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Bioscience II > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

the inability of the heart to pump blood at a rate that is proportionate with the requirements of the metabolizing tissues or can only do so from an elevated filling pressure

A

Heart Failure

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2
Q

You can have LVD but not have heart failure IF…

A

you can still meet the demands of the heart

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3
Q

Compensatory mechanisms

A 
natriuretic peptides
Frank-Starling mechanism
Myocardial hypertrophy
sympathetic reflexes
renin-angiotensin-aldosterone mechanism
        -all of these function in maintaining the cardiac output in a failing heart
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4
Q

Frank- Starling compensatory mechanisms

A

increased EDV
only works to a certain point
the more you put in, the more you get out

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5
Q

Myocardial hypertrophy compensatory mechanism

A

gradual change of the muscle cells and fibrous tissues that undergo hypertrophy
primary response is to generate an extra pump to go against the resistance
need more oxygen for more muscle but there is less wall stress with more muscle
*long term

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6
Q

Renin-angiotensin-aldosterone compensatory mechanism

A

The kidney produces renin which creates angiotensin to produce angiotensin II from ACE. Aldosterone is produced with helps with salt and water retention. This then increases the vascular volume therefore increasing venous return

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7
Q

Sympathetic reflexes compensatory mechanism

A

There is a high HR with heart failure which creates a ramped up sympathetic nervous system
These reflexes increase HR and contractility to improve cardiac output
*short term

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8
Q

Natriuretic peptides compensatory mechanism

A

counters overactivity of compensatory mechanisms
produced by the heart muscle cells in response to stretch
promotes excretion of Na+, water and potassium
inhibits aldosterone
acts as an antagonist for Ang II and inhibits NE therefore decreasing the volume of the heart to result in less stress

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9
Q

Causes of Heart Failure

A 
cardiomyopathies
myocarditis
coronary insufficiency
myocardial infarction
stenotic valces
regurgitant valves
congenital heart disease
systemic or pulmonary HTN
excessive intravenous fluid administration 
thyrotoxicosis
severe anemia
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10
Q

Normal symmetric hypertrophy

A

thickness of wall increases in proportion to the wall of the chamber

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11
Q

Concentric hypertrophy

A

disproportionate increase in wall thickness

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12
Q

Eccentric hypertrophy

A

disproportionate decrease in wall thickness
as the wall thins the chamber gets bigger
there is not enough pumping power with a stretched out wall therefore as wall stress increases so does oxygen demand

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13
Q

high output

A

usually caused by anemia

the heart keeps working and working but is not meeting the demands because oxygen content of the blood is insufficient

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14
Q

low output

A

more common classification

not generating sufficeint CO

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15
Q

systolic

A

more common classification

blood moving out

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16
Q

diastolic

A

blood filling

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17
Q

right sided heart failure

A

pressure backs up into the right atrium so that forces move into the systemic venous system

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18
Q

right sided HF symptoms

A 
fatigue
dependent edema (localized in a dependent area)
distention of the jugular veins
liver engorgement
ascites (fluid in peridinium accumulates)
loss of appetite
cyanosis
elevation in peripheral venous pressure
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19
Q

Left sided heart failure

A

more common
can cause right sided HF
blood backs up into the lungs causing pulmonary edema

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20
Q

Left sided HF symptoms

A

symptoms related to congestive HF
exertional dyspnea
orthopnea ( difficulty breathing while lying down)
paroxysmal nocturnal dyspnea (SOB suddenly at night)
cough
cyanosis
fatigue
elevation in pulmonary capillary wedge pressure

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21
Q

common signs and symptoms of HF

A 
fatigue
fluid retention and edema
pulmonary symptoms
altered exercise tolerance
cachexia (muscle wasting)
malnutrition
cyanosis (impaired oxygen delivery)
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22
Q

Treatment

A

turns down the influence of compensatory mechanisms that can worsen conditions
diuretics, ACE inhibitors/ARBs and Beta blockers are most popular and all lower BP

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23
Q

Diuretics

A

get rid of excess fluid (loop-diuretics) therefore decreasing stress on the heart

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24
Q

ACE inhibitiors/ARBs

A

produce less vasoconstriction and less fluid retention therefore decreasing stress and vascular volume of the heart

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25
Q

Beta blockers

A

decrease contractility of the heart by lowering sympathetic activity and concentration of NE to normalize cardiac function
metoprolol

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26
Q

digitalis (Digoxin)

