Acute Respiratory Acute Respiratory Failure Failure

Acute Respiratory Acute Respiratory

FailureFailure

• Classification of respiratory insufficiency according to L. Usenko (1993):• A. Primary (caused by disorders of external respiration). Reasons:• airway patency disorders (obstruction with tongue, vomit, mucus, gastric

contents, foreign bodies; laryngeal spasm, etc.) • central nervous system disorders (intoxication, brain injuries, haemorrhages,

inflammations, etc.) • disorders of respiratory muscles activity (myasthenia, botulism, tetanus, muscle

relaxants, etc.) • defects of chest structure or functional chest disorders ( chest injuries, limited

diaphragm mobility – for example due to enteroparesis) • disorders of pulmonary compliance (pneumonia, bronchiolitis, atelectasis,

“shock lung” syndrome, etc.) • disorders of ventilation-perfusion system (irregularity of ventilation and

perfusion during artificial ventilation, pulmonary oedema, etc.)

• B. Secondary (caused by inability of blood to contain enough oxygen for metabolic needs of tissues or disorders of transportation and cellular consumption).

• • Respiratory insufficiency is characterized with hypoxia (“lowering of the oxygen”).

Hypoxia occurs in case of:• 1. Inability of external respiration to provide arterial blood with enough amount of

oxygen (hypoxic hypoxia)• 2. Lowering of oxygen amount due to anaemia - decreased level of haemoglobin, red

blood cells or appearance of their atypical forms (haemic hypoxia).• 3. Inability of cardiovascular system to provide systemic and pulmonary circulation

enough for metabolic needs of the body (circulatory hypoxia).• 4. Disorders of oxidative phosphorylation on cellular level of different organs and

systems (tissue hypoxia). •

• Symptoms of acute respiratory failure are really various.• Central nervous system. Conscious patients can complain of breathlessness (feeling of the air-lack),

difficult inspiration or expiration. Due to development of hypoxia patients become restless, anxious, and sometimes euphoric; they can not evaluate critically their condition or environment. Terminal stages of insufficiency show total CNS inhibition – comatose state (hypoxic or hypercapnic). Quite often, especially in children, convulsions appear.

• Skin and mucosa are mirror of respiratory insufficiency: their changes are quite illustrative.• In case of external respiration disorders the amount of oxygenated haemoglobin is decreased and

thus quantity of reduced haemoglobin. Arterial blood becomes “venous” (dark): skin and mucosa become cyanotic (blue, purple). First of all their colour change lips, nail plates, earlobes, afterwards face and other body parts. In case of anaemic patients with haemoglobin level 60 grams per litre and lower skin stays pale even in terminal stages of respiratory insufficiency. In case of cyanic and carbon monoxide intoxication skin, nail plates and mucosa turn bright pink, although patients are greatly suffering from hypoxia. Hydrosis is quite significant feature of hypercapnia. Terminal respiratory insufficiency is characterized with dark-grey color cold skin covered with clammy sweat.

• Disorders of external respiration are the most obvious symptoms of respiratory insufficiency. Clinically in case of those patients next symptoms might be observed:

• complete breathing arrest (apnea);• low respiratory rate – less than 12 per minute (bradypnea);• high respiratory rate – more than 20 per minute (tachypnea);• shallow breathing (respiratory volume less than 5 ml per kilogram

of body weight);• respiratory “anarchy” (irregular breathing with pauses and uneven

amplitude of respiratory movements);

• pathological types of respiration: – Cheyne-Stokes breathing (periods of apnea, which are followed with chaotic

frequent breathing); – Biot’s breathing (periods of apnea which are followed with breathing of equal

amplitude); – Difficult breathing (noticeable at a distance, correlation between inspiration and

expiration is violated, with active participation of additional muscles): • 1. inspiratory dyspnea (difficult inspiration) – inspiration is prolonged,

intercostals spaces, jugular fossa and subclavian fossa are retracted; sometimes stridorous noise can be heard

• 2. expiratory dyspnea (difficult expiration) – patients should make a great physical effort in order to exhale; exhalation is prolonged, noisy, heard at a distance; chest is enlarged, becomes barrel shaped

Acute Respiratory FailureAcute 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 FailureAcute Respiratory Failure

• Hypercapnic v Hypoxemic respiratory failure

• ARDS and ALI

Hypercapnic Respiratory FailureHypercapnic Respiratory Failure

(PAO2 - PaO2)

