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RESPIRATORY - Coggle Diagram

- - - - superior to thyroid cartilage
        
        at level of C3
    - - can be felt as it is sup. to isthmus (2nd -4th tracheal rings can’t be felt as it is behind isthmus).
  - - - CUNEIFORM CAR.
        
        Rod shaped
        
        Located at posterior part of aryepiglottic fold
      - CORNICULATE CAR.
        
        Rod shaped
        
        Located at posterior part of aryepiglottic fold
      - ARYTENOID CAR.
        
        Three-sided pyramid shaped.
        
        Apex : corniculate cartilage  attached to aryepiglottic fold.
        
        Base : cricoid cartilage  forms the cricoarytenoid joint.
    - - EPIGLOTTIS
        
        post. to root of tongue + hyoid bone.
        
        Leaf-shaped fibrocartilage (provides flexibility to epiglottis)
        
        Superior end = broad, free end
        
        Inferior end = tapered, forms an angle with thyroid cartilage
      - CRICOID CARTILAGE
        
        Features:
        
        a) Signet ring shaped
        
        b) Anterior part --> arch
        
        c) Posterior part --> lamina
        
        *The only complete ring of cartilage that encircles the airway
        
        Articulates with arytenoid cartilages
        
        Permits a wide range of arytenoid motion
      - THYROID CAR.(largest)
        
        ANT FEATURE
        
        a) Left & right lamina :fuse ant.ly in median plane, forming...
        b) laryngeal prominence (Adam’s apple)
        
        POST FEATURE
        
        a) Post border : free, not attached
        
        b) Superior horns: + superior border of thyroid cartilage >> attached to hyoid bone by thyrohyoid membrane.
        
        c) Inferior horns : articulate with lat. surf of cricoid cartilage at cricothyroid joint
    - - Vocal process = provides post attachment for vocal ligaments.
        
        Muscular process = acts as levers to post & lat cricoarytenoid mm.
  - - - pierced by int laryngeal nn. & sup laryngeal vessel
  - - - Suprahyoid
        (Laryngeal elevators)
        
        mylohyoid,
        
        Ant belly of digastric*
        
        Post belly of digastric*
        
        stylohyoid
        
        geniohyoid
      - Infrahyoid
        (Laryngeal depressors)
        
        omohyoid
        
        sternohyoid,
        
        sternothyroid,
        
        thyrohyoid
    - - ABDUCTOR
        
        POST CRICOARYTENOID
      - ADDUCTOR
        
        LAT. CRCOARYTENOID
        
        TRANVERSE/ OBLIQUE ARYTENOID
      - TENSOR
        
        MED THYROARYTENOID
        
        CRICOTHYROID
      - RELAXER
        
        LAT. THYROARYTENOID
    - - VESTIBULAR FOLR
        
        False vocal cords
        
        Extending between the thyroid and arytenoid cartilages
        
        Function : not involved in voice production provide
        
        protection to the larynx
      - VOCAL FOLD
        
        TRUE vocal cords (source of sounds from the larynx).
        
        Attached anteriorly to the angle of the thyroid cartilage.
        
        Attached posteriorly to the vocal process of the arytenoid cartilage.
        
        Consist of vocal ligaments (thickened elastic tissue) and vocalis muscle.
        
        Function : Produce audible vibrations (when the free margins are not tightly closed)
        
        Main inspiratory sphincter of the larynx (when the free margins are tightly closed)
  - - - ALL intrinsic mm - innervated by RECURRENT LARYNGEAL N.
        
        except CRICOTHYROID - innervated by ext. branch of SUP LARYNGEAL N.
    - - Inferior/below the vocal folds --> RECURRENT LARYNGEAL N.
        
        Superior/above the vocal folds --> internal branch of SUP LARY. NN.
  - - - Larynx ends at superior border of 1st tracheal ring >> can be palpated >> for tracheostomy
- - - - • Gas exchange occurs only in respiratory bronchioles and alveoli (= respiratory zone)
        --> Alveoli are polyhedral in shape and clustered at ends of respiratory bronchioles, like units of honeycomb
        • All other structures constitute the conducting zone
    - - • Filters unwanted materials for circulation
        --> E.g. alveolar macrophages ingest inhaled bacteria & small particles
        • Bronchial secretions contain IgA
        --> Resist infections and maintain mucosal integrity
        • Blood reservoir (cardiac output of right heart)
        • To regulate blood acid-base level
        • Speech (air is taken into lungs and push out through glottis, vocal cords vibrate, creating sound)
    - - Angiotensin-converting enzyme (ACE)
        --> Converts angiotensin I (ATI) to angiotensin II (ATII)
        --> Degradation of bradykinin
        • Production & removal of arachidonic acid metabolites
        --> PGF2, PGF2α, leukotrienes
        • Phospholipid & protein synthesis
        --> Surfactant, collagen, elastin
  - - - FACTORS
        
        • Size of the lung – depends on the body posture
        --> prone position > supine & lateral
        • Degree of lung inflation
        --> Atelectasis (collapse) of some alveoli, ↓ lung compliance due to ↓ lung volume, requires higher pressure to inflate the alveoli
        
