Running a race at 12,000 feetRunning a race at 12,000 feet

Respiratory FailureRespiratory Failure

Dr. Sat SharmaDr. Sat Sharma

Univ of ManitobaUniv of Manitoba

RESPIRATORY FAILURERESPIRATORY FAILURE

““inability of the lung to meet the metabolic inability of the lung to meet the metabolic demands of the body. This can be from failure of demands of the body. This can be from failure of tissue oxygenation and/or failure of COtissue oxygenation and/or failure of CO2 2

homeostasis.” homeostasis.”

RESPIRATORY FAILURERESPIRATORY FAILURE

Definition Definition Respiration is gas exchange between the Respiration is gas exchange between the organism and its environment. Function of organism and its environment. Function of respiratory system is to transfer Orespiratory system is to transfer O22 from atmosphere from atmosphere

to blood and remove COto blood and remove CO22 from blood. from blood.

Clinically Clinically Respiratory failure is defined as PaORespiratory failure is defined as PaO22 <60 mmHg <60 mmHg

while breathing air, or a PaCOwhile breathing air, or a PaCO22 >50 mmHg. >50 mmHg.

Respiratory system includes:Respiratory system includes:

CNS (medulla) CNS (medulla) Peripheral nervous system (phrenic nerve) Peripheral nervous system (phrenic nerve) Respiratory muscles Respiratory muscles Chest wall Chest wall Lung Lung Upper airway Upper airway Bronchial tree Bronchial tree Alveoli Alveoli Pulmonary vasculature Pulmonary vasculature

Potential causes of Respiratory Failure

HYPOXEMIC RESPIRATORY HYPOXEMIC RESPIRATORY FAILURE(TYPE 1)FAILURE(TYPE 1)

PaOPaO22 <60mmHg with normal or low PaCO <60mmHg with normal or low PaCO2 2

normal or high pHnormal or high pH Most common form of respiratory failureMost common form of respiratory failure Lung disease is severe to interfere with Lung disease is severe to interfere with

pulmonary Opulmonary O22 exchange, but over all ventilation is exchange, but over all ventilation is

maintainedmaintained Physiologic causes: V/Q mismatch and shuntPhysiologic causes: V/Q mismatch and shunt

HYPOXEMIC RESPIRATORY FAILURE HYPOXEMIC RESPIRATORY FAILURE CAUSES OF ARTERIAL HYPOXEMIACAUSES OF ARTERIAL HYPOXEMIA

1.1. FiOFiO22

2.2. Hypoventilation Hypoventilation

(( PaCO PaCO22) Hypercapnic ) Hypercapnic

3. 3. V/Q mismatch V/Q mismatch Respiratory failure Respiratory failure (eg.COPD)(eg.COPD)

4. 4. Diffusion limitation ?Diffusion limitation ?

5. 5. Intrapulmonary shunt Intrapulmonary shunt - pneumonia - pneumonia

- Atelectasis - Atelectasis - CHF (high pressure pulmonary - CHF (high pressure pulmonary edema) edema) - ARDS (low pressure - ARDS (low pressure

pulmonary edema)pulmonary edema)

Causes of Hypoxemic Respiratory Causes of Hypoxemic Respiratory failurefailure

Caused by a disorder of heart, lung or blood. Caused by a disorder of heart, lung or blood.

Etiology easier to assess by CXR abnormality:Etiology easier to assess by CXR abnormality:

- Normal Chest x-ray - Normal Chest x-ray Cardiac shunt (right to left) Cardiac shunt (right to left)

Asthma, COPDAsthma, COPD

Pulmonary embolismPulmonary embolism

Hyperinflated Lungs : COPD

Causes of Hypoxemic Respiratory Causes of Hypoxemic Respiratory failure (cont’d.)failure (cont’d.)

• Focal infiltrates on CXRFocal infiltrates on CXR

AtelectasisAtelectasis

PneumoniaPneumonia

An example of intrapulmonary shunt

Causes of Hypoxemic Respiratory Failure Causes of Hypoxemic Respiratory Failure (cont’d.)(cont’d.)

