2 nd Year Revision Respiratory. Michael Hodkinson

Transcription

1 2 nd Year Revision Respiratory Michael Hodkinson

2 Before we start This is a quick run through of topics Obviously there will be more to learn than what s in these slides but hopefully it will provide a decent overview This is student to student teaching does not necessarily accurately reflect or override anything taught by QUB

3 Contents Basic Anatomy and Physiology of the Lungs PFTs ABGs COPD and Asthma Respiratory Tract Infections

4 Lung Anatomy Clinically The muscles in the thoracic wall alter the position of the ribs and sternum This changes the thoracic wall during breathing They also provide structural support

5 Right Lung

6 Left Lung

7 IVC/SVC From Body Pulmonary Vein From Lungs Right Atrium Left Atrium Tricuspid valve Right Ventricle Right Ventricle Mitral Valve Pulmonary Valve Aortic Valve Pulmonary Artery To Lungs Aorta Rest of the body

8 Lung Physiology Gaseous exchange Warming and humidifying gases Functions of the airways Protection of the lungs

9 Gaseous Exchange Flow of gas depends on Pressure gradient (alveoli and atmosphere) Resistance to flow Resistance to airflow is very low small pressure gradients required to move gas during ventilation Resistance is altered by bronchoconstriction/dilatation This is under AUTONOMIC NERVOUS CONTROL Adrenergic sympathetic nerves > dilatation Cholinergic parasympathetic > constriction

10 Lung Protection Air partially filtered by nasal hairs Mucus Continuous movement of cilia on the surface of trachea, bronchi and bronchioles transport mucus up to pharynx where it can be swallowed Vocal folds: reflexly close the glottis during swallowing, if this fails a cough reflex is triggered

11 Mechanism of Breathing INSPIRATION ACTIVE process Increase in thoracic volume Dome of diaphragm pulled down (contraction) thereby increasing the vertical height of the thorax PHRENIC NERVES from C3,4,5 Augmented by EXTERNAL intercostal muscles increasing the width of the thorax from front to back Accessory muscles (SCM and scalenus) during maximal inspiration: elevate sternum and 1 st two ribs Quiet EXPIRATION PASSIVE process Elastic recoil of stretched lungs Inspiratory muscles relax Can be accelerated by abdominal muscles INTERNAL intercostals actively pull the ribs downwards

12 Quick Fact Surfactant Surfactant : natural phospholipid protein produced by TYPE II PNEUMOCTYES it decreases the SURFACE TENSION of the lung thus requiring less NEGATIVE INTRAPLEURAL PRESSURE to keep the lung inflated thus INCREASING COMPLIANCE given to premature neonates to prevent Infant Respiratory Distress Syndrome Common EOP/Physiology Question

13 Gaseous Exchange 1 Alveolar membrane is the gas exchange surface BLOOD GAS barrier DEOXYGENATED Blood arrives from the heart via the pulmonary artery OXYGENATION occurs across the blood gas barrier and CARBON DIOXIDE is offloaded, this process is driven by partial pressure gradients (PaO2:PaCO2)

14 Spirometry Describe precisely what FEV1 and FVC FEV1 Forced expired volume in one second after full inspiration FVC (forced vital capacity) total forced expiratory volume after full inspiration

15 Spirometry cont. Spirometry indicates the presence of an abnormality if any of the following are recorded: FEV1 < 80% predicted FVC < 80% predicted FEV1/FVC ratio <0.7 Obstructive disorder: FEV1 reduced FVC is usually reduced but to a lesser extent than FEV1 FEV1/FVC ratio reduced (<0.7) Restrictive disorder: FEV1 reduced FVC reduced FEV1/FVC ratio normal (>0.7)

16 Asthma Reversible airway obstruction. SOB, cough, wheeze. Narrowing of large and small airways due to immune hyper reactivity. Bronchial smooth muscle contraction. Inflammation in the airway wall with a cellular infiltrate including eosinophils, mediator release and wall oedema Increased mucus production. Spirometry: FEV1 would be markedly reduced. FVC would be reduced to a lesser extent. FEV1 / FVC ratio <0.7 Obstructive defect, typically seen in asthma

17 Medications in Asthma B2 Agonists Salbutamol Acts on G protein coupled receptors (beta 2 receptors) leading to their activation and increasing camp in airway smooth muscle to produce bronchodilation Side effects include tremor, tachycardia, hypokalaemia