        PATHOLOGIC
        
        Increased fibrous tissues in the lung (pulmonary fibrosis) replace elastic tissue – stiff lung
        --> Decreased compliance due to reduction of the lung extracellular matrix and alteration of pulmonary surfactant
        
        Increased pulmonary venous pressure which leads to lung oedema
        --> Presence of fluid in alveolus – increases surface tension - hence reducing compliance
        
        Pulmonary emphysema
        --> Increased alveolar size – increased compliance
        --> Degeneration of lung tissue makes the lungs hard to expand
        
        NORMAL AGING
        
        Reduction in elastic tissues and vital capacity
        
        Restriction of chest movement (arthritic changes in the rib articulations & decreased flexibility of the costal cartilage)
        
        Lung compliance increases but thoracic wall compliance decreases
        
        ELASTICITY
        
        • Is tendency to return to initial size after distension
        • Due to high content of elastin proteins
        • Elastic tension increases during inspiration and is reduced by recoil during expiration
        
        ELASTIC RECOIL
        
        lung and balloon want to return to unstretched shape
        --> result of arrangement of fibres
        
        SURFACE TENSION
  - - - FXN
        
        (i) Prevents lung collapse--> [ Increase T ]– small alveoli will collapse
        (ii) To keep the alveoli ‘Dry’--> Without surfactant, increased surface tension will lead to fluid transudation (pulmonary oedema)
        
        To prevent lung collapse in newborn
        --> Lack of surfactant production in premature babies (surfactant secretion begins in late fetal life)
        --> In adults, septic shock may cause acute respiratory distress syndrome (ARDS) which decreases compliance and surfactant secretion
    - - CAUSE BY:
        • Heart surgery – use of O2 pump disrupt pulmonary circulation
        • Blockage of pulmonary artery
        • Long-term breathing 100% O2
        • Smoking
  - - - BOYLE'S LAW (P=1/V)
        
        Boyle’s Law describes the relationship between the pressure (P) and volume (V) of a gas at constant temperature.
        🔹 At constant temperature, the pressure of a gas is inversely proportional to its volume.
        
        PRESSURE
        
        Intrapleural pressure
        
        The opposing forces of the lung and P = - 4 mmHg the chest wall
        
        create a negative pressure (subatmospheric) in the intrapleural space
        
        Intrapleural pressure = 756 – 760mmHg = - 4 mmHg
        
        In pneumothorax (intrapleural pressure = atmospheric pressure)
        
        the lung will collapse and the chest wall will spring outward ~presence of airlithica pleural space
        
        At rest, alveolar pressure equals atmospheric pressure
        
        at sea level = 760 mmHg (1 atm) &
        
        Intrapulmonary pressure
        
        Implies that changes in intrapulmonary pressure occur as a result of changes in lung volume
        
        Pressure of gas is inversely proportional to volume
        
        Increase in lung volume decreases intrapulmonary pressure causing inspiration (more air moves in)
        
        Decrease in lung volume raises intrapulmonary pressure causing expiration
    - - Muscle of inspiration
        
        MAJOR
        
        Diaphragm - The most important muscle for inspiration
        
        Increases the vertical dimension of the chest cavity
        
        External intercostals - Increases the lateral & anteroposterior dimension
        
        PROCESS
        
        Internal intercostal muscles relax ↓
        
        External intercostal muscle contract ↓
        
        Rib cage moves upwards & outwards ↓
        
        Diaphragm contracts & flattens ↓
        
        Volume of thorax cavity increase ↓
        
        Pressure in alveoli decrease ↓
        
        Air moves in
        
        ACCESSORY
        
        Not used during quiet breathing
        • Used during exercise & in respiratory distress
        • Muscles that elevate the ribs:
        
        Scalene muscles elevate the first 2 ribs
        
        Sternocleidomastoids raise the sternum
        
        Pectoralis minor & serratus anterior
        • Alae nasi causes flaring of the nostrils
        • Small muscles in the neck and head
      - Muscle of expiration
        
        Expiration is normally passive
        • Relaxation of inspiratory muscles
        • Lung-chest wall system is elastic and tends to return to its resting position
        
        Expiratory muscles are used during forced expiration:
        • Exercise
        • Voluntary deep breathing
        • When airway resistance increased
        
        PROCESS
        
        Internal intercostal muscles contract ↓
        
        External intercostal muscle relax ↓
        
        Rib cage moves downwards & inwards ↓
        
        Diaphragm relaxes ↓
        
        Volume of thorax cavity decrease ↓
        
        Pressure in alveoli increase ↓
        
        Air moves out
        
        Active expiration
        
        Muscles that depress the ribs
        
        Internal intercostal muscles
        
        Pulling the ribs downward and inward
        
        Decreases the thoracic volume
        
        Stiffen the intercostal spaces to prevent them from bulging outward during straining
        
        Transversus thoracic muscle
        
        Pulls ribs towards the sternum during forced expiration, resulting in depression of those ribs
        
        Decreases the anteroposterior diameter of the thoracic cavity
        
        Abdominal muscles assist in expiration:
        
        Increases intra-abdominal pressure – pushes diaphragm upward
        
        Rectus abdominis, internal & external oblique muscles, transversus abdominis
        
        Also involved during coughing, vomiting, defecation
        
        The work of breathing
        
        Muscular effort (O2 & energy) required for ventilation
        
        The work done (W) by respiratory muscles to overcome
        
        resistance of airflow (28%)
        
        elastic recoil of the lung (65%)
        
        non-elastic tissue (7%)
        
        W during quiet breathing = 0.3 – 0.8 kgm/min
        
        2 more items...
        
