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Respiratory System 2

Understand key aspects of acid/base balance, respiratory control, and lung infection topics crucial throughout medical school. Learn about ABG interpretation, respiratory failure types, and the effects of sleep on breathing.

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Respiratory System 2

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  1. Respiratory System 2 Daniel Huddart 05/05/2019 CVS/Resp Weekend

  2. Acknowledgements - Thank you to Hussein Rajabali and Anam Malik for producing the slides

  3. Please note… • I don’t like preclinical medicine very much so will be aiming to make this relevant to not just this year but the rest of medical school and beyond • The more niche points I will provided slides but will focus on key things today • You’ll find some of what I say in the notes section of the powerpoint

  4. Lectures covered: • Acid/Base Balance • Control of breathing (Asleep) • Sensory aspects of Respiratory Disease • Respiratory Pathology • Lung Infection

  5. Topics you’ll return to throughout medicine • Acid/Base Balance • Control of breathing (Asleep) • Sensory aspects of Respiratory Disease • Respiratory Pathology • Lung Infection

  6. Acid/Base Balance

  7. LO’s • Explain the relationship between pH and hydrogen ion concentration • Explain the qualitative changes in arterial blood pH, PCO2 and base excess in: • Respiratory acidosisandmetabolic acidosis • Respiratory alkalosisandmetabolic alkalosis • Type IandII respiratory failure • Explain the effects of respiratory and renal compensation to correct acid-base imbalance

  8. Acids and Bases A greater concentration of H+ ions refers to a lower pH H2O + CO2 <-> H2CO3 <-> H+ + HCO3- This relationship is in an equilibrium. Increasing something on one side will push the equation in the opposite direction

  9. LO1 - Explain the relationship between pH and hydrogen ion concentration pH = -log10[H+] pH goes down, H+ ion concentration increases. That’s pretty much it…

  10. Physiology behind Acid/Base Balance • Organ systems to focus on for Acid/Base Balance: • LungsRESPIRATORY (blow off CO2 – excrete H+ ions) – Majority of the acid in the body is CO2 • KidneyMETABOLIC (produce HCO3 buffers, excrete H+ ions) – However this effect takes HOURS. H2O + CO2 <-> H2CO3 <-> H+ + HCO3-

  11. Now the nitty gritty… Acid/Base measured in an ABG – Arterial Blood Gas Main parameters: • pH • pO2 (Oxygen) • pCO2 (CO2) • Bicarbonate (HCO3) • Base Excess (BE)

  12. Interpreting ABGs • pH – Acidotic/Alkalotic/Normal – (7.35 - 7.45) • pCO2 – High/Low/Normal – (4.7 - 6.4 kPa) • Bicarbonate and Base Excess – High/Low/Normal – (22 – 26 mmol/l) and (-2 to +2) • pO2 – Normal/Low – (< 10.7 kPa)

  13. ROME

  14. Cases: • A patient with abdominal pain due to a duodenal ulcer was admitted to the medical ward with persistent vomiting (loss of HCl). He was also taking large quantities of sodium bicarbonate to ease the pain. A sample of arterial blood revealed: • pH 7.54 • pCo2 6.7 kPa (50 mmHg) • pO2 11.1 kPa (83 mmHg) • Bicarbonate: 37 mmol/l. • A 32 year old unconscious female presents to A&E. On examination, there were pin-point pupils and a blue-ish discolouration of the lips. An ABG is performed: • pH: 7.29 (7.35 – 7.45) • pCO2: 6.9 (4.7-6.0 kPa) • pO2: 10.2 (11-13 kPa) • Bicarbonate: 23 (22-26 mEg/L)

  15. What will these cause?

  16. Respiratory Failure • Hypoxia • If the PaO2 is <10 kPa on air – the patient is hypoxic. • If the PaO2 is <8 kPa on air – the patient is severely hypoxic and in respiratory failure. If so, we next look at the PaCO2 to determine if this is type 1 or type 2 respiratory failure.