A

less common
an antiarryhtmic taken by mouth to increase contractility and Ca2+
diminishes symptoms and creates better QOL

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27
Q

Aortic balloon pump

A

INFLATED to increased the driving pressure of blood flow during DIASTOLE
helium is sucked out to create a space and decrease demand in the artery during SYSTOLE

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28
Q

Impella

A

temporary

takes blood from one end and pumps it into another end

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29
Q

Thoratec HeartMate II LVAD

A

semi-permanent
pulls blood out of LV and puts it back in aorta so that LV doesn’t do much work
alternative to transplant

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30
Q

circulatory shock

A

failure of circulation to maintain adequate perfusion of vital organs. results in impairment in O2
patients tend to be hypotensive and tachycardic
there is a shift from aerobic—-> anaerobic metabolism
exhibit increased levels of lactic acid in the blood

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31
Q

circulatory shock- cardiogenic

A

impaired O2 delivery, contractility and CO
direct extension of heart failure
most commonly caused by MI
characteristic trait of low BP

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32
Q

circulatory shock- hypovolemic

A

diminished blood volume so that there is not enough to deliver adequate oxygen
can be caused by fluid shifts, burn injuries, hemorrhage or severe dehydration

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33
Q

circulatory shock- obstructive

A

not common
results from mechanical block of blood flow through the central circulation
there is impairment in heart filling (preload)
most frequent cause is pulmonary embolism
results in elevated right heart pressure

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34
Q

circulatory shock- vasodilatory (distributive)

A

there is so much vasodilation occurring that pressure gradients are decreased which results in anaphylatic shock

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35
Q

signs and symptoms of circulatory shock

A 
cool 
clammy (diaphoretic) 
cyanotic
poor renal output
altered mental state (confused, unresponsive)
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36
Q

mild hypovolemic shock

A

slight tachycardia
slight decrease in BP
15-25% volume loss

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37
Q

moderate hypovolemic shock

A

HR 100-120
SBP 90-100
pallor, oliguria (not making enough urine)
25-35% volume loss

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38
Q

severe hypovolemic shock

A

HR >120

SBP

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39
Q

septic shock

A 
most common type of vasodilatory shock
systemic vascular resistance problem
severe infection with low BP
linked to strong vasodilatory response
40% mortality
gram-negative bacteremia which is bacteria in the blood that initiates an inflammatory response
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40
Q

complications of shock

A

adult respiratory distress syndrome (ARDS)
-form of pulmonary edema
acute renal failure
gastrointestinal complications
disseminated intravascular coagulation (DIC)
multiple organ dysfunction syndrome (MODS)

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41
Q

general functions of the respiratory system

A

speaking
brings in O2
gets CO2 out
helps to regulate blood pH level

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42
Q

Which branches make up the Conducting Zone?

A

trachea, bronchi, bronchioles, terminal bronchioles

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43
Q

role of the conducting zone

A

takes air from the outside and brings it into the body
air is warmed to body temp and humidified
gas is filtered and cleaned via secreted mucus
NO gas exchange occurs here
ciliated epithelial tissue makes up this zone

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44
Q

role of respiratory zone

A

gas exchange with huge surface area

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45
Q

What occurs as you go down the branches of the respiratory system?

A

the amplification of division and number of structures gives a large surface area for gas exchange to occur

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46
Q

What important purpose do the bronchioles serve?

A

the control resistance and air flow through the lungs

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47
Q

difference between bronchi and bronchioles

A

bronchi have cartilaginous plates which give them structure

bronchioles do not which makes them much more susceptible to injury or disease

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48
Q

Type I alveolar cells

A

squamous epithelium involved in the process of gas exchange between the alveoli and blood.
cover 95% of alveoli surface

49
Q

Type II alveolar cells

A

Their function is of major importance in the secretion of pulmonary surfactant, which decreases the surface tension within the alveoli.
capable of cellular division
they are fewer in number

50
Q

structure of alveoli

A

“cluster of soap bubbles”
they share walls and have interconnectedness with adjacent alveoli
-this can help with pressure gradient and gas distribution

51
Q

parietal pleura

A

lines the inside of the rib cage

52
Q

visceral pleura

A

in direct contact with the lungs

53
Q

intrapleural space

A

has negative pressure which acts as a suction cup and is able to keep your lungs stuck to your rib cage
if there is a hole or cute here then your lung can collapse

54
Q

Palv

A

pressure in the alveoli

55
Q

Patm

A

atmospheric pressure
this changes with location
it is the reference point. Patm = 0

56
Q

For air to move from the room into the alveoli….