        Pulmonary Function Tests
        
        2 more items...
        
        Forced expiratory volume 1 (FEV1)
        • The volume of air that is forcefully exhaled in one second
        
        Forced vital capacity (FVC)
        • The volume of air that can be maximally forcefully exhaled
        
        FEV/FVC ratio
        • The percentage of FVC that can be expired in one second
        • 75-80% Normal
        • <70% Obstruction
  - - - EXT
        
        • Ventilation moves air in and out of lungs for gas exchange with blood
      - INT
        
        • Gas exchange between blood and tissues, and O2 use by tissues
        • Gas exchange is passive via diffusion
    - - • Warms and humidifies inspired air
        • Mucus lining filters and cleans the inspired air
        • Mucus moved by cilia to be expectorant
        
        PROPERTY
        
        PHYSICAL
        
        LUNG
        
        Its tendency to return to its resting volume after distention (collapse)
        
        INFLUENCED BY
        
        3 more items...
        
        CHEST WALL
        
        • Its tendency to return to its resting volume (expand)
        
        CHEMICAL
- - - - the amount of gas dissolved in fluid = Directly propor. to pressure of gas above solution
        
        depends on its:
        
        Solubility of the gas in the fluid
        
        Temperature of the fluid
        
        Partial pressure of the gas
    - - LAWS OF DIFFUSION
        
        Rate of diffusion of a gas (Vgas) is proportional to:
        
        Membrane surface area (A)
        
        Partial pressure difference (P1 – P2)
        
        Solubility of gas (sol)
        
        Rate of diffusion of a gas (Vgas) is inversely proportional to:
        
        Membrane thickness (T)
        
        Square root of molecular weight (MW)
        
        – the gas diffusion (Vgas) increases when...
        
        ↑ alveolar surface area (A)
        
        ↓ Membrane thickness (T) ↑ gas solubility (Sol)
        
        ↑ driving pressure across the membrane (P1-P2)
        
        ↓ molecular weight of gas (MW)
    - - EMPHYSEMA
        
        ↓ alveolar surface area (A)
        ↓ gas diffusion (Vgas)
      - PULMONARY FIBROSIS
        
        ↑ Membrane thickness (T)
        ↓ gas diffusion (Vgas)
  - - - Respiratory membrane is
        composed of several layers:
        
        Fluid lining the alveolus that contains surfactant
        
        Alveolar epithelium
        
        Epithelial basement membrane
        
        Interstitial space
        
        Capillary basement membrane
        
        Capillary endothelium
    - - Defined as volume of a gas diffuses through the membrane each minute for a pressure difference of 1 mmHg
        
        CO2 (440 ml/min/mmHg ) is 20 times greater than that of O2 (21 ml/min/mmHg)
        
        This is due to high solubility of CO2 in lipid membrane
        
        FACTORS
        
        Increases membrane thickness
        
        Pulmonary fibrosis, pulmonary oedema
        
        low solubility of O2 in lipid membrane
        
        Reduced surface area for gas diffusion
        
        Emphysema
        
        Partial pressure gradient
        
        High altitude (↓ PO2)
  - - - AMOUNT OF O2 DETERMINED BY
        
         Amount of dissolved O2
        
         Amount of Hb in blood
        
         Affinity of Hb for O2
    - - LOADING & UNLOADING
        
        DEPEND ON
        
        Affinity (bond strength) of Hb for O2 - ↓ affinity, ↑ O2
        loading
        
        PO2 of envi --> HIGH PO2 favours loading region
    - - Dissolved in plasma
        
        7% of CO2 transport
        
        As bicarbonate ion (70%)
        
        The first rx is very slow in plasma but fast in RBC due to presence of carbonic anhydrase (CA)
        
        The second rx is fast, without an enzyme
        
        23% combined with proteins (in plasma & Hb)
        
        CO2 combines with terminal amine groups to form carbamino compounds (mainly globin of Hb)
        
        CHLORIDE SHIFT
        
        70% HCO3- diffuses from RBC into plasma in exchange with Cl-
        
        More HCO3- diffuse into plasma, RBC gain more +ve charge
        
        Cl- moves into RBC to retain electrical neutrality of RBC 
        
        bicarbonate-chloride carrier protein shuttles the two ions in opposite direction at a high rate
        
        venous RBC contains higher Cl- than arterial blood
        
        H+ is buffered by Hb
        
        Binding of Hb to H+ promotes unloading of O2 to tissues
        
        BOHR EFFECT
        
        A shift of O2-Hb curve in response to changes in CO2 & H+
        
        At the lung, low PCO2 and H+ the curve shift to the left – increases Hb affinity for O2 --> Increases O2 transport
        
        At tissue, CO2 enters the blood, increased H+ -shift the curve to the right – Hb unload O2 to tissues
        
        Hb buffers H+ released by H2CO3
        
        Improves the ability to transport CO2
        
        HALDANE EFFECT
        
        2 more items...
        
