1.0 Overview.docx

1.0 Overview 1.1 Respiratory anatomy The conducting airways Air is inhaled through the nasopharynx and down into the trachea and then into the bronchi Right main bronchus almost forms a straight line with trachea (25 degrees) - most common for foreign bodies and aspiration - deep intubation L-...

1.0 Overview 1.1 Respiratory anatomy The conducting airways Air is inhaled through the nasopharynx and down into the trachea and then into the bronchi Right main bronchus almost forms a straight line with trachea (25 degrees) - most common for foreign bodies and aspiration - deep intubation L-mainstem bronchus is more angulated and less prone to these issues Bronchioles come off bronchi, end up in alveolar ducts and then into alveoli where gaseous exchange occurs Right lung Left lung Larger 3 lobes Smaller 2 lobes (plus lingula) Terminology Dyspnoea A subjective perception of shortness of breath Respiratory distress A term combining the patient's subjective sensation of dyspnea with signs indicating difficulty breathing. Hypoxia Insufficient delivery of oxygen to the tissues The brain is the most sensitive organ to hypoxia therefore is an early clinical sign. Hypoxemia Deficiency of oxygen in arterial blood Causes Hypoventilation Right to left shunt (intrapulmonary shunt) Ventilation-perfusion (V/Q) mismatch Diffusion impairment Low inspired oxygen Anoxia No oxygen Hypercapnia PaCO2 >45mmHg Normal 35-45mmHg Commonly caused by alveolar hypoventilation: slow, shallow breathing, small tidal volumes, under ventilation Rarely results from increased CO2 production alone Effects Seizures, coma, death Reduced myocardial and diaphragmatic contraction Arrhythmias, hypotension, cardio/respiraotry arrest, death Right shift on Oxy-Hb curve Decreased O2 affinity to Hb at the alveolus PaO2 The partial pressure of O2 in the blood This is dissolved oxygen in the blood, not bound to Hb SaO2 Measures the percentage of Hb saturated with O2 Accessory muscle use Important to see what muscles are being recruited in the laboured breathing patient Laboured inhalation Laboured exhalation (e.g. COPD, asthma) Muscles Scalenes Sternocleidomastoid Trapezius Intercostals Restrictive conditions Laboured Raise the ribs and sternum to increase the anterior posterior diameter Increase the AP diameter of the thorax Their contraction prevents collapse under high negative pressures Muscles Intercostals Obliques (internal/external) - contract trying to force air out of chest Obstructive lung disease Laboured The abdominal muscles are the most noticeable muscles of expiration Increase intra-abdominal pressure, thereby moving the diaphragm upward This helps with expiration against lower airway obstruction in obstructive lung disease Pulmonary compliance: refers to the amount of pressure that must be generated to expand the lungs with a given volume. E.g. some balloons are harder to inflate than others Good compliance Poor compliance Means you need little pressure to generate a big volume change Means you need a large pressure to create that same or less volume change - stiff lungs Lung volumes and capacities (sums of volumes) Tidal volume: the amount of air you inhale in a normal breath a rest Inspiratory reserve: amount you can possibly inhale over and above your tidal volume Expiratory reserve volume: amount you can possibly exhale below normal tidal volume Residual volume: prevents lungs from collapsing entirely Expiratory reserve + residual volume = functional residual capacity (FRC) Tidal volume + inspiratory reserve volume (IRV) = inspiratory capacity (IC) 1.2 Respiratory physiology Ventilation (V) Perfusion (Q) Volume of air that moves into and out of the mouth Minute ventilation = RR x TV FiO2 = fraction of inspired oxygen: an estimation of the oxygen content a person inhales and is thus involved in gas exchange at the alveolar level Flow of blood through the tissues or to an area E.g. CO = 6l/min = the lungs are perfused with 6L of blood per minute Under ideal conditions, ventilation should match perfusion (V = Q) Intrapulmonary shunt (occurs in bronchospasm) V/Q ratio decreases (<1) E.g. 5L air enters the lungs and CO=6l/min then 5/6 = 0.83 Result is decreased arterial oxygen concentration Dead space: volume of gas that does not take part in gaseous exchange (ventilated but not perfused) There are three types of dead space Alveolar dead space Alveoli that are ventilated but not perfused Changes from minute to minute Evident in shock states, emphysema, pulmonary embolism - little to no perfusion but still good ventilation Anatomical dead space Parts of respiratory tract that are ventilated but not perfused (trachea, bronchi, bronchioles) Fixed anatomy that does not change About 33% of every breath