Respiratory System Flashcards

1
Q

4 functions of respiratory system

A
  • Transfer of gases between air and blood
  • Regulation of body pH (regulate CO2)
  • Defense from inhaled pathogens
  • Vocalization
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2
Q

Structures of respiratory system

A

Upper respiratory tract:
- Nasal cavity
- Pharynx
- Tongue
- Vocal cords
- Esophagus
- Larynx
Lower respiratory tract
- Right lung
- Left lung
- Right bronchus
- Left bronchus
- Diaphragm

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3
Q

Respiratory muscles

A

Muscles of inspiration(breathe in)
- Sternocleidomastoid
- Scalenes
- External intercostals
- Diaphragm
Muscles of expiration(breathe out)
- Internal intercostals
- Abdominal muscles

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4
Q

Pleural sacs

A
  • Enclose the lungs and help with easier breathing
  • Fluid in between sacs kept at negative pressure
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5
Q

Airways connect external to internal environment

A
  • Warms air to 37C
  • Humidifies air to 100%
  • Filters air (with nose and respiratory cilia)
  • Alveoli (where air exchange occurs)
  • Trachea branches into two primary bronchi, primary bronchus divides 22 more times terminating in cluster of alveoli
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6
Q

Cilia

A
  • Lines airways and filters away pathogens
  • Cilia moves mucus to pharynx -> mucus layer traps inhaled particles -> watery saline layer allows cilia to push mucus towards pharynx -> goblet cell secretes mucus
  • Immune cells secrete antibodies and disables pathogens
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7
Q

Airways

A
  • Function is to distrubute air to large surface area of alveoli and lower air velocity so air exchange has enough time
  • 1st bifurcation: Right and left main bronchi, 2nd - 4th bifurcation: lobar bronchi. Have cartilage to maintain shape
  • 5th - 11th bifurcation: Segmental bronchi. 12th - 16th bifurcation: Terminal bronchioles. Stabilised by bronchiolar muscles. Contain smooth muscle cell, can change size
  • All above: Conducting airways (no gas exchange)
  • Constitute an anatomical dead space, always filled with air and doesn’t participate in gas exchange
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8
Q

Primary lobule

A
  • Region of gas exchange
  • Approximately 300 million alveoli
  • Total cross sectional area is enormous, at about 180 cm^2
  • Air velocity nearly 0
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9
Q

Alveoli

A
  • Contain type 1 and 2 alveolar cells
  • Where lungs and blood exchange O2 and CO2 during process of breathing in and out
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10
Q

Alveolar gas exchange

A
  • Occurs through passive diffusion between alveolar air space and plasma
  • Air can pass readily
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11
Q

Blood transportation to and from lungs

A

To lungs:
- Heart(right ventricle) -> pulmonary trunk -> pulmonary arteries -> pulmonary arterioles -> capillaries
From lungs:
- Capillaries -> pulmonary venules -> pulmonary veins -> heart(left atrium)
- High flow: 10% blood volume
- Low pressure: 25/8 mmHg

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12
Q

Pulmonary congestion in heart failure

A
  • Left side drop, right compensates (RV hypertrophy)
  • RV failure(decompensation)
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13
Q

Respiratory system must be protected from pathogens

A

Mechanisms:
- Filtering action of the nose
- Mucous and action of cilia lining the airways
- Antibodies secreted into respiratory surfaces
- Macrophages in respiratory tract and alveoli

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14
Q

Lung volumes

A
  • Inspiratory Reserve Volume(IRV): How much one can inspire, 3.5-6L
  • Vt(Tidal volume): Normal quiet breathing, 3-3.5L
  • Expiratory Reserve Volume(ERV): How much one can breathe out, 1.5-3L
  • Residual volume(RV): Volume that is always in lungs, 0-1.5L
  • Inspiratory Capacity(IC): How much inspire from normal exhale of 3L to max inhale level. Comprise of Vt and IRV
  • Functional residual capacity(FRC): How much air left in lungs after exhale, comprise of RV and ERV
  • Vital capacity(VC): How much air total. 1.5-6L. Comprise of ERV, Vt, and IRV
  • Total lung capacity(TLC): All volume total, comprise of RV, ERV, Vt, and IRV.
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15
Q