18 Medications cont.. Inhaled corticosteroid (Budesonide) Cause repression (decreased transcription) of proteins mediating inflammation, or activation (increased transcription) of proteins that suppress inflammation. Steroid side effects involve alteration of protein (skin thinning,osteoporosis, muscle wasting) carbohydrate( glucose intolerance, diabetes) and fat (buffalo hump, central obesity) metabolism. Inhaled candida

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20 COPD Chronic inflammatory condition causing progressive airflow obstruction secondary to parenchymal disease Symptoms SOB, cough, sputum, wheeze Causes Smoking, Alpha 1 antitrypsen deficiency (emphysema and cirrhosis)

21 Lung Volumes FEV1/FVC <0.7 obstructive Non reversible cf. asthma

22 Treatment Similar to asthma (inhaled b2 agonist/antimuscarinics) Stop smoking!

23 ABG s and Acid Base Balance

24 Acid Base Balance Common EOP question ABG analysis ph Pa02 PaCO >10kPA kpa HCO mmol/l Base Excess +2 to 2 N.B These values will vary in different resources normal values will always be given in the exam

25 Back to chemistry. Henderson Hasselbach CO 2 = ACIDIC HCO 3 = BASIC Reaction is catalysed by CARBONIC ANHYDRASE (H2CO3)

26 Interpretation Acid Base Quick guide 1. Are they Hypoxic? O 2 low? 2. ph: is the patient Acidotic or Alkalotic Acidosis can either be from too much CO 2 (Respiratory) or not enough HCO 3 (Metabolic) AlkalosisIs usually the result of too little acid (loss of H+) or too little CO2 (hyperventilation) 2. CO 2 :is the CO2 high or low? High CO 2 This is indicative of Respiratory acidosis the retention of CO 2 Low/Normal Look at thehco 3 / Consider Hyperventilation 3.HCO 3 :is the HCO3 high or low? Low HCO3 without high CO2 = Metabolic acidosis

27 Quick guide Condition Gas Changes Underlying Cause Respiratory Acidosis PaCO2 Respiratory Failure/COPD Respiratory Alkalosis PaCO2 +HIGH Pa02 Hyperventilation *Panic attack* Metabolic Acidosis HCO3 DKA,Renal Failure, Lactic Acidosis, Acid Ingestion Metabolic Alkalosis HCO3 Acid loss vomiting/diarrhoea Usually on the End of Phase paper there is a case of acidosis you must be able to tell the difference between a metabolic and respiratory acidosis i.e High CO2 or Low HCO3 respectively (then consider compensation) IF IN DOUBT GO BACK TO BASIC CHEM CO2 ACIDIC / HCO3 BASIC

28 Respiratory Failure Two types TYPE I = Hypoxia in isolation po2 TYPE II= Hypoxia plus Hypercapnia ( CO2 retention) po2 pco2

29 Clinical significance The drive to breath comes from CO2 levels in the body, however patients with longstanding COPD can loose this stimulation as they chronically retain CO2 thus they rely on a HYPOXIC DRIVE to maintain respiration Thus delivering these Type 2 patients with high levels of O2 can reduce the drive to breath thus reducing respiratory rate = NOT GOOD This is overcome by maintaning a lower target saturation and using special oxygen deliver devices like Venturi Masks

30 Respiratory Infections Pneumonia LRTI Lower Respiratory Tract infection Signs and Symptoms= SOB/ Fever/ Productive Cough/ Confusion/ Chest pain On Examination= Coarse crepitations in lung fields / Decreased Saturations / Pyrexia Investigations = WCC raised/ CRP raised/ CXR shows consolidation/ Sputum or Blood Culture +ve/ Urinary antigen for Legionella Two main types CAP = Community Acquired HAP= Hospital Acquired > 2 days after admission Causative Organisms CAP 1.Viral 2. Strep Pneumoniae 3.Humophilus Influenza 4.Staph Aureus Atypical Organisms = Mycoplasma Pneumonia and Legionella Pneumophillia

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32 Pneumonia Degree of severity of CAP quantified using CURB 65 score (don t think you need to know in detail). Score 1 for each Confusion: Abbreviated Mental Test: 8 or less Urea: >7 Respiratory Rate: >30 BP <90 systolic or <60 diastolic Age >65 At risk groups = Extremes of age Immunosuppressed (Iatrogenic/HIV etc) CF/COPD/Asthmatics

33 Treatment Non severe (score 1) Oral Amoxicillin Mild Moderate (score 2 3) IV Amoxicillin Severe (score 3+) IV Ceftriaxone Second line/alternative: if true penicillin allergy contract microbiology Life advice: In an OSCE, if in doubt always say I will prescribe according to local guidelines

34 Any Questions?