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Respiratory Failure/ ARDS Ian B. Hoffman, MD, FCCP Pulmonary & Critical Care Medicine September 4, 2013.

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Presentation on theme: "Respiratory Failure/ ARDS Ian B. Hoffman, MD, FCCP Pulmonary & Critical Care Medicine September 4, 2013."— Presentation transcript:

1 Respiratory Failure/ ARDS Ian B. Hoffman, MD, FCCP Pulmonary & Critical Care Medicine September 4, 2013

2 Laboratory studies: Hemoglobin13.2 g/dL (132 g/L) Leukocyte count10,000/µL (10 × 10 9 /L) Arterial blood gas studies (on an F IO 2 of 0.8): pH7.48 P CO 2 30 mm Hg (4.0 kPa) PO2PO2 60 mm Hg (8.0 kPa) A 32-year-old man is evaluated for persistent hypoxemia on mechanical ventilation in the intensive care unit. His medical history is significant for paraplegia and a chronic indwelling urinary catheter for neurogenic bladder. He presented to the emergency department 2 days ago with sepsis. At that time, he received piperacillin/tazobactam, normal saline, and vasopressors. He was endotracheally intubated for decreased level of consciousness. His initial chest radiograph was normal. On physical examination on the second day of hospitalization, temperature is 37.1 °C (98.8 °F), blood pressure is 90/50 mm Hg, pulse rate is 96/min, and respiration rate is 26/min. His need for supplemental oxygen has steadily increased; his oxygen saturation on an FIO 2 of 0.8 is 89%. Pulmonary examination reveals bilateral inspiratory crackles. Cardiac examination reveals distant, regular heart sounds. Urine and blood cultures are positive for Escherichia coli. A follow-up chest radiograph shows diffuse bilateral infiltrates without cardiomegaly. Central venous pressure is 8 mm Hg.

3 Which of the following is the most likely cause of this patient’s hypoxemia? A.Acute respiratory distress syndrome B.E. coli pneumonia C.Heart failure D.Eosinophilic pneumonia

4 Respiratory Failure Any disruption of function of respiratory system – CNS, nerves, muscles, pleura, lungs Any process resulting in low pO 2 or high pCO 2 – arbitrarily 50/50 Acute respiratory failure can be exacerbation of chronic disease or acute process in previously healthy lungs

5 History 1940’s – polio, barbiturate OD 1960’s – blood gas analysis readily available, aware of hypoxemia 1970’s – decreased hypoxic mortality, increased multiorgan failure (living longer) 1973 – relationship between resp muscle fatigue and resp failure

6 Types of Respiratory Failure Type 1 (nonventilatory) – hypoxemia with or without hypercapnia – disease involves lung itself (i.e, ARDS) Type 2 – failure of alveolar ventilation – decrease in minute ventilation or increase in dead space (i.e. COPD, drug OD)

7 Goals of Treatment Correct hypoxemia or hypercapnia without causing additional complications Noninvasive ventilation vs. intubation and mechanical ventilation Goal of mechanical ventilation is NOT necessarily to normalize ABGs

8 Ventilation–perfusion (V/Q) relationships and associated blood gas abnormalities Shunt

9 The influence of shunt fraction on the relationship between the inspired oxygen (FiO2) and the arterial PO2 (PaO2).

10 Ventilatory Failure Failure of respiratory pump to adequately eliminate CO 2 pCO 2 : V CO 2 determined by rate of total body metabolism V CO 2 VAVA

11 ALVEOLAR HYPOVENTILATION IN THE ICU

12 Respiratory Muscles Acute or acute-on-chronic overloading COPD, hyperinflation, fatigue Electrolyte imbalances Sepsis Shock Malnutrition Drugs Atrophy related to prolonged mechanical ventilation Hypothyroidism Myopathies

