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Physiology Pt. 3 - Coggle Diagram

- - - - Homeostasis for O2, CO2 and pH
      - Obtain O2 for energy proudction
      - Eliminate CO2 (acid-base balance)
      - External respiration
        
        O2 exchange between atmosphere and body
      - Internal respiration
        
        Cellular respiration and metabolism by mitochondria
    - - Pressure gradients formed by air inside and outside the lungs
        
        Inspiration
        
        Contraction of intercosal muscles + expanded throacic cavity
        
        Increased transpulmonary pressure gradient
        
        Lungs expand (subatmospheric) and air flows in
        
        Expiration
        
        Diaphram stop contacting + thoracic cage shrinks
        
        Transpulomanry pressure gradient back to preinspiratory
        
        Lungs recoil (above atmospheric) + air flows out
      - Work of Breathing
        
        3% of total body expenditure
        
        Affected by:
        
        Elastic properties of the chest wall
        
        Elastic properties of the lung (ie surfactant)
        
        Resistance of flow through the airways
        
        F (Flow) = P /R
        
        nb: R ~ 1/r4 (reduce the radius by half, and increase the resitance by x16
        
        This increases the energy required to maintain flow rate (ie more foceful contractions)
        
        Regulation of airways resistance
        
        Neural control (P/SNS)
        
        contracts bronchiole sm = constricts
        
        1 more item...
        
        Local factors (irritants, allergens, inflammation)
        
        contracts bronchiole smooth muscle
        
        Physiological obstructions (odema, mucous, FB)
        
        contracts bronchiole smooth muscle
        
        Endocrine (SNS - adrenaline)
        
        Relaxtaion of sm = dilation
        
        1 more item...
        
        Alveolar ventilaton = Tidal volume - dead space volume x RR
  - - - Major Inspiratory
        
        External Intercostal + Diaphragm
      - Active Expiration
        
        Internal Intercostal muscles +abdominal muscles
      - Accessory muscles of inspiration
        
        Sternocleidomastoid + Scalene m.
    - - Trachea
        
        Bronchi x2
        
        Bronchioles
        
        Terminal bronchioles
        
        Alveolar ducts
        
        Alveolar sacs
      - Dead Space
        
        volume of air in conudcting airways (stale air) with no gas exchange
      - Blood-Gas Barrier
        
        Alveolar Epithelium and Capilllary endothelium are in intimate contact, their basement membranes separated only my an ISF space allowing for diffisuion of gases
        
        Fick's Law
        
        V = Area x Diffusion constant x P / thickness
        
        Deoxygenated blood has a lower partial pressure of O2 and higher CO2 than the alveolus allowing for equilibration and exchange
        
        Gas exchange affected by:
        
        Partial pressure gradients of O2 and CO2
        
        Surface area (nb: in emphysema SA is reduced)
        
        Thickness of the barrier (nb: in pnuemonia odema increases thickness)
      - Gas Transport
        
        Oxygen = Haemoglobin (98.5%), Dissolved (1.5%)
        
        O2 carrying capacity of blood is influenced by Hb content
        
        Hb dissication curve
        
        Hb saturation follow an s curve: the partial pressure of PO2 affects the affinity of Hb for O2
        
        Increased temp, pCO2, acidity, and 2,3-BPG concentration shift the dissociation curve to the right
        = important for exercise as it facilitates the release of O2 by Hb
        
        CO2 = HCO3 (60%), Hb (30%), dissolved (10%)
        
        CO2 + H20 <--> H2CO3 <--> H+ + HCO3-
    - - Room Air
        
        O2 (20%), N2 (80%)
        
        O2 (160mmHg) N2 (600mmHg), CO2 (0 mmHg)
      - Alveolar gas
        
        O2 (13%), CO2 (5%), N2 (75%)
        
        O2 (100 mmHg), CO2 (40mmHg), N2 (570 mmHg)
  - - - Hypoxic hypoxia
        
        = low arteial PO2 w/ poor Hb sats (Poor gase exchnage or low O2 enviornment)
      - Anemic Hypoxia
        
        low O2 carrying capacity
        
        RBC, Hb poisioning (PO2 is normal)
      - Cirulatory hypoxia
        
        reduced blood flow and O2 delivery
        
        CHF, Cirulatory shock, Vascular occlusion
  - - - PaO2, PaCO2, and H+
      - Carotid and aortic bodies - CNIX & X
    - - Medulla
      - H+ in CSF/brainECF
        
        ie. increase CO2 + H20 --> H2CO3 --> H+ + HCO3-
    - - Medulla oblongata
        
        PaCO2 is the most important minute-minute regulator
        
        high PaCO2 is detected in the brain via the H+ w/ HCO3- equilibrium coffient--> medulla/periph are stimulated = increase ventillation (rate and depth), which will reduce arterial PCO2 to restore to set point
        
