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BUPA Physiology > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the function of turbinates?

A

To humidify and warm air to body temperature

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2
Q

What are the directions of the muscle fibers in the external and internal intercostal muscles?

A

External intercostals - “hands in front pocket”

Internal intercostals - “hands in back pocket”

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3
Q

The amount of air brought in during normal breathing

A

Tidal volume

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4
Q

The amount of air brought in during a maximal inhalation

A

Maximal inspiratory effort

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5
Q

The difference between the tidal volume and maximal inspiratory effort

A

Inspiratory reserve volume

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6
Q

The amount of air breathed out during a maximal exhalation

A

Maximal expiratory effort

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7
Q

The difference between the tidal volume and the maximal expiratory effort

A

Expiratory reserve volume

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8
Q

Maximal breath in and maximal breath out as hard and as fast as a person can in 1 sec

A

Forced expiratory volume

FEV1

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9
Q

MIE + TV + MEE

A

Vital capacity

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10
Q

Maximal breath in and maximal breath out as hard and as fast as a person can

A

Forced vital capacity

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11
Q

The volume of air that is in the lung when the person is relaxed (no inspirations or expirations)

A

Functional residual capacity

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12
Q

How much air is left in the lung after you have maximally expired

A

Residual volume

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13
Q

RV + VC

OR

RV + ERV + TV + IRV

A

Total lung capacity

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14
Q

What are the features of the conducting zone of the lungs?

A
  • Contains the first 16 generations of bronchial branches
  • no alveoli
  • anatomical dead space
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15
Q

What are the features of the transitional zone of the lungs?

A
  • Contains generations 17-19 of bronchial branches

- some alveoli

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16
Q

What are the features of the respiratory zone of the lungs?

A
  • Contains generations 20+ of bronchial branches
  • many alveoli
  • major site of gas exchange
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17
Q

Why isn’t the cartilage of the trachea complete?

A

To allow swallowing in the esophagus

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18
Q

Why do bronchi have irregular cartilage plates in addition to a muscle layer and elastic fibers

A

To allow for constriction/dilation

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19
Q

Why do bronchioles have a tendency to collapse?

A
  • No cartilage

- progressively thinner muscle layer

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20
Q

Alveolar septa are interconnected via collagen/elastin fibers to provide what? How is this beneficial?

A

Lateral traction

Keeps the alveoli open —> one alveolus can’t change shape without affecting its neighbors

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21
Q

What are the two main secretory cells in the airway tract? What do they secrete and what does it do?

A

Goblet cells - mucus; traps harmful substances

Clara cells - CCSP (clara cell secretory protein); anti-inflammatory/immunomodulatory

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22
Q

Which cells proliferate in the alveolar-capillary units during injury and why?

A

Type II cells to maintain epithelial surface integrity

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23
Q

Immune cell present in the lung to phagocytize foreign particles

A

Alveolar macrophages

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24
Q

What part of the CNS controls “autonomic” breathing?

A

Medullary Respiratory Center (Medulla)

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25
Q

What are the 5 main functions of the respiratory system?

A
  1. Gas exchange
  2. Acid-base balance
  3. Phonation
  4. Pulmonary defense
  5. Pulmonary metabolism
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26
Q

What is the acid-base balance equation?

A

CO2 + H2O H2CO3 H+ + HCO3-

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27
Q

What does the CNS have sensors for in order to control breathing?

A

CO2 and H+

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28
Q

How is sound produced?

A

CNS control of respiratory muscles causes air to flow through the vocal cords and mouth

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29
Q

What size particles are filtered out in the nasal passages and how?

A

10-15 um

Nasal hairs + turbulence in air flow

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30
Q

What size particles are filtered out in the small airways via sedimentation (due to gravity)?

A

2-5 um

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31
Q

What size particles are filtered out via entrapment in the mucus?

A

> 2 um

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32
Q

Traps and “sweeps” foreign materials up toward the pharynx

A

Mucociliary escalator

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33
Q

How does a cough/sneeze contribute to pulmonary defense? How are they triggered?

A

Particles mechanically/chemically trigger cough (in trachea) or sneeze (in nose/pharynx)

Forced expired air produces a high air flow that rubs against walls and forces mucus up through the airway

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34
Q

What role do immature mononuclear phagocytic cells play in the airways?

A

They engulf bacteria and other antigens that causes them to mature

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35
Q

What role do mature dendritic cells play in the airways?

A

The migrate to lymphoid tissue where they present the antigen they engulfed and either activate T cells/immune response/inflammation or they promote antigen tolerance/suppress the immune response (depending on the antigen)

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36
Q

Where are dendritic cells located in the immune system?

A

From trachea to alveoli

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37
Q

What role do alveolar macrophages play in the respiratory system?

A
  • Engulf and destroy antigens with lysosomes
  • engulf non-degradable particles and migrate to mucociliary escalator for removal
  • role in immune/inflammatory response
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38
Q

How does cigarette smoke damage the airways?