        (promoting O2 transport)
  - - - FACTOR
        
        Blood pH
        
        LOW PCO2 --> LOW pH --> decreases affinity (Bohr effect)
        
        deoxyHb binds H+ more actively than does HbO2
        
        Blood temperature
        
        HIGH temperature – lower the affinity
        
        [2,3-BPG]
        
        HIGH [2,3-BPG] – lower the affinity
        
        2,3-biphosphoglycerate (2,3-BPG)
        = 2,3-diphosphoglycerate (2,3-DPG)
        
        aka 2,3-diphosphoglycerate (2,3-DPG)
        
        plentiful in RBC
        
        Product of glycolysis in RBC
        HbO2 + 2,3-BPG Hb-2,3BPG + O2
        
        Factors that affect [2,3-BPG]
        
        Chronic hypoxia – at high altitude, chronic lung disease, increases 2,3-BPG
        
        Anaemia – increases 2,3-BPG
        
        Acidosis – inhibit glycolysis, hence reduces 2,3-BPG
- - - - Activities of medullary rhythmicity center are influenced by centres in pons
        • These two centres modify the inspiratory depth & rate established by medullary centres
        • Central respiratory centres are composed of 3 main groups of neurons:
      - 1) apneustic centre - stimulate inspiratory neuron in VRG pneumotaxic centre ventral group
        
        antagonise apneustic centre & inhibit respiration
        
        helps to control the rate & pattern of breathing 3
        
        Inhibit DRG and thus control the filling phase of respiratory cycle
    - - dorsal respiratory groups (DRG) - forms inspiratory (I) neurons
        
        generate inspiratory action potentials to stimulate phrenic nerve to the diaphragm
        
        responsible for basic rhythm of respiration (automatic breathing)
        
        receive input from chemoreceptor and from other receptors in the lung to regulate ventilation (CN IX & X)
        
        Ventral respiratory groups (VRG) - contain both I & expiratory (E) neurons
        
        I neurons stimulate spinal interneurons
        
        activate spinal motoneurons of respiration
        
        rostral nucleus retroambiguus
        
        E neurons inhibit motoneurons of phrenic nerve during expiration
        
        nucleus retrofacialis & caudal nucleus retroambiguus
        
        inactive during quiet breathing
  - - - CENTRAL - located in ventrolateral surface of MO
        
        Aka medullary chemoreceptors
        • Stimulated by high [H+] in CSF and brain interstitial fluid
        • Blood-brain barrier is impermeable to plasma H+
        • Blood CO2 can easily cross BBB
        CO2 + H2O H2CO3 --> H+ + HCO3-
      - PERIPHERAL
        
        AORTIC BODY - around the aortic arch via vagus
        nerve (CNX)
        
        CAROTID BODY- in each common carotid artery via
        glosso-pharyngeal nerve (CNIX)
        
        Receive enormous blood supply & have high metabolic rate
        • They respond to
        
        hypotension – reduced blood flow
        
        hypoventilation
        • stimulated by increased PaCO2 & [H+]
        
        decreased PaO2 < 60 mmHg (fall to about half normal)
        
        cyanide poisoning
        
        K+ - increased during exercise induces hyperpnoea
        • not stimulated in
        
        Anaemia, CO poisoning (PaO2 maintains at a normal level in the carotid bodies)
        
        PROCESS
        
        hypoxia closes O2 sensitive K+ channel --> depolarisation of glomus cell --> voltage gated Ca2+ channel opening --> Ca2+ entry in glomus cell --> NT release (dopamine) --> nerve stimulation (increase ventilation)
        
        Effects of Blood PCO2 and pH
        on Ventilation
        
        BRAIN
        
        Brain chemoreceptors are responsible for greatest effects on ventilation
        
        H+ can't cross BBB but CO2 can, which is why it is monitored and has greatest effects CO2 cross BBB
        
        Rate and depth of ventilation adjusted to maintain arterial PCO2 of ~40 mm Hg
        
        Chemoreceptors modify ventilation to maintain normal CO2, O2, and pH levels
        
        PCO2 is most crucial because of its effects on blood pH • H2O + CO2  H2CO3  H+ + HCO3 -
        • Hyperventilation causes low CO2 (hypocapnia)
        • Hypoventilation causes high CO2 (hypercapnia)
        
        Low blood PO2 (hypoxemia) has little effect on ventilation
        
        It influences chemoreceptor sensitivity to PCO2
        
        PO2 has to fall to about half normal before ventilation is significantly affected
      - Lung receptors
        
        J receptors (juxtapulmonary
        capillary receptors)
        
        endings of nonmyelinated C fibres in alveolar walls close to capillaries
        
        results in rapid shallow breathing & dyspnoea (difficult breathing)
        
        e.g. left heart failure, interstitial lung disease
        
        Pulmonary stretch receptors
        
        present in smooth muscles of the airways
        • involved in Hering-Breuer reflex
        
        prevents over-inflation of the lung
        
        signal from receptors sent via vagus to DRG to “switch off” inspiration
        
        Irritant receptors
        
        stimulated by noxious gases, cigarette smoke, dust, cold air
        • results in bronchoconstriction and hyperpnoea
        