13 What factors leading to respiratory muscle weakness can be reversed? Reduce respiratory load treat asthma, COPD, upper airway problems treat pneumonia, pulm edema, reduce dynamic hyperinflation, drain large pleural effusions, evacuate PTX Replace K, Mg, PO 4, Ca Treat sepsis Nutritional support w/o overfeeding Rest muscles hrs, then exercise Stop aminoglycosides Rule out hypothyroidism, oversedation, critical illness myopathy/neuropathy

14 To intubate or not Decision to mechanically ventilate is clinical Some criteria: Decreased level of consciousness (ER always tells us that GCS = 3 and pt tubed to protect airway!) Vital capacity <15 ml/kg Severe hypoxemia Hypercarbia (acute or acute-on-chronic) Vd/Vt >0.60 NIF < -25 cm H 2 0

15 ARDS – Acute Respiratory Distress Syndrome

16 ARDS - Definition Severe end of the spectrum of acute lung injury Diffuse alveolar damage Acute and persistent lung inflammation with increased vascular permeability – inflammatory cytokines Diffuse infiltrates Hypoxemia No clinical evidence of elevated left atrial pressure (PCWP <18 if measured)

17 ARDS – History/Definitions 1967 – Ashbaugh described 12 pts with acute respiratory distress, refractory cyanosis, decreased lung compliance, diffuse infiltrates; 7 of the 12 died 1988 – 4 point lung injury score (level of PEEP, pO 2 /FiO 2, lung compliance, degree of infiltrates) 1994 – acute onset, bilateral infiltrates, no direct or clinical evidence of LV failure, pO 2 /FiO 2 )

18 1994 American European Consensus Acute onset Bilateral infiltrates c/w pulmonary edema No clinical evidence of left-sided CHF (PCWP <18) paO 2 /FiO 2 ratio <300 Acute onset Bilateral infiltrates c/w pulmonary edema No clinical evidence of left-sided CHF (PCWP <18) paO 2 /FiO 2 ratio <200 Acute Lung InjuryARDS 100/0.40 = /0.60 = 167

19 New Definition of ARDS Acute onset (within 7 days of some defined event) Bilateral infiltrates (on CXR or CT) No need to exclude heart failure (respiratory failure “not fully explained by CHF”) Hypoxemia – mild, moderate, severe

20 Severity of ARDS (2012) ARDS Severity PaO 2 /FiO 2 (on PEEP 5) Mortality Mild % Moderate % Severe<10045%

21 ARDS - Incidence Annual incidence 75 per 100,000 (1977) 9% of American critical care beds occupied by pts with ARDS

22 ARDS - Diagnosis Clinically and radiographically resembles cardiogenic pulmonary edema PCWP can be misleading – should be normal or low, but can be high 20% of pts with ARDS may have LV dysfunction

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24 ARDS - Causes Direct injury to the lung Indirect injury to the lung in setting of systemic process Multiple predisposing disorders substantially increase risk Increased risk with alcohol abuse, chronic lung disease, acidemia

25 ARDS - Causes Direct Lung Injury Pneumonia Gastric aspiration Lung contusion Fat emboli Near drowning Inhalation injury Reperfusion injury Indirect Lung Injury Sepsis Multiple trauma Cardiopulm bypass Drug overdose Acute pancreatitis Blood transfusion

26 ARDS - Physiologic Derangements Inflammatory injury producing diffuse alveolar damage Alveolar epithelium (eg, aspiration) Vascular endothelium (eg, sepsis) Proinflammatory cytokines (TNF, IL-1, IL-8) Neutrophils recruited – release toxic mediators Normal barriers to alveolar edema are lost, protein and fluid flow into air spaces, surfactant lost, alveoli collapse; inhomogeneous process Impaired gas exchange Decreased compliance Pulmonary hypertension

27 ARDS – Features Severe initial hypoxemia Increased work of breathing (decreased compliance) – generally a prolonged need for mechanical ventilation Initial exudative stage Proliferative stage resolution of edema, proliferation of type II pneumocytes, squamous metaplasia, collagen deposition Fibrotic stage

