resp (1).pptx
- 1. Moderator- Dr.John Israel By- Dr.Ranjith Kumar Dr.Spandana
- 2. ⦁ a condition in which the respiratory system fails in one or both of its gas-exchanging functions ⦁ a syndrome of inadequate gas exchange due to dysfunction of one or more essential components of the respiratory system
- 3. CNS (medulla) Peripheral nervous system (phrenic nerve) Respiratory muscles Chest wall Lung Upper airway Bronchial tree Alveoli Pulmonary vasculature
- 4. ⦁ Rhythmic respiration - initiated by a pacemaker cells in the pre-Bötzinger complex on either side of the medulla between the nucleus ambiguus and the lateral reticular nucleus ⦁ RESPIRATORY CENTER-Brain stem ⦁ Incl. (a)DRG (b)VRG (c)PRG/Pneumotaxic center-PONS (d)Apneustic center MEDULLA
- 5. ⦁ DRG-responsible for the basic rhythm of respiration. ⦁ VRG-When the respiratory drive for increased pulmonary ventilation becomes greater than normal,respiratory signals spill over into the ventral respiratory neurons
- 6. ⦁ Pneumotaxic center - limits inspiration, which has a secondary effect of increasing the rate of breathing ⦁ Apneustic center- slows down the inhibitory signals from pneumotaxic center-regulates intensity of respiration
- 8. ⦁ Chemosensitive area in the respiratory center-beneath the ventral surface of medulla Sensitive to changes in blood PCO2/pH Acute rise in PCo2 stimulates chemosensitive area which inturn stimulates inspiratory area
- 9. ⦁ Decreased stimulatory effect of CO2 after the first 1 to 2 days ⦁ Part of this decline results from renal readjustment of the H+ ion concentration towards normal. ⦁ Over a period of hours, the HCO3- ions also slowly diffuse through the blood-brain and blood–CSF barriers and combine directly with the hydrogen ions adjacent to the respiratory neurons
- 11. ⦁ Incl: The Carotid and the Aortic bodies ⦁ The Carotid bodies are located bilaterally in the bifurcations of the common carotid arteries. ⦁ Their afferent nerve fibers pass through Hering’s nerves to the glossopharyngeal ⦁ nerves and then to the dorsal respiratory area of the medulla.
- 12. ⦁ The aortic bodies are located along the arch of the aorta ⦁ Their afferent nerve fibers pass through the vagi, also to the dorsal medullary respiratory area. ⦁ Decreased Arterial Oxygen Stimulates the Chemoreceptors
- 14. ⦁ Reason for acclimatization is that, within 2 to 3 days, the respiratory center in the brain stem loses abt. four fifths of its sensitivity to changes in PCO2 and hydrogen ions. ⦁ Therefore, the excess ventilatory blow-off of CO2 that normally would inhibit an increase in respiration fails to occur, and low O2 can drive the respiratory system to a much higher level of alveolar ventilation than under acute conditions.
- 15. ⦁ Type-I : Hypoxemic respiratory failure ⦁ Type-II : Hypercapnic respiratory failure ⦁ Type-III : Perioperative respiratory failure ⦁ Type-IV : Respiratory failure in shock
- 16. ⦁ defined as an arterial pO2(paO2) less than 55 mm Hg when the fraction of oxygen in inspired air (FiO2) is 0.60 or greater Seen in ⦁ Alveolar hypoventilation, ⦁ Ventilation–perfusion mismatch, ⦁ Shunt and ⦁ Diffusion limitation ⦁ Low FiO2 (high altitude)
- 17. ⦁ HYPOXEMIC RESP. FAILURE INCREASED ALVEOLAR GRADIENT NORMAL ALVEOLAR GRADIENT O2 responsive V/Q mismatch Non responsive Shunt PaCo2 Normal Airway Ds. 1.COPD 2.Asthma 3.CF ILD Pulm Vasc. Ds. PE Intracard.Shunt ASD,VSD,PFO Intrapulm shunt Pulm AVM Alveolar filling Pulm edema, ARDS, TRALI, pneumonia, Aspiration Alv. H’ge Alv. proteinosis Alveolar hypoventilation High altitude Low inspired O2
- 18. ⦁ defined as an arterial pCO2 (paCO2) greater than 45 mmHg ⦁ Results from: ⦁ (a) an increase in CO2 production, ⦁ (b) a decrease in minute ventilation, and ⦁ (c) an increase in dead-space ventilation
- 19. 🞂 CNS Anterior Horn Cells Motor Nerves RESP. PUMP FAILURE NMJ Muscles Airways Excessive & Alveoli work of breathing Drugs Medullary CVA OSA Hypothyroi dism Ondine’s curse(idiop athic) ALS Polio Cervical spine injury GBS Crtical illness polyneuro pathy Diphth. Fish toxins Tick paralysis M.Gravis LEMS Botulism OP Poisoning tis Dermato myositis Muscular dystrophi es Myopathy COPD Drugs CF Polymyosi Asthma PF P.Edema Chestwall disorders Scoliosis Obesity Sepsis, M.acidosis Tense ascites, AC syndr. Upper airway obstruc.