A

Palv must be lesser than the room

57
Q

For there to be no air movement…

A

Palv=Patm

58
Q

Pip

A

pressure of the interpleural fluid
keeps the alveoli inflated
always negative

59
Q

Transpulmonary pressure

A

Palv – Pip
pressure difference across the wall of the alveoli
the bigger the difference the greater the alveoli expansion

60
Q

What generates pressure changes during a normal respiratory cycle?

A

muscle activity

61
Q

What happens when Palv drops below Patm?

A

inspiration

62
Q

What happens when Palv > Patm as we breathe?

A

exhalation

63
Q

Palv = Patm

A

no change in breathing

64
Q

during inhalation…..

A

Pip becomes more negative while the transpulmonary Pressure increases therefore allowing alveoli to expand

65
Q

during exhalation…

A

Pip becomes less negative

66
Q

Diaphragm and inhalation

A

as the it contracts it drops down and increases the thoracic volume while decreasing the pressure creating a pressure gradient for air to move in
Pip decreases and becomes more negative while the transpulmonary pressure increases to increase alveoli

67
Q

relaxation of the diaphragm causes?

A

transpulmonary pressure to decrease and the size of the alveoli to decrease

68
Q

Role of pulmonary surfactant

A

produced by Type II alveolar cells

- reduces surface tension of water molecules in alveoli
- makes them more compliant; ease of lung inflation
- helps keep alveoli dry
- prevents pulmonary edema
69
Q

Describe what it means that our lungs are compliant

A

This means that they have ease with stretching and don’t need to work hard to expand alveoli
- the ease of inflating
-determined by the elastic properties
of the lung, its water content, and surface tension

70
Q

What decreases lung compliancy?

A

diminished by conditions that reduce the natural
elasticity of the lung, increase the surface tension in
the alveoli, or impair the flexibility of the thoracic cage

71
Q

A lung that is more compliant loses what ability?

A

loses the ability to recoil; return to its original shape

This is because the overstretched tissues are easier to inflate but more difficult to deflate

72
Q

What makes up pulmonary surfactant?

A

mixture of phospholipids, neutral lipids, and proteins made by Type II alveolar cells
developed in the 26-27th week of gestation which is why many premature babies have pulmonary issues since their surfactant has not been fully produced

73
Q

Why do we encourage our bed-ridden patients to cough?

A

deep breathe enhances the spreading
of surfactant, allowing for a more even distribution
of ventilation and prevention of atelectasis

74
Q

What is atelectasis?

A

partial or complete collapse of a lung

75
Q

During what action is there more resistance of the airways?

A

During exhalation
-This is because elastic-type fibers connect the outside of the airways to the surrounding lung tissues. As a result, these airways are pulled open as the lungs expand during inspiration, and they become narrower as the lungs deflate
during expiration

76
Q

What happens to the airway radius during inspiration?

A

It is greater therefore resistance to flow is decreased

77
Q

Resistance to flow is inversely related to….

A

airway raidus

78
Q

What is the effect of exercise on airway resistance?

A

it significantly increases it with forced expiration

79
Q

What happens to Pip during forced exhalation (coughing)

A

it becomes positive and dynamic compression of small airways occurs

80
Q

What happens to the airway radius during exhalation?

A

airway radius is less therefore resistance to flow is increased

81
Q

What happens to the lungs if Pip exceeds Palv greatly?

A

It can cause the lungs to collapse
palv — PIP = – Tp
compression

82
Q

Airway diameter is narrowed as a result of?

A

a negative transpulmonary pressure

83
Q

Airway diameter is greater at…

A

larger lung volumes

84
Q

Higher expiatory flow rates can be achieved with?

A

higher lung volume

85
Q

What factors increase resistance to flow?

A 
bronchiolar constriction
  -caused by parasympathetic stimulation
histamine
   -allergic response
decreased PCO2 levels
expiration
86
Q

What factors give less airway resistance?

A 
brochiolar dilation
  -caused by sympathetic stimulation
epinephrine and analogs
    -B2 stimulation
increased Pco2 levels
inspiration
87
Q

What does high PO2 mean?

A

it means good ventilation locally so arterioles DILATE to increase local blood flow

88
Q

What does low PO2 mean?

