CO 2 Removal. Is it an Important goal in Ventilation? Yes (& No)

Transcription

1 CO 2 Removal Is it an Important goal in Ventilation? Yes (& No)

2 Basic Considerations CO 2 REMOVAL IN VENTILATION

3 Variable CO 2 : What s the Problem? CO 2 largest end product of metabolism (200ml/min) Major determinant of ph CO 2 levels very tightly controlled by central & peripheral CO 2 & ph sensors Can be blunted by drugs or disease CO 2 regulation must evolutionarily be very important for such an intricate system to be naturally selected ph control necessary for metabolic activity PaCO 2 important in CNS & pulmonary auto-regulation of blood flow For routine MV, target a mild hypocarbia to blunt respiratory drive

4 Basic Considerations: CO 2 & Ventilation Permissive Hypercapnia: A strategy to limit adverse effects secondary to mechanical ventilation Contraindications to permissive high CO 2 Brain injury? Case Report of papilledema and raised ICP even with normal brain in extreme hypercapnia Pregnancy (? Up to 60 mmhg) Other conditions with extreme acidosis and hyerkalemia Caution with targeted hypocapnea Hyperventilation in Raised ICP /TBI Temporarily decreases CBF CBV ICP Worse functional neurological outcomes Sub group analysis At 3 & 6 but not at 12 months

5 Basic Considerations: CO 2 & Ventilation Clinical Syndromes Chronic CO 2 retention Acute hypoventilatory failure Severe ARDS Dual/tricky situations CNS + RS injury Poly trauma Post CPR + aspiration CVA & chest infection? Poisoning

6 Approach to high CO 2 on Ventilator Target: CO 2 or ph Normal vs other? Ventilatory options to high CO 2 Increase RR &/or TV Tracheostomy / Remove dead space O 2 insufflation through ETT Is hypercapnia or effects of MV worse Baro-Trauma & Ventilator Associated Lung Injury Hemodynamic worsening-map/peepi

7 CO 2 in Spontaneous modes of Ventilation (NIV or tracheal tube) Common error in intubated & ventilated patient Patient on PSV Low minute volume or apnoea alarm goes off Doctor switches patient back to Control Mode Unnecessary delays in weaning & extubation Correct approach Check if patient comfortable & check PaCO 2 If awake and hypocapnic / normocapnic & alkalotic decrease PSV or wean and extubate If drowsy, high CO 2 / acidosis Control mode and evaluate

8 Chronic CO 2 Retention Syndromes CO 2 REMOVAL IN VENTILATION

9 NIV (BiPAP) in Chronic Progressive Neuromuscular Disease MND & muscular dystrophy Low SaO 2 (air) + normal lungs = Hypoventilation Many symptoms attributed to hypoxia are due to hypoventilation & hypercarbia O 2 will not relieve & may worsen these effects NIV with room air will usually correct hypoxemia NIV will relieve symptoms secondary to hypercarbia

10 NIV in Progressive Neuromuscular Disease Main indications are clinical Day time drowsiness & other CNS symptoms Respiratory symptoms Main aim is to give symptomatic relief Some evidence of prolonging life Focus must be on Quality of Life

11 NIV in Progressive Neuromuscular Disease Two main Strategies Elective Nocturnal Ventilation To relieve day time symptoms of drowsiness or impaired cognition Day time Ventilation To relieve respiratory symptoms Not elective Liberally as needed

12 NIV in Chronic Non-Progressive Hypoventilation Syndromes OSA & Obesity Hypoventilation syndrome Similar considerations as in neuromuscular disease Elective nocturnal NIV Prevents nocturnal desaturation, hypercapnea & repeated arousal Improves day time symptoms? Reversible risk factor for CAD & CCF COPD Usually need ventilation for acute exacerbation

13 CO 2 Target in Chronic Hypercarbic Diseases Best NOT to set a CO 2 target Avoid routine ABGs Use Spontaneous mode of ventilation PSV or BiPAP Patient matches ventilatory pattern to need The Correct CO 2 is the one which the patient is alert and comfortable on ph can guide to acute or chronic hypercarbia

14 Evidence Systematic review of non-invasive positive pressure ventilation for chronic respiratory failure. AU Hannan LM, Dominelli GS, Chen YW, Darlene Reid W, Road J SO Respir Med. 2014;108(2):229. BACKGROUND: This systematic review examined the effect of noninvasive positive pressure ventilation (NIPPV) on patient reported outcomes (PROs) and survival for individuals with or at risk of chronic respiratory failure (CRF). METHODS: Randomised controlled trials (RCTs) and prospective non-randomised studies in those treated with NIPPV for CRF were identified from electronic databases, reference lists and grey literature. Diagnostic groups included in the review were amyotrophic lateral sclerosis/motor neuron disease (ALS/MND), Duchenne muscular dystrophy (DMD), restrictive thoracic disease (RTD) and obesity hypoventilation syndrome (OHS).