28 ARDS – Course Early Inciting event pulmonary dysfunction (worsening tachypnea, dyspnea, refractory hypoxemia) Nonspecific labs CXR – diffuse alveolar infiltrates Subsequent Eventual improvement in oxygenation Continued ventilator dependence Complications Large dead space, high minute ventilation requirement Organization and fibrosis in proliferative phase

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30 ARDS - Complications Ventilator induced lung injury Sedation and neuromuscular blockade Nosocomial infection Pulmonary emboli Multiple organ dysfunction

31 ARDS - Prognosis Improved survival in recent years – mortality was % for many years, now 35-40% Improvements in supportive care, improved mechanical ventilatory management Early deaths (3 days) usually from underlying cause of ARDS Later deaths from nosocomial infections, sepsis, MOSF Respiratory failure only responsible for ~16% of fatalities Long-term survivors usually show mild abnormalities in pulmonary function (DLCO)

32 Question 2 A 63-year-old man with acute respiratory distress syndrome (ARDS) is evaluated in the intensive care unit. He has just been intubated and placed on mechanical ventilation for ARDS secondary to aspiration pneumonia. Before intubation, his oxygen saturation was 78% breathing 100% oxygen with a nonrebreather mask. On physical examination, temperature is 37.0 °C (98.6 °F), blood pressure is 150/90 mm Hg, and pulse rate is 108/min. His height is 150 cm (59 in) and his weight is 70.0 kg (154.3 lb). Ideal body weight is calculated to be 52.0 kg (114.6 lb). Central venous pressure is 8 cm H 2 O. Cardiac examination reveals normal heart sounds and no murmurs. Crackles are auscultated in the lower left lung field. The patient is sedated. Neurologic examination is nonfocal. Mechanical ventilation is on the assist/control mode at a rate of 18/min. Positive end-expiratory pressure is 8 cm H 2 O, and FIO 2 is 1.0.

33 Which of the following is the most appropriate tidal volume? A.300 ml B.450 ml C.700 ml D.840 ml

34 Ventilatory Goals in ARDS Provide adequate oxygenation without causing damage related to: Oxygen toxicity Hemodynamic compromise Barotrauma Alveolar overdistension Alveolar shear

35 Mechanical Ventilation in ARDS Reliable oxygen supplementation Decrease work of breathing Increased due to high ventilatory requirements, increased dead space, and decreased compliance Recruitment of atelectatic lung units Decreased venous return can help decrease fluid movement into alveolar spaces

36 Ventilator Induced Lung Injury Known for decades that high levels of positive pressure ventilation can rupture alveolar units In 1950’s became known that high FiO 2 can produce lung injury More recently, effects of alveolar overdistension, shearing, cyclical opening and closing have become apparent

37 Ventilator Induced Lung Injury Macrobarotrauma Pneumothorax, interstitial emphysema, pneumomediastinum, SQ emphysema, pneumoperitoneum, air embolism ? resulting from high airway pressures, or just a marker of severe lung injury Higher PEEP predicts barotrauma

38 Ventilator Induced Lung lnjury Microbarotrauma Alveolar overinflation exacerbating and perpetuating lung injury – edema, surfactant abnormalities, inflammation, hemorrhage Less affected lung accommodates most of tidal volume – regional overinflation Cyclical atelectasis (shear) – adds to injury Low tidal volume strategy (initial tidal volume 6 ml/kg IBW, plateau pressure <30) – lower mortality

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40 Ventilatory Strategies Therapeutic target of mechanical ventilation in patients with ARDS has shifted from maintenance of "normal gas exchange” to the protection of the lung from ventilator-induced lung injury Low tidal volume, plateau pressure <30 peak pressure = large airways plateau pressure = small airways/alveoli PEEP – enough, not too much Pressure controlled vs. volume cycled Prolonging inspiratory time (increase mean airway pressure and improve oxygenation) APRV Recent data suggests high frequency oscillation is bad Permissive hypercapnia Secondary effect of low tidal volumes Maintain adequate oxygenation with less risk of barotrauma Sedation/paralysis often necessary

41 The only method of mechanical ventilation that has been shown in randomized controlled trials to improve survival in patients with ARDS is low tidal volume ventilation.