- 20. ⦁ Results from lung atelectasis ⦁ also called perioperative respiratory failure. ⦁ After general anesthesia, decrease in FRC leads to collapse of dependent lung units.
- 21. ⦁ Rx: ⦁ frequent changes in position,chest physiotherapy, upright positioning, incentive spirometry. ⦁ Noninvasive positive-pressure ventilation may also be used to reverse regional atelectasis.
- 22. ⦁ results from hypoperfusion of respiratory muscles in patients in shock ⦁ Normally, respiratory muscles consume <5% of total cardiac output and oxygen delivery. ⦁ Patients in shock often experience respiratory distress due to pulmonary edema (e.g., in cardiogenic shock), lactic acidosis, and anemia.
- 23. ⦁ In this setting, up to 40% of cardiac output may be distributed to the respiratory muscles. ⦁ Intubation and mechanical ventilation can allow redistribution of the cardiac output away from the respiratory muscles and back to vital organs while the shock is treated
- 25. ⦁ Acute hypercarbic resp failure is accompanied by change in pH i.e. acidemia ⦁ Chronic condition result in renal compensation & increased serum HCO3- conc.
- 26. ⦁ Acute and chronic hypoxemic respiratory failure may not distinguished based on ABG values ⦁ Markers of chronic hypoxemia- polycythemia or cor pulmonale provides clues to a long- standing disorder ⦁ Abrupt changes in mental status suggest an acute event.
- 27. ⦁ The diagnosis of acute or chronic respiratory failure begins with clinical suspicion of its presence ⦁ Confirmation of the diagnosis is based on arterial blood gas analysis. ⦁ Evaluation for an underlying cause must be initiated early, frequently in the presence of concurrent treatment for acute respiratory failure
- 28. ⦁ Sepsis - fever, chills ⦁ Pneumonia - cough, sputum production, chest pain ⦁ Pulmonary embolus - sudden onset of SOB or chest pain ⦁ COPD exacerbation – H/O heavy smoking, cough, sputum production ⦁ Cardiogenic pulmonary edema - chest pain, PND, and orthopnea
- 29. ⦁ Noncardiogenic edema - the presence of risk factors including sepsis, trauma, aspiration, and blood transfusions ⦁ Accompanying sensory abnormalities /symptoms of weakness- neuromuscular respiratory failure, H/O an ingestion or administration of drugs or toxins. ⦁ Additional exposure history may help diagnose asthma, aspiration, inhalational injury and some interstitial lung diseases
- 30. ⦁ Hypotension usually with signs of poor perfusion- severe sepsis or massive pulmonary embolism ⦁ Wheezing suggests airway obstruction • Fixed upper or lower airway pathology • Secretions • Pulmonary edema (“ cardiac asthma”) • Bronchospasm
- 31. ⦁ Stridor suggests upper airway obstruction ⦁ JVP suggests RV dysfunction due to accompanying pulmonary hypertension ⦁ Tachycardia and arrhythmias may be the cause of cardiogenic pulmonary edema
- 32. ⦁ ABG ⦁ Quantifies magnitude of gas exchange abnormality ⦁ Identifies type and chronicity of respiratory failure
- 33. ⦁ Complete blood count ⦁ Anemia may cause cardiogenic pulmonary edema ⦁ Polycythemia suggests may chronic hypoxemia ⦁ Leukocytosis, a left shift, or leukopenia suggestive of infection ⦁ Thrombocytopenia may suggest sepsis as a cause
- 34. ⦁ Cardiac serologic markers ⦁ Troponin, Creatine kinase- MB fraction (CK- MB) ⦁ B-type natriuretic peptide (BNP) ⦁ Microbiology ⦁ Respiratory cultures: sputum/tracheal aspirate/broncheoalveolar lavage (BAL) ⦁ Blood, urine and body fluid (e.g. pleural) cultures
- 35. ⦁ Chest radiography ⦁ Identify chest wall, pleural and lung parenchymal pathology; ⦁ Distinguish disorders that cause primarily V/Q mismatch (clear lungs) vs. Shunt (intra- pulmonary shunt; with opacities present) ⦁ Electrocardiogram ⦁ Identify arrhythmias, ischemia, ventricular ⦁ Dysfunction ⦁ Echocardiography ⦁ Identify right and/or left ventricular dysfunction
