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Anatomy and Physiology > respiratory iii > Flashcards

respiratory iii Flashcards

1
Q

Gas exchanges bt blood, lungs, and tissues

A

external respiration = diffusion of gases in lungs

Internal respiration = diffusion of gases at body tissues

Both involve

  • physical properties of gases
  • composition of alveolar gas
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2
Q

Dalton’s law of partial pressures

A

Total pressure exerted by mixture of gases = sum of pressures exerted by each gas

Partial pressure

  • pressure exerted by each gas in mixture
  • directly proportional to its percentage in mixture
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3
Q

Henry’s law

A

Gas mixtures in contact with liquid

  • each gas dissolves in proportion to its partial pressure
  • at equilibrium, partial pressures in two phases will be equal

amount of each gas that will dissolve depends on

  • solubility: CO2 is 20 timese more soluble in water than O2 –> little N2 dissolves in water
  • Temp: as temp rises, solubility decreases
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4
Q

Composition of alveolar gas

A

Alveoli contain more CO2 and water vapor than atmospheric air

  • gas exchanges in lungs
  • humidification of air
  • mixing of alveolar gas with each breath
N2 = 75%
O2 = 14%
CO2 = 5%
H2O = 6%
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5
Q

Nitrogen

A

Even though the air we breathe is mostly N2, very little dissolves in blood due to low solubility
-can be overcome by increasing pressure - hyperbaric environment

Decompression sickness (beds) due to rapid decreasing of barometric pressure allowing dissolved nitrogen bubble out of blood

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6
Q

External respiration

A

exchange of O2 and CO2 across respiratory membrane

Influenced by

  • thickness and surfac area of respiratory membrane
  • partial pressure gradients and gas solubilities
  • ventilation-perfusion coupling
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7
Q

Thickness and surface area of respiratory membrane

A

Respiratory membranes

  • 0.5 to 1 um thick
  • large surface area (40 times that of skin) for gas exchange

Thickens if lungs become waterlogged and edematous –> gas exchange inadequate

Reduced surface area in emphysema (walls of adjacent alveoli break down), tumors, inflammation, mucus

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8
Q

Partial pressure gradients and gas solubilities: O2

A

Steep partial pressure gradient for O2 in lungs

venous blood O2 pressure = 40 mm Hg

alveolar O2 pressure = 104 mm Hg

  • drives oxygen flow to blood
  • equilibrium reached across respiratory membrane in 0.25 s, about 1/3 time of a rbc in pulmonary capillary –> adequate oxygenation even if blood flow increases 3x
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9
Q

Partial pressure gradients and gas solubilities: CO2

A

Partial pressure gradient for CO2 in lungs less steep

  • venous blood CO2 pressure = 45 mm Hg
  • Alveolar CO2 pressure = 40 mm Hg

Though gradient not as steep, CO2 diffuses in equal amounts with oxygen
-CO2 is 20 times more soluble in plasma than oxygen

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10
Q

Ventilation-perfusion coupling

A

Perfusion = blood flow reaching alveoli

Ventilation = amt of gas reaching alveoli

Ventilation and perfusion matched (coupled) for efficient gas exchange

  • never balanced for all alveoli due to:
    1. regional variations due to effect of gravity on blood and air flow
    2. some alveolar ducts plugged with mucus
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11
Q

ventilation-perfusion coupling: at alveolar level with dif gasses

A

Changes in O2 pressure in alveoli cause changes in diameters of arterioles

  • where alveolar O2 is high, arterioles dilate
  • where alveolar O2 is low, arterioles constrict
  • directs most blood to where alveolar oxygen is high

Changes in CO2 pressure in alveoli cause changes of diameters of bronchioles

  • where alveolar CO2 is high, bronchioles dilate
  • where alveolar CO2 is low, bronchioles constrict
  • allows elimination of CO2 more rapidly
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12
Q

Internal respiration

A

capillary gas exchange in body tissues

Partial pressures and diffusion gradients reversed compared to external respiration

  • tissue O2 pressure always lower than in systemic arterial blood –> oxygen from blood to tissues
  • CO2 from tissues to blood
  • venous blood oxygen pressure = 40 mm HG and CO2 pressure = 45 mm Hg
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13
Q

O2 transport in blood

A

molecular O2 carried in blood

  • 1.5% dissolved in plasma
  • 98.5% loosely bound to each Fe of hemoglobin in RBCs (4 O2 per Hb)
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14
Q