42 ARDS Network Trial Initial tidal volume of 6 ml/kg IBW and plateau pressure <30 vs. Initial tidal volume of 12 ml/kg IBW and plateau pressure <50 Reduction in mortality of 22% (31% vs 40%) NEJM 2000; 342:

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44 Ventilator management in patients with acute respiratory distress syndrome or acute lung injury N Engl J Med 2000; 342:1301

45 A 25-year-old woman is admitted to the intensive care unit (ICU) for a 6-hour history of respiratory distress. She has acute lymphoblastic leukemia and received cytotoxic chemotherapy 2 weeks before ICU admission. She has had fever and leukopenia for 7 days. On physical examination, she is in marked respiratory distress. Temperature is 39.0 °C (102.2 °F), blood pressure is 110/70 mm Hg, pulse rate is 130/min, and respiration rate is 42/min. Weight is 50.0 kg (110.2 lb). Ideal body weight is calculated as 50.0 kg (110.2 lb). Acute respiratory distress syndrome is diagnosed. She is intubated and started on mechanical ventilation in the assist/control mode at a rate of 12/min, tidal volume of 300 mL, positive end-expiratory pressure (PEEP) of 5 cm H 2 O, and FIO 2 of 1.0. An arterial blood gas study on these settings shows a pH of 7.47, PCO 2 of 30 mm Hg (4.0 kPa), and PO 2 of 45 mm Hg (6.0 kPa). Peak airway pressure is 26 cm H 2 O, and the plateau pressure is 24 cm H 2 O. Question 3

46 Which of the following is the most appropriate treatment to improve this patient’s oxygenation? A.Increase PEEP to 10 cm H2O B.Increase respiratory rate to 18/min C.Increase tidal volume to 500 ml D.Start inhaled nitric oxide

47 PEEP in ARDS Increases FRC (volume of air remaining in lungs following a normal tidal exhalation) – recruits “recruitable” alveoli, increases surface area for gas exchange Decreases shunt, improves V/Q matching No consensus on optimal level of PEEP

48 ALVEOLI trial High PEEP vs. low PEEP Low tidal volume for all (6 ml/kg predicted weight) Higher PEEP patients had better oxygenation, but no difference in mortality, duration of mechanical ventilation, duration of non-pulmonary organ failure No benefit from recruitment maneuvers (CPAP cm H 2 0 for 30 seconds) – but other studies suggest that recruitment maneuvers do help NEJM 2004; 351:

49 Prone Positioning Thought to improve oxygenation and respiratory mechanics by: alveolar recruitment redistribution of ventilation toward dorsal areas resulting in improved V/Q matching elimination of compression of the lungs by the heart reduction of parenchymal lung stress and strain

50 Prone Positioning Several studies demonstrate improved oxygenation, but no overall reduction in mortality Greatest benefit of prone positioning occurs in the sickest patients if used early after the diagnosis of ARDS

51 Other modalities - None of these have proven superior to more standard techniques APRV High-frequency ventilation Partial liquid ventilation Inverse ratio ventilation ECMO Nitric Oxide, prostacyclin Ketoconazole, ibuprofen Glutathione (anti-oxidant) Surfactant Steroids Intravenous beta-agonists (increases clearance of alveolar edema) – needs more study

52 APRV

53 Pharmacotherapy - Nitric Oxide Selectively dilates vessels that perfuse better ventilated lung zones, resulting in improved V/Q matching, improved oxygenation, reduction of pulmonary hypertension Less benefit in septic patients No clear improvement in mortality

54 Pharmacotherapy - Surfactant First tried in 1980’s No benefit in adult population One study did demonstrate improvement in oxygenation and mortality in children

