOAM cells formed?
macrophages ingest deposited cholesterol from LDLs; making "plaque"
99
What does the build up of plaque lead to?
hypertrophy
100
What does LDL do?
deposits cholesterol
101
What happens when plaque ruptures?
a blood clot forms at the site & the muscle in that area of the blocked artery starts to die
102
What causes things like CVD, PVD, & cerebral issues?
inadequate tissue perfusion; disruption of supply & demand
103
What are the symptoms of inadequate tissue perfusion?
coronary issues - stable angina - unstable angina peripheral disease - claudication cerebral - TIA - CVA
104
What is present in stable angina?
a significant fixed lesion?
105
What is present in unstable angina?
unstable plaque that could break off causing clotting and an acute MI; AKA acute coronay syndrome (ACS)
106
What are the three main reperfusion strategies when an MI has occurred?
- pharmacologic agents (fibrinolytic therapy) - percutaneous coronary intervention - CABG
107
What are the types of PCIs that can be performed?
- percutaneous transluminal coronary angioplasty (PTCA) - stents - artherectomy - thrombectomy
108
What is a CABG?
Coronary Artery bypass graft; a healthy blood vessel is attached to the aorta to bypass a blockage
109
What is a stent?
a small device that is put into a vein or artery to keep it open

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