Acute Respiratory Failure Lecture 2014-2015 (5!1!14) FINAL

Acute Respiratory Failure

Matthew Karulf, MD Pulmonary & Critical Care Medicine

Michigan State University College of Human Medicine

Spectrum Health Medical Group

Hypoxemic Respiratory Failure Type I Respiratory Failure

• Definition

– Impairment of respiratory function characterized by the presence of hypoxemia as diagnosed by a reduced partial pressure of oxygen in arterial blood.

– PaO2 <= 60 mmHg

• Acute vs. Chronic

– Acute hypoxemia occurs over period of hours to days.

– Chronic hypoxemia occurs over a period of weeks to months.

Murray & Nadel’s Textbook of Respiratory Medicine (5th ed.)

PaO2 <= 60 is chosen because below this Hgb saturation falls rapidly.


Anatomic Differential


(A-a) gradient

• Normal (A-a) gradient increases with age.

= Approx 10-20 (depending on age of patient)

• Alveolar gas equation 100 = 0.21 X [760 – 47] – [40/0.8] = 150 - 50

• (A-a) gradient = PAO2 – PaO2

• Differential of a Normal (A-a) gradient

– Normal – Pure Hypoventilation – Low FIO2

Common Causes with an abnormal (A-a) gradient

• Cardiogenic pulmonary edema

• Pneumonia

• Sepsis

• Aspiration

• Trauma

• Multiple transfusions

– TRALI/TACO

Case #1

• 48 yo woman complains of 3 days of dyspnea, cough, fevers, malaise and left-sided pleuritic chest pain.

• Vital Signs

– Temp 39.2 Celsius HR 95 BP 100/60 RR 35

– Room Air O2 saturation 82%

• What is your differential diagnosis for this patient?

Differential Diagnosis

• Pneumonia

• Pericarditis

• Influenza

• Infective Endocarditis with septic emboli

• Empyema

• Venous Thromboembolic Disease

What are your initial diagnostic and therapeutic steps?

HPI

• Symptoms began 3 days prior with cough, fevers and malaise.

• Progressively worsening

• No hemoptysis

• No syncope, trauma

• No significant past medical or surgical history

• Works as a grade school teacher without recent sick contacts aside from students with colds.

• Non-smoker, No EtOH or illicit drug use

• What risk factors identify a patient who may have multidrug resistant pathogens?

Initial Evaluation

• ABC’s!

• Supplemental Oxygen is placed

– O2 saturation improves to 90% on NRBM

• Physical Exam

– Appears in acute distress

– Lung auscultation reveals rhonchi over left base

• IV access, fluid challenge, labs and CXR

Interpret the following labs

• Na 136 Cl 100 BUN 30 • K 3.8 HCO3 18 Cr 1.4

• WBC 4.2 (36% Bands) • Lactate 2.7

• Room Air ABG

– 7.36/28/47 • PAO2 = 0.21 x [760 – 47] – [28/0.8] = 115

= 150 - 35

• (A-a) gradient = PAO2 – PaO2 = 115 – 47 = 68 – Normal (A-a) gradient for this patient = 2.5 + (0.21 * Age) = 13

Case #1 Working Diagnosis

• Previously healthy 48 yo woman with

– Community Acquired Pneumonia

– Severe Sepsis

– Acute Respiratory Failure with Hypoxemia

– Acute Kidney Injury

– Lactic Acidosis

– Elevated Anion Gap Metabolic Acidosis

– Respiratory Alkalosis

• Why is this patient hypoxemic?

• Why does pneumonia cause hypoxemia?

