Approximately 50% of the time a patient spend on a mechanical ventilator is in the process of weaning
opposite way to which we commencement of mechanical ventilation.
ETT blockage, if no proper care.
The amount of sedatives used must be minimized and the patient wakened daily.
by using a nerve stimulator
Have you ever tried to inflate a completely deflated balloon: it’s really difficult to inflate initially, then you feel a give and the rest is a cinch! Inflating alveoli is like this. A more appropriate approach would be to let the balloon (alveolus) deflate to just above the point where inflation becomes easy (the lower inflection point of the pressure-volume curve), then reinflation is much less work. This is the concept behind CPAP
Increased intrathoracic pressure will have adverse effect on CVS
Less useful in Pt. on prolonged ventilation & in elderly.
Unless the patient is being ventilated for post-operative care, in which case the lungs are usually normal,
Describe how you would evaluate this patient for weaning from mechanical ventilation?
1. Why the patient was intubated2. For how long he remained on artificial ventilation3. How much sedation was given
Nosocomial Pneumonia (VAP) Stretch injury and barotrauma Airway trauma Prolonged Sedation Obvious increase in associated cost Ventilator dependency
Hypoxemia & hypercarbia Sympathetic discharge – cardiovascular stress. Muscular fatigue and acidosis Loss of airway protection (aspiration). Reintubation into an edematous airway (risk of hypoxic brain injury etc).
Prolonged sedation, reduces respiratory drive and prolongs ventilation. Psychological dependence on the ventilator follows prolonged usage. A number of factors will reduce central respiratory drive. As CO2 is the main stimulus for ventilation, the pt’s PaCO2 must be returned to a normal level. Metabolic or respiratory alkalosis reduces hydrogen ion concentration in the brainstem, and thus the stimulus to breath. For weaning the patient must be awake and co-operative and able to protect his airway.
It is essential to rule out the possibility of a persistent neurological injury such a phrenic nerve palsy, due to surgery. Some drugs such as aminoglycosides can mimic NMBs. Prolonged critical illness may lead to the development of a critical illness polyneuropathy, due to axonal degeneration.
Muscular atrophy due to malnutrition, prolonged muscle relaxants or critical illness myopathy may limit weaning.
Chest Wall – flail chest: is the pain under control? Does the patient have a compliant chest wall? If the patient has to work hard just to lift the chest wall - for example extensive edema, large fat pads, tight dressings, increased abdominal pressure - due to bowel swelling, packs, blood etc, then weaning will be very difficult. Pleural effusions – are they present, can they be drained? Does the patient have a chest drain in – is there much coming in.
Airways – airway obstruction – mucus plug, excessive secretions or bronchospasm? Is there laryngeal edema Abdomen: does the patient have a compliant abdominal surface. The presence of ascites, distended bowel, abdominal hypertension, packs or tight surgical dressings may interfere with ventilation.
Avoid being drawn into the “minute volume looks” the ability to ventilate is related to alveolar ventilation, not minute ventilation.
“Why A patients PaCO2 so high when he has a minute ventilation of 20 liters per minute?"
Clearance of carbon dioxide is determined by the alveolar ventilation and the physiologic dead space. This is a common trap to fall into: confusing alveolar ventilation (difficult to measure) with minute ventilation (always measured). The difference between the two is determined by the anatomical dead space. BEWARE OF TACHYPNEA WITH SMALL TIDAL VOLUMES
Patient A taking 20 breaths of 500ml tidal volume. Patient B taking 50 breaths of 200ml tidal volume.
Pt. A has a normal blood gas.Pt. B has a significant respiratory acidosis. Vd/Vt ratio Patient A Vd/Vt < 30% Patient B Vd/Vt 75%. ???? In the case of patient B, 75% of his respiratory effort is being wasted, leading to severe muscular fatigue and acidosis.
Alveolar dead space: A patient can be receiving tidal volumes of 500ml and still have a dead space / tidal volume ratio of 75%.How??? Alveolar dead space is caused by increased volume of zone 1 (zone 1 is where alveolar pressure exceeds the perfusion pressure to the lung unit: alveoli are ventilated but not perfused):
Zone 1:PA > Pa > PvZone 2:Pa > PA > PvZone 3:Pa > Pv > PA
Hypoperfusion - low pulmonary blood volume-pressure leads to underperfusion of non dependent lung segments. Overdistension of lung by excessive PEEP Vd/Vt = PaCO2 - PetCO2/PaCO2
The patient is able to ventilate The patient is able to oxygenate The patient is able to protect his airway
Alveolar Ventilation keeps PaCO2 < 50 mmHg Production of CO2 can be controlled by reducing the carbon load in the diet (high fat), minimize agitation, pain, fever, shivering muscle workload.
diffusion abnormalities, ventilation-perfusion mismatch, dead space and shunt persistent lower respiratory tract infection, alveolar edema, airway/lobar collapse, lung fibrosis
The commonest cause of airway collapse is absorption atelectasis, distal to mucus plugs Good quality of chest physiotherapy is required to mobilize secretionsIf the patient is requiring moderate to high levels of PEEP to oxygenate , then weaning is unlikely.