A
  • damages cilia in mucociliary escalator

- inhibit activity of alveolar macrophages

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39
Q

What role do surface enzymes and mucus play in pulmonary defense?

A

Contain antibacterial components that inactivate bacterial enzymes and factors

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40
Q

What major role does the pulmonary system play in circulation besides oxygenating blood?

A

It traps substances/clots in pulmonary capillaries and the immune system removes them

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41
Q

Cells that cause bronchoconstriction, immune responses, and cardiopulmonary reflexes

A

Mast Cells

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42
Q

What substances do mast cells release?

A 
Histamine
Lysosomal Enzymes
Prostaglandins
Leukotrienes
Platelet activating factors
Neutrophil and eosinophils chemotactic factors
Serotonin
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43
Q

What immunologically active substances produced by the lung tissue can end up in the blood?

A 
Bradykinin
Histamine
Serotonin
Heparin
PGE2 and PGF2alpha
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44
Q

Substance produced by Type II alveolar cells that reduces surface tension in alveoli

A

Surfactant

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45
Q

Tidal volume * frequency of breaths

A

Minute ventilation

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46
Q

Makes lungs tend to empty/collapse or expand

A

Lung elastic recoil

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47
Q

Makes the rib cage tend to expand or collapse

A

Thoracic cage elastic recoil

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48
Q

Equal to Paw (pressure of air way) at rest OR the combined compliance of zero

A

functional residual capacity

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49
Q

What two forces contribute to the negative intrapleural pressure?

A

Lung elastic recoil

Thoracic cage elastic recoil

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50
Q

Before inspiration, what forces are acting on the respiratory system and what is Paw and Pip?

A

Lung elastic recoil = Thoracic cage elastic recoil

Pip = lung elastic recoil

Paw = 0

No air flow.

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51
Q

During inspiration, inspiratory muscles are active. What forces are acting on the respiratory system and what is Paw and Pip?

A

Lung elastic recoil <
Thoracic cage elastic recoil + muscle forces

Pip = more negative

Paw = negative

Air flows in.

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52
Q

At the end of inspiration, inspiratory muscles are actively holding lung at increase volume. What forces are acting on the respiratory system and what is Paw and Pip?

A

Lung elastic recoil = thoracic cage elastic recoil + muscle forces

Pip = negative = lung elastic recoil

Paw = 0

No air flow.

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53
Q

During expiration, inspiratory muscles are inactive. What forces are acting on the respiratory system and what is Paw and Pip?

A

Lung elastic recoil > thoracic cage elastic recoil

Pip = less negative = lung elastic recoil

Paw = increases

Air flows out.

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54
Q

What is the equation for transpulmonary pressure and what does it represent?

A

Changes in alveolar distending pressure

Transpulmonary pressure = Palv - Pip

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55
Q

Why does increased transpulmonary pressure lead to increased lung volume?

A

It is the pressure difference between the alveoli and the intrapleural space. If it that pressure difference increases, it means the lungs will be pulled open and lung volume will increase

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56
Q

What is the equation for the chest wall’s distending pressure?

A

Distending pressure = Pip-Patm

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57
Q

What is the equation for compliance?

A

C = change in volume/change in pressure

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58
Q

What will high compliance show vs low compliance?

A

High compliance = small pressure change with large volume change

Low compliance = large pressure change with small volume change

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59
Q

Ease of stretch or distensibility

A

Compliance

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60
Q

Tendency to oppose stretch or dissension; ability to return to original after stretching

A

Elasticity

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61
Q

What is hysteresis?

A

A difference in the PV curve where inflation is at a lower totally lung volume that expiration - due to surfactant

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62
Q

What is the equation for lung compliance?

A

Change in lung volume / transpulmonary pressure

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63
Q

What is the equation for chest wall compliance?

A

Change in lung volume / chest wall’s distending pressure

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64
Q

What is the equation for combined (lung + chest wall) compliance?

A

Change in lung volume / (alveolar pressure - atmospheric pressure )

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65
Q

What can cause changes in chest wall compliance?

A

Pregnancy or obesity - Decrease range of motion of diaphragm

Musculoskeletal disorders - decrease motion of rib cage

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66
Q

What is the Law of LaPlace?

A

P = 2T/r

Where:
T = wall tension
R = radius

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67
Q

What happens to the intrapleural pressure if lung elasticity decreases (due to aging or disease)?

A

It becomes less negative

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68
Q

Why do smaller alveoli have higher pressure?

A

Because surface tension is the same for all alveoli so the driving force for pressure is dependent on radius (smaller radius = higher pressure)

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69
Q

How does surfactant work to keeps the lungs from collapsing?

A
  • decreases surface tension
  • increases lung compliance
  • breaks up water molecules and is more effective in smaller alveoli
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70
Q

What is surfactant made out of?

