Acute Respiratory Failure

Acute Respiratory Failure

Failure in one or both gas exchange functions: oxygenation and carbon dioxide elimination
In practice: PaO2<60mmHg or PaCO2>46mmHg Derangements in ABGs and acid-base status

Acute Respiratory Failure

Hypercapnic v Hypoxemic respiratory failure

ARDS and ALI

Hypercapnic Respiratory Failure

PaCO2 >46mmHg Not compensation for metabolic alkalosis (PAO2 - PaO2)
normal increased

Alveolar Hypoventilation
PI max Central Hypoventilation Neuromuscular Problem

V/Q abnormality
Nl VCO2 V/Q Abnormality VCO2 Hypermetabolism Overfeeding

The Case of Patient RV

71M s/p L AKA revision. PMH: CAD s/p CABG, COPD on home O2 and CPAP, DM, CVA, atrial fibrillation PACU: L pleural effusion, hypotension, altered mental status. Sent to ICU for monitoring. POD#1: RR overnight, intermittently hypoxic. BiPAP 40%: 7.34/65/63/35/+10 Preintubation: 7.28/91/81/43

Hypercapnic Respiratory Failure

PaCO2 >46mmHg Not compensation for metabolic alkalosis (PAO2 - PaO2)
normal increased

Alveolar Hypoventilation
PI max Central Hypoventilation Neuromuscular Problem

V/Q abnormality
Nl VCO2 V/Q Abnormality VCO2 Hypermetabolism Overfeeding

Hypercapnic Respiratory Failure

nlPI max Central Hypoventilation Brainstem respiratory depression Drugs (opiates) Obesity-hypoventilation syndrome

Alveolar Hypoventilation

PI max Neuromuscular Disorder

Critical illness polyneuropathy Critical illness myopathy

Hypophosphatemia Magnesium depletion Myasthenia gravis Guillain-Barre syndrome

Hypercapnic Respiratory Failure

PaCO2 >46mmHg Not compensation for metabolic alkalosis (PAO2 - PaO2)
normal increased

Alveolar Hypoventilation
PI max Central Hypoventilation Neuromuscular Disorder

V/Q abnormality
Nl VCO2 V/Q Abnormality VCO2 Hypermetabolism Overfeeding

Hypercapnic Respiratory Failure

V/Q abnormality
Increased Aa gradient Nl VCO2

VCO2

V/Q Abnormality

Hypermetabolism Overfeeding

Hypercapnic Respiratory Failure

V/Q abnormality
Increased Aa gradient Nl VCO2

VCO2

V/Q Abnormality Increased dead space ventilation advanced emphysema PaCO2 when Vd/Vt >0.5 Late feature of shunt-type edema, infiltrates

Hypermetabolism Overfeeding

Hypercapnic Respiratory Failure

V/Q abnormality
Increased Aa gradient Nl VCO2

VCO2

V/Q Abnormality

Hypermetabolism Overfeeding

VCO2 only an issue in pts with ltd ability to eliminate CO2 Overfeeding with carbohydrates generates more CO2

Hypoxemic Respiratory Failure

Is PaCO2 increased?
Yes

No

Hypoventilation
(PAO2 - PaO2) Hypovent plus another mechanism

(PAO2 - PaO2)?
Yes Is low PO2 correctable with O2? No Shunt Yes V/Q mismatch No Inspired PO2 High altitude FIO2

Hypoventilation alone Respiratory drive Neuromuscular dz

The Case of Patient ES

77F s/p MVC. Injuries include multiple L rib fxs, L hemopneumothorax s/p chest tube placement, L iliac wing fx. PMH: atrial arrhythmia, on coumadin. INR>2 HD#1 RR 30s and shallow. Pain a/w breathing deeply. Placed on BiPAP overnight PID#1 BiPAP 80%: 7.45/48/66/32/+10

Hypoxemic Respiratory Failure

Is PaCO2 increased?
Yes

No

Hypoventilation
(PAO2 - PaO2) Hypovent plus another mechanism

(PAO2 - PaO2)?
Yes Is low PO2 correctable with O2? No Shunt Yes V/Q mismatch No Inspired PO2 High altitude FIO2