is anatomical dead space Apparatus dead space From equipment such as filter and EtCO2 Don't add unnecessary apparatus as this increases dead space and traps CO2 1.3 Acid base disorders, O2 delivery and O2 dissociation Main buffer system: lungs and kidneys must work together to keep or restore balance (normal pH 7.4) CO2 + H2O > H2CO3 > H+ + HCO3- Lungs: acid is excreted as carbon dioxide Kidneys: bicarbonate is altered to counteract altered CO2 Respiratory acidosis Respiratory alkalosis Definition High PaCO2/EtCO2 Retained CO2 = increase resp rate to blow off CO2 (hyperventilation) Leads to formation of carbonic acid when CO2 combines with water, more H+ ions, lower pH Lower CO2 = decreased resp rate to retain CO2 (hypoventilation) Low PaCO2/EtCO2 Less carbonic acid, thus less H+ in blood, pH increase Causes Lung disease causing impaired gas exchange and CO2 retention Opioid overdose Head injury Any condition resulting in hypoventilation (cardiac arrest) ROSC target CO2 is lower end of normal (35-40) to reduce acidosis from no respiration Salicylate overdose High fever Hysteria/voluntary over breathing Passive over ventilation by hand delivered ventilations via BVM or incorrectly adjusting the mechanical ventilator Any condition resulting in hyperventilation Oxygen delivery to tissues Partial pressure of gas: the total pressure of a mix of gases is equal to the sum of their own individual pressures Dalton’s law states that the total pressure exerted by a mixture of non-reacting gases is equal to the sum of the partial pressures of each individual gas in the mixture. Henry’s law states that the amount of a gas dissolved in a liquid is directly proportional to the partial pressure of that gas above the liquid. It describes the relationship between the concentration of a gas in a solution and its partial pressure. Ficks law states that the rate of gas diffusion across a permeable membrane is determined by The partial pressure gradient of the gas The thickness of the membrane (APO, fibrosis) - important The surface area of the membrane (COPD, fibrosis) - important Chemical features of the gas and the membrane The Bohr effect refers to the phenomenon in which the affinity of haemoglobin for oxygen is reduced under conditions of low pH (acidic environment) and high levels of carbon dioxide (CO2). Oxygen dissociation The O2-Hb dissociation curve is an S shaped curve that illustrates the % of Hb saturated with O2 at different partial pressure levels of arterial oxygen. Left shift Right shift Hb holds tighter onto O2 and does not easily release to the tissues Hb holds less tightly to the O2 and releases it easily to the tissues 1.4 Patient assessment and treatment General RSA RIPAP assessment for all patients with respiratory compromise Normal Mild/moderate Severe Life-threatening Conscious state Alert Alert May be altered Altered or unconscious General appearance Calm, quiet Calm, mildly anxious Distressed Distressed, anxious, fighting to breathe, exhausted, catatonic Speech Clear and steady sentences Full sentences, pausing to catch breath Short phrases only Words only, or unable to speak Skin Normal, pink Normal, may be pale, sweaty Pale, sweaty, may be cyanosed (cyanosis SpO2 <90) Pale, sweaty, cyanosed Work of breathing (inspect use of accessory muscles) Normal chest movement (nil accessory muscles) Slight increase in normal chest movement Marked chets movement + use of accessory muscles Marked chest movement with accessory muscle use, intercostal retraction +/- tracheal tugging (suprasternal retractions) or exhaustion SaO2 88-92% for COPD patients is normal - ask what patients normal sats is 94-98% >94% 90-94% <90% Rate/rhythm 12-16 Regular event cycles 20-25 Asthma may have slightly longer expiratory phase >25 Asthma prolonged expiratory phase >25 or <8 Asthma prolonged expiratory and inspiratory phase Inspect Symmetrical rise and fall of chest bilaterally, nil scars, patches N/A N/A Asymmetrical rise and fall of chest, unilateral/bilateral hyperinflation (tension pneumo) Palpation N/A N/A N/A N/A Auscultation Usually quiet, no wheeze Normal vesicular sounds Asthma: mild expiratory wheeze +/- inspiratory wheeze LVF: may be some fine crackles at bases, progresses to mid zone Athma: expiratory wheeze +/- inspiratory wheeze LVF: fine crackles - full field with possible wheeze Upper airway obstruction: inspiratory stridor Silent chest, faint adventitious sounds Percussion Resonance: normal Dull: fluid filled compartment, solid organ Hyperresonant: air field compartment Resonant bilaterally N/A N/A Hyperresonance with tension pneumothorax Percussion sounds Hyperresonant Hollow sound Air filled cavity = pneumothorax which can progress to tension pneumothorax Normoresonant Between