        Bronchial C fibres
        
        reflex response - rapid shallow breathing, bronchoconstriction and mucus secretion
        
        response to chemicals in bronchial circulation
        
        other
        
        Nose & upper airway receptors
        • respond to mechanical & chemical stimulation
        • results in reflex response – sneezing, coughing bronchoconstriction
        
        Joint & muscle receptors
        • impulses from limbs stimulate ventilation during exercise
        
        Gamma system
        • in airway obstruction (e.g. asthma), large respiratory effort required to move the lung and chest wall Y
        • muscle spindles in intercostal muscles and diaphragm are stimulated
        • reflex control on the strength of contraction
        
        Arterial baroreceptors
        • An increase in arterial BP can cause reflex hypoventilation & apnea
        • A decrease in arterial BP results in hyperventilation (through unknown pathways) Itemporary cessation of breathing)
        
        Receptors for pain & temperature
        • Pain often causes a period of apnea followed by hyperventilation
        • Heating the skin may also result in hyperventilation
  - - - 1) Hypoxic hypoxia
        
        PaO2 is significantly reduced
        o Peripheral chemoreceptor stimulated
        
        Causes: Physiologic – high altitude
        
        PATHOLOGIC
        
        i. Hypoventilation - e.g. COPD, myasthenia gravis, poliomyelitis
        
        Caused by - Defect anywhere along respiratory control pathway
        
        Severe thoracic cage abnormalities
        
        Major obstruction of upper airway
        • Results in hypoxemia that is always accompanied by an increase in PaCO2
        
        ii. V:Q inequality - e.g. airway obstruction, pulmonary embolism
        
        Occurs in COPD and many other lung diseases
        • PaCO2 may be normal or increased (depending on how much ventilation is reflexly stimulated)
        
        iii. Impaired gas diffusion - e.g. pulmonary oedema
        
        Results from: – thickening of alveolar membranes
        
        reduced surface area
        
        Blood PO2 and alveolar PO2 fail to equilibrate carterial
        
        PaCO2 either
        – normal - CO2 diffuses more readily across blood-air barrier than O2
        – or reduced – hypoxemia reflexly stimulates ventilation
        
        iv. Right-left shunt - e.g. congenital heart disease
        
        Results from - Anatomic abnormality of the CVS [ blood from the right ventricle passes the left ventricle ]
        
        mixed venous blood bypasses ventilated alveoli
        
        Intrapulmonary defect --> mixed venous blood perfuses unventilated alveoli
        
        PaCO2 is not raised
        --> The effect is counterbalanced by increased ventilation stimulated by hypoxemia
      - 2) Anaemic hypoxia
        
        [Hb] is significantly reduced
        
        Reduced total O2 content in the blood
        
        But arterial PO2 is normal (O2 dissolved in plasma)
        --> thus peripheral chemorec not stimulated
        
        Causes - Large amount of blood loss
        
        Reduced Hb synthesis
        
        vit B12 and folate deficiencies --. Abnormal Hb synthesis due to genetic defect --. sickle cell anaemia Ithalassemia
        
        Carbon monoxide (CO) poisoning --. Hb has higher affinity for CO, thus preventing binding of O2 to Hb
      - 3) Stagnant / static / ischemic hypoxia
        
        Results of low blood flow
        • Normal PAO2 & PaO2
        • e.g. congestive heart failure
        
        reduced cardiac output to all tissues including peripheral chemoreceptors alredar arterial
        
        Reduced O2 delivery to tissues
      - 4) Cytotoxic / histotoxic hypoxia
        
        Normal PAO2 & PaO2 but tissues unable to use O2
        • Mainly due to poisoning of oxidative enzymes of the cells
        • e.g. cyanide poisoning
        • Venous PO2 is abnormally high
        • Peripheral chemoreceptors cannot use O2, so they detect as though O2 is insufficient
    - - O2 treatment
        
        O2-rich gas mixtures
        • Very limited value in stagnant, anaemic & histotoxic/cytotoxic anaemia Expoxia Of cannot bind ; can help but not much
        • in severe pulmonary failure
        
        hypercapnia is so high that it depresses ventilation
        
        ventilation is stimulated by hypoxia
- - - - LACTATE THRESHOLD
        
        Is maximum rate of O2 consumption before blood lactic acid levels rise as a result of anaerobic respiration
        – occurs when 50-70% maximum O2 uptake has been reached
        • Endurance-trained athletes have higher lactate threshold, because of higher cardiac output
        – have higher rate of O2 delivery to muscles and greater numbers of mitochondria and aerobic enzymes
    - - NEUROGENIC
        
        Sensory nerve activity from proprioceptors stimulates respiratory centres to increase ventilation
        
        Input from cerebral cortex may stimulate respiratory centres to modify ventilation
      - HUMORAL
        
        – PCO2 and pH in the region of chemoreceptors may be different from the values in blood – this cyclic changes may stimulate CHEMORECEPTORS
  - - - Involves increased ventilation, increased 2,3-BPG, and increased Hb levels etc.
        
