Respiratory Insufficiency Respiratory Failure L.Dadak inspired by www.aic.cuhk.edu.hk https://emedicine.medscape.com/article/167981overview Interpretation of arterial blood gases ● ● ● Oxygenation Ventilation Acid base status Oxygenation ● ● What is the PaO2? Is this is adequate for the amount of inspired oxygen? ● Does the ABG result agree with the saturation probe? pH PaCO2 PaO2 HCO3Base excess Saturation Oxygenation ● ● ● ● ● ● Normal PaO2 breathing air (FiO2 = 21%) is 12-13.3 kPa ; small reduction with age Lower values constitute hypoxaemia PaO2 <6.7 kPa on room air = respiratory failure PaO2 should go up with increasing FiO2 A PaO2 of 13.3 kPa breathing 60% O2 is not normal You need to know the FiO2 to interpret the ABG Oxygenation ● ● Correlate the ABG result with the saturation probe result If there is a discrepancy: ● ● Is there a problem with the probe (poor perfusion? etc) Is there a problem with the blood gas (is it a venous sample?) Oxygenation ● ● Is the PaO2 is lower than expected? Calculate the A-a gradient to assess if the low PaO2 is due to: ● ● Low alveolar PAO2 Structural lung problems causing failure of oxygen transfer Oxygenation The alveolar gas equation: PAO2 = [94.8 x FIO2] – [PaCO2 x 1.25] The alveolar-arterial oxygen difference (A-a) PO2 = PAO2 - PaO2 Aa Gradient = [FiO2*(Patm-PH2O)-(PaCO2/0.8) ] - PaO2 Aa Gradient = (713 x FiO2) – (pCO2 / 0.8) – (paO2) [mmHg] A-a difference ● ● is less than 10 (15) mmHg. 1,3kPa (2kPa) Normally, the A-a gradient increases with age. For every decade a person has lived, their A-a gradient is expected to increase by 1 mmHg. Oxygen dissociation curve 100 Saturation % 75 50 3.5 5.3 13.3 PO2 kPa Oxygen dissociation curve 100 88 Saturation % 75 50 3.5 5.3 6.7 13.3 kPa PO2 Oxygen cascade Dry atmospheric gas: 21 kPa Humidified tracheal gas: 19.8 kPa Alveolar gas: 14 kPa Arterial blood: 13.3 kPa Capillary blood: 6-7 kPa Mitochondria: 1-5 kPa Venous blood: 5.3 kPa PaCO2 5,3 kPa ● The arterial pCO2 is normally maintained at a level of about 40 mmHg by a balance between production of CO2 by the body and its removal by alveolar ventilation. If the inspired gas contains no CO2 then this relationship can be expressed by: paCO2 is proportional to VCO2 / VA VCO2 is CO2 production by the body VA is Alveolar ventilation ● where: ● ● An increase in arterial pCO2 can occur by one of three possible mechanisms: ● ● ● Presence of excess CO2 in the inspired gas Decreased alveolar ventilation Increased production of CO2 by the body Respiratory Insuf. = Resp.Failure Definition ● The condition in which the lungs cannot take in sufficient oxygen and/or expell sufficient carbon dioxide to meet the needs of the cells of the body. Also called pulmonary insufficiency, respiratory failure. In practice, respiratory failure is defined as a PaO2 value of less than 60 mmHg (8kPa) while breathing air or a PaCO2 of more than 50 mmHg (6.6kPa). Need of arterial blood gasses ● ● ● RF Classification ● ● ● Acute / Chronic hypoxemic or hypercapnic Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3. Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased. The distinction between acute and chronic hypoxemic respiratory failure cannot readily be made on the basis of arterial blood gases. The clinical markers of chronic hypoxemia, such as polycythemia or cor pulmonale, suggest a longstanding disorder. ● ARF ARF is not a specific disease but a reaction to an underlying condition, e.g. trauma, sepsis or pneumonia. Due to different definitions, the incidence and mortality rates for ARF vary across studies. In addition, the underlying condition strongly influences prognosis. 16 Respiratory failure Acute respiratory failure (ARF) is a common and important indication for critical care with a substantial mortality. It is defined as all acute lung conditions with the exception of chornic obstructive lung disease that require active therapy. Pump failure or lung failure ? The respiratory system can be modelled as a gas exchanger (the lungs) ventilated by a pump. The dysfunction of each of the two parts, pump or lungs, may cause respiratory failure defined as inability to maintain adequate blood gases while breathing ambient air. 18 Pump failure Pump failure primarily results in alveolar hypoventilation, hypercapnia and respiratory acidosis. 