dull and hollow Air filled alveoli Hyporesonant Dull sound Fluid filled cavity For hyper resonant and hyperresonant sound, the potential space between the visceral pleura and parietal pleura becomes an actual space as the layers separate due to being filled with air or fluid. Pneumothorax COPD can cause bullae which is a rupture/tear in visceral pleura which leads to pneumothorax Pneumothorax Tension pneumothorax Hemodynamically stable Hemodynamically unstable History Chief complaint Allergies Medications Past medical Hx Last email Events proceeding What's been going on today? When did the symptoms start? Did it come on suddenly or has it gotten worse? Duration? Gotten better or worse? Always there or does it come and go? SOB only on exertion or at rest as well? Pain = OPQRST Cough Dry or productive cough? Acute <3 weeks Subacute 3-8 weeks Chronic >8 weeks Presence of blood or precipitants? Can develop after starting new medications such as ACE inhibitors Occupational Hx Work exposures e.g. smoke, asbestos, silica, coal mine dust Social Hx Alcohol, drug use, smoking history Travel Hx High risk areas? India, Pakistan, Africa Recent long haul flights = PE Sputum Frothy, sometimes with a pink tinge’ think purulent: congestive heart failure, pulmonary oedema Yellow or green: infectious Brown: tobacco smokers, old blood Clear or white: Viral bronchitis, COPD, asthma Blood streaked: tumour, tuberculosis, pulmonary oedema, trauma from coughing Volume/viscosity Auscultation Term Acoustic characteristics Description Course crackle Discontinuous sound: loud, low in pitch Pulling apart strips of velcro Predominantly heard during inspiration Loudest in the bases Fine crackles Discontinuous sound: sift, higher pitch, shorter duration Unilateral crackles = infection (pneumonia) can be secondary to COPD Wheeze Continuous sound: high pitched, dominant High/low pitched, continuous musical sound Stridor Loud, musical sound of definite and constant pitch Identical to wheezing except for following characteristics Confined to inspiration Always louder over neck where wheezing is loudest (wheezing is louder over the chest) Pleural rub Discontinuous sound: low or high pitch. Short duration Predominantly during expiration Confined mostly to expiration Loud grating or rubbing sounds Sometimes had crackling character, resembles parenchymal crackles Arterial Blood Gas Analysis Only pO2 will be different between arterial and venous, the other parameters will be the same. pH Normal 7.35 to 7.45 Changes depending on level of CO2/bicarbonate PaO2 Normal >75mmHg Hypoxia kill first before hypercarbia PaCO2 Normal 35 to 45mmHg Oxygen can absorb without ventilation while CO2 requires ventilation to blow off Bicarb Normal 22 to 26 mmol Bicarb increases slowly over hours to weeks to compensate for acidosis therefore usually only evident in chronic conditions Acute conditions: no change to bicarb due to time to change COPD is chronic and shows high bicarb due to metabolic system working hard to compensate for acidosis Respiratory/ventilatory failure Occurs when the lungs and ventilatory muscles cannot move enough aim in and out of the alveoli to adequately oxygenated arterial blood and eliminate carbon dioxide. Type 1 (hypoxemic) Type 2 (hypercapnic) PaO2 <60mmHg with normal or subnormal PaCO2 E.g. APO/CAPO, pneumonia PaCO2 >50mmHg E.g. respiratory pump failure Diagnosis template Respiratory acidosis/alkalosis (depending on pH) with or without metabolic compensation (depending on bicarb) the patient is in type I/II respiratory failure Ventilation strategy Adult Paediatric One breath every 5-6 seconds 10-12bpm One breath every 3-5 seconds 12-20bpm Start in guideline and titrate to effect based on Alveolar plateau - alveolar is empty - end of expiration Good rise and FALL (no breath stacking) AND SpO2 EtCO2 “Supplement the patient's breath and stick 2 breaths in between giving a resp rate of 18/min” “I want to increase the patient's minute volume (resp rate x tidal volume)” Tidal volume aim: 6-8 ml/kg One breath over 1 second Gas trapping/breath stacking: air accumulates due hyperventilation where inspiratory volume exceeding expiratory volume (due to expiratory outflow issue) Shark fin on capnography: air is struggling to get out - prolonged expiratory phase - no alveolar plateau Permissive hypoxia/hypercapnia: settling for lower respiratory rate to prevent breath stacking Hyperventilation complications Barotrauma Gastric inflation - causes regurgitation to aspiration to pneumonia Increase in intrathoracic pressure causes a decrease in BP O2 delivery systems Mask Litres per minute Nasal cannula 1 to 6 Simple face mask 5 to 10 Nebuliser 8 Non-rebreather 10 to 15 BVM 10 to 15 CPAP 5 cm H2O 8 10 cm H2O 12 15 cm H2O 15