A

85-90% lipids and 10-15% proteins

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71
Q

What contributes to pulmonary resistance?

A 
Lung Tissue resistance (20%)
Airway resistance (80%)
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72
Q

Where is the largest resistance in the lungs?

A

In the LARGER segmental bronchi (no cartilage, less surface area)

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73
Q

What is Poiseuille’s Law?

A

R is proportional to (n*L)/r^4

F = deltaP/R

F is proportional to (deltaP * r^4)/(n*L)

F = flow 
R = resistance
DeltaP = pressure difference
r = radius
n = viscosity
L = length
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74
Q

What happens to resistance during inspiration and expiration?

A

As lung expands, radius of alveoli increases and resistance decreases

Small changes in radius = big changes in resistance (r^4)

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75
Q

What factors affect resistance in the airway?

A 
Transpulmonary pressure (indirectly related)
Lateral traction/elastic recoil (directly)
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76
Q

What determines the radius of alveoli?

A

Transpulmonary pressure gradient

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77
Q

Describe dynamic airway compression.

A

As air moves out, it rubs against the walls of the airway ad pressure drops on the way out.
At the equal pressure point (EPP), the pressure equalizes with the intrapleural pressure and the. Airway can collapse (if not reinforced by cartilage)

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78
Q

Why is dynamic airway compression more likely to happen at low lung volumes than high lung volumes?

A

It happens in low lung volumes because the alveolar pressure is lower and closer to the intrapleural pressure and so the EPP shifts down and if it ends up in non-cartilaginous bronchi the airway will collapse

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79
Q

At what point of VC is dynamic airway compression?

A

High risk of airway compression in low lung volumes (<60%)

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80
Q

Why do we see “pursed-lip” breathing in patients with lung diseases of increased compliance?

A

“Pursed lips” will increase airway resistance and thus airway pressure, moving the EPP higher and reducing the risk of airway collapse

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81
Q

Volume at which airway closure begins during forced expiration

A

Closing capacity

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82
Q

The volume expired from closing capacity to residual volume

A

Closing volume

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83
Q

How does emphysema affect closing capacity?

A

Decreased in elastic recoil —> decrease in lateral traction to help get air out —> increased closing capacity

Airways close at higher volumes + trap gas

Patient breaths at higher volumes to increase recoil

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84
Q

What is Henry’s Law and what does it measure?

A

C = P * S

C = concentration
P = partial pressure
S = solubility
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85
Q

What is Fick’s Law and what does it measure?

A

V = DSA(P1-P2)/deltaX

D = diffusion coefficient
S = solubility
A = surface area of barrier
P1-P2 = partial pressure gradient
DeltaX = thickness of barrier

Volume of gas diffusing through alveolar-capillary barrier per unit of time

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86
Q

The diffusion coefficient is indirectly proportional to what?

A

The molecular weight (aka. The bigger the molecule, the slower it diffuses)

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87
Q

Why does CO2 diffuse faster than O2 despite having a lower diffusion coefficient?

A

It’s is 24x more soluble due to the bicarbonate system

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88
Q

What is Dalton’s law and what does it measure?

A

Pgas = Ptotal * Fgas

Determines partial pressure of a gas

IN LUNGS:

Pgas = (Ptotal - PH2O) * Fgas

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89
Q

How much pressure does water vapor exert always?

A

47 mm Hg

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90
Q

How does the rate of diffusion change along the length of the capillary at the alveolus?

A

It decreases

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91
Q

The changes in blood partial pressures for oxygen and CO2 are +60mmHg and -6mmHg respectively but the amounts of gas moved are roughly the same… how is this possible?

A

CO2 has a high solubility so a small pressure difference can move a large amount of gas where as oxygen is less soluble

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92
Q

Why is there still a lot of CO2 left in the blood after gas exchange?

A

Due to bicarbonate which plays a role in blood pH

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93
Q

When and won’t you see equilibrium in gas exchange?

A 
Perfusion-limited = equilibrium
Diffusion-limited = no equilibrium
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94
Q

What is the equation for the diffusing capacity of the lung?

A

DL = DSA/deltaX

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95
Q

What gas is diffusion capacity measured with and why?

A

Carbon monoxide because it binds immediately with hemoglobin and doesn’t accumulate in the blood (partial pressure is 0); diffusion limited

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96
Q

What is PAO2 determined by?

A

Balance between removal of O2 and replenishment by ventilation

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97
Q

What is PACO2 determined by?

A

Balance between addition of CO2 and removal by ventilation

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98
Q

What is the alveolar ventilation equation?

A

VA = VCO2*(Pb - 47mmHg)/PACO2)

VA = volume of alveolar gas
VCO2 = volume of CO2 produced
Pb = barometric pressure
PACO2 = pressure of alveolar CO2
99
Q

What is the alveolar gas equation?