A source of ventilation-perfusion mismatch: this leads to hypoxemia and hypercarbia. Tremendously difficult to reinflate: leading to a huge increase in the work of breathing & oxygen consumption.
How much to give ?Insufficient PEEP is of little benefit.Excessive PEEP problems:- barotrauma wasted ventilation Increased intrathoracic pressure Ideal level of PEEP is that which prevents derecruitment of the majority of alveoli, while causing minimal over distension
Auto-PEEP is gas trapped in alveoli at end expiration, due to inadequate time for expiration, bronchoconstriction or mucus plugging. It increases the work of breathing.
Rapid Shallow Breathing Index f/VT RSBI OF < 105
Controlled Ventilation Partial ventilator support The objective of PVS is to allow the patient to interact with the ventilator as the neuro-mechanical cause of respiratory failure resolves. The disease process and ICU interventions (sedation), do not allow for immediate movement from full support to extubation.
Although partial support modes arewidely used, there is no evidence thatthey are superior to multiple daily T-piece trials. The most effective methodof PVS is targeted pressure support. SIMV + PS Pressure Assist control PSV
Ensure that patient is suitable for weaning Communicate to the patient Conduct the trials early in the morning, when the patient is fully rested and there is a full supporting staff available. During these trials the patient should be awake and co-operative, afebrile and on minimal pressor support
Place the patient in the upright or semi- upright position and explain what you are attempting to do. Suction out the tube, airway and oropharynx.
For How longhave to monitor the weaning process with SBT
Criteria Description Objective o Adequate oxygenation (eg, PaO2 >60 mm Hg on FIO2 > 0.4; PEEP <5cmmeasurements H2O; PaO2/FIO2 >150–300); o Stable cardiovascular system (HR <140; stable BP; (no or minimal vasopressors) o Afebrile (temperature < 38 C) o No significant respiratory acidosis o Adequate hemoglobin o Adequate mental status (arousable, no continuous sedative Infusions) o Stable metabolic status (acceptable electrolytes) Subjective clinical o Resolution of disease acute phase; physician believes discontinuation assessment possible; adequate cough reflex
Two parts to weaning: weaning to partial ventilator support weaning to discontinuation. There is little evidence that partial modes are more effective than T-piece trails. Of these modes, pressure support is the best.
If it is possible to wean a patient to extubation, but the patient cannot protect his airway. It is best to perform tracheotomy.
It may be difficult to wean a patient if ongoing inflammatory processes persist in the lungs: consolidation fibrosis auto-PEEP diffusion defects
A 77 year old male F/c Lapratomy. Complicated by perioperative MI, systemic sepsis required insertion of a pulmonary artery catheter, volume loading and vasopressors, and moderate renal dysfunction, with s.creatinine 3.3. He is now at 14 days postop on ventilator Currently he is difficult to arouse, on a sedation of fentanyl 50μg/hr & medazolam His temperature is 37.8. Pulse is 76 and regular, B.P. is 130/70 and CVP is 12.
lungs are clear on auscultation, CXR reveals some patchy infiltrates, atelectasis and a left sided pleural effusion. On SIMV rate 8, pressure support 16 and PEEP 5 cmH2O, FIO2 35% . ABG :- pH 7.52, PaO2 72, PaCO2 44, BE +8, SaO2 94%. Abdomen is tense, with a wound closed with tension sutures and two drains, currently draining very little. LFT: normal except for an albumin of 1.6 . He has edema of lower limb, sacral and scrotal area. His fluid balance is even over the past five days. Hb 8.1, WBC 18.5, Plat 1.2 Lac, Na 148, K 3.1, Urea37,Creat 1.2, MgSO4 3.2, PO4 1.5, Ca 2.0. The patient is completing a 14 day course of ampi., genta. & metronidazole.
CNS – he remains sedated with medazolam and fentanyl. These will both reduce level of consciousness and impair central respiratory drive. These agents must be aggressively weaned. PNS – although he has only been ventilated for two weeks, he is doing little work himself, and may have some muscular atrophy. In addition, the combination of a low serum potassium, magnesium and phosphate need to be supplemented for muscular function.
CVS – the patchy infiltrates on CXR and the history of MI are worrisome, this indicates that this patient will not easily tolerate the autotransfusion associated with moving from positive to negative pressure ventilation. It is essential to do an echocardiogram, assess cardiac performance and consider the use of an agent that remodels the ventricle and reduced preload and afterload – an ACE inhibitor. We must be cautious in this circumstance with the history of renal failure. Alternative therapies would be the introduction of either nitrates or dobutamine in the hours peri-extubation.