Obstructive and restrictive lung diseases

A
  • Obstructive lung disease(asthma): more airway resistance, increase RV, lower lung capacity
  • Inspiratory restrictive lung disease(pulmonary fibrosis): Less compliant lung, lung stiff, low IRV
  • Expiratory restrictive lung disease(obesity): Organs push diaphragm upwards, ERV low
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16
Q

Forced expiratory volume

A
  • Following maximal inhalation
  • Forced expiratory volume(FEV) = volume of air forcefully exhaled in 1st second
  • Forced vital capacity(FVC) = volume of air forcefully exhaled
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17
Q

FEV and FVC in obstructive lung disease(asthma)

A
  • Very low FEV: Problem with air escaping lungs, especially at high velocities
  • Low FVC: Problem with air escaping at all points
  • Improved with bronchodilators
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18
Q

FEV and FVC in restrictive lung disease(fibrosis)

A
  • Low FEV: lung damage
  • Low FVC: low compliance
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19
Q

Boyle’s Law

A
  • Increase volume, decrease pressure
  • Decrease volume, increase pressure
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20
Q

Changes in lung volumes drive pressure gradient and air flow

A
  • At rest, diaphragm relaxed
  • When diaphragm contracts, thoracic volume increases
  • When diaphragm relaxes, thoracic volume decreases
  • Inspiration atmospheric pressure > alveolar pressure
  • Expiration alveolar pressure > atmospheric pressure
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21
Q

Muscles of inspiration increase lung volumes

A
  • Sternocleidomastoids
  • Scalenes
  • External intercostals
  • Diaphragm
  • Increase size of thoracic cavity
  • Inspiratory muscles active when breathing at rest
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22
Q

Muscles of expiration decrease lung volumes

A
  • Internal intercostals
  • Abdominal muscles
  • Expiratory muscles inactive when breathing at rest
  • Become active when breathing frequency is high
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23
Q

Intrapleural pressure sucks lungs to the ribs

A
  • Fluid lubricates outside of lung
  • Negative pressure created by elastic recoil of ribcage(outward) and elastic recoil of ribcage(inward)
  • Allows lungs to fill thorax without anatomical attachment
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24
Q

