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Respiratory Failure and the Need for Mechanical Ventilation

Respiratory Failure and the Need for Mechanical Ventilation. RES 300 Winter 2011. What is Respiratory Failure?. Defined as the inability to maintain oxygen delivery to the tissues or adequate removal of carbon dioxide from the body. Criteria PaO 2 < 60 mm Hg and/or PaCO 2 > 45 mm Hg

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Respiratory Failure and the Need for Mechanical Ventilation

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  1. Respiratory Failure and the Need for Mechanical Ventilation RES 300 Winter 2011

  2. What is Respiratory Failure? • Defined as the inability to maintain oxygen delivery to the tissues or adequate removal of carbon dioxide from the body. • Criteria • PaO2 < 60 mm Hg and/or • PaCO2 > 45 mm Hg • In individuals on room air at sea level • 36% hospital mortality

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

  4. Which one is refractory hypoxemia?

  5. Clinical Presentation: V/Q Mismatch . • By definition patient has low PaO2 and 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

  6. Clinical Presentation: V/Q Mismatch (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

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

  8. Clinical Presentation: Shunt • Shunt presents very similarly to V/Q match. • Shunt usually presents with a white radiograph. • ARDS would be the classic example. • Shunt is differentiated from V/Q mismatch by lack of response in PaO2 as the FIO2 is increased.

  9. 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

  10. 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 and symptoms of hypoxemia may present. • Treat with oxygen

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

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

  13. Oxygen Indices • PaO2/PAO2 • Advantage- remains stable with FIO2 changes • Normal is 0.8-0.9 • <0.75 = pulmonary dysfunction (V/Q mismatch, shunt or diffusion defect) • Ex: PaO2 of 55 mmHg /PAO2 120 mmHG = .46

  14. Oxygen Indices • PaO2/FIO2 • Advantage- Does not require PAO2 • < 200 = large shunt (ARDS) • Ex: PaO2 of 50 mmHg /FIO2 of .70 = 71.4

  15. Deadspace • What is deadspace? • Ventilation without Perfusion • Total deadspace = anatomic + alveolar (all terminal respiratory units that are overventilated relative to their perfusion) • Anatomic = 1 cc/lb of ideal body weight • So, VE = Alveolar Ventilation + Deadspace Ventilation • VD/VT =(PaCO2 – PECO2)/PaCO2 • Normal is < 0.3 or 30% • Increased in Pulmonary Embolism • Increased in ARDS

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

  17. Ventilatory Failure: Decreased Ventilatory Drive • Ventilatory drive is most commonly diminished by: • Drug overdose or sedation • Brainstem lesions • Diseases of the CNS • Multiple sclerosis or Parkinson’s disease • Hypothyroidism • Morbid obesity • Sleep apnea • Clinical hallmark is bradypnea (<12 beats/min) and ultimately apnea.

  18. Ventilatory Failure: Neurologic Diseases • CNS signals fail to reach the 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)

  19. Neurologic Diseases 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 they commonly result in respiratory muscle fatigue and ventilatory failure (elevated CO2).

  20. Ventilatory Failure: Increased Work of Breathing • Ventilatory failure may occur if the 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 work of breathing (WOB) • May also be caused by • Pneumothorax, rib fractures, pleural effusions • Hypermetabolic states such as burns

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

  22. Chronic Respiratory Failure (Type I and Type II) • Over months and years, acute respiratory failure will become a chronic condition. • Body develops compensatory mechanisms. • Chronic type I failure (hypoxemic) • Polycythemia and 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

  23. Acute-on-Chronic Respiratory Failure • Chronic failure complicated by acute failure. • This is most commonly brought about by • Bacterial or viral infections • CHF • Pulmonary embolus • Chest wall dysfunction • Medical noncompliance • Key: Treat aggressively to prevent further exacerbations.

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

  25. Clinical Presentation of Acute Respiratory Failure • Respiratory muscle fatigue presents • Tachypnea: cardinal sign of increased WOB • Worsening fatigue RR starts falling, bradypnea occurs and, with progression, apnea • Respiratory alternans (normal/paradoxical breathing) • With full ventilatory failure • ABG: hypercapnia with acidosis

  26. Indications for Ventilatory Support Goal of Mechanical Ventilation • Supportive therapy until underlying problem resolves OR • Provide long-term support for patients with chronic ventilatory failure • Support will be aimed at the patient’s specific needs • A pneumonia patient’s ventilatoryneeds will differ markedly from that of a patient with a C1 spinal cord injury.

  27. Indications for Ventilatory Support (cont.) • Values that indicate mechanical ventilation • handout

  28. Assessment of Respiratory Muscle Weakness • Commonly occurs in neuromuscular disease (NMD) patients, but also COPD and kyphoscoliosis. • Tests to assess respiratory muscle strength • MIP of >20 is inadequate, but watch trends. • In NMD the trend of MIP becoming less negative indicates impending ventilatory failure

  29. Respiratory Muscle Weakness, Fatigue, and Failure • Weakness, fatigue, and failure overlap and may result in acute or chronic failure. • Excessive WOB is the most common cause of respiratory muscle fatigue and failure to wean from MV. • Imposed WOB in ventilated patients is due to: • ETT • Ventilator circuit • Auto-PEEP • Disease process

  30. Non-Invasive Ventilation RES 300 Winter 2011

  31. Are there alternatives? • Noninvasive positive-pressure ventilation provides support without intubation. • Methods • CPAP- one continuous pressure • used for oxygenation and stinting airway in OSA • BiPAP- one pressure for inspiration and one for expiration • used for ventilation, oxygenation and stinting airway in OSA