A

PAO2 = PIO2 - (PACO2/R)

PAO2 = pressure of alveolar O2
PIO2 = pressure of inspired oxygen
PACO2 = pressure of alveolar CO2
R = respiratory exchange quotient
100
Q

What is minute ventilation (VE)?

A

VE = (VDf) + (VAf)

101
Q

What is the equation for tidal volume?

A

VT = VD + VA

VD = volume of an atomic dead space
VA = volume of alveoli
102
Q

How much time does blood spend in the pulmonary capillaries? How long does it normally take for O2 to reach equilibrium?

A
  1. 75 sec

0. 3 sec

103
Q

Alveoli that can not be perfused

A

Alveolar dead space

104
Q

What is physiologic dead space?

A

Alveolar dead space + anatomical dead space

105
Q

How is physiologic dead space measured? What is the equation?

A

Simplified Bohr Equation:

VD/VT = (PACO2 - PECO2)/PACO2

VD = volume of physiologic dead space
VT = tidal volume
PACO2 = pressure of alveolar CO2
PECO2 = pressure of expiratory CO2
106
Q

Low oxygen delivery to tissues

A

Hypoxia

107
Q

Low oxygen content in blood

A

Hypoxemia

108
Q

What are the causes of hypoxemia?

A

Hypoventilation
Diffusion impairment
Shunt
V-Q mismatching

109
Q

Describe compliance at the apex vs. the base of the lung.

A

Due to gravity, the intrapleural pressure is higher at the top of the lung (alveoli are more distended) so compliance is lower

110
Q

Describe perfusion at the apex vs. the base of the lung.

A

Due to gravity, there is a drop in hydrostatic pressure at every level above the heart —> decrease BP —> less distended vessels —> reduced radius —> increased resistance —> decreased blood flow

111
Q

Why is a normal V/Q 0.8 and not 1.0?

A

Perfusion usually has a steeper gradient and makes more of a difference (due to gravity)

112
Q

Capillaries that have no gas exchange in the lungs; function is to dilate as lung expands to reduce resistance

A

Extraalveolar capillaries

113
Q

Capillaries in the lung that constrict during inhalation leading to more resistance

A

Alveolar capillaries

114
Q

What leads to decreased vascular resistance during inhalation?

A

Extraalveolar capillaries

Lateral traction

115
Q

Poorly ventilated lung units that equilibrate to near mixed venous blood

A

Shunt

116
Q

Poorly perfused lung units that equilibrate to near inspired air

A

Dead space

117
Q

What is V/Q at the apex of the lung compared to the base?

A

Apex - high V/Q

Base - low V/Q

118
Q

How do the different V/Q regions of the lung affect arterial blood?

A

The blood at the base is “wasted perfusion because it is better perfused than ventilated. The blood at the apex is “wasted ventilation” because it is better ventilated than perfused.

119
Q

How do the oxygen partial pressures compare at the apex of the lung?

A

PA>Pa>Pv

120
Q

How do the oxygen partial pressures compare at the base of the lung?

A

Pa>Pv>PA

121
Q

What are some examples of hypoxia?

A

Anemia
Blood loss
Decreased cardiac output

122
Q

What are some examples of hypoxemia that would cause a normal A-a gradient? Is it responsive to O2?

A

Hypoventilation
Altitude

Responsive to O2.

123
Q

What are some examples of hypoxemia that would cause a increased A-a gradient? Is it responsive to O2?

A

Shunt/V-Q mismatch
diffusion problem
R—>L shunt

Not responsive to O2.

124
Q

What is a normal A-a gradient?

A

4-10 mmHg

125
Q

When would we see perfusion-limited oxygenation?

A

Exercise (normal)

126
Q

When would we see diffusion/ventilation-limited oxygenation?

A

In a pathological condition (ie. shunt, V/Q mismatch, etc.)

127
Q

How is diffusion tested?

A

DCLO - tests diffusion with CO because it binds immediately with Hb

128
Q

What is the cause of NATURAL shunts?

A

Mismatching of ventilation and blood flow in various parts of the lungs

129
Q

What is the normal V/Q ratio and what does it mean?

A

0.8

Normal VA = 4 L/min
Normal pulmonary blood flow = 5 L/min

130
Q

What are examples of normal R—>L shunts?

A
  • returning bronchial circulation to left heart via pulmonary veins
  • Returning coronary venous blood to the left ventricle via thebesian veins
131
Q

What can cause a physiologic R—>L shunt?

A

Congenital heart disease (atrial septal defects, patent foramen ovale)

Pulmonary disease (cor pulmonale)

132
Q

abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels

A

Cor pulmonale

133
Q

Why wouldn’t supplemental O2 be useful for shunts?

A

Hb carries most of the oxygen in blood and they are already usually fully saturated. Only a small amount is dissolved as well. Blood is shunted so it never sees the extra oxygen anyway.

