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Chapter 41 Respiratory Failure and the Need for Ventilatory Support. Learning Objectives. Define acute respiratory failure. Differentiate between hypoxemic (type I) and hypercapnic (type II) respiratory failure Discuss the causes of acute respiratory failure.
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Chapter 41Respiratory Failure and the Need for Ventilatory Support
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.
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.
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
. . 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
All of the following are causes of hypoxemia, except? • Shunt • Alveolar hyperventilation • Diffusion impairment • Decreased inspired oxygen
. • . . . . . . . . . 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
. • . Mismatch (cont.) V/Q
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
. . 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
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
. . . . 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
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
. . . . . . 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
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 cracklespulmonary fibrosis • Jugular distention, edemapulmonary hypertension
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
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
. . V/Q Differentiating Between Causes of Hypoxemic Respiratory Failure • Focus on three main causes: • Hypoventilation • Normal P(A a)O2: 1025 mm Hg • mismatch • Significant response to oxygen therapy • Shunt • Little or no improvement even on 100% O2
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
Hypercapnic Respiratory Failure (Type II) • aka “pump failure” or “ventilatory failure” • Elevated PaCO2 results in uncompensated respiratory acidosis
. . 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
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
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)
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)
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
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
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
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
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
Acute-on-Chronic Respiratory Failure (cont.) • 49% mortality within 2 years of acute exacerbation • Key: Treat aggressively to prevent further exacerbations
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
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
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
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
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
. . 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
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
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
All of the following can increase WOB on ventilated patients, except: • Artificial airway • Ventilator circuit • Pressure support • Underlying pulmonary disease
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)
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
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
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
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
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
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
All of the following can occur if PaCO2 is normalized in patients with chronic respiratory failure, except? • Metabolic acidosis • Hypokalemia • Seizures • Arrhythmias