O2 and hemoglobin

A

Oxyhemoglobin = hemoglobin-O2 combo

Reduced hemoglobin = deoxyhemoglobin = hemoglobin that has released O2
-Deoxyhemoglobis is usually still 75% saturated

Loading and unloading of O2 facilitated by change in shape of Hb

  • as O2 binds, Hb affinity for O2 increases
  • as O2 is released, Hb affinity for O2 decreasies
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15
Q

Things that affect rate of loading and unloading of O2

A

Oxygen pressure
temp
blood ph
Carbon dioxide pressure

Concentration of BPG –> produced by RBCs during glycolysis; levels rise when oxygen levels are chronically low, so that hemoglobin’s affinity for O2 will decrease

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16
Q

Oxygen pressure’s effect on hemoglobin saturation

A

Oxygen-hemoglobin dissociation curve

Hemoglobin saturation plotted against oxygen pressure is not linea; S-shaped curve
-binding and release of O2 influenced by oxygen pressure

17
Q

Oxygen pressure’s effect on hemoglobin saturation: arterial blood

A

In arterial blood

  • oxygen pressure = 100 mm Hg
  • contains 20 ml oxygen per 100 ml blood (20% volume)
  • Hb is 98% saturated

Further increases in PO2 (breathing deeply) produce minimal increases in O2 binding

18
Q

Oxygen pressure’s effect on hemoglobin saturation: venous blood

A

In venous blood

  • PO2 = 40 mm Hg
  • Contains 15% volume oxygen
  • Hb is 75% saturated

Venous reserve = oxygen remaining in venous blood

19
Q

Other things’ effect on Hemoglobin saturation

A

Increases in temp, H+, PCO2, and BPG

  • modify structure of hemoglobin; decrease its affinity for O2
  • occur in systemic capillaries
  • enhance O2 unloading from blood
  • shift O2-hemoglobin dissociation curve to right

Decrease in these factors shift curve to left –> decreases O2 unloading from blood

20
Q

Factors that increase release of O2 by hemoglobin

A

As cells metabolize glucose and use O2

  • PCO2 and H+ increase in capillary blood
  • Declining blood ph and increasing PCO2 –> bohr effect = hb-O2 bonds weaken and oxygen unloading where needed most
  • heat production increases –> directly and indirectly decreases Hb affinity for O2 –> increased oxygen unloading to activate tissues
21
Q

Hypoxia

A

inadequate O2 delivery to tissues (cyanosis = blue skin)

  • Anemic hypoxia = too few RBCs; abnormal or too little Hb
  • Ischemic hypoxia = impaired/blocked circulation
  • histotoxic hypoxia = cells unable to use O2 as in metabolic poisons
  • hypoxemic hypoxia = abnormal ventilation; pulmonary disease
  • Carbon monoxide poisoning = especially from fire; 200x greater affinity for Hb than O2
22
Q

Carbon dioxide transport

A

happens in 3 forms

  • 7 to 10% dissolved in plasma
  • 20% bound to globin of hemoglobin (carbaminohemoglobin)
  • 70% transported as bicarbonate ions (HCO3-) in plasma
23
Q

Transport and exchange of CO2

A

CO2 combines with water to form carbonic acid (H2CO3) which quickly dissociates

Occurs primarily in RBCs where carbonic anhydrase reversibly and rapidly catalyzes the reaction

24
Q

Transport and exchange of CO2 in systemic capillaries

A

HCO3- quickly diffuses from RBCs into plasma

-chloride shift occurs –> outrush of HCO3- from RBCs balanced as CL- moves into RBCs from plasma

25
Q

transport and exchange of CO2 in pulmonary capillaries

A
  • HCO3- moves into RBCs (while Cl- moves out); binds with H+ to form H2CO3
  • H2CO3 split by carbonic anhydrase into CO2 and water
  • CO2 diffuses into alveoli
26
Q

Haldane effect

A

Amount of CO2 transported affected by PO2

  • reduced hemoglobin (less O2 saturation) forms carbaminohemoglobin and buffers H+ more easily
  • lower PO2 and hemoglobin saturation with O2; more CO2 carried in blood

Encourages CO2 exchange in tissues and lungs

At tissues, as more CO2 enters blood

  • more oxygen dissociates from hemoglobin (bohr effect)
  • as HbO2 releases O2, it more readily forms bonds with CO2 to form carbaminohemoglobin
27
Q

