Chapter 41 Respiratory Failure and the Need for Ventilatory Support

1. Chapter 41Respiratory Failure and the Need for Ventilatory Support

2. Learning Objectives • Define acute respiratory failure. • Differentiate between hypoxemic (type I) and hypercapnic (type II) respiratory failure • Discuss the causes of acute respiratory failure. • Contrast chronic respiratory failure and acute-on-chronic respiratory failure.

3. Learning Objectives (cont.) • Identify the complications of respiratory failure. • Discuss the indications for ventilatory support. • Describe the general management principles of hypoxemic and hypercapnic respiratory failure. • Discuss the indications for noninvasive ventilation.

4. Introduction: Respiratory Failure • Inability to maintain oxygen delivery to tissues or adequate removal of carbon dioxide from body • Criteria • PaO2 < 60 mm Hg and/or • PaCO2 > 50 mm Hg • In individuals on room air at sea level • 36% hospital mortality

5. . . V/Q Hypoxemic Respiratory Failure (Type I) • Causes of hypoxemia • mismatch (most common cause) • Shunt • Alveolar hypoventilation • Diffusion impairment • Perfusion/diffusion impairment (rare) • Decreased inspired oxygen • Venous admixture

6. All of the following are causes of hypoxemia, except? • Shunt • Alveolar hyperventilation • Diffusion impairment • Decreased inspired oxygen

7. . • . . . . . . . . . V/Q V/Q V/Q V/Q Mismatch V/Q • Normal physiology • High at apices of lung • Low at bases of lung • Disease worsens mismatch impairing ventilation, while perfusion remains adequate • Obstructive lung disease (asthma, COPD) • Infection, heart failure, inhalation injury • Partially collapsed or fluid-filled alveoli

8. . • . Mismatch (cont.) V/Q

9. Clinical Presentation • Patient has low PaO2 & SaO2 • Presents with • Nonspecific: dyspnea, tachycardia, tachypnea • Accessory muscle use (important sign) • Nasal flaring • Pedal edema (RF is cardiac in origin) • Cyanosis (peripheral or central) • Confusion to coma if CNS dysfunction

10. . . V/Q Clinical Presentation (cont.) • Auscultation • Bilateral wheezing • Bronchospasm, fluids, or upper airway disease • Breath sounds diminished bilaterally • Common finding with emphysema • Unilateral abnormalities important • Wheezing one lung may signify lesion • Absence of B/S one lung: collapse, effusion • Unilateral crackles: alveolar filling process

11. Clinical Presentation (cont.) • Radiographically can present as “black” or “white” • Black radiograph • Hyperinflated lungs characteristic of obstructive lung disease • White radiograph • Evidence of partial or total alveolar filling • Characteristic of restrictive lung disease

12. . . . . V/Q V/Q Shunt • Normal anatomic shunt ~2-3% of cardiac output • Pulmonary shunt occurs when NO ventilation to match perfusion • Always pathologic • Leads to hypoxemia as alveoli collapse or filled with fluid or exudate • Atelectasis, pulmonary edema, pneumonia • Major difference between shunt & mismatch • mismatch responds to oxygen therapy unlike shunt which is refractory

13. Which of the following is the major difference between of V/Q mismatch and a shunt? • V/Q mismatch responds to oxygen therapy unlike shunt which is refractory • Shunt responds to oxygen therapy unlike V/Q mismatch which is refractory • Pulmonary shunt occurs when there is ventilation to match perfusion • Shunt leads to hyperxemia as alveoli collapse

14. Shunt (cont.)

15. . . . . . . V/Q V/Q V/Q Clinical Presentation • Shunt presents very similar to mismatch • Usually presents with white radiograph • ARDS is classic example • mismatch often presents with black radiograph • Differentiated from mismatch by lack of response in PaO2 as FIO2 is increased

16. Diffusion Impairment • Most pronounced on exertion • Impairment can be caused by • Thickened/scarred: fibrosis, asbestosis • Alveolar destruction: emphysema • Pulmonary vascular abnormalities • Anemia, pulmonary emboli or hypertension • Clinical presentation depends on disease • Dry cough, fine bibasilar cracklespulmonary fibrosis • Jugular distention, edemapulmonary hypertension

17. Decreased Inspired Oxygen • Clinically uncommon • High altitude while mountain climbing • Airlines pressurized cabins but not to 1 atm • Travelers with pulmonary disease may require supplemental oxygen or more supplemental oxygen than normal • Signs & symptoms of hypoxemia may present • Treat with oxygen