        Hypoxic ventilatory response initiates hyperventilation → decreases PCO2
        
        chronic hypoxia increases nitric oxide (NO) production in lungs causes vasodilation
        
        NO binds to Hb and is unloaded in tissues where it may also increase dilation and blood flow
        
        NO may also stimulate CNS respiratory centers
        
        Altitude increases 2,3-BPG, causing Hb-O2 curve to shift to the right
        
        Hypoxia causes kidneys to secrete erythropoietin (EPO) which increases RBCs
        
        Acute mountain sickness (AMS)
        
        Common at altitude >5,000 ft
        
        Cardinal symptoms: – Headache
        
        low PaO2 --> vasodilation in pia mater --> HIGH BF & HIGH BP in skull
        
        Hyperventilation --> LOW PaCO2 --> cerebral vasoconstriction
        
        Malaise, anorexia, nausea & fragmented sleep
        
        Pulmonary oedema occurs at altitude > 9,000 ft
        
        Cerebral oedema normally occurs at altitude > 10,000 ft
        
        Both conditions are potentially dangerous & should be alleviated by descending to a lower ALTITUDE
  - - - A. Cerebral oedema
      - B. Pulmonary oedema
      - C. With time the right ventricle may hypertrophy
      - D. Blood viscosity increases
      - E. The oxyhaemoglobin dissociation curve shifts to the
      - right
- - - - • Begins in neck - level of C6 as continuation of larynx
        • Ends – sternal angle (T4/T5) in thorax
        
        the beginning of Respiratory tree
        
        wide tube with fibroelastic wall with C-shaped hyaline cartilages that keep the lumen patent
        
        the gap of the C- shape cartilage is bridged by smooth muscle called Trachealis m - complete lumen
        
        BIFURCATE (aka carina)
        
        RIGHT
        
        R PRIMARY Bronchus
        = Main bronchus = Principal bronchus
        
        • Shorter, wider & more vertical
        • Divide to 3 secondary bronchi
        
        SECONDARY bronchi (lobar bronchi)
        
        R lung has 3 lobes = 3 secondary bronchi (sup, middle & inf)
        
        3' bronchi (Segmental bronchi)
        
        Each 30 bronchi will pass into a
        BRONCHOPULMONARY SEGMENT
        
        LEFT
        
        L PRIMARY Bronchus
        
        •Longer, narrower & more horizontal
        •Divide to 2 secondary bronchi
        
        SECONDARY bronchi (lobar bronchi)
        --> divide into 3o bronchi & then to quaternary bronchi
        & continue dividing until about 23 branchings
        
        L lung has 2 lobes = 2 secondary bronchi (sup & inf)
        
        3' bronchi (Segmental bronchi)
        
        Each 30 bronchi will pass into a
        BRONCHOPULMONARY SEGMENT
        
        Trachea ends – at the level of
        T4/5 (sternal angle)
      - BRONCHIOLE
        
        Branches of the bronchi & <1 mm in diameter
        • Bronchioles divide until they become terminal bronchioles (end of the conducting part of the respiratory system)
        
        • beginning of respiratory portion (gaseous exchange occurs)
        • have sporadic alveoli on their walls
        • branches into alveolar ducts → alveolar sacs
    - - LUNGS
        
        essential organ of respiration
        • located in the pulmonary chambers on each side of mediastinum
        
        • Pulmonary chambers with pleural cavities
        • Heart with pericardial cavity
        
        RIGHT
        
        R Lung is larger, heavier but
        • shorter & wider than the L lung
        • Due to: R dome of diaphragm is higher
        --> Pericardium bulge more to the L Lung
        
        LOBES= 3
        
        FISSURES= 2
        
        SIZE = LARGER
        
        WEIGHT = HEAVIER
        
        LENGHTH = SHORTER
        
        WIDTH = WIDER
        
        LINGULA, CARDIAC ARCH= -
        
        MAJOR STRUCT
        
        5 more items...
        
        LEFT
        
        MAJOR STRUC
        
        •Heart
        
        •Aortic arch
        
        •Thoracic aorta
        
        •Oesophagus
        
        STRUCTURE
        
        •Shape: half-cone
        
        • covered with visceral pleura
        
        •Base = Concave in shape- sits on the diaphragm
        
        •Surfaces
        
        •Costal surfaces
        
        •Mediastinal surfaces
        
        •Diaphragmatic surface/base
        
        HILUM
        
        – depression on the mediastinal surface where the parietal pleura is continuous with the visceral pleura
        • Pleura is a continuous sac
        • Visceral pleura is continuous with the parietal pleura at the hilum of the lung
        
        • Roots
        
        • A short tubular collection of structures: bronchi, vessels & nerves that enter & leave the lung
        • Root - covered by a sleeve of pleura
        
        • Lobes & Fissures
        
        R
        
        3 lobes (SUP, MIDDLE & INF)
        2 fissures (Horizontal & Oblique)
        
        L
        
        2 lobes (SUP & INF)
        1 fissure (Oblique)
        
        FISSURE
        
        Horizontal fissure
        • Oblique fissure
        
        •Apex
        
        Blunt apex – projects 2.5 cm above the medial 1/3 of clavicle
        
        LINGULA
        
        •Thin, tongue-like process at lower part of SUP lobe of L lung
        
        ARTERY
        
        Pulmonary a
        
        bring deO2 blood from the heart to the lungs
        
        Bronchial a
        
        nutrition to pulmonary tissues (bronchial walls & glands, wall of large vessels, visceral pleura)
        