        EFFERENT: Somatic Motor Neurons for Inspiration and Expiration
        
        AFFERENT: Volunatry controls/limbic + Co2 (medullary + periph) + O2/pH (periph) ---> input in CPG
    - - Accessory breathing muscles activated
      - Dysponea
        
        SOB + Air hunger
        
        usually high pCO2 and work of breathing
      - Wheeze
        
        Prolonger expiratoiry phase due to airways resistance
      - Cyanosis
        
        Late sign - colour of deoxyHb
  - - - Mucociliary escalator
        
        Cilia are coverd by a mucous (Gel and Sol layer) the cilia beat in the sol layer in the direction of the pharyn to remove inhalnats
        
        Cilia can be paralysed by toxous gases and cigarette smoke
      - Alveolar macrophages (immue response)
      - Swallowing
    - - Swallowing and Gagging (Oropahrynx)
      - Sneezing (Nasopharnx) - trigemenal afferents
        
        Similar to cough reflex
        
        deep inspiration --> glottis closes, uvula depresses to deflect outflow --> expiratory muscles contarct glottis opens --> high pressure air expelled through nose and mouth
      - Laryngeal spasm (larygngopharnx) - vagus afferents
        
        triggered by mechanical/chemical stimulation of the laryngeral afferents
        
        spasm = stridor on inspiration
      - Coughing
        
        mechanical/chemical receptors --> Nuclus tratus solitaris/medulla resp centre = forceful inspiration and expiratory contraction w/ closure of the glottis/chords --> increase in lung pressure, chords open and COUGH! ---> removing FB
- - - - 45% Cells (RBCs, Lucocytes [1%])
      - 55% Plasma (water proteins, elctrolytes, nuttrients, gases, waste products)
      - 5.5L in Males vs 4.5 L in Females
    - - Venous Return = Cardiac Output, therefore increase in return increases CO
      - 4 mm Hg in Vena cava VS 104 mm Hg in the Aorta
      - nb: Cerebral blood flow maintains constant flow in mL/min
    - - MABP = CO x TPR
      - CO = SV x HR
      - Changes to resistance to flow: Vasoconstriction = affected by sympathetic stimulation ie NA, Vasopressin, Angiotensin II Vasodilation = affected by sympathetic with histamine or heat
      - Autonomic NS = vasomotor/cardioregulatory mechanism controls: P/SNS control the heart, SNS controls the heart, blood vessels
    - - Contraction regulated by the Ca++ & troponin/tropomyosin system (Actin/myosin)
        
        Stroke Volume
        
        Intrinsic Regulation: Stretch of atria = incrrease force contraction (Frank-Startling mechanism)
        
        Extrinsic Regulation: more Ca++, increases MyosinATPase= increases force and rate of contraction
      - Intercalated discs join iberes end-end, gap junctions allow for transfer of molecules for widespread contraction
      - Pacemaker cells initiate contractions = 250ms period
        
        SA node 70 bpm
        
        AV node 50bpm
        
        Purkinje Fibers 30 bpm
      - Sympathetic fibers = b1 agernergic receptors, G-coupled AMP receptors
        
        Act on SA node -> increased pacemaker discharge rate = positive "chronotropic" action ~HR increased
        
        HR increased = increases strength of myocardial contraction, positive "inotropic" action
      - Parasympathetic Fibers = vagus nerve SA node/R atrium
        
        slowed rate of discharge from the SA node = negative "chronotropic" action ~HR reduced
        
        Negative inotropic action on heart atria – via regulating calcium in the heart
  - - - Aortic and Carotid baroreceptors (Afferent Stretch Receptors) - carried by Vagus (aortic) glossopharyngeal (carotid)
      - Regulated in the medulla
        
        Efferents to the SNS or P/SNS to alter HR and force of contraction, and TPR
      - Vena cava and R atrium (venous return/blood volume) = vagus nerve
        
        Ex. Orthostatic Hypotension
        
        Reduced BP on standing up, pooling of venous blood in extremities causes reduced venous return, reduced SV&CO, and reduces MABP, reduced MABP detected via arterial baroreceptors, baroreflex (SNS activation) increases vasocontstriction/TPR, contratility, increase venous tone/EDV and SV and HR to restore MABP
    - - Trans-capillary fluid shift
        
        STARLINGS FORCES: Colloid Osmotic pressure (IN force) & Hydostatic pressure (OUT)
        
        Venous end: fluid moves IN (reasbsorption)
        
        Arterial End: fluid moves OUT (ultrafiltration)
        