19 Pump failure  Insufficient alveolar ventilation may result from a number of causes intrinsically affecting one or more of the elements of the complex chain that starts from: the respiratory centres (pump controller) central and peripheral nervous ways chest wall, the latter including both the respiratory muscles and all the passive parts that couple the muscles with the lungs. 2 Pump failure  Insufficient alveolar ventilation may even take place in the absence of any intrinsic problem of the pump, when a high ventilation load overcomes the natural capacity of the pump.  Excessive load can be caused by airway obstruction, respiratory system stiffening or high ventilation requirement, and finally results in intrinsic pump dysfunction due to respiratory muscle fatigue. 2 Lung failure  Lung failure results from any damage of the natural gas exchanger: alveoli, airways and vessels.  Lung failure involves impaired oxygenation and impaired CO2 elimination depending on a variable combination of: True intrapulmonary shunt Increased alveolar dead space  Lung damage also involves increased ventilation requirement and mechanical dysfunctions resulting in high impedance to ventilation. 22 Cause  intoxikation, cerbral insult  sy Guillain Barré, trauma, poliomyelitis  myastenia, neuritis, tetanus, botulism  PNO, haemothorax  upper airway obstruction  asthma, COPD, bronchiolitis, fibrosis, ARDS, aspiration  cardiology 23 Pathophysiologic causes of acute respiratory failure ● ● ● Hypoventilation, V/Q mismatch, shunt Hypoventilation ● usually occurs from depression of the CNS from drugs or neuromuscular diseases affecting respiratory muscles. Hypoventilation is characterized by hypercapnia and hypoxemia. V/Q mismatch ● most common cause of hypoxemia. V/Q units may vary from low to high ratios in the presence of a disease process. The low V/Q units contribute to hypoxemia and hypercapnia in contrast to high V/Q units, which waste ventilation but do not affect gas exchange unless quite severe. The low V/Q ratio may occur either from a decrease in ventilation secondary to airway or interstitial lung disease or from overperfusion in the presence of normal ventilation. The overperfusion may occur in case of pulmonary embolism, where the blood is diverted to normally ventilated units from regions of lungs that have blood flow obstruction secondary to embolism. ● ● ● Administration of 100% oxygen eliminates all of the low V/Q units, thus leading to correction of hypoxemia. Hypoxemia increases minute ventilation by chemoreceptor stimulation, but the PaCO2 level generally is not affected. ● PEEP is less toxic than 100% O2 Shunt ● is defined as the persistence of hypoxemia despite 100% oxygen inhalation. The deoxygenated blood (mixed venous blood) bypasses the ventilated alveoli and mixes with oxygenated blood that has flowed through the ventilated alveoli, consequently leading to a reduction in arterial blood content. The shunt is calculated by the following equation: QS/QT = (CCO2 – CaO2)/CCO2 – CvO2) ● Symptoms: ● ● Fatigue ... Exercise intolerance Dyspnea = an uncomfortable sensation of breathing, shortness of breath Cyanosis, a bluish color of skin and mucous membranes, indicates hypoxemia. Visible cyanosis typically is present when the concentration of deoxygenated hemoglobin in ● the capillaries or tissues is at least 5 g/dL. ● ● ● Heavy breathing Rapid / slow breathing confusion and somnolence .. coma Imaging Studies: ● Chest radiograph Chest radiography is essential because it frequently reveals the cause of respiratory failure. However, distinguishing between cardiogenic and noncardiogenic pulmonary edema often is difficult. heart size, vascular redistribution, peribronchial cuffing, pleural effusions, septal lines, and perihilar bat-wing distribution of infiltrates suggest hydrostatic