A

it means poor ventilation locally so arterioles CONSTRICT to divert blood to areas of the lung that are well ventilated

89
Q

Ventilation Perfusion Ratio (V/Q)

A

a measurement used to assess the efficiency “V” – ventilation – the air that reaches the alveoli and “Q” – perfusion – the blood that reaches the alveoli.
Our goal is to maximize this

90
Q

How can you maximize V/Q?

A

……..?

91
Q

Tidal Volume

A

500 mL

the amount of air that moves into and out of the lungs during a normal breath

92
Q

Inspiratory Reserve Volume

A

2000 mL
maximum amount of air that
can be inspired in excess of the normal TV

93
Q

Expiratory Reserve Volume

A

1200 mL
maximum amount that can be exhaled in excess of
the normal TV

94
Q

Residual Volume

A

1200 mL

air that remains in the lungs after forced expiration

95
Q

Total Lung Capacity

A

4900 mL
TV +RV + ERV + IRV
sum of all the volumes in the lungs

96
Q

Functional Residual Capacity

A

2400 mL
RV + ERV
it is the volume of air that remains in the lungs at the end of normal expiration

97
Q

Vital Capacity

A

3700 mL
IRV +TV +ERV
amount of air that can be exhaled from the point of maximal inspiration

98
Q

Why are these lung values greater in men and taller individuals?

A

these populations have greater lung volumes and capacities which is why they have higher values

99
Q

What is total minute volume?

A

the amount of air exchanged in one minute

Ve = Vtidal x f (respiratory rate)

100
Q

What is Valv?

A

volume of gas that can be used to get O2 and lose CO2

101
Q

Why is shallow breathing fatiguing?

A

You must breathe faster to maintain Valv so it is less efficient due to the constant dead space volume
There is reduced oxygen and blood circulation in the lungs with shallow breathing

102
Q

Flow-Volume Loop

A

air flow rate vs. lung volume during a forced expiratory maneuver

103
Q

If there is ventilation without perfusion….

A

V/0
increases dead space
gas exchange is impaired with lack of blood flow
you end up being ventilated with no gas exchange

104
Q

If there is perfusion without ventilation….

A

0/Q
shunting
alveoli of the lungs are perfused with blood as normal, but ventilation (the supply of air) fails to supply the perfused region

105
Q

Obstructive airway disease

A

persons usually find it less difficult to inflate their
lungs but expend more energy in moving air through the
airways. As a result, these persons tend to take deeper
breaths and breathe at a slower rate to achieve their oxygen needs

106
Q

persons with stiff and noncompliant lungs

A

expansion of the lungs is difficult for persons
with stiff and noncompliant lungs, they usually find
it easier to breathe if they keep their TV low and breathe
at a more rapid rate to achieve their minute volume

107
Q

What is dead space?

A

the volume of gas that fills conducting airways
does not participate in gas exchange
150 mL

108
Q

What happens with hyperventilation?

A

it increases PO2 in the alveoli
it decreases PCO2 in the alveoli
-you breathe deeper and more rapidly

109
Q

Partial pressures of deoxygenated venous blood

A

lower pO2 and higher pCO2

110
Q

Components of hypoventilation

A

slow breathing
CO2 accumulates in the alveoli while O2 is removed
changes seen in arterial blood
PO2 is lower while PCO2 is higher

111
Q

factors affecting gas exchange at the lung

A 
concentration difference
surface area
diffusion distance
altitude
supplemental oxygen
112
Q

Which diseases have increased diffusion distance?

A

pulmonary edema and fibrosis of the lungs

-this slows down diffusion

113
Q

Levels of the lung and V/Q

A

upper lung = more ventilation
middle lung = V=Q
lower lung= more perfusion

114
Q

the oxygen-Hb dissociation curve

A

shows how much O2 has Hb bound to it

the goal is to keep patients in the plateau region where they are well saturated

115
Q

Shifts in the O2-Hb dissociation curve

A

with exercise the muscles produce more CO2, there is an increase in temperature and RBC 2,3 di-PG
There is a shift to the right as things increase but there is lower Hb saturation

116
Q

lower Hb saturation means?

A

more readily to let of O2

117
Q

Left shifts in the O2-Hb curve

A

increased saturation so Hb is less likely to give up O2

118
Q

Effect of anemia on the O2-Hb cuve

A

someone with anemia does not have enough Hb therefore they have low oxygen levels

Bioscience II (10 decks)

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