Diffuse infiltrates on CXRDiffuse infiltrates on CXR Cardiogenic Pulmonary EdemaCardiogenic Pulmonary Edema Non cardiogenic pulmonary edema (ARDS)Non cardiogenic pulmonary edema (ARDS) Interstitial pneumonitis or fibrosisInterstitial pneumonitis or fibrosis InfectionsInfections

Diffuse pulmonary infiltrates

Hypercapnic Respiratory Failure Hypercapnic Respiratory Failure (Type II)(Type II)

PaCOPaCO22 >50 mmHg >50 mmHg

Hypoxemia is always presentHypoxemia is always present pH depends on level of HCOpH depends on level of HCO33

HCOHCO33 depends on duration of hypercapnia depends on duration of hypercapnia

Renal response occurs over days to weeksRenal response occurs over days to weeks

Acute Hypercapnic Respiratory Failure Acute Hypercapnic Respiratory Failure (Type II)(Type II)

AcuteAcute Arterial pH is lowArterial pH is low CausesCauses

- sedative drug over dose- sedative drug over dose- acute muscle weakness such as myasthenia gravis- acute muscle weakness such as myasthenia gravis- severe lung disease: - severe lung disease: alveolar ventilation can not be maintained (i.e. Asthma or alveolar ventilation can not be maintained (i.e. Asthma or

pneumonia) pneumonia)

• Acute on chronic:Acute on chronic: This occurs in patients with chronic COThis occurs in patients with chronic CO2 2 retention who worsen and retention who worsen and

have rising COhave rising CO2 2 and low pH.and low pH. Mechanism: respiratory muscle fatigueMechanism: respiratory muscle fatigue

Causes of Hypercapnic Respiratory failureCauses of Hypercapnic Respiratory failure

Respiratory centre (medulla) dysfunctionRespiratory centre (medulla) dysfunction Drug over dose, CVA, tumor, hypothyroidism,central Drug over dose, CVA, tumor, hypothyroidism,central

hypoventilationhypoventilation Neuromuscular disease Neuromuscular disease

Guillain-Barre, Myasthenia Gravis, polio, spinal injuriesGuillain-Barre, Myasthenia Gravis, polio, spinal injuries Chest wall/Pleural diseases Chest wall/Pleural diseases kyphoscoliosis, kyphoscoliosis,

pneumothorax, massive pleural effusionpneumothorax, massive pleural effusion Upper airways obstruction Upper airways obstruction tumor, tumor,

foreign body, laryngeal edemaforeign body, laryngeal edema Peripheral airway disorder Peripheral airway disorder

asthma, COPDasthma, COPD

Clinical and Laboratory ManifestationClinical and Laboratory Manifestation

(non-specific and unreliable)(non-specific and unreliable)

Cyanosis Cyanosis - bluish color of mucous membranes/skin indicate - bluish color of mucous membranes/skin indicate

hypoxemiahypoxemia - unoxygenated hemoglobin 50 mg/L - unoxygenated hemoglobin 50 mg/L

- not a sensitive indicator - not a sensitive indicator Dyspnea Dyspnea

- secondary to hypercapnia and hypoxemia - secondary to hypercapnia and hypoxemia Paradoxical breathingParadoxical breathing Confusion, somnolence and comaConfusion, somnolence and coma ConvulsionsConvulsions

ASSESSMENT OF PATIENTASSESSMENT OF PATIENT Careful historyCareful history Physical ExaminationPhysical Examination ABG analysis ABG analysis

-classify RF and help with cause -classify RF and help with cause

1) PaCO1) PaCO22 = = VCOVCO22 x 0.863 x 0.863 VAVA

2) P(A-a)02) P(A-a)022 = (PiO = (PiO22 - - PaCOPaCO22) – PaO) – PaO22

RR Lung function Lung function

OVP vs RVP vs NVPOVP vs RVP vs NVP Chest RadiographChest Radiograph EKG EKG

Clinical & Laboratory ManifestationsClinical & Laboratory Manifestations

Circulatory changesCirculatory changes

- tachycardia, hypertension, hypotension- tachycardia, hypertension, hypotension

Polycythemia Polycythemia - chronic hypoxemia - erythropoietin - chronic hypoxemia - erythropoietin synthesissynthesis

Pulmonary hypertensionPulmonary hypertension Cor-pulmonale or right ventricular failureCor-pulmonale or right ventricular failure

Management of Respiratory Failure Management of Respiratory Failure PrinciplesPrinciples