Hypoventilation alone Respiratory drive Neuromuscular dz

Hypoxemic Respiratory Failure

V/Q mismatch
PvO2>40mmHg PvO2<40mmHg

V/Q mismatch

DO2/VO2 Imbalance DO2: anemia, low CO VO2: hypermetabolism

Hypoxemic Respiratory Failure

V/Q mismatch

SHUNT V/Q = 0

Atelectasis Intraalveolar filling Pneumonia Pulmonary edema

ARDS Interstitial lung dz Pulmonary contusion

DEAD SPACE V/Q =

Intracardiac shunt Vascular shunt in lungs

Pulmonary embolus Pulmonary vascular dz Airway dz (COPD, asthma)

Hypoxemic Respiratory Failure

V/Q mismatch

SHUNT V/Q = 0

Atelectasis Intraalveolar filling Pneumonia Pulmonary edema

ARDS Interstitial lung dz Pulmonary contusion DEAD SPACE V/Q =

Intracardiac shunt Vascular shunt in lungs

Pulmonary embolus Pulmonary vascular dz Airway dz (COPD, asthma)

Hypoxemic Respiratory Failure

Acute Respiratory Distress Syndrome

Severe ALI B/L radiographic infiltrates PaO2/FiO2 <200mmHg (ALI 201-300mmHg) No e/o L Atrial P; PCWP<18

Hypoxemic Respiratory Failure

Acute Respiratory Distress Syndrome

Develops ~4-48h Persists days-wks Diagnosis:

Distinguish from cardiogenic edema History and risk factors

Inflammatory Alveolar Injury

Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8)

Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8)

Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium

Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8)

Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium Fluid in interstitium and alveoli

Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8)

Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium Fluid in interstitium and alveoli
Impaired gas exchange Compliance PAP

Hypoxemic Respiratory Failure

Acute Respiratory Distress Syndrome

Exudative phase
Diffuse alveolar damage

Proliferative phase

Fibrotic phase

Hypoxemic Respiratory Failure

Acute Respiratory Distress Syndrome Direct Lung Injury Infectious pneumonia Aspiration, chemical pneumonitis Pulmonary contusion, penetrating lung injury Fat emboli Near-drowning Inhalation injury Reperfusion pulmonary edema s/p lung transplant

Hypoxemic Respiratory Failure

Acute Respiratory Distress Syndrome Indirect Lung Injury Sepsis Severe trauma with shock/hypoperfusion Burns Massive blood transfusion Drug overdose: ASA, cocaine, opioids, phenothiazines, TCAs. Cardiopulmonary bypass Acute pancreatitis

Hypoxemic Respiratory Failure

Acute Respiratory Distress Syndrome Complications Barotrauma Nosocomial pneumonia Sedation and paralysis persistent MS depression and neuromuscular weakness

Management of Respiratory Failure Principles

Hypoxemia may cause death in RF Primary objective is to reverse and prevent hypoxemia Secondary objective is to control PaCO2 and respiratory acidosis Treatment of underlying disease Patients CNS and CVS must be monitored and treated

Risks of Oxygen Therapy

O2 toxicity: - very high levels(>1000 mmHg) CNS toxicity and seizures - lower levels (FiO2 > 60%) and longer exposure: - capillary damage, leak and pulmonary fibrosis - PaO2 >150 can cause retrolental fibroplasia - FiO2 35 to 40% can be safely tolerated indefinitely CO2 narcosis: - PaCO2 may increase severely to cause respiratory acidosis, somnolence and coma - PaCO2 increase secondary to combination of a) abolition of hypoxic drive to breathe b) increase in dead space

MECHANICAL VENTILATION
Non invasive with a mask Invasive with an endobronchial tube MV can be volume or pressure cycled For hypercapnia: - MV increases alveolar ventilation and lowers PaCO2, corrects pH - rests fatigues respiratory muscles

For hypoxemia: - O2 therapy alone does not correct hypoxemia shunt - Most common cause of shunt is fluid filled or alveoli (Pulmonary edema)

caused by
collapsed

POSITIVE END EXPIRATORY PRESSURE (PEEP)

PEEP increases the end expiratory lung volume (FRC) PEEP recruits collapsed alveoli and prevents recollapse FRC increases, therefore lung becomes more compliant Reversal of atelectasis diminishes intrapulmonary shunt Excessive PEEP has adverse effects decreased cardiac output barotrauma (pneumothorax, pneumomediastinum) increased physiologic dead space increased work of breathing