  17. Respiratory Failure • Type 1 vs type 2 respiratory failure • Type 1 respiratory failure involves hypoxia (PaO2 <8 kPa) with normocapnia (PaCO2 <6.0 kPa). • Type 2 respiratory failure involves hypoxia (PaO2 <8 kPa) with hypercapnia (PaCO2 >6.0 kPa). • 1 – V/Q mismatch • 2 – alveolar hypoventilation

  18. Control of Breathing (asleep)

  19. LOs • LO1 - Describe the effect of sleep on breathing and blood gases in healthy people • LO2 - How does sleep affect oxygen and CO2 levels. What mechanisms lead to these changes? • LO3 - Describe the apnoeic threshold that can lead to central sleep apnoea • LO4 - Describe the influences of sleep on the upper airway that can lead to obstructive sleep apnoea. • LO5 - Know at least two upper airway muscles that reduce their activity during sleep. • LO6 - Know the other major cardio-respiratory diseases (one cardiac, one respiratory) that are exacerbated by sleep-related changes in the control of breathing; briefly explain why sleep is detrimental to these patients.

  20. LO1 - Describe the effect of sleep on breathing and blood gases and in healthy people The changes that can be seen between wakefulness and sleep are: • A decrease in tidal volume • A decrease in ventilatory rate • A decrease in alveolar ventilation • A decrease in oxygen saturation

  21. LO1 - Describe the effect of sleep on breathing and blood gases and in healthy people • In healthy people: • O2 sats don’t change too much because of the O2 sats curve. • In COPD patients: • O2 sats already on the steep bit of curve, if they drop sats any more, it can be critical.

  22. LO1 - Describe the effect of sleep on breathing and blood gases in healthy people

  23. LO3 - Describe the apnoeic threshold which in some people leads to central sleep apnoea. • Apnoeic threshold is the pCO2 that must be exceeded during sleep. • Below threshold, pCO2 is too low to cause stimulation of resp centres - so stop breathing, i.e. apnoea

  24. LO3 - Central sleep apnoea. • The brain stops sending signals to breathe • As a result, pCO2 rises, and O2 falls. • Causes: • Stroke / central lesion • Congenital hypervenilationsyndome. • Association: • Heart Failure – will discuss soon

  25. LO4/5 – Sleep and the upper airway. • REM sleep – paralysis: • Muscles – tongue, levator palatini, tensor palatine in back of throat relax and obstruct upper airway • Stiffening of pharynx and prevention of collapse. • Collapse in disease states. • Causes pharyngeal resistance to increase during sleep. • Main cause: Obesity • Patient still tries to ventilate (thorax and abdomen are putting in effort)

  26. Obstructive Sleep Apnoea

  27. LO4/5 – Sleep and the upper airway.

  28. Why care about sleep apnoea?

  29. LO6 –Know the other major cardio-respiratory diseases (one cardiac, one respiratory) that are exacerbated by sleep-related changes in the control of breathing; briefly explain why sleep is detrimental to these patients. • COPD: • O2 sats are low, but drop even further and cause respiratory difficulty in these patients. • Accessory muscles paralysed in REM sleep (need more effort inspiring and expiring) • Heart Failure: • Associated with central sleep apnoea. • HF  Pulmonary congestion  irritation of J receptors in lung  chronic hyperventilation  patient gets closer to apnoeic threshold  apnoea

  30. SBA • Which of the following describes a change that occurs within sleep, with respect to being awake? • A) Increase in tidal volume • B) Reduced pCO2 • C) Reduced alveolar ventilation • D) Increased bicarbonate release from the kidneys • E) Increased pO2

  31. SBA • Which of the following describes a change that occurs within sleep, with respect to being awake? • A) Increase in tidal volume • B) Reduced pCO2 • C) Reduced alveolar ventilation • D) Increased bicarbonate release from the kidneys • E) Increased pO2

  32. LOs - Cough • Describe the mechanics of a cough. • Briefly explain how this manoeuvre serves to (i) protect the lungs from inhaled noxious materials and (ii) clear excessive secretions from the lower respiratory tract • Identify the type and location of sensory receptors with the airways indicating how they are stimulated to give rise to cough. Identify the neural pathways which transmit this afferent neural information to the brain. • Describe in outline which regions in the brain are involved in generating the co-ordinated neural activity that results in the act of cough. Identify the efferent (motor) neural pathways and the main muscle groups which produce cough. • Explain the concept of the sensitised cough reflex in disease as the basis for chronic cough. • Discuss ways of controlling unnecessary cough.