Alveolar Hypoventilation

V/Q abnormality

PI max

increasednormal

Nl VCO2

PaCO2 >46mmHgNot compensation for metabolic alkalosis

CentralHypoventilation

NeuromuscularProblem

VCO2

V/Q Abnormality

HypermetabolismOverfeeding

The Case of Patient RVThe 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/+10Preintubation: 7.28/91/81/43


(PAO2 - PaO2)


V/Q abnormality

PI max

increasednormal

Nl VCO2



NeuromuscularProblem

VCO2

V/Q Abnormality




Brainstem respiratory depression Drugs (opiates) Obesity-hypoventilation syndrome

PI max


NeuromuscularDisorder

nlPI max

Critical illness polyneuropathyCritical illness myopathy

HypophosphatemiaMagnesium depletion

Myasthenia gravisGuillain-Barre syndrome


(PAO2 - PaO2)


V/Q abnormality

PI max

increasednormal

Nl VCO2



NeuromuscularDisorder

VCO2

V/Q Abnormality



V/Q abnormalityIncreased Aa gradient

Nl VCO2

VCO2

V/Q Abnormality




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



Nl VCO2

VCO2

V/Q Abnormality


• VCO2 only an issue in pts with ltd ability to eliminate CO2

• Overfeeding with carbohydrates generates more CO2

Hypoxemic Respiratory FailureHypoxemic Respiratory Failure

Is PaCO2 increased?

Hypoventilation (PAO2 - PaO2)?

Hypoventilation alone

Respiratory driveNeuromuscular dz

Hypovent plus another

mechanism

Shunt

Inspired PO2

High altitudeFIO2

(PAO2 - PaO2) No

NoYes

Is low PO2 correctable

with O2?

V/Q mismatch

No Yes

Yes

The Case of Patient ESThe 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#1BiPAP 80%: 7.45/48/66/32/+10


Is PaCO2 increased?

Hypoventilation (PAO2 - PaO2)?

Hypoventilation alone

Respiratory driveNeuromuscular dz

Hypovent plus another

mechanism

Shunt

Inspired PO2

High altitudeFIO2

(PAO2 - PaO2) No

NoYes

Is low PO2 correctable

with O2?

V/Q mismatch

No Yes

Yes


V/Q mismatch

V/Q mismatch DO2/VO2 Imbalance

PvO2>40mmHg PvO2<40mmHg

DO2: anemia, low COVO2: hypermetabolism


V/Q mismatch

SHUNTV/Q = 0

DEAD SPACEV/Q = ∞

AtelectasisIntraalveolar filling Pneumonia Pulmonary edema

Pulmonary embolusPulmonary vascular dzAirway dz (COPD, asthma)

Intracardiac shuntVascular shunt in lungs

ARDSInterstitial lung dzPulmonary contusion


V/Q mismatch

SHUNTV/Q = 0

DEAD SPACEV/Q = ∞

AtelectasisIntraalveolar filling Pneumonia Pulmonary edema

Pulmonary embolusPulmonary vascular dzAirway dz (COPD, asthma)

Intracardiac shuntVascular shunt in lungs

ARDSInterstitial lung dzPulmonary contusion


Acute Respiratory Distress Syndrome

• Severe ALI• B/L radiographic

infiltrates• PaO2/FiO2 <200mmHg

(ALI 201-300mmHg)• No e/o L Atrial P;

PCWP<18



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

– Distinguish from cardiogenic edema

– History and risk factors

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




Fluid in interstitium and alveoli

• Impaired gas exchange Compliance PAP





Exudative phase Fibrotic phaseProliferative phase

Diffuse alveolar damage



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



Indirect Lung Injury• Sepsis• Severe trauma with shock/hypoperfusion• Burns• Massive blood transfusion• Drug overdose: ASA, cocaine, opioids, phenothiazines,

TCAs. • Cardiopulmonary bypass• Acute pancreatitis



Complications• Barotrauma

• Nosocomial pneumonia

• Sedation and paralysis persistent MS depression and neuromuscular weakness



• 861 patients, 10 centers• Randomized• Tidal Vol 12mL/kg PDW,

PlatP<50cmH2O• Tidal Vol 6mL/kg PDW,

PlatP<30cmH2O• NNT 12

• 31% mortality v 39.8%• 65.7% breathing without assistance by day 28 v 55%• Significantly more ventilator-free days• Significantly more days without failure of nonpulmonary

organs/systems

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Acute Respiratory Acute Respiratory Failure Failure