134
Q

What are some examples of diffusion impairment?

A
  • Diffuse interstitial fibrosis
  • Asbestosis
  • Fluid build up/thickening of alveolar walls (pneumonia)
135
Q

Why do athletes sometimes have widened A-a gradients?

A

Huge cardiac output —> short transit time of blood —> blood not fully oxygenated —> decreased PcO2 and widened A-a gradient

136
Q

How to allosteric properties contribute to Hb binding of O2?

A

They make each consecutive oxygen easier to bind and vice versa

137
Q

What happens when you increased PAO2 to 600mmHg?

A

Increase in total oxygen but minimal — most of the gain is in dissolved oxygen because Hb already fully saturated

138
Q

What are the Bunsen solubility coefficients for O2, CO2, and N2?

A

O2: 0.003 mL/100ml/mmHg
CO2: 0.075 mL/100mL/mmHg
N2: 0.0017 mL/100mL/mmHg

139
Q

How does temperature affect the Hb sat curve?

A

Increased temp shifts it to the right —> decreases affinity (favors unloading of oxygen)

140
Q

How does pH affect the Hb sat curve? Why does this occur?

A

Decrease in pH (increase in H+ ions) shifts it to the right —> decreased affinity

                                                                                                      higher hydrogen ion concentration causes an alteration in amino acid residues that stabilises deoxyhaemoglobin in a state (the T state) that has a lower affinity for oxygen
141
Q

How does PCO2 affect the Hb sat curve? Why does this occur?

A

Increased pCO2 shifts it to the right —> decreases affinity (favors unloading of oxygen)

Increased CO2 —> signals hypoxia —> decreased affinity for O2

142
Q

How does 2,3-DPG affect the Hb sat curve? Why does this occur?

A

Increased 2,3-DPG shifts it to the right —> decreases affinity (favors unloading of oxygen)

Chronic hypoxia, anemia, acclimation to altitude —> low RBC PO2 —> increased glycolysis and 2,3-DPG —> lowers hemoglobin’s affinity for oxygen by binding preferentially to deoxyhemoglobin

*Glycolysis is part of both anaerobic and aerobic pathway but produces 2 ATP so it is essential for keeping energy up

143
Q

How does myoglobin differ from hemoglobin?

A
  • found in tissues
  • high affinity for O2
  • last ditch oxygen reserve in cells (mostly muscle)
  • regular curve vs. sigmoidal
144
Q

How does anemia change the hemoglobin sat curve?

A

Maintains sigmoidal curve but its lowered because anemic blood can’t carry as much oxygen

145
Q

How does CO poisoning change the Hb sat curve?

A

Shifts to a regular curve (comparable to myoglobin curve); CO binds to Hb 200x better that O2 —> Hb carries less oxygen and reduces O2 delivery to tissues

146
Q

How is CO poisoning treated?

A
  • High flow O2

- Hyperbaric oxygen chamber (increased pressure decreases binding of CO-Hb)

147
Q

What is the chemical equation for CO2 transport in blood?

A

CO2 + H2O —> H2CO3 —> H+ + HCO3-

148
Q

What happens to CO2 transport in tissues?

A

increased CO2 —> increase H+ + HCO3-

HCO3 is pumped out using an HCO3-/Cl- transporter

H+ binds with histidines on hemoglobin and decreased affinity for oxygen

149
Q

What happens to CO2 transport in the lungs?

A

Decreased PCO2 —> decreased H+ and HCO3-

HCO3- is pumped back into the RBC to make CO2

H+ un-binds from RBC, increasing affinity for O2

150
Q

Which enzyme is responsible for converting CO2 to H2CO3 and vice versa?

A

Carbonic anhydrase

151
Q

What role to carbamino compounds in RBCs play in increased PCO2 (tissues)?

A

CO2 bind with Hb-NH2 to form Hb-NH-COO- and H+

H+ binds to histidine on Hb and decreases affinity for oxygen

152
Q

What are the ratios of transported forms of CO2?

A

Carbonate - 60%
Carbamino - 30%
Dissolved - 10%

153
Q

The more CO2 bound to hemoglobin the less affinity for oxygen and vice versa

A

Haldane Effect

154
Q

Why is deoxygenated blood able to carry more CO2 that oxygenated blood?

A

Carbamino

155
Q

The increase in frequency of impulses from respiratory muscle nerves at the onset of inspiration and rapid decrease near the end of inspiration

A

Augmenting

156
Q

What 3 things increase the depth of respiration?

A
  • increased impulses from each motor unit
  • recruitment of motor units
  • longer duration of burst of impulses
157
Q

How are TV and RR related?

A

Inversely proportional

158
Q

Respiratory center in the Nucleus of the Solitary Tract in the medulla associated with inspiration only

A

Dorsal Respiratory Group (DRG)

159
Q

Respiratory center in the medulla associated with inspiration AND expiration

A

Ventral respiratory group (VRG)

160
Q

Respiratory center in the upper pons associated with early cut off of respiration

A

Pneumotaxic center (pontine respiratory group)

161
Q

What results in apneustic breathing?