Renal – renal function is reasonably good now, metabolic alkalosis indicate sodium bicarbonate use – seen in the high serum sodium. This alkalosis can be corrected with judicious use of sodium chloride (the chloride will correct the alkalosis by returning to electro-neutrality) or increasing enteral free water delivery. Gastrointestinal/Abdomen – a tense tight abdomen will interfere with diaphragmatic excursion, and thus respiratory mechanics. We have little control over this. It is worth asking, nonetheless, with a tense abdomen and nothing draining, if the drains are blocked. Does the patient have ascites? If so, it may be worth draining this to reduce intra- abdominal pressure.
Extremities – peripheral edema and a low serum albumin, as the patient probably also has soggy lungs, from sepsis induced capillary leak (low oncotic pressure and fluid extravascation). There is little that can be done about this edema, the fact that it is resistant to diuretics is interesting. Has the patient been given adequate prophylaxis against deep venous thrombosis and pulmonary embolism? Pulmonary function – the x-ray findings indicate patchy consolidation (difficult to oxygenate) and a pleural effusion (difficult to ventilate). The effusion can be drained if necessary. Think for a possible nosocomial pneumonia – because of persistent leucocytosis, lung infiltrates and a low grade temperature.
The patient has not been covered for pseudomonas or MRSA pneumonia, and it is essential to rule out this possibility by performing a broncho-alveolar lavage at this time. How long have the pt’s lines been in – is that the source? This patient will probably tolerate a pressure support mode of ventilation fairly well, although his electrolytes and acid base status require correction. If there is no movement towards minimal ventilator settings within 48 hours, a prolonged wean is probably likely (due to low physiological reserve) and the patient will require a tracheostomy.
Cardiovascular – pulmonary edema due to left ventricular failure or volume overload decreases lung compliance and will make weaning more difficult. When mechanical ventilation is discontinued, significant physiological changes occur which will influence cardiovascular performance: change from positive pressure to negative pressure ventilation, reduced mean intrathoracic pressure, increased preload and afterload. This may lead to critical loading of myocardial fibers and provoke ischemia – failure and edema. Gastroinestinal – recurrent aspiration pneumonitis, ascites or abdominal wounds leading to diaphgramatic splinting. Abdominal distension or hypertension, for any reason (massive fluid resuscitation, surgical packs etc), will reduce chest wall compliance and lead to failure to ventilate.
Nutrition -protein malnutrition leading to muscular atrophy, which affects the diaphragm and intercostals. Acid base – metabolic alkalosis, particularly due to use of diuretics reduces respiratory drive. Conversely, muscles perform poorly in an acidic environment. Metabolic acidosis is caused by excessive amounts of measured anions (chloride) or unmeasured anions (lactate - from hypoperfusion), ketones and renal acids. Electrolytes– hypophosphatemia, hypomagnesemia, hypokal emia, hypocalcemia: these all affect muscular function and protein metabolism.
Endocrine – muscle weakness due to hypothyroidism or steroid induced myopathy. Oxygen delivery capacity – the circulating hemoglobin concentration: anemia increases respiratory drive and cardiac output in order to maintain oxygen delivery. Pain control – it is very difficult to wean patients who are in pain, particularly from upper abdominal or thoracic surgery or injuries. If a patient has a flail chest, it may be necessary to insert a thoracic epidural prior to extubation
Indicators of deterioration are:1. respiratory rate >35/mt.2. falling tidal volume <5ml/kg3. PaO2 <55mm Hg; Rising PaCO24. fall in blood pressure5. tachycardia, cardiac arrythmias, sweating -increased sympathetic activity6. altered mental status - restlessness, anxiety, confusion
The Cuff leak test: The ventilator is used in Assist Control mode with a tidal volume of 10-12ml/kg. The expired tidal volume is measured with the cuff inflated. The cuff is then deflated and after elimination of artefacts due to cough, four to six consecutive breaths are used to compute the average value for the expiratory tidal volume. The difference in the tidal volumes with the cuff inflated and deflated is the leak. A value of 130ml (12% of inspiratory tidal volume) gave a sensitivity of 85% and a specificity of 95% to identify patients with an increased risk of post extubation stridor.
Cough / Leak test: In spontaneously breathing patientsThe tracheal cuff is deflated and monitored for the first 30 seconds for cough. Only cough associated with respiratory gurgling (heard without a stethoscope and related to secretions) is taken into account.The tube is then obstructed with a finger while the patient continues to breath. The ability to breathe around the tube is assessed by the auscultation of a respiratory flow.