Pneumothorax

A
  • Apply wet dressing (re-establish continuous layer of pleural fluid)
  • Add positive pressure to mouth (inflate lungs)
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25
Pressure changes during quiet breathing
- Changes in lung volume drive changes in pressure - Intrapleural pressure is always sub-atmospheric but changes - Thoracic pressure changes more quickly than alveolar pressure - Alveolar pressure changes initially due to chest volume changes - Alveolar pressure reverses A2-A3 and A4-A5 due to air entering/leaving alveoli
26
Lung compliance
- How much lung volume changes when intrapleural pressure changes - Influenced by elastin fiber network, surface tension in alveoli
27
Elastin fibers influence lung compliance
- Elasticity of the lungs decrease as age - More elastic -> more compliance - Less elastic -> less compliance
28
Lung compliance curves change with different diseases
- Emphysema curve is above normal, higher lung volume - Fibrosis curve is below normal, lower lung volume
29
Surface tension influences compliance
- Surface tension shrinks volume of alveolus - Pressure in alveolus increases - Must overcome pressure when inflating lungs - Surface tension within alveoli increases elasticity - Surfactant reduced surface tension
30
Surface tension equalized among alveoli of different sizes
- Law of LaPlace: P=2T/r - P = pressure - T = surface tension - r = radius - If two bubbles have same surface tension, smaller bubble will have higher pressure
31
Architecture of airways provide resistance
- 90% airway resistance due to trachea and bronchi - Bronchioles: large cross sectional area so low resistance, but can change diameter - Bronchioconstriction: diameter gets smaller (eg. histamine) - Bronchodilation: diameter gets larger, eg. CO2, epinephrine binding to B2 adrenergic receptors
32
How much air is moved in and out of lungs per minute
- Normal Vt = 500 mL/breath - Normal respiration rate = 12 breaths/min - Dead space volume = 150 mL/breath - Total pulmonary ventilation = tidal vol (Vt) x respiratory rate - Normal minute ventilation = 500 mL/breath x 12 breaths/min = 6000 mL/min - Alveolar ventilation = (Vt - dead space volume) x respiratory rate - Alveolar ventilation = (500 mL/breath - 150 mL/breath) x 12 breaths/min = 4200 mL/min
33
How much air gets to the alveoli
- At end of inspiration, dead space filled with fresh air. 2700mL + 150 mL - Exhale 500 mL(tidal volume). 2200 mL + 150 mL(dead space) - At end of expiration, dead space filled with stale air from alveoli - During inhalation, inhale 500 mL of fresh air (tidal volume). 2200 mL + 500 mL + 350mL of fresh air reaches alveoli
34
How much oxygen and CO2 in air
- Total atmospheric pressure = sum of all partial pressures - PO2 = FO2 x PB - PB is atmospheric pressure - FO2 is fraction conc of oxygen - PB is normally 760 mmHg - FO2 = 21% - FCO2 = 0.04%
35
Pressure of humified air
- Pressure of humified air = 760 mmHg - 47 mmHg = 713 mmHg - Water vapour pressure contributes to overall pressure (PH2O = 47 mmHg) - Because water vapor has a partial pressure, PO2 and PCO2 go down when air is humidified in respiratory tract
36
What determines amount of gas in solution
- Partial pressure of gas - Solubility of gas - Temperature of solution
37
Gas exchange occurs by passive diffusion
Fick's Law of Diffusion: - Gas transfer = Constant x Partial pressure gradient x Area/Wall thickness - Maximize partial pressure gradient area and minimize area
38
Gas exchange can be affected in many diseases
- Low arterial PO2 causes: - Low blood O2 concentration - Smaller gradient between blood and tissues - Low O2 delivery to tissues - Poor tissue function and disease - Pulmonary edema: Increase diffusion distance due to fluid buildup
39
How much O2 and CO2 in blood
- Alveolar air: PO2 = 100, PCO2 = 40 - Arterial blood: PO2 = 100, PCO2 = 40 - Tissues: PO2 = 40, PCO2 = 46 - Venous blood: PO2 = 40, PCO2 = 46 - Atmospheric air: PO2 = 160, PCO2 = 0.3
40
How is oxygen transported in the blood
- O2 dissolved in plasma <2%, 3mL of O2/L of blood - Carried in red blood cells > 98%, 197mL of O2/L of blood
41
Structure of hemoglobin
- 4 globin chains, each centred around a heme group - Each heme group has a porphyrin ring with an iron atom at centre
42
Oxygen - hemoglobin dissociation curve
- At alveoli: 98% of Hb is saturated with O2 - At tissues: 73% of Hb is saturated with O2 - Therefore 25% is released at tissues at rest - During exercise, PO2 at tissues = 20 mmHg, so 55% O2 offloaded at tissue
43
Hemoglobin saturation affected by pH, temperature, and PCO2