A

Lesion of BOTH the pneumotaxic respiratory group and the vagus nerve

162
Q

What part of the respiratory center is responsible for the self-cycling circuits of respiration?

A

DRG

163
Q

What part of the respiratory center is responsible for the pacemaker activity of respiration?

A

Pre-Botzinger complex in the ROS trail portion of the VRG

164
Q

Describe the process of the self-cycling circuit in respiration.

A

DRG/VRG activate —> B medullary neurons (DRG also activates motor neurons in cervical spinal cord and external intercostals) —> C inhibitory neurons —< DRG

165
Q

How does the pontine respiratory group affect the self-cycling respiratory circuit?

A

It activates the C neurons which inhibit DRG (end inspiration)

166
Q

How does the vagus nerve affect the self-cycling respiratory circuit?

A

It’s activates the medullary B neurons, which activated C neurons, which inhibit DRG

167
Q

Pulmonary stretch receptors in the airway smooth muscle layer detect lung inflation and stimulate vagus nerve activity (inhibit inspiration)

A

Hering-Breuer reflex

168
Q

Where are the peripheral chemoreceptors located?

A

Carotid (carotid sinus) and aortic bodies

169
Q

Where are the central chemoreceptors located?

A

Ventral surface of the medulla

170
Q

Changes in oxygen and pH stimulate which receptors? What about CO2?

A

O2/pH - peripheral

CO2/CSF pH - central

171
Q

What difference in PCO2 will double ventilation?

A

3 mmHg

172
Q

What is the maximum PCO2 that the central chemoreceptors will respond to? Why?

A

70-80 mmHg

Toxic effects of high CO2 on central neuronal function will decrease ventilation

173
Q

What happens with chronically elevated PCO2 levels?

A

Chronically decreased pH of CSF —> compensatory increase in HCO3- (shifts equilibrium left)

Also decreased sensitivity of central chemoreceptors

174
Q

What happens with chronically reduced PCO2 levels (high altitude)?

A

Chronically increased pH of CSF —> compensatory decrease in HCO3- (shifts equilibrium right)

Also increased sensitivity of central chemoreceptors

175
Q

What is the most important peripheral chemoreceptor?

A

Carotid bodies

176
Q

At what change in fractional atmospheric O2 will we see an increase in ventilation?

A

A fraction of less than 10%

Blood: ~60 mmHg

177
Q

Which cells in the peripheral chemoreceptors respond to O2 levels? How so?

A

Type 1 Glomus cells —> O2 sensitive channels sense decreased PO2/blood flow/pH —> K+ channels close —> depolarization

178
Q

What happens if you lesion the peripheral chemoreceptors?

A

Complete loss of respiratory response to changes in arterial PO2 (PCO2 response intact)

179
Q

How do central chemoreceptors respond to pH? How do H+ ions cross the BBB?

A

They respond to LARGE changes in pH; however, pH only has a small effect

“breaks” in the BBB allow H+ to cross

180
Q

What are the other inputs to the respiratory centers aside from the peripheral and central chemoreceptors (6)?

A
  • cerebral cortex: voluntary control
  • hypothalamic center/limbic system: emotional states
  • hypothalamic/skin temperature receptors: helps lose body heat
  • muscular/join receptors: exercise
  • medullary reflexive areas: swallowing/vomiting
  • baroreceptors: increase RR with decreased BP and vice versa
181
Q

At what age is the Hering-Breuer inflation reflex strongest?

A

In un-anesthetized infants during the first 5 days of life

182
Q

Where are irritant receptors in the airway located and what do they respond to?

A

Between epithelial cells

Noxious gases, ammonia, cigarette smoke, histamine

183
Q

Where are J (juxtacapillary) receptors in the airway located and what do they respond to? What nerve to they travel in?

A

Conducting airways and alveoli

Chemical and mechanical stimulation

Vagus nerve (slowly conducting, unmyelinated, C fibers)

184
Q

What is Cheynes-Stokes breathing and what causes it?

A

Hyperventilation followed by deep respiration excursions that diminish to the point of apnea

Caused by abnormally long delay for transport of arterial gases from pulmonary circulation to the brain

185
Q

What is apneustic breathing and what causes it?

A

Deep inspirations lasting from 30-90 seconds followed by brief periods of expiratio

Cause by damage to pons or medulla

186
Q

What is sleep apnea and how is it treated?

A

Mechanical blockage of airways prevents inspiration —> rise of PACO2 a d fall of PO2 levels leads to arousal and opening of airway

Treated with nasal CPAP

187
Q

What is the equilibrium equation for blood pH?

A

PH = pKD + log [AC-]/[HAc]

188
Q

When optimal buffering occurs, what is true about pH?