        Balance of these forces determines the movement of fluyid in the blood vessels
        
        A pathology seen in these forces results in odema
        
        The small amount of fluid that is filtered out of the vessles is collected by the lymphatics
      - RAAS
        
        Kidney
        
        reduced MABP/NaCl detected by afferent arterioles
        
        Renin
        
        is released from the JGA
        
        Angiotensinogen released from the Liver is cleaved to Angiostensin I
        
        Angiotensin I moves via circulation to the Lungs where ACE converts it into Angiotensin II
        
        Angiotensin II
        
        Arteriole Vasocontriction
        
        Hypothalamus
        
        Increases thirst (behavioural)
        
        Increase fluid intake
        
        Post. Pituiraty gland to release vasopressin/ADH
        
        Increases H2O reasorption in kidneys
        
        Water retained without salt
        
        Adrenal Cortex
        
        Aldosterone
        
        Increases Na+ reabsoption
        
        passively Cl- reabsorption
        
        Water is retianed in ECF
    - - intravascular fluid volume mointoring
      - Regulation of ESF volume & renal renal fluid output
  - - - Short Term = Baroreceptors/Chemoreceptor reflexes mediated by ANS
        
        Reduced P/SNS to heart, increased SNS to heart
        
        Increased HR, Contratility, Venous return = SV = CO
        
        Capillaries favour reabsorprtion into plasma
      - RAAS
        
        Renin (Kidneys) --> Angiotensiongen (liver) ~~> circulation --> Ang I --> ACE (lungs) --> Ang II
        
        Ang II
        
        Hypothalamus
        
        Thirst
        
        Vasoconstriction
        
        Aldosterone
        
        Na+ reabsorb/Cl reabsorb
        
        Water retention
        
        1 more item...
        
        ADH (post. pit)
        
        Water retention
        
        Erythropoieiin is relasesd from kidney to replace RBCs
      - Circulatory Shock
        
        The inital -ve feedback mechanisms fail and a postive feedback loop ensues
        
        RESULTING SHOCK OR REDUCED MABP
        
        Hypolavemic
        
        Blood volume loss/haemorrhage
        
        Cardiogenic
        
        ie MI or CHF (weakend heart)
        
        Vasogenic
        
        Septic shock/Anaphylatic shock = reduced TPR
- - - - Stress Response
        
        Stressor act on the hypothalamus -->
        
        Posterior Pituitry Gland --> Vasopressin
        
        CRH ---> Anterior pituitary --> ACTH --> Adrenal cortex --> Cortisol
        
        Increase blood glucose, ffa, amino acids
        
        SNS
        
        Adrenal medulla
        
        Epinephrine
        
        Pancreas --> increase glucacogn reduce insulin
        
        Smooth muscle --> vasconstriction
        
        1 more item...
    - - exacerbated by stress
    - - allergic reactions or overdoese
  - - - Cardiac
        
        Orthostatic Hypotension
        
        Standing up = blood pools in the legs
        
        Reduced venous return/CO/MABP
        
        Inadequate baroreflex response --> medulla stimulates SNS + reduces P/SNS = reduced cerebral perfusion/syncope
        
        Compensation = Vasocons-- incrTPR --> incrDBP --> IncrHR&CO --> incSBP (+ venostriction)
        
        Predisposing effects: Drugs (hypotensives), prolonged supine, Warm temperature, dehydration, age
        
        Vasovagal Syncope
        
        transient faint due to loss of consciousness
        
        Psychogenic (anxiety and fear)
        
        Emotional Stress
        
        Iniaites fight or flight (HYPOTH)
        
        Tachycardia, vasoconstriction, w/ increase in muslce blood flow
        
        Absence of flight (reduced venous return) --> reduced BP (baroreflex --> SNS activity maintains then sudden withdrawal of SNS for P/SNS
        
        Vasodilation (less SNS and less TPR) bradycardia, reduced CO --> drop in MABP
        
        Reduced cerebral perfusion --> transient unconsciousness (when laid supine)
        
        Angina Pectoris
        
        Transient chest pain from MI
        
        C fiber pain (crushing, dull ache)
        
        Relieved by nitroglycerine (vasodilator = reduces preload/afterload on the heart)
        
        Stable angina should be <15mins, assume MI if it is new, or >15mins
        
        If MI is suspected - administer 300mg aspirin to reduce cardiac damage (antiplatelet)
        
        Types:
        
        Stable = Classic, emotional/exertive, 1-15min duration, good w/ GTNs
        
        Variant = Atypical, Coronary artey spasm, varied duration, Good response to GTNs
        
        Unstable = cresendo, any or nil, upto 30mins, poor w/ GTNS
        
        Cardiac Arrest
        
        Types:
        