Factors that decrease affinity of hemoglobin for oxygen: - Lower pH -> release more O2 - Increase temperature -> decrease dissociation of O2 - Increase PCO2 -> offload more O2 - 2,3- DPG
44
Different forms of hemoglobin
- Most adult hemoglobin is HbA (2 alpha and 2 beta chains) - Fetal hemoglobin is HbF (2 alpha and 2 gamma chains) - Fetal Hb has greater affinity for oxygen than maternal Hb - Fetal Hb improves fetal survival by increasing O2 uptake from mother
45
How is CO2 transported in blood
- Converted to bicarbonate -> diffuse into blood - Carbonic anhydrase catalyzes formation of carbonic acid - Hemoglobin buffers hydrogen ion - In order for bicarbonate to leave the cell, chloride must enter
46
How is CO2 released at lungs
- Carbonic anhydrase catalyzes breakdown of carbonic acid - Hydrogen ion dissociates from hemoglobin - For bicarbonate to enter, chloride must leave cell
47
Haldane effect
- As PO2 increases, amount of CO2 carried decreases - Oxygenated blood carries less CO2, and allows CO2 to be offloaded at lungs - In deoxygenated state, venous blood carries more CO2
48
Pulmonary ventilation is matched to metabolic demand
- Consume a lot of O2, release a lot
49
Feedback regulation of breathing
- Gas exchange -> PCO2, PO2 -> Chemoreflexes -> Ventilation
50
Chemoreceptors located in the brain and large vessels
- Medulla oblongata(central chemoreceptors): Detect H+ in cerebrospinal fluid - Carotid chemoreceptors: Detect H+ in blood. Sensitive when PO2 falls
51
How do chemoreceptors influence ventilation
- Central chemoreceptors detect H+ -> Medulla oblongata and pons as respiratory control centre -> Somatic motor neurons for inspiration/expiration -> Lung muscles - Peripheral chemoreceptors(carotid and aortic) detect H+ and O2 -> Afferent sensory neurons -> Medulla oblongata and pons as respiratory control centre -> Somatic motor neurons for inspiration/expiration -> lung muscles
52
Central chemoreceptors
- Cerebral capillary carries oxygenated blood and measures level of PCO2 - High level of CO2 diffuse from capillary to cerebrospinal fluid (doesn't allow H+ to go through, only CO2) - High level of CO2 comverted to carbonic acid -> bicarbonate ions and H+ -> measured at central chemoreceptors - Central chemoreceptors signal respiratory control centers -> increase ventilation and decrease CO2 levels
53
Central chemoreflex responds to PCO2
- Ventilation increases with greater PCO2 - Central chemoreflex provides most our drive to breathe
54
Peripheral chemoreflex stimulated by low PO2
- As PO2 levels drop, increase in ventilation - Response affected by low levels of circulating O2, does not usually occur under normal conditions
55
Peripheral chemoreceptor function modulated by low O2
- Carotid receptor sense low PO2 -> K+ channels close -> Depolarization of cell -> Ca2+ channels -> Exocytosis of dopamine containing vesicles -> Action potential to signal to medullary centers to increase ventilation
56
Chemoreflex negative feedback loops
- Peripheral chemoreceptors only activated when plasma O2 < 60 mmHg - Respiratory control centers -> increase in ventilation -> increase PO2 and decrease PCO2 - Negative feedback loop on PO2 < 60 mmHg -> turn of peripheral chemoreceptors - Negative feedback loop on high PCO2 --> turn off central chemoreceptors
57
How is blood pH regulated
- PCO2 controlled by respiratory system, response time is 5-10 min, eliminates 10,000 mmol of carbonic acid per day - HCO3- controlled by renal and other systems, response time is 8-12 hours, eliminates 100 mmol of fixed acid per day
58
Dysregulation of pH in disease
Acidosis: high H+, low pH - Respiratory: reduced CO2 excretion. eg. lung disease(doesn't secrete O2, damage to alveoli), overdose of sedatives - Metabolic: gain of H+ or loss of HCO3-. eg. ketoacidosis, diarrhea Alkalosis: low H+, high pH - Respiratory: excessive CO2 excretion. eg. hyperventilation -> drive level of CO2 down -> lower H+ ions - Metabolic: loss of H+ or gain of HCO3-. eg. vomiting, excessive antacid drugs
59
Compensation of acidosis
- Problem is high H+ - Bicarbonate reserves breakdown sodium bicarbonate to form bicarbonate -> bicarbonate + H+ -> carbonic acid -> increase respiratory rate to lower PCO2 - Other buffer systems absorb H+, H+ secreted as NH4+ in kidneys
60
Compensation for alkalosis
- Problem is too little H+ - Decrease respiratory rate to elevate PCO2 (inactivation of chemoreceptors) -> carbonic acid -> H+ and bicarbonate - Other buffer systems release H+ - Secretion of HCO3- in kidneys to generate H+
61
Spinal motoneurons that control the respiratory muscles