        VENOUS
        
        SVC - AZYGOUS VEIN - HEMIAZYGOUS V. - ACC. HEMIAZYGOUS V
        
        NERVE
        
        Sympathetic & Parasympathetic – Vagus nerve via Ant & Post Pulmonary Plexus
- - - - Pulmonary ventilation = respiratory minute volume
        
        amount of air inspired per minute
        
        Uneven ventilation occurs in different pulmonary regions
        
        Tidal volume (VT or TV) = the volume of air moved into or out of the lungs in one breath
        
        Healthy young adult, TV = 500 ml per inspiration at rest or 7ml/kg of body mass
        
        Respiratory minute volume (RMV)
        
        It measures pulmonary ventilation
        = respiratory rate x tidal volume
        = RR x VT
        = 12/min x 500 ml
        = 6000 ml (6L)/min
        
        normal range of RMV = 4000 – 6000 ml/min
        
        RR = respiratory rate (12 breaths/min)
        
        VT = tidal volume (500 ml)
        
        6L of air moves in and out of the respiratory tract every minute, but the whole volume of air is not utilized for gas exchange
      - PULMONARY CIRCULATION
        
        Rate of blood flow through pulmonary circuit equals flow through systemic circulation
        
        Pumped at lower pressure (about 15 mmHg)
        
        Pulmonary vascular resistance is low
        
        Low pressure produces less net filtration than in systemic capillaries --> avoids pulmonary oedema
        
        PERFUSION
        
        Pressure in various parts of the lung varies
        
        Pressure gradient in pulmonary system ≈ 7 mmHg (compared to systemic circulation ≈ 90 mmHg)
        
        Gravity affects pulmonary circulation
    - - Rate of alveolar ventilation = total volume of new air entering the alveoli per minute
        
        VA = RR(VT – VD)
        = 12(500 – 150)
        = 4200 ml (4.2L)/min
        
        RR = respiratory rate (12 breaths/min)
        
        VT = tidal volume (500 ml)
        
        VD = dead space (150 ml)
        
        • Alveolar ventilation - volume of air subjected to gas exchange
        • Air trapped in the respiratory passage (dead space) does not take part in gas exchange = wasted air
        
        DEAD SPACE
        
        ANATOMICAL (VD)
        
        • The conducting airways where gas exchange does not take place
        • Normal volume = 150 ml (increases slightly with age)
        • 30% of normal tidal volume (500ml)
        
        FACTORS
        
        Body size: increased size --> increased VD
        
        Body posture: 150 ml sitting, 100 ml supine
        
        AGE: loss of elastic tissue
        
        GENDER: male (>)
        
        TRACHEOSTOMY: decreases VD
        
        CHEMICALS: adr cause bronchodilation --> increase VD
        
        histamine/Ach --> bronchoconstriction --> decrease VD
        
        PHYSIOLOGICAL (Vp)
        
        Anatomical dead space + alveolar dead space (regions of the lung that are ventilated but no perfusion)
        
        FACTORS
        
        Physiological dead space ↑ during respiratory diseases, which affects the pulmonary blood flow or the alveoli
        
        Affected by changes in alveolar ventilation & perfusion
        
        Reduced pulmonary perfusion (gas exchange does not take place during inadequate blood supply)
        --> Pulmonary embolism, pulmonary congestion
        
        Decreased O 2 diffusion due to reduced surface area for gas exchange --> Emphysema
        
        Wasted ventilation – the volume of air that ventilates physiological dead space
        
        Under normal conditions,
        physiological dead space (VP) = anatomical dead space (VD)
    - - HYPOVENTILATION
        
        • Inadequate alveolar ventilation in relation to metabolic demands
        • CO2 removal does not keep up with CO2 production causing hypercapnia (PaCO2 > 44 mmHg)
        • P(A-a)O2 is normal
        • Results in hypoxemia
      - HYPERVENTILATION
        
        • Alveolar ventilation exceeds metabolic demands
        • Lung removes CO2 at faster rate than it is produced resulting in hypocapnia (PaCO2 < 36 mmHg)
        • Both hypoventilation & hyperventilation can be determined by arterial blood gas (ABG) analysis
  - - - UNEVEN PULMO PERF
        
        GRAVITY
        
        For every 1 cm away from the heart, MAP change = 0.77 mmHg - Decreased in any vessel above the level of the heart due to the gravitational effect
        
        Apex of the lung has lower arterial pressure
        
        Base of the lung has higher arterial pressure
        
        Intrapleural (Pip) and intrapulmonary pressures
        
        During inspiration, Pip is more negative due to the recoil of the lung away from the chest to keep the lung inflated.
        