        Pulseless electrical = beatsing but too weak
        
        Ventricular tachy (pulseless) = inneffective pumping
        
        Ventricular fibrilation
        
        chaotic contractions
        
        Common after an MI = lead to death
        
        Aystole - hypoxia to heart
        
        Management
        
        AED = restore effective ECG rhythm
        
        25% people have no clinical symptoms prior to onset
        
        Survival imporves w/ immediate CPR, early defib, early ATCL (amioderone IV if possible)
      - Metabolic
        
        Drug ingestion/administartion
        
        Anaphylaxis
        
        Following drug administartion (ie penicillian, opioids, LA, latex)
        
        S&S: Mins-Hours: hives, odema, SOB, wheeze/stridor
        
        type 1 HS = Mediated by histamine, bradykinin, prostaglandins
        
        Caused by vasodiltation, vascular leakage, sm. spasm, itch
        
        Immediate Mx: Remove exposure, DRS ABC, Epipen
        
        Adrenaline = vasonstriction to increase TPR, CO to imporve MABP, and breaks bronchospasm (beta2) and laryngeal odema (alpha1)
        
        LA overdose
        
        Signs: Tinnitis, periooral tingliness, drowsniess
        
        Management: Adminmster oxygen and monitor vital signs (sometimes due to intravascular injection)
        
        MAX ligno w/ adren = 7mg/kg
        
        Blood Glucose
        
        Hyperglycemia
        
        Elevated BGL = caused by untreated DM/insulin OD
        
        Dehydration, hypovalemia, ketoacidosis (RR and acetone breath)
        
        Mx: Supportive management --> as per for known or unknown diabetic
        
        Hypoglycemia
        
        Depressed BGL = failure to eat, OD insulin, or alcohol
        
        Cerebral dysfunction, hypotension, tachy
        
        Management: Adminster glucose orally (glucagon IM and adrenaline if unconscious)
        
        Cortisol/Adrenal Insuffiency
        
        Caused: Addison's Disease, LT steriod therapy
        
        vasomotor reponse is reduced due to inadequate cortisol secretion from the adrenal cortex
        
        S&S: confusion, bradycardia, hypotension, weakness, hypoglycemia, dehydration, collapse and cardiac arrest
        
        Consult w/. GP --> possible Steroid prophylactic dosing
      - Respiratory
        
        Respriatory Depression
        
        Causes: GAs, sedatives, alcohol, opiates
        
        Signs due to hypercapnia and hypoxia
        
        CNS = anxiety and unciousness
        
        CVS = tachy, HTN, hypoxia, dysponea
        
        Management
        
        Position - supine, legs lifted
        
        Airway - clear, head/tilt chin-lift
        
        Breathing - High flow O2
        
        Circulation - CPR if needed
        
        Definitive care = help, antidotes, IV lines ect
        
        Airways obstruction
        
        Stridor & dysponea
        
        URT: tongue FB, infections and laryngospasm
        
        Remove FB (back blows)
        
        LRT: bronchospasm, anaphylaxis, drugs
        
        inhaling B2 (salbutamol) or intramusc Adrenaline
        
        Asthma
        
        Intermittent & reversible airway changes
        
        Extrnsic (Atopic) Asthma
        
        Type 1 - IgE mediated response = mast cells degranulate --> histamine, PGs, bradykinin, -> sm contraction and = Airway narrowing
        
        Intrinsic asthma
        
        Non-allergic (exericse, irritants) --> cause a vagal reflex of the bronchioles for contriction
        
        Management
        
        reliever inhaler (4 puffs:4 breaths:4 mins waiting) β2-adrenergic agonist
        
        SABA e.g salbutamol (reilver)
        
        status asthmaticus - no imporvement w/ 2-3 doses w/ Beta2
        
        Chronic inflammation from eosinophils
        
        Acute Ventilation
        
        Acute Anxiety
        
        Respiratory control centre --> Incr rate/depth of breathin, hypocapnia, alkolosis, incrraeses mucles excitability and causes muscle spasms and dizziness (cerebral ischaemia)
        
        Cardiovasc contol centre --> Incre SNS --> elevated BP, HR, adreanline, causes chest pain and palpatations
        
        Management: rebreath their own CO2, raise PCO2 which reveres the hypocapnia
      - Nervous
        
        Seizures
        
        Disrupted electrical firing in the brain
        
        Types: abscent, atonic, febrile, generalised tonic-clonic, and myoclonic
        
        Management: Note time siezure start, protect head, nnothing in mouth, side-stable poision, talk until regained consciouness, reassure until recovered
        
        If first time - refer to GP, if regular - refer to GP for for consultation on medications ect