A

Optimal buffering: pH = pKD

[Ac-]/[HAc] = 1

189
Q

What are the 3 main buffering systems in the body?

A

Phosphate buffer system
Proteins (hemoglobin)
Carbonate buffer system

190
Q

What is the equation and pKD of the phosphate buffer system?

A

NaHPO4-2 + H+ —> NaH2PO4-

pKD = 6.8

191
Q

What is the pKD for the hemoglobin buffer system? Which amino acid is the main contributor to this buffer?

A

Histadine

The pKD = 7.0-7.8

192
Q

What organs regulate the carbonate system?

A

Kidneys and lungs

193
Q

A pH of 7.4 in the blood is equal to which concentration of protons?

A

40 nMol

194
Q

If acid is added to the blood, how does it affect the pH and buffer concentrations?

A

Most of it binds with buffers but some remains dissolved = deacreased pH

The ratios for ALL buffers are still independently in equilibrium with the new pH

195
Q

What is the normal bicarbonate concentration for a blood pH of 7.4?

A

24 mMol

196
Q

What happens during metabolic acidosis? What are the compensatory mechanisms?

A

Increased H+/removal of HCO3- (diarrhea) —> shift eq right —> decrease pH —> detection by peripheral chemoreceptors —> increase ventilation —> lowers PCO2 —> drives reaction back to left

**brain senses low CO2 levels but not pH —> opposes hyperventilation (doesn’t completely compensate)

197
Q

When all buffers in a solution are in equilibrium with the same H+ concentration

A

Isohydric principle

198
Q

What happens during metabolic alkalosis? What are the compensatory mechanisms?

A

Addition of HCO3-/removal of H+(vomiting) —> shift eq left —> increase pH —> detection by peripheral chemoreceptors —> decrease ventilation —> raises PCO2 —> drives reaction back to right

**brain senses higher CO2 levels but not pH —> opposes hypoventilation (doesn’t completely compensate)

199
Q

What happens during respiratory acidosis? What are the compensatory mechanisms?

A

Decreased ventilation —> increased CO2 —> shifts eq right —> increased H+ —> increased formation of bicarbonate in kidneys to shift eq back left

200
Q

What happens during respiratory alkalosis? What are the compensatory mechanisms?

A

Increased ventilation —> decreased CO2 —> shifts eq left —> decreased H+ —> decreased formation of bicarbonate in kidneys to shift eq back right

201
Q

The proportion of whole blood that is composed of red blood cells

A

Hematocrit (normal: 45-50%)

202
Q

When blood is centrifuges, this layer is the one that contains leukocytes and platelets

A

Buffy coat

203
Q

How much Hb is is RBCs? Why does it need to be in RBCs?

A

30 g/dL

Hb has a short half-life in circulation and packaging in RBCs shields it from rapid removal

204
Q

What are some unique characteristics of RBCs?

A
  • Has no nucleus, ribosomes, ER, or mitochondria
  • No protein synthesis once mature
  • 120 day lifespan
205
Q

Formed in slow flowing blood when RBCs stack up/stick together

A

Rouleaux

206
Q

Why is the biconcave shape beneficial for a RBC?

A

Needs to deform to pass through capillaries —> more flexible

207
Q

What protein is responsible for the shape of RBCs?

A

Spectrin

208
Q

What does a deficiency of spectrin result in?

A

Spherocytosis - sphere-shaped RBCs with much shorter half-lives

209
Q

What happens if RBC gets depleted of ATP?

A

RBC becomes crenated (shrivels up). ATP important in maintaining cell shape

210
Q

How is ATP made in RBCs?

A

Anaerobic glycolysis

211
Q

How does the RBC get glucose?

A

It readily diffuses into the cell (not insulin required)

212
Q

Where does most of the RBCs energy go?

A

ATPase pumps

Also some to Ca+2 pumps to pump calcium out

213
Q

What happens if Ca+2 accumulates in the RBC?

A

RBCs form “spikes” and becomes an echinocyte

214
Q

What occurs with sickle cell anemia?

A

Change in a single Hb amino acid —> low O2/pH causes HbS to crystallize and aggregate to form long rigid rods —> leads to “sickle” shape

215
Q

Why are sickle cells problematic?

A
  • not flexible

- blocks vasculature (which deceases O2 even more and propagates the problem)

216
Q

What happens in a sickle cell crisis?

A

Build up of sickle cells becomes irreversible, non-functional, and leads to breakdown and removal of RBCs

217
Q

Why is oxidation harmful to RBCs?

A
  • damages Hb

- Fe2+ can be oxidized to ferric iron Fe3+ (methemoglobin) which is non-functional

218
Q

Enzyme in the RBCs that restores iron to Fe+2 form using NADH as a cofactor

A

Methemoglobin reductase

219
Q

How does H2O2 damage hemoglobin? What is the defense mechanism against this?