18. Venous Admixture • Decreased mixed venous oxygen • Clinically patient’s lung must add more oxygen to blood; presence of pulmonary disease may prevent • Heart failure is most common cause • Decreased cardiac output: tissues extract more oxygen • Clinically presents with signs & symptoms of CHF and/or underlying pulmonary disease

19. . . V/Q Differentiating Between Causes of Hypoxemic Respiratory Failure • Focus on three main causes: • Hypoventilation • Normal P(A  a)O2: 1025 mm Hg • mismatch • Significant response to oxygen therapy • Shunt • Little or no improvement even on 100% O2

20. Which of the following is a form of hypoxemia that would occur in the face of a normal P(A – a)O2 • Shunting • V/Q mismatch • Hyperventilation • Hypoventilation

21. Hypercapnic Respiratory Failure (Type II) • aka “pump failure” or “ventilatory failure” • Elevated PaCO2 results in uncompensated respiratory acidosis

22. . . V Hypercapnic Respiratory Failure (Type II) (cont.) • PaCO2 & alveolar ventilation are inversely proportional. Mathematically: PaCO2 = (0.863 VCO2)/ A A = MV (1  VD/VT) VA = alveolar ventilation; VCO2 = CO2 production MV = minute volume; VD/VT = dead space-to-tidal volume

23. Impairment in Respiratory Control • Ventilatory drive most commonly diminished by: • Drug overdose or sedation • Brainstem lesions • Diseases of CNS • Multiple sclerosis or Parkinson’s disease • Hypothyroidism • Morbid obesity • Sleep apnea • Clinical hallmark is bradypnea (<12 beats/min) & ultimately apnea

24. Impairment in Respiratory Effectors • Neurologic Diseases • CNS signals fail to reach ventilatory muscles due to: • Spinal trauma • Motor neuron disease (ALS or polio) • Motor nerve disorders (GBS) • Neuromuscular junction disorders (MG or botulism) • Muscular diseases (MD, myositis)

25. Clinical Presentation • Varied presentation • Drooling, dysarthria, weak cough - ALS • Lower extremity weakness progressing upward – GBS • Ocular muscle weakness, ptosis, diplopia, dysphagia – Myasthenia gravis • Different clinical presentations, yet commonly result in respiratory muscle fatigue & ventilatory failure (elevated CO2)

26. Increased Work of Breathing • Ventilatory failure may occur if imposed workload cannot be overcome • Most commonly occurs secondarily to • Increased VD/VT in COPD • Elevated Raw in asthma • Both cause intrinsic PEEP, which generates excessive WOB • May also be caused by • Pneumothorax, rib fractures, pleural effusions • Hypermetabolic states such as burns

27. Clinical Presentation • Rapid shallow breathing is indication of impending ventilatory failure • Shallow breathing increases VD/VT ratio & results in hypercapnia • Diminished B/S in young asthmatic is ominous not moving adequate air • Irritability, confusion, & coma are signs of worsening hypercapnia • Muscle tremors & papilledema

28. Chronic Respiratory Failure(Type I & Type II) • Over months & years, acute respiratory failure will become chronic condition • Body develops compensatory mechanisms • Chronic type I failure (hypoxemic) • Polycythemia & oxy-Hb shift to right • Cerebral blood flow enhanced by increased PaCO2 • Chronic ventilatory failure (hypercapnic) • Renal response: retain HCO3 to normalize pH • Will be incomplete but will raise pH toward normal

29. All of the following are clinical presentations of worsening respiratory failure, except? • Decreased VD/VT ratio • Diminishing breath sounds • Irritability, confusion, and coma • Muscle tremors and papilledema

30. Acute-on-Chronic Respiratory Failure • Chronic failure complicated by acute failure • Most commonly brought about by • Bacterial or viral infections • CHF • Pulmonary embolus • Chest wall dysfunction • Medical noncompliance

31. Acute-on-Chronic Respiratory Failure (cont.) • 49% mortality within 2 years of acute exacerbation • Key: Treat aggressively to prevent further exacerbations

32. Complications of Acute Respiratory Failure • Complications add significantly to morbidity & mortality • ARDS- more patients die of complications (sepsis, MSOF) than of original disease • Emboli, barotrauma, & infection common • Nonpulmonary complications include • Cardiac: arrhythmias, hypotension • Gastrointestinal: hemorrhage, dysmotility • Renal failure and/or positive fluid balance

33. Clinical Presentation of Acute Respiratory Failure • Respiratory muscle fatigue presents • Tachypnea: cardinal sign of increased WOB • Worsening fatigue RR starts falling, bradypnea occurs, & apnea • Respiratory alternans • Full ventilatory failure • ABG: hypercapnia with acidosis