55 Pharmacotherapy - Steroids No consensus on effectiveness – no clear benefit, some risks ARDSnet - NEJM 2006; 354: some benefit in subgroups, but not overall; increased mortality if started after 14 days; neuromyopathy Meduri - Chest2007; 131: improvement in pulmonary and extrapulmonary organ dysfunction, reduction in duration of mechanical ventilation and ICU length of stay – (small sample size, imbalance in treatment arms)

56 Fluid management in ARDS Increased extravascular lung water associated with poor outcome Reduction in PCWP associated with increased survival

57 Fluid and Catheter Treatment Trial (FACTT) Liberal vs conservative fluid management CVP just as good as PCWP Conservative management group did better (more ventilator free days, fewer ICU days, trend toward lower mortality) No difference in incidence of hypotension or need for renal replacement therapy NEJM 2006 Excluded patients with shock, was initiated later in ICU course (mean time 43 hrs) – early aggressive fluid resuscitation appropriate Liberal group gained ~1 liter/day, conservative had net zero balance over 1 st 7 days

58 MAP > 60, no vasopressors for > 12 hrs CVPPCWPAverage urine output 0.5 cc/kg/hr >8>12Lasix; reassess in 1 hrLasix; reassess in 4 hrs Rapid fluid bolus; reassess 1 hrLasix; reassess in 4 hrs <4<8Rapid fluid bolus; reassess 1 hrNo intervention; reassess in 4 hrs Simplified Algorithm for Conservative Fluid Management (Target CVP <4 or PCWP <8)

59 Supportive Care Treat predisposing factors Prophylaxis for GI bleeding DVT prophylaxis Prevent and treat nosocomial pneumonia – most important causes are microaspiration, biofilm formation (VAP bundle?) Nutritional support Blood sugar control ?Transfusion (Hgb >7 adequate) Decrease oxygen utilization - antipyretics, sedatives, paralysis

60 VAP Bundle – ?truly evidence based Elevate head of bed (helpful) Daily sedation vacation and assessment of readiness to extubate (shorter duration on vent, should be less pneumonia) Daily chlorhexidine mouth rinse (questionable benefit) PPI or H2 antagonists (can increase risk) DVT prophylaxis (nothing to do with pneumonia) Potentially helpful: subglottic suctioning, lateral head- down positioning, silver-coated ET tubes, “mucus shaver”

61 “There is nothing so useless as doing efficiently that which should not be done at all.” (Peter Drucker)

62 A 50-year-old man is evaluated in the intensive care unit for acute respiratory distress syndrome secondary to severe community- acquired pneumonia. He is intubated and placed on mechanical ventilation. He was previously healthy and took no medications before his hospitalization. On physical examination, temperature is 38.3 °C (100.9 °F), blood pressure is 120/60 mm Hg, and pulse rate is 110/min. The patient weighs 60.0 kg (132.3 lb); ideal body weight is 60.0 kg (132.3 lb). He is sedated and is not using accessory muscles to breathe. Central venous pressure is 8 cm H 2 O. Other than tachycardia, cardiac examination is normal. There are bilateral inspiratory crackles. Initial ventilator settings are volume control with a rate of 18/min, a tidal volume of 360 mL, positive end-expiratory pressure (PEEP) of 10 cm H 2 O, an FIO 2 of 0.8, a peak pressure of 34 cm H 2 O, and a plateau pressure of 32 cm H 2 O. Oxygen saturation by pulse oximetry is 96%. Question 4

63 Which of the following is the most appropriate next step in management? A.Decrease respiratory rate B.Decrease tidal volume C.Increase FiO2 D.Increase PEEP

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67 CVPOliguric Non-Oliguric >9VasopressorDiureticDiuretic 4-8Fluid bolusFluid bolusDiuretic <4Fluid bolusFluid bolusKVO fluid Shock No Shock Simplified Algorithm for Conservative Fluid Management

68 Flow diagram for the evaluation of hypoxemia P V O 2 = mixed venous pO 2 VO 2 = oxygen consumption DO 2 = oxygen delivery

69 Flow diagram for the evaluation of hypercapnia VCO 2 = CO 2 production


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