- Phrenic motoneurons whose axons make up the phrenic nerve, drives the diaphragm. Found in cervical spinal cord segments C3, C4, and C5 - Motoneurons whose axons make up the intercostal nerves which drive the intercostal muscles are found in the thoracic spinal cord segments T1 and T12
62
Relationship between tidal volume and phrenic nerve activity
- During inspiration, tidal volume increasing, and number of active inspiratory neurons also increases
63
Brain areas that control respiratory rhythm
- Higher brain centers -> Pontine Respiratory Group (PRG) -> Nucleus Tractus Solitarius (NTS) -> Dorsal Respiratory Group (DRG) -> Output primarily to inspiratory muscle - Ventral respiratory group -> output to expiratory, some inspiratory, pharynx, larynx, and tongue muscles - Pre-motor neurons in the VRG and the DRG activate respiratory motoneurons (phrenic and intercostal) in the spinal cord
64
Firing patterns in breathing
- Hypoglossal nerve: firing during inspiration, no firing during expiration - Phrenic nerve: Firing during inspiration, no firing during expiration - Rostral VRG: Firing during inspiration, no firing during expiration - preBotzinger complex: firing during inspiration, no firing during expiration - Botzinger complex: no firing during inspiration, firing during expiration
65
Rhythmic breathing can be influenced by 8 factors
- Voluntary control (speech) from motor cortex - Chemoreceptors (chemical control of breathing) - Reflexes like sneezing and coughing - Posture affects intercostal and abdominal muscles - Startling events - Emotions like fear, anxiety, sorrow - Exercise immediately increases breathing - Pain increases breathing All of these signals involve CNS and signal to medulla and pons
66
General organization
- Cough (medulla), Voluntary control (motor cortex), Posture (cerebellum) and Rhythym generator (medulla) converge to respiratory motoneurons - Emotions (forebrain) -> limbic system, Sensory stimuli (pain) -> reticular formation -> Rhythm generator (medulla) -> respiratory motoneurons
67
Feedback pathway that regulates breathing
Afferent pathway: Relay sensory information fron respiratory system to brain - Airway and lung receptors (controlled by vagus nerve) -> medullary respiratory neurons - Peripheral chemoreceptors via glossopharyngeal nerve -> medullary respiratory neurons - Central chemoreceptors -> medullary respiratory neurons - Muscle receptors -> spinal respiratory motoneurons Efferent pathways: Carry motor command from brain to respiratory muscles - Medullary respiratory neurons -> Upper airway muscles and airway smooth muscle via vagus nerve - Medullary respiratory neurons -> spinall respiratory motoneurons -> respiratory muscles -> muscle receptors or pulmonary ventilation, pulmonary ventilation -> airway and lung receptors or PO2 and H+
68
Airway and lung receptors tell brain about breathing
- Receptors are found in all lobes of lungs and airways - Irritant receptors: respond to irritants in lungs
69
Stretch receptors
- Locations: - Found from trachea to bronchioles - Sends info through vagus nerve - Main functions: - Controls breathing pattern: tidal volume and frequency - Response to dyspnea(shortness of breath): mismatch between actual ventilation (stretch receptors) and ventilation demands (peripheral chemoreceptors)
70
Hering - Breuer Reflex
- Slow, deep breathing: - Early inflation activates rapidly-adapting receptor afferent activity(RAR) -> Later hyperinflation activates slowly-adapting receptor afferent activity -> Increase BP activates baroreceptors - 8 beats/inhalation, 5 beats/exhalation -> high respiratory sinus arrhythmia (RSA) - Normal breathing: - Weak inflation activates RARs -> SARs remain mostly inactive -> slightly increased BP weakly activate baroreceptors -> 4 beats/inhalation, 4 beats/exhalation -> low RSA
71
Irritant receptors
- Found throughout airway and lung - Trigger breathing and bronchoconstriction - Initiates several reflexes Reflexes: - Sneeze -> nasal receptor -> trigeminal nerve - Aspiration -> Epipharyngeal receptor -> Glossopharyngeal nerve - Cough -> Laryngeal or Tracheal receptor -> Vagus nerve - Breathing -> Juxtapulmonary receptor -> Vagus nerve
72
Factors that regulate breathing
- Higher brain centers -> Respiratory centers (medulla and pons) -> Peripheral chemoreceptors in low O2, high CO2 and H+ positively regulate breathing Central chemoreceptors in high CO2 and H+ positively regulate breathing Receptors in muscles and joints (exercise) positively regulate breathing Stretch receptors in lungs negatively regulate breathing -> lung isn't overstretched Irritant receptors negatively regulate -> to not inhale more irritant