34. Indications for Ventilatory Support • Goal of MV is constant • Supportive therapy until underlying problem resolves • Provide long-term support for patients with chronic ventilatory failure • Support aimed at patient’s specific needs • ARDS patient’s ventilatory needs will differ markedly from patient with C1 spinal cord injury

35. Indications for Ventilatory Support (cont.)

36. Hypoxemic Respiratory Failure • Refractory hypoxemia is common indication for intubation & MV • Indices to assess need include: • P(A  a)O2 > 350 on 100% oxygen • P/F ratio (PaO2/FIO2) < 200 • Frequently, hypoxemic and hypercapnic respiratory failure occur simultaneously

37. Hypercapnic Respiratory Failure • Elevated PaCO2 may or may not indicate need for ventilatory support • PaCO2 > 55 with pH < 7.20; acute process probably requires ventilation • PaCO2 > 55 with pH near normal; chronic failure with renal compensation probably does not require MV • The trend for PaCO2 & pH is very useful

38. . . V V Significance of an Elevated PaCO2 • Normally increased CO2 is matched by increased A so PaCO2 should not change • Elevated PaCO2 indicates 1 of 3 problems • Respiratory center dysfunction • Nerve transmission problems • Lungs & chest are incapable of providing adequate ventilation due to disease or weakness

39. Assessment of Respiratory Muscle Weakness • Commonly occurs in neuromuscular disease (NMD) patients, but also COPD & kyphoscoliosis • Tests to assess respiratory muscle strength • MIP of >20 is inadequate, but watch trends • In NMD trend of MIP becoming less negative indicates impending ventilatory failure • VC & MMV have limited value in ICU setting as patients are generally too SOB to cooperate

40. Respiratory Muscle Weakness, Fatigue, & Failure • Weakness, fatigue, & failure overlap & may result in acute or chronic failure • Excessive WOB is most common cause of respiratory muscle fatigue & failure to wean from MV • Imposed WOB in ventilated patients due to: • ETT • Ventilator circuit • Auto-PEEP • Disease process • If patient’s WOB is <0.8 J/L, 96% successfully extubate

41. All of the following can increase WOB on ventilated patients, except: • Artificial airway • Ventilator circuit • Pressure support • Underlying pulmonary disease

42. Ventilatory Support Strategy: NIV • Noninvasive ventilation provides support without intubation • Types of NIV include • CPAP • Pressure support ventilation • Volume ventilation (A/C or SIMV) • Pressure ventilation (A/C or SIMV)

43. Ventilatory Support Strategy: NIV (cont.) • Clinical situations that may respond to NIV • Acute exacerbations of COPD (good evidence) • Cardiogenic pulmonary edema (reversibility) • Acute asthma (use is controversial) • Acute type I failure: improved P/F ratio but no patient important outcomes (i.e., LoS, M/M) • Chronic type II failure particularly NMD: improves & prolongs life & cognitive function; reduces pneumonia & hospitalization

44. Invasive Ventilatory Support • IPPV indicated for • Severe hypoxemia caused by disease that is slow to resolve, i.e., ALI • Patients needing support who cannot tolerate or are contraindicated for NPPV • Effective for hypoxemic & hypercapnic respiratory failure

45. Ventilatory Support: ARDS • Patients have very noncompliant lungs • Best to ventilate patients with small VT (~6 ml/kg) • This strategy • Reduces complications • Improves survival • Often use permissive hypercapnia strategy • Allow CO2 to slowly rise, maintaining pH > 7.2 to 7.25

46. Ventilatory Support: Head Injury • Ventilation patients with increased ICP • Short term can hyperventilate (PaCO2 25 to 30 mm Hg) to alleviate spikes in ICP • Long term support: PaCO2 30 to 40 mm Hg • PEEP may increase CVP, deceasing pressure gradient for cerebral venous drainage which in turn elevates ICP • Alleviate affects by raising head of bed • If patient is unstable, may require invasive ICP monitoring

47. Ventilatory Support: COPD • Ventilator settings optimized • Low VT of 6 to 8 ml/kg IBW • Moderate RR • High inspiratory flow rates (70 to 100 L/min) • These reduce IT, prolong ET • These minimize auto-PEEP • Set PEEP to alleviate imposed WOB & asynchrony associated with auto-PEEP

48. Ventilatory Support: Chronic Ventilatory Failure • Goal is to normalize pH but not PaCO2 • If PaCO2 is normalized, may cause • Metabolic alkalosis, which can produce • Hypokalemia • Seizures • Arrhythmias • May prolong weaning from mechanical ventilation

49. All of the following can occur if PaCO2 is normalized in patients with chronic respiratory failure, except? • Metabolic acidosis • Hypokalemia • Seizures • Arrhythmias