- 36. ⦁ Pulmonary function tests/bedside spirometry ⦁ Identify obstruction, restriction, gas diffusion abnormalities ⦁ May be difficult to perform if critically ill ⦁ Bronchoscopy ⦁ Obtain biopsies, brushings and BAL for histology, cytology & microbiology ⦁ Results may not be available quickly enough to avert respiratory failure ⦁ Bronchoscopy may not be safe in the if critically ill
- 37. ⦁ ABC’ s ⦁ Ensure airway is adequate ⦁ Ensure adequate supplemental oxygen and assisted ventilation, if indicated ⦁ Support circulation as needed
- 38. ⦁ Treatment of a specific cause when possible ⦁ Infection ⦁ Antimicrobials, source control ⦁ Airway obstruction ⦁ Bronchodilators, glucocorticoids ⦁ Improve cardiac function ⦁ Positive airway pressure, diuretics, vasodilators, ⦁ morphine, inotropy, revascularization
- 39. ⦁ Mechanical ventilation is used to assist or replace spontaneous breathing. ⦁ Types: ⦁ 1.NIV ⦁ 2.Conventional MV ⦁ 3.Non-Conventional MV
- 40. ⦁ usually is provided with a tight-fitting face mask or nasal mask ⦁ if patient can protect airway and is hemodynamically stable) NIV has proved highly effective in patients with respiratory failure arising from acute exacerbations of COPD It is most frequently implemented as BiPAP ventilation or Pressure Support Ventilation ⦁ Both modes, which apply a preset positive pressure during inspiration and a lower pressure during expiration at the mask, are well tolerated by a conscious patient and optimize patient- ventilator synchrony.
- 41. ⦁ Limitations of NIV ⦁ Patient intolerance ⦁ Tight fitting mask req for NIV can cause both physical and pysh. discomfort ⦁ Once NIV is initiated, patients should be monitored;a reduction in respiratory frequency and a decrease in the use of accessory muscles (scalene, sternomastoid, and intercostals) are good clinical indicators of adequate therapeutic benefit
- 42. 1. COPD exacerbation 2. Cardiogenic pulmonary edema 3. Obesity /hypoventilation syndrome 4. NIV may be tried in selected pts with asthma or non-cardiogenic hypoxemic respiratory failure
- 43. ⦁ Cardiac or respiratory arrest ⦁ Severe encephalopathy ⦁ Upper airway obstruction ⦁ Severe UGI bleeding ⦁ Inability to protect airway
- 44. ⦁ Hemodynamic instability ⦁ Inability to clear secretions ⦁ High risk for aspiration ⦁ Unstable cardiac rhythm ⦁ Nonrespiratory organ failure ⦁ Facial surgery, trauma, or deformity
- 45. ⦁ Conventional MV is implemented once a cuffed tube is inserted into the trachea to allow conditioned gas(warmed, oxygenated, and humidified) to be delivered to the airways and lungs at pressures above atmospheric pressure. ⦁ Care should be taken during intubation to avoid brain-damaging hypoxia
- 46. ⦁ Admin. of mild sedatives-opioids, BZD ⦁ Shorter-acting agents etomidate and propofol have been used for both induction and maintenance of anesthesia in ventilated patients because they have fewer adverse hemodynamic effects ⦁ Great care must be taken to avoid the use of neuromuscular paralysis during intubation of patients with renal failure, tumor lysis syndrome, crush injuries, medical conditions associated with elevated serum K+ levels, and muscular dystrophy syndromes
- 47. ⦁ To optimize oxygenation while avoiding ventilator-induced lung injury due to overstretch and collapse/re-recruitment. ⦁ Normalization of pH through elimination of CO2 is desirable but the risk of lung damage associated with the large volume and high pressure. ⦁ This has led to the acceptance of permissive hypercapnia. This condition is well tolerated when care is taken to avoid excess acidosis by pH buffering.