Five Mechanisms of Hypoxemic Respiratory Failure

• Normal (A-a) gradient

– Decreased Inspired Oxygen Pressure

– Hypoventilation

• Abnormal (A-a) gradient

– Impaired Diffusion

– Right-to-Left Shunt

– Ventilation-Perfusion Mismatch


• Decreased Inspired Oxygen Pressure

– Reduction in FIO2 (suffocation)

– Altitude



• Hypoventilation

– As alveolar CO2 increases Alveolar O2 decreases

– Opioid Overdose • Will see a normal (A-a) gradient



• Hypoventilation

• Impaired Diffusion

– Unlikely to be sole cause of respiratory failure

– Often coexists with other mechanisms

– Pulmonary Edema • Cardiogenic

• Non-Cardiogenic

Significant reserve overcomes many diffusion impairments




• Hypoventilation


• Right-to-Left Shunt

– Intrapulmonary • Atelectasis or Consolidation with loss of hypoxic vasoconstriction

• Pulmonary arteriovenous malformation

– Intracardiac • ASD with eisenmeinger’s physiology



• Hypoventilation


• Right-to-Left Shunt

• Ventilation-Perfusion Mismatch

– A Small V/Q mismatch is normal and explains the normal (A-a) gradient.

– Pulmonary Embolus

The two most common mechanisms of acute hypoxemic respiratory failure.


Clinical Approach


Case #1 Working Diagnosis

• Previously healthy 48 yo woman with

– Community Acquired Pneumonia

– Severe Sepsis

– Acute Respiratory Failure with Hypoxemia

– Acute Kidney Injury

– Lactic Acidosis

– Elevated Anion Gap Metabolic Acidosis

– Respiratory Alkalosis

Case #1(cont.)

• Pt. remains distressed, complaining of dyspnea, despite the non-rebreather mask. – Temp 39.2 Celsius HR 112 BP 100/60 RR 38

– 90% Non-Rebreather Mask

• What additional management steps should be implemented now? – Intubation

– Empiric antibiotics for CAP in the ICU

– Early Sepsis Resuscitation

What clinical syndrome of respiratory failure does this patient have?

• Acute Respiratory Distress Syndrome (ARDS)

• Berlin Criteria 2012

• Acute onset (within 7 days of insult)

• PaO2/FiO2 < 300 (with a minimum PEEP of 5) – Mild 200-300

– Moderate 100-200

– Severe <100

• Bilateral opacities consistent with pulmonary edema (on either CXR or CT)

• Not fully explained by cardiac failure or volume overload

When should mechanical ventilation be initiated?

When hypoxemic or hypercapneic respiratory failure cannot be treated by less aggressive

methods.

Non-Invasive Positive Pressure Ventilation (NIPPV) or Invasive.

What is the mechanical ventilation strategy in ARDS?

Low Tidal Volume Ventilation.

(6ml/kg PBW)

• 861 patients w/ ALI randomized – 4-6ml/kg PBW vs. 12ml/kg PBW

– Goal Pplat <30 cm H2O

• Main Outcomes – Mortality

The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000;342:1301-1308

• What information is needed in order to determine the appropriate tidal volume?

– Gender and Height

– Not the measured weight!

FIO2/PEEP titration

• Why do patients with ARDS benefit from a low tidal volume and PEEP strategy?

• Limits ventilator associated lung injury.

• Decreases biomechanical factors contributing to multisystem organ failure and death.

Slutsky AS, Ranieri VM. N Engl J Med 2013;369:2126-2136.

Protective Ventilation

Malhotra A. N Engl J Med 2007;357:1113-1120

Lung Protective Ventilation

Slutsky AS, Ranieri VM. N Engl J Med 2013;369:2126-2136.

Case #2

• 68 yo man presents with 5 days of progressive dyspnea and increased cough productive of purulent sputum.

• Vital Signs

– Temp 37.9 Celsius HR 95 BP 100/60 RR 35

– Room Air O2 saturation 82%

• What is your differential diagnosis?

Differential Diagnosis

• Acute Exacerbation of Chronic Bronchitis

• Pneumonia

• Venous Thromboembolic Disease

• Acute Myocardial Infarction

HPI (cont.)

• History of COPD, FEV1 47% predicted.

• Ongoing 50 pack year history of Tobacco Abuse.

• Two “pneumonias” in the past year treated with prednisone and azithromycin.