15 Evidence RESULTS: Eighteen studies were included and overall study quality was weak. ALS/MND had improved somnolence and fatigue as well as prolonged survival with NIPPV. OHS, improvements in somnolence and fatigue, dyspnoea and sleep quality were demonstrated, while for RTD, measures of dyspnoea, sleep quality, physical function and health, mental and emotional health and social function improved. There was insufficient evidence to form conclusions regarding the effect of NIPPV for those with DMD. CONCLUSIONS: This review has demonstrated that NIPPV influences PROs differently depending on the underlying cause of CRF. These findings may provide assistance to patients and clinicians to determine the relative costs and benefits of NIPPV therapy and also highlight areas in need of further research.

16 Acute CO 2 Retention Syndromes CO 2 REMOVAL IN VENTILATION

17 Acute CO 2 Retention AE-COPD Acute Severe Asthma Due to neurological conditions /drugs Consider OP/NP airway or ETT for airway patency NIV or ETT as per clinical status rather than CO 2 level No validated cut-off for CO 2 level or rate of rise of CO 2 to guide intubation On A-C Ventilation: Target mild alkalosis / hypocapnea Obstructed Tracheal Tube: Correct appropriately

18 Ventilation & CO 2 in AE-COPD NIV-Standard mainline treatment Based on symptoms & not on CO 2 Intubation for failed NIV Respiratory fatigue rather than CO 2 level Use spontaneous modes if feasible Avoid rapid correction of chronic hypercarbia when using Assist-Control Ventilation Acute (metabolic) alkalosis with high HCO 3 Acute hypokalemia acute arrhythmias COPD (between exacerbations) NIV as per symptoms not CO 2 Role of day/night time or long term elective NIV unclear

19 NIV in COPD Lightowler. Et al Meta-Analysis BMJ 2003 Composite End point: Mortality, ETT, Intolerance to Rx

20 NIV in COPD Lightowler. Et al Meta-Analysis BMJ 2003 Mortality Risk for intubation

21 Acute Severe Asthma Anaesthesia and Intensive Care. 1991;19:119

22 Circulatory Arrest Induced by Intermittent Positive Pressure Ventilation in a Patient with Severe Asthma 36-year-old woman with asthma since childhood The patient presented by ambulance with acute severe asthma after three days of worsening dyspnoea and wheeze. Twenty-five minutes after presentation, she was intubated Hand ventilation was commenced by an anaesthetist experienced in these techniques at a rate of 14/min and an estimated tidal volume of ml. The Sp02 initially increased to 94%. However, the blood pressure started to fall Five minutes after intubation BP was unrecordable.

23 Circulatory Arrest Induced by Intermittent Positive Pressure Ventilation in a Patient with Severe Asthma External cardiac massage was commenced and IPPV was continued at the same rate and tidal volume. The patient was given 0.5 mg of intravenous adrenaline, 8 mg of intravenous pancuronium 1000 mcg of salbutamol via the endotracheal tube. During the next fifteen minutes of cardiopulmonary resuscitation the patient remained in apparent electromechanical dissociation, with sinus rhythm on the electrocardiograph monitor and no evidence of cardiac output. Received 3 mg adrenaline.

24 Circulatory Arrest Induced by Intermittent Positive Pressure Ventilation in a Patient with Severe Asthma Twenty-five minutes after intubation the situation was considered irretrievable. External chest compression and ventilation were ceased and the endotracheal tube was disconnected from the ventilation bag. Three minutes after cessation of treatment heart rate had increased to 115/minute (sinus rhythm). Five minutes after treatment had ceased, carotid and femoral pulses became palpable although the blood pressure was still unrecordable.

25 Circulatory Arrest Induced by Intermittent Positive Pressure Ventilation in a Patient with Severe Asthma Ventilation was recommenced at a rate of fifteen breaths per minute and within fifteen seconds the carotid pulse was again impalpable. Ventilation was reduced to a rate of six to eight per minute, with a short inspiratory phase and a prolonged expiratory phase. Within three minutes the pulse rate was 150/ minute (sinus rhythm) and the systolic blood pressure returned to 110 mmhg.

26 Circulatory Arrest Induced by Intermittent Positive Pressure Ventilation in a Patient with Severe Asthma When ventilation was transiently increased on three subsequent occasions to rates greater than ten per minute, the blood pressure became unrecordable on each occasion. Seventy-five minutes after initial intubation the blood pressure was 165/80 mmhg, the pupils were reactive to light, and the patient was starting to move spontaneously. Circulatory state remained satisfactory without the need for volume expansion or inotrope support. The patient subsequently showed satisfactory resolution of asthma. Severe cerebral ischaemic damage was initially present By six months she was functioning independently at home with minimal persisting neurological deficit.

27 Mechanical Ventilation in Severe Asthma

28 Mechanical Ventilation in Severe Asthma With recognition of danger of PEEPa, ICU mortality has decreased Review of 1223 ventilated asthmatics 80% deaths associated with CPR prior to ICU Crit Care Med 2004;8:R

29 Role of NIV in Asthma Five studies have reported on the use of NIV for patients with asthma who had persistent hypercapnia or excessive work of breathing despite treatment with bronchodilators and corticosteroids. Only 19 / 112 patients required intubation.