- 48. ⦁ Ventilation strategy that allows PaCO2 to rise by accepting a lower alveolar minute ventilation ⦁ to avoid specific risks: ⦁ Dynamic hyperinflation (“auto- peep”) and barotrauma in patients with asthma ⦁ Ventilator-associated lung injury, in patients with, or at risk for, ALI and ARDS ⦁Contraindicated in patients with increased intracranial pressure such as head trauma
- 50. 1. Assisted Control MV ⦁ an inspiratory cycle is initiated either by the patient’s inspiratory effort or, if none is detected within a specified time window, by a timer signal within the ventilator. ⦁ Every breath delivered, whether patient- or timer-triggered, consists of the operator-specified tidal volume. ⦁ Ventilatory rate is determined either by the patient or by the operator-specified backup rate, whichever is of higher frequency. ⦁ commonly used for initiation of MV because it ensures a backup minute ventilation in the absence of an intact respiratory drive and allows for synchronization of the ventilator cycle with the patient’s inspiratory effort.
- 51. ⦁ Patients with tachypnea due to nonrespiratory or nonmetabolic factors, such as: Anxiety, Pain, and Airway irritation. ⦁ Respiratory alkalemia may develop and trigger myoclonus or seizures.
- 52. ⦁ Dynamic hyperinflation leading to increased intrathoracic pressures (so-called auto-PEEP) may occur-inadequate time is available for complete exhalation between inspiratory cycles. ⦁ Auto-PEEP can limit venous return, decrease cardiac output, and increase airway pressures, predisposing to barotrauma
- 53. ⦁ The number of mandatory breaths of fixed volume to be delivered by the ventilator are set ⦁ Between those breaths, the patient can breathe spontaneously. ⦁ In the most frequently used SIMV, mandatory breaths are delivered in synchrony with the patient’s inspiratory efforts.
- 54. ⦁ If the patient fails to initiate a breath, the ventilator delivers a fixed-tidal-volume breath and resets the internal timer for the next inspiratory cycle. ⦁ SIMV differs from ACMV in that only a preset number of breaths are ventilator-assisted. ⦁ SIMV allows patients with an intact respiratory drive to exercise inspiratory muscles between assisted breaths; thus it is useful for both supporting and weaning intubated patients ⦁ difficult in patients with tachypnea because they may attempt to exhale during the ventilator- programmed inspiratory cycle.
- 55. ⦁ This form of ventilation is pt triggered, flow- cycled, and pressure-limited. ⦁ It provides graded assistance and differs from the other two modes in that the operator sets the pressure level (rather than the volume) to augment every spontaneous respiratory effort.
- 56. ⦁ The level of pressure is adjusted by observing the patient’s respiratory frequency ⦁ With PSV, patients receive ventilator assistance only when the ventilator detects an inspiratory effort. ⦁PSV is often used in combination with SIMV to ensure volume-cycled backup for patient whose respiratory drive is depressed.
- 57. ⦁ Pressure Control Ventilation ⦁ Inverse Ratio Ventilation ⦁ CPAP-The ventilator provides fresh gas to the breathing circuit with each inspiration and sets the circuit to a constant, operator specified pressure. ⦁ CPAP is used to assess extubation potential in pts who have been effectively weaned
- 58. ⦁ High frequency oscillatory Ventilation ⦁ Airway Pressure Release Ventilation ⦁ Extracorporeal Membrane Oxygenation ⦁ Partial Liquid Ventilation ⦁ Proportional Assist ventilation ⦁ Neurally Adjusted Ventilatory Assist ventilation
- 59. ⦁ (1) Set a target tidal volume close to 6 mL/kg of ideal body weight. ⦁ (2) Prevent plateau pressure (static pressure in the airway at the end of inspiration > 30 cm H2O. ⦁ (3) Use the lowest possible Fio2 to keep the Sao2 at ≥90%. ⦁ (4) Adjust the PEEP to maintain alveolar patency while preventing overdistention & closure/reopening.