Objective Findings

• Oxygen saturation improves to 89% on 3L

• Appears distressed, speaks in 4 word sentences.

• Intercostal retractions, pursed lip breathing

• Lung auscultation reveals diffuse expiratory wheezes.

ABG on 3L 7.24/80/78 Na 139 Cl 99 BUN 25 K 3.8 HCO3 34 Cr 1.2

• What is your patient suffering from?

• Acute on Chronic Hypercarbic Respiratory Failure

• Acute Exacerbation of Chronic Bronchitis

Acute Hypercarbic Respiratory Failure

• PaCO2 is elevated.

• Total minute ventilation is the sum of alveolar ventilation

and dead space ventilation.

• A decrease in total minute ventilation or an increase in dead space ventilation can reduce alveolar ventilation.

• Any decrease in or increase in with constant results in increased PaCO2.

= CO2 production

= Alveolar ventilation

Acute Hypercarbic Respiratory Failure

• The absolute PaCO2 level is not diagnostic.

– Many conditions result in chronic hypercapnia.

• “Acute” implies that PaCO2 rises faster than the kidneys are able to retain bicarbonate, resulting in acute respiratory acidosis.

• The diagnosis requires an arterial blood gas!

Physiologic mechanisms of acute ventilatory failure


Won’t Breathe Can’t Breathe

Reduced Ventilatory Drive “Won’t Breathe”

• Pharmacologic disruption – Drug overdose

• Consider reversal agents (naloxone for opioids and flumazenil for benzodiazepines)

• Acquired Defect – Stroke

– Neoplasm

– Obesity-Hypoventilation syndrome

• Myxedema

Inadequate Ventilation despite effort “Can’t Breathe”

• Neuromuscular weakness – Cervical spinal cord injury – Myasthenia gravis (Monitor Vital Capacity)

• Restrictive Chest Wall disease – Kyphoscoliosis

• Airway Obstruction – Upper – foreign body, vocal cord paralysis – Lower – COPD, Status Asthmaticus

• Increased Dead-space ventilation – High V/Q – COPD (Emphysema) – Generalized pulmonary hypoperfusion – shock

• Increased CO2 production (unable to compensate) – Fever, sepsis, burns, trauma, seizures

Case #2 (cont.)

• What is your next step in the management of your patient with an acute exacerbation of COPD?

– ABC’s

– Bronchodilators

– Systemic Glucocorticoids

– Antibiotics

– NiPPV

Noninvasive Mechanical Ventilation

• Invasive mechanical ventilation for COPD (i.e. Intubation) exacerbations is associated with high morbidity and mortality.

• Noninvasive Positive Pressure Ventilation (NIPPV – e.g. BiPAP or CPAP) reduces intubation rates and in-hospital mortality for COPD exacerbations

• Plant et al. Lancet, 2000.

– NIPPV vs. standard therapy

– reduced intubation rates (15% vs. 27%, P = .02)

– Reduced mortality (10% vs. 20%, P = .05)

What are the indications for NIPPV?

• Hypoxemic respiratory failure

– Cardiogenic pulmonary edema

– Immunocompromised patients

• Hypercapnic respiratory failure

– Acute exacerbation of COPD

– Acute Asthma exacerbation

What are the contraindications to NIPPV?

• Uncooperative patient

• Inability to protect airway

• High risk for aspiration

• Cardiac or respiratory arrest

• Hemodynamic instability

• Myocardial ischemia

• Facial trauma, surgery, burns

Is post-extubation NIPPV beneficial in preventing reintubation?

• NIPPV for patients who develop respiratory distress within 48 hours of extubation may not prevent reintubation and may be harmful.

• Preemptive use of NIPPV (extubating to BiPAP) may prevent reintubation.

• Review on Liberation from mechanical ventilation: – McConville JF, Kress JP. N Engl J Med 2012;367:2233-2239

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Acute Respiratory Failure Lecture 2014-2015 (5!1!14) FINAL

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