edema; the lack of these findings suggests acute respiratory distress syndrome (ARDS). ECG ● ● ● supra ventricular tachycardia MI Cor Pulmonale after diltiazem Cor Pulmonale ● ● ● right ventricular hypertrophy (RVH) Right axis deviation R/S amplitude ratio in V1 greater than 1 (an increase in anteriorly directed forces may be a sign of posterior infarction) R/S amplitude ratio in V6 less than 1 P-pulmonale pattern (an increase in P wave amplitude in leads 2, 3, and aVF) S1 Q3 T3 pattern and incomplete (or complete) right bundle branch block, especially if pulmonary embolism is the underlying etiology Low-voltage QRS because of underlying COPD ● ● ● ● Echocardiography ● is a useful test when a cardiac cause of acute respiratory failure is suspected. (The findings of left ventricular dilatation, regional or global wall motion abnormalities, or severe mitral regurgitation support the diagnosis of cardiogenic pulmonary edema. ) ● Pulmonary Function Tests Normal values of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) suggest a disturbance in respiratory control. ● A decrease in FEV1 -to-FVC ratio indicates airflow obstruction, whereas a reduction in both the FEV1 and FVC and maintenance of the FEV1 -to-FVC ratio suggest restrictive lung disease. Respiratory failure is uncommon in obstructive diseases when the FEV1 is greater than 1 L and in restrictive diseases when the FVC is more than 1 L. ● Therapy: The goal: ● PaO2 of 60 mmHg or an arterial oxygen saturation (SaO2) of greater than 90%. Experts believe that hypercapnia should be tolerated until the arterial blood pH falls below 7.2 ● O2: [nasal, mask, m+ reservoar] fiO2 up to 40% Arteficial Ventilation ● NonInvasive / Invasive ECMO Case #1: ● 70 y.o. male has been treated for chronic obstructive pulmonary disease (COPD) for 14 years. Now he is being treated for exacerbation at internal department. Despite full therapy, his status is worsening progressively: he is in increasing respiratory distress and his consciousness worsens. ● #1 COPD acute exacerbation ● You find the patient on a standard ward, hardly breathing O2 via facemask (15l/min, FiO2 1,0), unresponsible, on painful stimulus he distracts arm and opens his eyes. BP 170/70, TF 130/min, sat 99%, RR 12/min. laboratory?? What next?? ● #1 COPD acute exacerbation Arterial blood gases: pH=7.11, pO2=16kPa, pCO2=14 kPa, BE=+16 mM Determine the type of acid-base disorder, incl. compenstation if present. What is the cause of hypercapnia? Describe the regulation of minute ventilation during both normal status and chronic hypercapnia. What was wrong in the treatment of this patient? #1 COPD acute exacerbation Arterial blood gases: pH=7.11, pO2=16kPa, pCO2=14 kPa, BE=+16 mM Describe typical physical findings on a chest of patient with bronchial obstruction. Describe also typical spirometry finding in bronchial obstruction. What is FEV1/FVC? http://www.worldcme.com/webpages/members_only/Asthma/case5/c5post.htm OTI ?? Should this patient be intubated and mechanically ventilated? Determine Glasgow Coma Score of this patient. Ethical aspects ● If this patient had expressed the wish not to be intubated before this episode, would you accept it and provide sympthomatic treatment only (i.e. morphin, fluids)? Explain terms witholding and withdrawing treatment. ● Pathophysiology: obstructive and restrictive disorders of ventilation, incl. spirometric findings Pathology: COPD, chronic bronchitis, emphysema Example 2. A 33 male patient with ARDS has a saturation of 91% on Fi02 0.4 ● ● pH PaCO2 PaO2 HCO3Base excess 7.43 4.76 8.1 23 -0.6 Is he hypoxic? Is there an acid base or ventilation problem? Saturation 90% Is he hypoxic? YES. The SpO2 and calculated saturation agree pH PaCO2 PaO2 HCO3Base excess 7.43 4.76 8.1 23 -0.6 Saturation 90% Is he hypoxic? YES. (A-a) PO2 = 23.9 kPa There is major problem with oxygen transfer into the lung pH PaCO2 PaO2 HCO3Base excess 7.43 4.76 8.1 23 -0.6 Saturation 90% Is there an acid base or ventilation problem? pH PaCO2 PaO2 PaCO2 Base excess 7.43 4.76 8.1 23 -0.6 Saturation 90% Is there