30 CO 2 Removal in Acute Asthma In Acute severe asthma, the risk of PEEPa is greater than that of hypercarbia It is acceptable to target a lower CO 2 as long as there is no increase in PEEPa hemodynamic worsening May have to compromise if CPR has previously occurred & patient not recovered consciousness PaCO 2 should not be used to decide about intubation Apnea or Unresponsive Progressive fatigue despite maximal medical therapy Failed trial of NIV

31 ARDS CO 2 REMOVAL IN VENTILATION

32 Permissive Hypercarbia in Asthma & ARDS Widespread appreciation of risks of mechanical ventilation & role of permissive hypercapnia in acute asthma Understanding that mechanical ventilation requires trade offs between various parameters Growing appreciation of the baro-trauma, volutrauma or stretch-trauma in ARDS Baby lung & Sponge lung The concept of protective ventilation Gentle ventilation Low Tidal volumes & airway pressure

33 ARDS: Pathophysiology Insights

34 ARDS & Hypercarbia The underlying pathophysiology of shunt & V/Q mismatch does not usually cause CO 2 retention as hyperventilation will clear the CO 2 from the normally functioning lung High CO 2 in a self ventilating patient is a sign of impending fatigue High CO 2 in a ventilated patient is a sign of a severe ARDS Hypercapnea in ventilated ARDS is an independent predictor of a poor outcome

35 ARDS & Permissive Hypercarbia Hickling KG Henderson SJ, Jackson R. Low mortality associated with low volume pressure limited ventilation with permissive hypercapnea in severe adult respiratory distress syndrome. Intensive Care Med 1990;16:372-7 Retrospective analysis of 50 patients with Severe ARDS SIMV: Low Pressures, TV and Min volumes regardless of CO 2 Mean max PaCO 2 = 62 mmhg, Highest CO 2 = 129 mmhg SMR Actual vs predicted (APACHE II) mortality 16.0/39.6% Mortality 2/ 10 in subgroup with ~ 100% predicted mortality (ventilator score > 80) We suggest that this ventilatory management may substantially reduce mortality in ARDS, particularly from respiratory failure.

36 ARDS: The Definitive Trial (N Engl J Med 2000;342:1301-8) TV: 12 ml/kg PIP < 50 vs 6ml/kg & PIP < 30 Lower mortality: 31% vs 39.8%, P = Five basic components Volume Control Ventilation (Any mode but target TV) Low tidal volume 6 ml/kg ideal body weight Low plateau airway pressure < 30 cm H 2 O Simultaneous escalating of FIO 2 & PEEP Prevent hypoxemia Avoidance of hypercarbia & acidosis Increase Respiratory Rate Correct acidosis with HCO 3

37 ARDS & Permissive Hypercarbia "ARTERIAL ph and PaCO2 / EtCO2 Goal: ph = Leave the respiratory rate at the current settings Acidosis management: ph Increase ventilator rate until ph > 7.30 or PaCO2 < 25 Maximum set ventilator rate is 35 bpm Acidosis Management: ph < 7.10 Increase the set ventilator rate to 35 bpm If ph remains < 7.10, tidal volume may be increased in 1ml/kg IBW steps until ph > 7.10

38 ARDS & Permissive Hypercarbia Mortality ARDS-Net: 31% Default setting in control arm of subsequent trials Very low mortality: % Given this low mortality (in RCTs) it is sensible to use the whole ARDS-Net protocol as the default strategy for ventilating ARDS Hypercapnea should be avoided, but not at the cost of high TV or airway pressure

39 The PHARLAP Study (ANZICS-CTG) Permissive Hypercapnia, Alveolar Recruitment and Low Airway Pressure Pilot: Critical Care 2011, 15:R133 This study examines the effectiveness and safety of a novel open lung strategy, which includes permissive hypercapnia,.. This open lung strategy was associated improved oxygenation and lung compliance over seven days RCT: ClinicalTrials.gov Identifier:NCT Currently recruiting patients

40 ECMO & ECCOR ECMO? Positive trial (CESAR) ICUs with ECMO option have better outcome ECCOR: No definitive trial Critical Care 2014, 18:222 Extracorporeal carbon dioxide removal for patients with acute respiratory failure secondary to the acute respiratory distress syndrome: a systematic review Evidence for a positive effect on mortality and other important clinical outcomes is lacking. Practical options but need experienced centers or in the context of RCTs

41 Conclusions CO 2 is very tightly controlled physiologically & variations are poorly tolerated and rapidly corrected CO 2 management with mechanical ventilation occurs in various clinical settings Generally target a mild hypocarbic alkalosis Chronic hypercapnia syndromes Spontaneous and non invasive modes preferred Target symptoms not CO 2 levels Home BiPAP improves quality of life, daytime symptoms and may decrease CAD & CCF

42 Conclusions In acute hypoventilation, NIV or ETT + ventilation till situation reserved In severe acute asthma, target PEEPa and hemodynamic parameters and not normocarbia Unless CPR has occurred In ARDS try to maintain normal ph but not at cost of high TV or PAP Consider Extracorporeal options

43 Concluding Thought Is CO 2 Removal an Important goal in Ventilation? Yes (& No) Always, treat the patient and not the number