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 • PaO2 < 60 mm Hg and/or • PaCO2 > 45 mm Hg • In individuals on room air at sea level • 36% hospital mortality
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
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
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
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
Clinical Presentation: Shunt • Shunt presents very similar 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.
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 and symptoms of hypoxemia may present. • Treat with oxygen
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
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
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
Hypercapnic Respiratory Failure (Type II) • aka “pump failure” or “ventilatory failure” • An elevated PaCO2 results in uncompensated respiratory acidosis.
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.
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)
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).
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
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 ominousnot moving adequate air • Irritability, confusion, and coma are signs of worsening hypercapnia. • Muscle tremors and papilledema
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
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.
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
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 • With full ventilatory failure • ABG: hypercapnia with acidosis
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.
Indications for Ventilatory Support (cont.) • Values that indicate mechanical ventilation • handout
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
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
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
NPPV • Indications • Allows patient to be supported while other therapeutic maneuvers can help the patient while decreasing the WOB • Disorders that can be rapidly reversed • Clinical situations that may respond to NPPV • Acute exacerbations of COPD (good evidence) • Cardiogenic pulmonary edema (reversibility) • Acute asthma (use is controversial) • Acute type I failure: improved PaO2/FiO2 ratio but no patient improvement outcomes (i.e., LoS, M/M) • Chronic type II failure particularly NMD: improves and prolongs life and cognitive function and reduces pneumonia and hospitalization
What if our problem is oxygenation alone? • Can try CPAP and/or Vapotherm