        Pulmonary arteries & veins distended – central venous P LOW (pressure in great vein at the entrance of right atrium)
        
        Diaphragm contracts and pulls downward --> INCREASE the size of the thoracic cavity --> DECREASE intrapulmonary pressures
        
        Intraabdominal P HIGH – inferior vena cava compressed – squeezes blood toward the heart
        
        HIGH VR --> HIGH SV --> HIGH CO --> increases lung perfusion
        
        During expiration,
        
        Pip is less –ve oIntrapulmonary P +ve
        
        Thoracic veins are compressed, increasing central venous pressure
        
        Diaphragm relaxes – low intraabdominal P
        
        LOW VR --> LOW SV --> LOW CO --> decreases lung perfusion
    - - Sympathetic nerve does not play an important role (reduces blood flow by 30%)
        
        Influenced by local factors; PaO2 & PaCO2
        
        e.g. bronchus or bronchiole obstruction
        
        LOW PaO2 / HIGH PaCO2 – pulmonary vasoconstriction (hypoxic vasoconstriction)
        
        shunting blood away from low ventilated area
        
        Circulating humoral agents:
        
        PULMO VASODILATOR - bradykinin, histamine,
        atrial natriuretic peptide
        
        PULMO VASOCONSTRICTOR - thromboxane, serotonin
      - UPRIGHT POSITION
        
        The heart pumps against gravity to perfuse the lung
        
        Blood pressure in the apex is lower than at the base
        
        Increased pressure will increase perfusion
        
        So, the base of the lung is better perfused compared to the apex
        
        DISTRIBUTION OF V & Q
        
        The lung is divided into 3 zones based on the relationships among PA, Pa & Pv
        
        Pulmonary capillary bed is surrounded by air-filled alveoli; perfusion is affected by alveolar pressure
        
        PA – alveolar pressure
        
        Pa – arterial pressure
        
        Pv – venous pressure
        
        Zone 1 (apex): PA > Pa > Pv
        
        Pip is more –ve --> greater transpulmonary P --> larger alveoli
        
        Area is higher than heart level --> LOW Pa
        
        Capillary bed collapses; decreased perfusion
        
        Zone 2 (middle): Pa > PA > Pv
        
        Fair perfusion
        
        Zone 3 (base): Pa > Pv > PA
        
        Small alveoli
        
        Blood flow is determined by the arterial-venous pressure difference (Pa – Pv)
        
        Good perfusion
        
        V & Q MISMATCH
        
        Both V & Q is better at the base, however they are not perfectly matched at any zones
        
        at the base, Q exceeds V --> low V:Q
        
        at the apex, V exceeds Q --> high V:Q
        
        Normal V:Q = 0.8
        
        Effect of V:Q on PCO2 and PaO2
- - - - THORACIC CAGE
        
        • Sternum
        
        PARTS
        
        Manubrium
        
        Body
        
        Xiphoid process / Xiphisternum
        
        IMP LANDMARK
        
        Suprasternal notch/ Jugular notch (at the level of T2/T3)
        
        Sternal angle/Angle of Louis (at the level of T4/T5)
        
        xiphisternal joint (T9/T10)
        
        Sternal angle/ Angle of Louis
        
        • at the level of T4/T5
        • Divide superior & inferior mediastinum
        • >> clinical relevance = CPR (marks the articulation of the 2nd rib)
        -->. Chest compression position (on the lower half of the sternum, just below the Angle of Louis) --> to maximize cardiac output
        
        • 12 pairs of ribs & associated costal cartilages
        
        • True ribs (1-7)
        
        • are the ribs that have direct articulation with sternum
        • connected anteriorly to sternum via costal cartilage
        • connected posteriorly to thoracic vertebrae
        
        • False ribs (8-10)
        
        • ribs 8,9 & 10 : do not articulate directly with sternum
        •They articulate with costal cartilage of the 7th rib.
        
        • Floating ribs(11-12)
        
        ribs 11 & 12
        
        do not have an attachment to sternum at all.
        
        RIBS
        
        TYPICAL [3-9]
        
        • Head: has 2 facets articulates with bodies of thoracic vertebrae
        • Neck
        • Tubercle : articulates with transverse process of thoracic vertebra.
        • Costal groove : lodges intercostal vessels & nerves
        •Angle : a point lateral to tubercle, where shaft bends sharply forward
        
        ATYPICAL [1,2,10,11,12]
        
        1 - shortest, flat, broadest & most curved
        
        Head : has only ONE facet
        
        2 - tubercle for attachment of serratus anterior muscle
        
        10 - head has only ONE facet
        
        11 , 12 - no neck & tubercle head has only ONE facet
        
        intercostal spaces
        
        HOW TO LOCATE?
        
        • An intercostal space is the space between two ribs
        • 12 ribs = 11 intercostal spaces
        
        Sternal angle – same level to 2nd costal cartilage
        
        NERVE
        
        derived from ventral rami of thoracic spinal nerves (T1-T11) Intercostal nerves
        
        Main motor supply to muscles of thoracic wall (intercostal muscles)
        
        ARTERY
        
        Subclavian a
        
        Internal thoracic a (1)
        ant intercostal a
        
        Descending thoracic Aorta- Post intercostal a (4)
        
        Axillary a
        
        Sup thoracic a (2)
        Lat thoracic (3)
        
        VENOUS
        
        Ant intercostal v drain into internal thoracic v(1) --> brachiocephalic v.
        
        R Post intercostal v drain into azygous vein (2) → Sup Vena Cava
        
        L Post intercostal v drain into hemiazygous v (3) / accessory hemiazygous v(4) --> AZYGOUS V --> SUP VENA CAVA
        
        • 12 thoracic vertebrae & intervertebral disc