- 60. ⦁ As improvement in respiratory function is noted, the first priority is to reduce the level of mechanical ventilatory support. ⦁ Patients on full ventilatory support should be monitored frequently, with the goal of switching to a mode that allows for weaning as soon as possible ⦁ Patients whose condition continues to deteriorate after ventilatory support is initiated may require increased O2, PEEP, or one of the alternative modes of ventilation.
- 61. ⦁ Sedation and analgesia to maintain an acceptable level of comfort-lorazepam, midazolam, diazepam, morphine,and fentanyl ⦁ Subcutaneous heparin and/or pneumatic compression boots to avoid DVT ⦁ To prevent decubitus ulcers- frequent changes in body position , use of soft mattress overlays and air mattresses ⦁ Prophylaxis against diffuse GI mucosal injury is indicated for patients undergoing MV-H2 receptor antagonists, antacids, and cytoprotective agents such as sucralfate
- 62. ⦁ Nutritional support - enteral feeding through either a nasogastric or an orogastric tube should be initiated and maintained whenever possible. ⦁ Delayed gastric emptying is common in critically ill patients taking sedative medications but often responds to promotility agents such as metoclopramide.
- 63. ⦁ Pulmonary: ⦁ Barotrauma ⦁ Nosocomial pneumonia ⦁ Oxygen toxicity ⦁ Tracheal stenosis ⦁ Intubated patients are at high risk for ventilator- associated pneumonia as a result of aspiration from the upper airways through small leaks around the endotracheal tube cuff; ⦁ The most common organisms - Pseudomonas aeruginosa, enteric gram-negative rods, and Staphylococcus aureus. 🞂
- 64. ⦁ Hypotension resulting from elevated intrathoracic pressures with decreased venous return is almost always responsive to intravascular volume repletion. ⦁ Gastrointestinal effects of positive-pressure ventilation include stress ulceration and mild to moderate cholestasis
- 65. ⦁ The decision to wean: ⦁ (1) Lung injury is stable or resolving. ⦁ (2) Gas exchange is adequate, with low PEEP/Fio2 (<8 cmH2O) and Fio2(<0.5). ⦁ (3) Hemodynamic variables are stable, and the patient is no longer receiving vasopressors). ⦁ (4) The patient is capable of initiating spontaneous breaths.
- 66. ⦁ SPONTANEOUS BREATHING TRIAL ⦁ The SBT is usually implemented with a T- piece using 1–5 cmH2O, CPAP with 5– 7cmH2O ⦁ Once it is determined that the patient can breathe spontaneously, a decision must be made about the removal of the artificial airway, which should be undertaken only pt has the ability to protect the airway, is able to cough and clear secretions, and is alert enough to follow commands
- 68. ⦁ Several studies suggest that NIV can be used to obviate reintubation, particularly in patients with ventilatory failure secondary to COPD exacerbation ⦁ In this setting, earlier extubation with the use of prophylactic NIV has yielded good results.
- 69. ⦁ Prolonged Ventilation- >21 days. ⦁ A tracheostomy is thought to be more comfortable, to require less sedation, and to provide a more secure airway and may also reduce weaning time. ⦁ In patients with long-term tracheostomy, complications include tracheal stenosis, granulation, and erosion of the innominate artery. ⦁ MV for more than 10–14 days, a tracheostomy is indicated
- 70. ⦁ Mortality in hypoxemic respiratory failure depends on the underlying cause ⦁ Mortality in ARDS appears to have improved in recent years, but it remains high in the elderly -mortality is 60%. ⦁ Patients who develop sepsis after trauma have a lower mortality than do patients with sepsis that complicates medical disorders.
- 71. ⦁ Higher mortality in patients admitted with hypercapnic respiratory failure ⦁ For patients hospitalized with an acute exacerbation of COPD, overall mortality is 8% to 12%, but it may be as high as 28% for those with significant comorbidities