Hypoxemia may cause death in RFHypoxemia may cause death in RF Primary objective is to reverse and prevent Primary objective is to reverse and prevent

hypoxemiahypoxemia Secondary objective is to control PaCOSecondary objective is to control PaCO22 and and

respiratory acidosis respiratory acidosis Treatment of underlying diseaseTreatment of underlying disease Patient’s CNS and CVS must be monitored and Patient’s CNS and CVS must be monitored and

treatedtreated

Oxygen TherapyOxygen Therapy

Supplemental OSupplemental O22 therapy essential therapy essential titration based on SaOtitration based on SaO22, PaO, PaO22 levels and PaCO levels and PaCO22

Goal is to prevent tissue hypoxiaGoal is to prevent tissue hypoxia Tissue hypoxia occurs (normal Hb & C.O.) Tissue hypoxia occurs (normal Hb & C.O.)

- venous PaO- venous PaO22 < 20 mmHg or SaO < 20 mmHg or SaO22 < 40% < 40% - arterial PaO- arterial PaO22 < 38 mmHg or SaO < 38 mmHg or SaO2 2 < 70%< 70%

Increase arterial PaOIncrease arterial PaO22 > 60 mmHg(SaO > 60 mmHg(SaO22 > 90%) or > 90%) or venous SaOvenous SaO22 > 60% > 60%

OO22 dose either flow rate (L/min) or FiO dose either flow rate (L/min) or FiO22 (%) (%)

Risks of Oxygen TherapyRisks of Oxygen Therapy OO22 toxicity toxicity: - : -

very high levels(>1000 mmHg) CNS toxicity and very high levels(>1000 mmHg) CNS toxicity and seizures - seizures - lower levels (FiOlower levels (FiO22 > 60%) and longer exposure: - > 60%) and longer exposure: - capillary capillary damage, leak and pulmonary fibrosis damage, leak and pulmonary fibrosis - PaO - PaO2 2 >150 can cause retrolental fibroplasia >150 can cause retrolental fibroplasia - FiO - FiO22 35 to 40% can be safely tolerated indefinitely 35 to 40% can be safely tolerated indefinitely

COCO22 narcosis: narcosis: - - PaCO PaCO22 may increase severely to cause respiratory may increase severely to cause respiratory acidosis, acidosis, somnolence and comasomnolence and coma

- PaCO- PaCO2 2 increase secondary to combination of increase secondary to combination of a) abolition of hypoxic drive to breathe a) abolition of hypoxic drive to breathe b) increase in dead space b) increase in dead space

MECHANICAL VENTILATIONMECHANICAL VENTILATION Non invasive with a maskNon invasive with a mask Invasive with an endobronchial tube Invasive with an endobronchial tube MV can be volume or pressure cycled MV can be volume or pressure cycled

For hypercapnia: For hypercapnia: - MV increases alveolar ventilation and lowers - MV increases alveolar ventilation and lowers

PaCOPaCO22, corrects pH , corrects pH

- rests fatigues respiratory muscles - rests fatigues respiratory muscles

For hypoxemia: For hypoxemia: - O - O22 therapy alone does not correct hypoxemia therapy alone does not correct hypoxemia caused by shuntcaused by shunt- Most common cause of shunt is fluid filled or - Most common cause of shunt is fluid filled or collapsed alveoli (Pulmonary edema)collapsed alveoli (Pulmonary edema)

POSITIVE END EXPIRATORY POSITIVE END EXPIRATORY PRESSURE (PEEP)PRESSURE (PEEP)

PEEP increases the end expiratory lung volume (FRC)PEEP increases the end expiratory lung volume (FRC) PEEP recruits collapsed alveoli and prevents recollapsePEEP recruits collapsed alveoli and prevents recollapse FRC increases, therefore lung becomes more compliantFRC increases, therefore lung becomes more compliant Reversal of atelectasis diminishes intrapulmonary shuntReversal of atelectasis diminishes intrapulmonary shunt Excessive PEEP has adverse effects Excessive PEEP has adverse effects

- decreased cardiac output - decreased cardiac output - barotrauma (pneumothorax, - barotrauma (pneumothorax, pneumomediastinum) - increased physiologic pneumomediastinum) - increased physiologic dead space - increased work dead space - increased work of breathingof breathing