an acid base or ventilation problem? NO. pH PaCO2 7.43 4.76 8.1 23 -0.6 pH, PaCO2 and PaCO2 are normal This is pure hypoxaemic respiratory failure PaO2 PaCO2 Base excess Saturation 90% Example 9. Is he hypoxic? pH pH PaCO2 PaCO2 PaO2 PaO2 HCO3HCO37.5 7.23 6.2 3.3 10.6 10.6 38 8 Base excess +8 Base excess -10 Saturation Saturation 96% 96% Example 9. Is he hypoxic? pH pH PaCO2 PaCO2 7.5 7.23 6.2 3.3 10.6 10.6 38 8 NO. This is a normal PaO2 for a patient this age breathing room air PaO2 PaO2 HCO3HCO3- Base excess +8 Base excess -10 Saturation Saturation 96% 96% Emergency department : ● ● ● consciousness, sitting, haevy breathing, sweating. What to do? Examination> Airway Breathing Circulation Disability Electrolytes Fluids Gut Hematology Infection Lines Med, Nutrition, .... A B C D ... Problem: Plan: Physical Examination> Airway Breathing Ciruculation Disability Electrolytes Fluids Gut Hematology Infection … today topic A open, clear, cough / upper airway obstruction, OTI, TS O2 mask B Lung Auscultation – vesicular / wheezes tubular / gurgling... SpO2, Ventilation ... Problem: Plan: Respiratory Failure O2 mask / NIV / OTI treat the cause Questions: Essential: ● ● Problem> Patient history monitoring: ● SpO2, ECG, NIBP O2 mask Asthma A unable to converse, accessory muscles of respiration are used, sitting position B tachypneic, Loud expiratory wheezing, SpO2 92 on air C s.r. 100/min, pulsus paradoxus D ... Problem: Plan: Asthma A unable to converse, accessory muscles of respiration are used, sitting position B tachypneic, Loud expiratory wheezing, SpO2 92 on air C s.r. 100/min, pulsus paradoxus D ... Problem: Moderate asthma Plan: Asthma A unable to converse, accessory muscles of respiration are used, sitting position B tachypneic, Loud expiratory wheezing, SpO2 92 on air C s.r. 100/min, pulsus paradoxus Problem: Moderate asthma Plan: SABA á 20min, á 3h + corticoid (p.os) Asthma 2 A sitting, suprasternal retractions; B breathless during rest; Loud biphasic (expiratory and inspiratory) wheezing SpO2 85 on Air C s.r. 130/min, hypertension, sweating D confused... Problem: Plan: Asthma 2 A sitting, suprasternal retractions; B breathless during rest; Loud biphasic (expiratory and inspiratory) wheezing SpO2 85 on Air C s.r. 130/min, hypertension, sweating D confused... Problem: Life-Threatening Asthma Plan: Astma 2 A sitting, suprasternal retractions; B breathless during rest; Loud biphasic (expiratory and inspiratory) wheezing SpO2 85 on Air C s.r. 130/min, hypertension, diaphoresis = sweating D confused... Problem: Life-Threatening Asthma Plan: OTI + sedation, vent. ● SABA á 20min, á 3h + corticoid i.v. Asthma ● Do NOT administer metylxantins (tachykardia) Asthma = obstruction http://www.rtjournalonline.com/Life%20threatening%20Asthma%20Physiology%20and%20Management.pdf MET call A spont. vent., O2 mask (40% O2) B 30/min, SpO2 85% C 110/min, 80/40mmHg D somnolence … sopor I: 39°C, 2D stand.wards. Augmentin iv. Problem: Plan: MET call A B C 110/min, 80/40mmHg D somnolence … sopor I: 39°C, 2D stand.wards. Augmentin iv. Problem: bronchopneumonia Plan: ATB, OTI, Vent. MET call A O2 mask B rapid, shallow breading, SpO2 90%, crackles C s.r. + Norepinephrine D somnolence ... Problem: pancreatitis Plan: rtg ARDS = acute respiratory distress syndrome ● Clinical presentation - Tachypnea and dyspnea; crackles upon auscultation Clinical setting - Direct insult (aspiration) or systemic process causing lung injury (sepsis) Radiologic appearance - Three-quadrant or 4quadrant alveolar flooding Lung mechanics - Diminished compliance (< 40 mL/cm water) Gas exchange - Severe hypoxia refractory to oxygen therapy (PaO2/FIO2 < 200) ● ● ● ● ● End. COPD Signs ● ● ● ● barrel chest, pursed-lip breathing, productive cough, cyanosis. Barrel Chest ● lungs become enlarged, the diaphragm is displaced downward and is unable to contract efficiently. Furthermore, the chest wall is enlarged, making accessory breathing muscles (muscles in the neck, upper chest, and between the ribs) less efficient as well. These changes contribute to shortness of breath.