Acute Respiratory Acute Respiratory Failure Failure.
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Transcript of 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
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
Hypercapnic Respiratory FailureHypercapnic Respiratory Failure
Alveolar Hypoventilation
Brainstem respiratory depression Drugs (opiates) Obesity-hypoventilation syndrome
PI max
CentralHypoventilation
NeuromuscularDisorder
nlPI max
Critical illness polyneuropathyCritical illness myopathy
HypophosphatemiaMagnesium depletion
Myasthenia gravisGuillain-Barre syndrome
Hypercapnic Respiratory FailureHypercapnic Respiratory Failure
(PAO2 - PaO2)
Alveolar Hypoventilation
V/Q abnormality
PI max
increasednormal
Nl VCO2
PaCO2 >46mmHgNot compensation for metabolic alkalosis
CentralHypoventilation
NeuromuscularDisorder
VCO2
V/Q Abnormality
HypermetabolismOverfeeding
Hypercapnic Respiratory FailureHypercapnic Respiratory Failure
V/Q abnormalityIncreased Aa gradient
Nl VCO2
VCO2
V/Q Abnormality
HypermetabolismOverfeeding
Hypercapnic Respiratory FailureHypercapnic Respiratory Failure
V/Q abnormalityIncreased Aa gradient
Nl VCO2
VCO2
V/Q Abnormality
HypermetabolismOverfeeding
• Increased dead space ventilation• advanced emphysema• PaCO2 when Vd/Vt >0.5
• Late feature of shunt-type• edema, infiltrates
Hypercapnic Respiratory FailureHypercapnic Respiratory Failure
V/Q abnormalityIncreased Aa gradient
Nl VCO2
VCO2
V/Q Abnormality
HypermetabolismOverfeeding
• 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
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
Hypoxemic Respiratory FailureHypoxemic Respiratory Failure
V/Q mismatch
V/Q mismatch DO2/VO2 Imbalance
PvO2>40mmHg PvO2<40mmHg
DO2: anemia, low COVO2: hypermetabolism
Hypoxemic Respiratory FailureHypoxemic Respiratory Failure
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
Hypoxemic Respiratory FailureHypoxemic Respiratory Failure
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
Hypoxemic Respiratory FailureHypoxemic 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 FailureHypoxemic 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
Fluid in interstitium and alveoli
Pro-inflmm cytokines (TNF, IL1,6,8)
Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium
Inflammatory Alveolar Injury
Fluid in interstitium and alveoli
• Impaired gas exchange Compliance PAP
Pro-inflmm cytokines (TNF, IL1,6,8)
Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium
Hypoxemic Respiratory FailureHypoxemic Respiratory Failure
Acute Respiratory Distress Syndrome
Exudative phase Fibrotic phaseProliferative phase
Diffuse alveolar damage
Hypoxemic Respiratory FailureHypoxemic 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 FailureHypoxemic 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 FailureHypoxemic Respiratory Failure
Acute Respiratory Distress Syndrome
Complications• Barotrauma
• Nosocomial pneumonia
• Sedation and paralysis persistent MS depression and neuromuscular weakness
Hypoxemic Respiratory FailureHypoxemic Respiratory Failure
Acute Respiratory Distress Syndrome
• 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