PULMONARY EDEMAPULMONARY EDEMA Pulmonary edema is an increase in extravascular lung Pulmonary edema is an increase in extravascular lung

waterwater Interstitial edema does not impair functionInterstitial edema does not impair function Alveolar edema cause several gas exchange abnormalitiesAlveolar edema cause several gas exchange abnormalities Movement of fluid is governed by Starling’s equation Movement of fluid is governed by Starling’s equation

QF = KF [(PQF = KF [(PIVIV - P - PISIS ) + ) + ( ( ISIS - - IVIV ) )

QF = rate of fluid movement QF = rate of fluid movement KF = membrane permeability KF = membrane permeability P PIVIV & P & PISIS are intra vascular and interstitial hydrostatic are intra vascular and interstitial hydrostatic pressures pressures ISIS and and IVIV are interstitial and intravascular are interstitial and intravascular oncotic pressures oncotic pressures reflection coefficientreflection coefficient

Lung edema is cleared by lymphaticsLung edema is cleared by lymphatics

Adult Respiratory distress Syndrome Adult Respiratory distress Syndrome (ARDS)(ARDS)

Variety of unrelated massive insults injure gas Variety of unrelated massive insults injure gas exchanging surface of Lungsexchanging surface of Lungs

First described as clinical syndrome in 1967 by First described as clinical syndrome in 1967 by Ashbaugh & Petty Ashbaugh & Petty

Clinical terms synonymous with ARDS Clinical terms synonymous with ARDS Acute respiratory failure Acute respiratory failure

Capillary leak syndrome Capillary leak syndrome Da Nang Lung Da Nang Lung Shock Lung Shock Lung Traumatic Traumatic wet Lung wet Lung Adult hyaline membrane diseaseAdult hyaline membrane disease

Risk Factors in ARDSRisk Factors in ARDS

Sepsis 3.8% Sepsis 3.8% Cardiopulmonary bypass 1.7% Cardiopulmonary bypass 1.7% Transfusion 5.0% Transfusion 5.0% Severe pneumonia 12.0% Severe pneumonia 12.0% Burn 2.3% Burn 2.3% Aspiration 35.6% Aspiration 35.6% Fracture 5.3% Fracture 5.3% Intravascular coagulopathy 12.5% Intravascular coagulopathy 12.5% Two or more of the above 24.6% Two or more of the above 24.6%

PATHOPHYSIOLOGY AND PATHOPHYSIOLOGY AND PATHOGENESISPATHOGENESIS

Diffuse damage to gas-exchanging surface Diffuse damage to gas-exchanging surface either alveolar or capillary side of either alveolar or capillary side of membrane membrane

Increased vascular permeability causes Increased vascular permeability causes pulmonary edemapulmonary edema

Pathology: fluid and RBC in interstitial Pathology: fluid and RBC in interstitial space, hyaline membranesspace, hyaline membranes

Loss of surfactant: alveolar collapse Loss of surfactant: alveolar collapse

CRITERIA FOR DIAGNOSIS OF CRITERIA FOR DIAGNOSIS OF ARDSARDS

Clinical history of catastrophic event Clinical history of catastrophic event Pulmonary or Non pulmonary (shock, multi system Pulmonary or Non pulmonary (shock, multi system trauma) trauma)

Exclude Exclude chronic pulmonary diseases chronic pulmonary diseases left left ventricular failure ventricular failure Must have respiratory distress Must have respiratory distress tachypnea >20 breath/minute tachypnea >20 breath/minute

Labored breathing Labored breathing central cyanosis central cyanosis CXR- diffuse infiltrates CXR- diffuse infiltrates PaOPaO22 <50mmHg FiO <50mmHg FiO22 >O.6 >O.6 Compliance <50 ml/cm HCompliance <50 ml/cm H22O increased O increased shunt and shunt and dead space dead space

ARDSARDS

MANAGEMENT OF ARDSMANAGEMENT OF ARDS

Mechanical ventilation Mechanical ventilation corrects hypoxemia/respiratory acidosiscorrects hypoxemia/respiratory acidosis

Fluid management Fluid management correction of anemia and hypovolemiacorrection of anemia and hypovolemia

Pharmacological intervention Pharmacological intervention Dopamine to augment C.O. Dopamine to augment C.O.

Diuretics Diuretics Antibiotics Antibiotics Corticosteroids - no Corticosteroids - no demonstrated benefit demonstrated benefit early disease, early disease, helpful 1 week laterhelpful 1 week later

Mortality continues to be 50 to 60%Mortality continues to be 50 to 60%