  33. WHY DO WE COUGH? Protection from: 1. inhaled foreign material 2. excessive mucous secretion

  34. WHY DO WE COUGH? Coughing leads to mucociliary clearance – this mechanism is less effective in those with lung disease Expulsive phase of cough – generates a high velocity of airflow – facilitated by: 1. bronchoconstriction 2. mucous secretion

  35. Identify the type and location of sensory receptors with the airways indicating how they are stimulated to give rise to cough.

  36. Identify the neural pathways which transmit this afferent (sensory) neural information to the brain. Vagus nerve Superior laryngeal nerve Impulses integrated in a ‘cough’ center in the medulla oblongata Activates suppression from medial prefrontal cortex

  37. Identify the efferent (motor) neural pathways and the main muscle groups which produce cough.Discuss ways of controlling unnecessary cough. • Cerebral cortex – negative effect on coughing • Cough centre in the medulla – positive effect on coughing • Glottis. Accessory muscles of inspiration, external intercostals, diaphragm.

  38. Explain the concept of the sensitised cough reflex in disease as the basis for chronic cough. Cough paroxysms difficult to control (not throat clearing) • Triggers: Deep breath, laughing, talking too much, vigorous exercise; Smells (perfumes, vinegar); Cigarette smoke; Eating crumbles (biscuits); Cold air ‘Cough Hypersensitivity Syndrome’ via INCREASED EXPRESSION OF TRPV-1 1 – this is a Calcium-permeable channel • Activated by capsaicin, endocannabinoid, noxious heat & H+ and 12-lipoxygenase metabolites • Expressed in sensory neurones of dorsal root and trigeminal ganglia

  39. Discuss ways of controlling unnecessary cough.

  40. LOs – Chest Pain Chest pain: • Identify the type and location of sensory receptors with the thoracic cavity that when stimulated give rise to chest pain. Identify the neural pathways which transmit this afferent neural information to the brain. • Describe in outline which regions in the brain are involved in the perception of pain. • Discuss the concept of referred pain in the chest. • Describe different typical patterns of chest pain that can help in diagnosing the cause of pain.

  41. Identify the neural pathways which transmit afferent neural information to the brain. • Nose • Trigeminal (V) • Pharynx • Glossopharyngeal (IX) Vagus (X) • Larynx • Vagus (X) • Lungs • Vagus (X) • Chest wall • spinal nerves

  42. 1° somato - sensory cortex 1° somato - sensory cortex thalamus thalamus sP(AIN)ino-thalamic tract dorsal columns A, A viadorsal horn A, Cvia dorsal horn Describe in outline which regions in the brain are involved in the perception of pain. Touch Pain cerebral cortex midbrain pons rostral medulla cord

  43. Discuss the concept of referred pain in the chest. • Visceral pain - from organs eg heart, gi tract, bronchial wall •  fewer afferents than number of somatic afferents •  difficult to localise • diffuse in character •  referred to somatically innervated structures • Pain arising from various viscera in the thoracic cavity and from the chest wall is often qualitatively similar and both can cause referred pain in similar areas difficulties in diagnosis.

  44. Describe different typical patterns of chest pain that can help in diagnosing the cause of pain Chest wall: muscular or rib fractureSkin: Herpes zosterPleural pain (pulmonary infarction; pneumonia)Deep seated, poorly-localised painNerve root pain/Intercostal nerve painReferred pain: shoulder-tip pain of diaphragmatic irritation

  45. Describe different typical patterns of chest pain that can help in diagnosing the cause of pain • Musculoskeletal disorders -injury to ribs or thoracic muscles • Cardiovascular disorders - myocardial ischaemia, dissecting aortic aneurysm • Gastrointestinal disorders - Gastro-oesophageal reflux

  46. SBA • What type of sensory nerve would be activated after inhalation of capsaicin (chilli extract)? • A) Slowly Adapting Stretch Receptors • B) J-receptors • C) Rapidly Adapting Stretch Receptors • D) Trigeminal Nerve • E) C-fibres

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