  32. BiPAP Vision/ BiPAP S/T

  33. What if our problem is oxygenation alone? • CPAP and/or Vapotherm

  34. Diseases That Can Use NPPV • COPD (good evidence) • Cardiogenicpulmonary edema • Asthma • Atelectasis • Restrictive chest wall diesease • Pneumonia • post-extubation respiratory failure • DNR • Obstructive Sleep Apnea • Obesity Hypoventilation • Upper airway Obstruction Sleep ApneaArds • Near drowning • Neuromuscular disease

  35. Benefits of NPPV • Avoidance of endotracheal tube • Decreased duration of ventilation • Decreased incidence of pneumonia • Better communications • Ability to eat or drink • Preservation of effective cough (nasal NPPV) • Decreased need for sedation

  36. Contraindications for NPPV • Apnea • Need for immediate intubation • Facial burns or trauma • Uncontrolled vomiting • Inability to clear secretions • Inability to cooperate • Hemodynamic instability • Uncontrolled vomiting • Gastric bleed

  37. Potential Risks of NPPV • Facial skin necrosis (use padding) • Increased aspiration risk • Increased duration of ventilation in patients who fail NPPV • Mucus plugging (keep hydrated, humidified and suctioned) • Decreased ability to cough ( full face mask) • Increased myocardial ischemia in CPE • Difficulty providing adequate calories enterally

  38. Initial Settings: according to one hospital protocol • Mode:Bipap S/T IPA P= 10 cm H20EPA P= 4 cm H20Rate= 10FiO2 - titrate to keep SpO2 greater than or equal to 92% (Patient should be connected to continuous oximeter) • Increasing the IPAP will increase the tidal volume and reduce the PaCO2; however, IPAP increases may be limited by patient intolerance. • The EPAP assists in maintaining airway patency during expiration and increases PaO2.

  39. Procedure • Check order, if no settings by MD, what settings would you use? IPAP EPAP and O2 (Initial settings: S/T 10/4, 10/5)? When would you choose BiPAP vs. CPAP • Gather equipment- NPPV machine, circuit (connect pressure line), filter, mask (a couple of sizes if unsure), a chin strap if using a nasal mask, Oxygen tubing and port adapter if no blender, minineb adapter if needed • Talk to the patient about the procedure and confirm understanding. What would you say if the patient says they will not wear it? • Asses the patient’s vital signs, SpO2 (CPO), breath sounds, ventilatory status

  40. Procedure (Cont.) 5. Fit the mask- Use plastic sizing tool, Use sizing gauge to determine appropriate size mask. Select the smallest size mask to comfortably fit the patient. • Nasal Mask: The mask will fit from the bridge of the nose to just below the nares and rest above the upper lip. • Full-face Mask: The full-face mask will fit from the bridge of the nose to the chin. • Use spacer to fill in any gaps-starting with the smallest spacer first, in between the forehead and mask. Select the size that fills the gap between the forehead and mask. 6. Assemble the circuit and bleed in oxygen. Oxygen must be bled into some machines, others have blenders. Oxygen should be bled into the circuit at the mask or as close to the mask as possible to minimize loss through the continuous leak (in the “Respironics” circuit the continuous leak is through the “Whisper swivel”). 7. Turn machine on a low beginning pressure or use Ramp-allows pressure to rise gradually (Occlude circuit to set pressure) 8. Secure the mask (not too tight) and put in settings

  41. Procedure (cont.) • Check for leaks; what is appropriate? (25-50) • Set alarms • High pressure- 10-15 above pressure • Low pressure- 2-3 below • Delay or apnea- 15-20 seconds • Reassess the patient, (if needed use padding with mask to prevent any skin breakdown) • Obtain ABG 1 hour after initiation of NPPV

  42. ADJUSTMENT OF SETTTINGS • Adjust to control symptoms and follow ABG results • Adjust IPAP level in increments of 2cm H20 (to a maximum level of 25 cm H20) to relieve symptoms of respiratory distress. • Adjust EPAP level in increments of 2 cmH20 (to a maximum level of 10 cm H20) and FiO2 *Increasing EPAP will decrease the pressure support level, therefore the IPAP must also be changed to the complementary level to maintain the desired level of ventilation (for example, if EPAP is increased by 2 cm H20, IPAP should be increased by 2 cm H20 also, in order to keep pressure support level the same.) Minimum pressure support should be maintained at least 5 cm H20.

  43. Monitoring the Patient • Monitor for leaks • Monitor amount of ventilation actually provided • Physical exam for synchrony • Work of breathing • Depth of breathing • Decreased respiratory rate • Increase pressures to increase tidal volumes

  44. Criteria for Termination of NPPV • Decreased level of consiousness • Worsening of ABG’s • Tachypnea • Hemodynamic instability • Inability to tolerate

  45. Weaning the Patient • Reduce the level of pressure • Increased periods if time off NPPV • Gives time for eating • Give time for expectoration • Reduced necrosis of skin tissue

  46. Pulmonary Edema Cardiogenicvs Non Cardiogenic • Heart failure (CHF) • Coronary artery disease with left ventricular failure. • Cardiac arrhythmias • Fluid overload -- for example, kidney failure. • Cardiomyopathy • Obstructing valvular lesions -- for example, mitral stenosis • Myocarditis and infectious endocarditis *BNP (B-type natriuretic peptide The heart secretes BNP in high levels when it's overworked. A large amount of BNP in the blood may indicate congestive heart failure. • Smoke inhalation. • Overwhelming sepsis. • Overwhelming aspiration • Near-drowning *Due to changes in capillary permeability Pathophysiology Fluid first accumulates in and around the capillaries in the interlobular septa (typically at a wedge pressure of about 15 mm Hg) Further accumulation occurs in the interstitial tissues of the lungs Finally, with increasing fluid, the alveoli fill with edema fluid (typically wedge pressure is 25 mm Hg or more)

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