A

H2O2 cross-links cysteine of Hb and inactivated it

Presence of GSH - reacts with H2O2 to protect Hb

220
Q

How does GSH (glutathione) get reduced back to normal?

A

Glutathione reductase uses NADPH to reduce glutathione

221
Q

Where does NADPH in RBCs come from?

A

Glucose-6-phosphate dehydrogenase

222
Q

What would happen if a patient had a deficiency in G6PD?

A

Hemolytic anemia

223
Q

Why is 2,3-DPG important in RBCs?

A

In low levels of O2, 2,3-DPG binds to Hb and reduces the affinity for O2 to increase tissue delivery

224
Q

Where are RBCs made in the fetus? What about at birth? As an adult?

A

Fetus: yolk sac/liver/spleen
Birth: bone marrow only
Adult: axial skeleton

225
Q

How does bone marrow make RBCs?

A

Marrow precursors (stem cells) —> 4 divisions —> normoblasts —> Hb synthesis for 4-5 days —> Hb reaches mature levels —> nucleus/mitochondria extruded —> reticulocyte —> enters circulation and Hb synthesis continues for about 2 days before RNA/ribosomes/ER break down —> mature RBC

226
Q

How is the formation of RBCs regulated?

A

Low O2 detected by JG apparatus in the kidney —> kidney releases erythropoietin (EPO) —> EPO stimulates formation and maturation of RBC precursors

227
Q

% of RBCs that are reticulocytes

A

Reticulocyte index

228
Q

What would cause the reticulocyte index to increase?

A

Increased production of RBCs (indicative of anemia)

229
Q

What is required for Hb formation? Where does Hb production occur?

A

Occurs in normoblast

Iron-dependent: recycled from old RBCs, body stores, and GI tract

230
Q

How is Hb formed?

A

Transferrin binds recycled iron —> uptake of transferrin by normoblast —> iron released into cell —> iron moves into mitochondria and made into heme while alpha and beta chains are made by the ribosomes

231
Q

How is iron stored in the normoblast until it is ready to be used?

A

Stored in hemosiderin

232
Q

What happens when RBCs are near their end of life?

A

Become senescent —> lose flexibility and denatured Hb forms lumps) —> recognized by macrophages and engulfed, mainly in spleen

233
Q

How does the spleen aid in filtering out old RBCs?

A

Old RBCs are less flexible and get stuck in crevices of spleen

234
Q

Breakdown or lysis of RBCs in macrophages

A

Extravascular hemolysis

235
Q

What happens during extravascular hemolysis?

A

RBC broken down into heme chain (recycled via transferrin), goblin (broken down into amino acids), and porphyrin ring (broken down to bilirubin, which is bound to albumin, taken to liver, and excreted in feces)

236
Q

What happens during intramuscular hemolysis?

A

Hemoglobin released into blood:

  1. Hb becomes oxidized to methemoglobin - globin becomes amino acids and heme group bound by hemopexin and brought to liver where its broken down
  2. Hb split into dimer —> binds with haptoglobin —> brought to liver to be broken down (if no haptoglobin available, dimers are excreted in urine by kidneys)
237
Q

What are some signs of intravascular hemolysis?

A
  • low levels of haptoglobin (seen after 5 days)

- hemoglobinuria - hemoglobin in urine (last for 2 days)

238
Q

What are some causes for hypoproliferative anemia?

A
  • iron deficiency
  • acute bleeding (losing recyclable iron)
  • inflammation (macrophage hangs onto iron, iron feeds bacteria)
  • bone marrow damage
  • inability to release EPO (signaling molecule for erythropoiesis
239
Q

What are some examples of hemolytic anemias?

A
  • G6PD deficiency - increases RBC sensitivity to oxidative agents
  • Sickle cell - RBCs deformed + trapped in spleen
  • Hereditary spherocytosis - RBCs suffer damage when passing through spleen
240
Q

Anemia caused by vitamin B12 deficiency

A

Pernicious anemia

241
Q

When alpha and beta globin chains are not synthesized in equal amounts —> destruction of RBC precursors in marrow

A

Thalassemia

242
Q

Describe what happens in a mother who is Rh-negative with an Rh-positive fetus.

A

Red cells from baby introduce D antigen to maternal circulation at birth —> mother forms antibodies —> second Rh+ fetus —> Rh antibodies attack fetal RBCs

243
Q

Hemolytic disorder of the fetus due to Rh antibodies; effects may be irreversible (high bilirubin can cause fetal brain damage)

A

Erythroblastosis fetalis

244
Q

How is Erythroblastosis fetalis treated/prevented?

A

Treated:

  • fetal transfusion
  • plasma exchange for mother (to dilute antibodies)

Prevented:
-Rhogam (antibodies to D antigen that rapidly remove it from maternal circulation at birth)

BUPA Physiology (3 decks)

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