Influence of CO2 on Blood pH (buffer system)

A

Carbonic acid- bicarbonate buffer system –> resists changes in blood pH

  • if H+ concentration in blood rises, excess H+ is removed by combining with HCO3- –> H2CO3
  • If H+ concentration begins to drop, H2CO3 dissociates, releaseing H+
  • HCO3- is alkaline reserve of carbonic acid-bicarbonate buffer system
28
Q

Influence of CO2 on Blood pH: respiratory rate

A

Slow, shallow breathing –> increased CO2 in blood –> drop in pH

Rapid, deep breathing –> decreased CO2 in blood –> rise in pH

Changes in ventilation can adjust pH when disturbed by metabolic factors

29
Q

Control of respiration

A

involves higher brain centers, chemoreceptors, and other reflexes

Neural controls

  • neurons in reticular formation of medulla and pons
  • clustered neurons in medulla important: ventral respiratory group and dorsal respiratory group
30
Q

Medullary respiratory center (VRG)

A

rhythm-generating and integrative center

  • sets eupnea (12-15 breaths/min) = normal
  • its inspiratory neurons excite inspiratory muscles via phrenic (diaphragm) and intercostal nerves (external intercostals)
  • expiratory neurons inhibit inspiratory neurons
31
Q

Medullary respiratory centers DRG

A

near rood of cranial nerve IX

Integrates input from peripheral stratch and chemoreceptors; sends into –> VRG

32
Q

Pontine respiratory centers

A
  • influence and modify activity of VRG
  • smooth out transition between inspiration and expiration and vice versa
  • transmit impulses to VRG –> modify and fine-tune breathing rhythms during vocalization, sleep, exercise
33
Q

Factors influencing breathing rate and depth

A
  • Depth determined by how actively respiratory center stimulates respiratory muscles
  • rate determined by how long inspiratory center active

Bothe modified in response to changing body demands

  • most important are changing levels of CO2, O2, and H+
  • sensed by central and peripheral chemoreceptors
34
Q

Chemical factors affecting breathing rate and depth (CO2)

A

Influence of PCO@ (most potent; most closely controled)

  • if blood PCO2 levels rise (hypercapnia), CO2 accumulates in brain
  • CO2 in brain hydrated –> carbonic acid –> dissociates, releasing H+ –> pH drops
  • H+ stimulates central chemoreceptors of brain stem
  • chemoreceptors synapse with respiratory regulatory centers –> increased depth and rate of breathing –> lower blood PCO2 –> pH rises
35
Q

Hyperventilation and apnea

A

Hyperventilation = increased depth and rate of breathing that exceeds body’s need to remove CO2
-decreased blood CO2 levels (hypocapnea) –> cerebral vasoconstriction and cerebral ischemia –> dizziness and fainting

Apnea = breathing cessation; may be due to abnormally low PCO2

36
Q

Chemical factors affecting depth and rate of breathing (PO2)

A

Peripheral chemoreceptors in aortic and carotid bodies - arterial O2 level sensors
-when excited, cause respiratory centers to increase ventilation

Declining PO2 normally slight effect on ventilation

  • huge O2 reservoir bound to Hb
  • Requires substantial drop in arterial PO2 (to 60 Hg to stimulate increased ventilation)
37
Q

Chemical factors: influence of arterial pH

A
  • can modify respiratory rate and rhythm even if CO2 and O2 levels are normal
  • mediated by peripheral chemoreceptors
  • decreased pH may reflect CO2 retention, accumulation of lactic acid; excess ketone bodies
  • respiratory system controls attempt to raise pH by increasing respiratory rate and depth
38
Q

Higher brain center influences: Hypothalamic and Cortical

A

Hypothalamic controls act through limbic system to modify rate and depth of respiration (e.g. breath holding that occurs in anger or gasping with pain)

Rise in body temp increases respiratory rate

Cortical controls - direct signals from cerebral motor cortex that bypass medullary controls (e.g. voluntary breath holding –> brain stem reinstates breathing when blood CO2 critical)

39
Q

Pulmonary irritant reflexes

A

Receptors in bronchioles respond to irritants
-communicate with respiratory centers via vagal nerve afferents

Promote reflexive constriction of air passages

Same irritant –> cough in trachea or bronchi; sneeze in nasal cavity

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