1. IN THE NAME OF GOD

2. Acute Respiratory Failure
Dr.h-kayalha
Anesthesiologist

3. 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
Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory failure is defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 mm Hg. Furthermore, respiratory failure may be acute or chronic. While acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.

4. Acute Respiratory Failure
Hypercapnic
Hypoxemic
Mixed
ARDS and ALI

5. Hypercapnic Respiratory Failure
PaCO2 >46mmHg
Not compensation for metabolic alkalosis
(PAO2 - PaO2)
normal
increased
Alveolar Hypoventilation
V/Q abnormality
Nl VCO2
VCO2
PI max
Central
Hypoventilation
Neuromuscular
Problem
V/Q
Abnormality
Hypermetabolism
Overfeeding

6. Hypercapnic Respiratory Failure
Alveolar Hypoventilation
nlPI max
PI max
Central
Hypoventilation
Neuromuscular
Disorder
Brainstem respiratory depression
Drugs (opiates)
Obesity-hypoventilation syndrome
Critical illness polyneuropathy
Critical illness myopathy
Hypophosphatemia
Magnesium depletion
Myasthenia gravis
Guillain-Barre syndrome
Alveolar hypoventilation can cause both hypoxemia and hypercapnia.
In trauma, we see this acutely when pts splint from painful rib fxs - tire out, need intubation.
Maximum inspiratory pressure.

7. Hypercapnic Respiratory Failure
V/Q abnormality
Increased Aa gradient
VCO2
Nl VCO2
Hypermetabolism
Overfeeding
V/Q
Abnormality
Increased dead space ventilation
advanced emphysema
PaCO2 when Vd/Vt >0.5
Late feature of shunt-type
edema, infiltrates
VCO2 is rate of CO2 production. Nl is 90 to 130 L/min/m2, which is 80% of VO2.

8. Hypercapnic Respiratory Failure
V/Q abnormality
Increased Aa gradient
VCO2
Nl VCO2
Hypermetabolism
Overfeeding
V/Q
Abnormality
VCO2 only an issue in pts with limited ability to eliminate CO2
Overfeeding with carbohydrates generates more CO2
VCO2 is rate of CO2 production. Nl is 90 to 130 L/min/m2, which is 80% of VO2.

9. Hypoxemic Respiratory Failure
Is PaCO2 increased?
Yes No
Hypoventilation
(PAO2 - PaO2)?
(PAO2 - PaO2)
Yes No
Hypovent plus another mechanism
Is low PO2 correctable with O2?
V/Q mismatch No
Yes
Inspired PO2
Hypoventilation alone
High altitude
FIO2
This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.
Respiratory drive
Neuromuscular dz
Shunt

10. Hypoxemic Respiratory Failure
V/Q mismatch
PvO2>40mmHg
PvO2<40mmHg
DO2/VO2 Imbalance
V/Q mismatch
DO2 oxygen delivery; VO2 oxygen uptake. Imbalance can aggravate hypoxemia caused by abnl gas exchange in lungs.
DO2: anemia, low CO
VO2: hypermetabolism

11. Hypoxemic Respiratory Failure
V/Q mismatch
Atelectasis
Intraalveolar filling
Pneumonia
Pulmonary edema
ARDS
Interstitial lung dz
Pulmonary contusion
SHUNT
V/Q = 0
DEAD SPACE
V/Q = ∞
Pulmonary embolus
Pulmonary vascular dz
Airway dz
(COPD, asthma)
Intracardiac shunt
Vascular shunt in lungs

12. Hypoxemic Respiratory Failure
Acute Respiratory Distress Syndrome
Severe ALI
B/L radiographic infiltrates
PaO2/FiO2 <200mmHg (ALI mmHg)
* pulmonary oedema
* normal vascular pedicle
* no cardiomegaly or upper lobe blood diversion
* when pulmonary vessels can be distinguished they are often constricted
* septal lines usually absent because capillary leak occurs directly into alveolar spaces (cf cardiogenic pulmonary oedema)
* progressive lung destruction and transition from alveolar to interstitial opacities
Chronic phase
* fibrosis
* focal emphysema

13. Hypoxemic Respiratory Failure
Acute Respiratory Distress Syndrome
Develops ~4-48h
Persists days-wks
Diagnosis:
Distinguish from cardiogenic edema
History and risk factors
* pulmonary oedema
* normal vascular pedicle
* no cardiomegaly or upper lobe blood diversion
* when pulmonary vessels can be distinguished they are often constricted
* septal lines usually absent because capillary leak occurs directly into alveolar spaces (cf cardiogenic pulmonary oedema)
* progressive lung destruction and transition from alveolar to interstitial opacities
Chronic phase
* fibrosis
* focal emphysema

14. Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells
Increased permeability of alveolar capillary membrane
Influx of protein rich edema fluid and inflammatory cells into air spaces
Dysfunction of surfactant

15. Inflammatory Alveolar Injury
Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells
Increased permeability of alveolar capillary membrane
Influx of protein rich edema fluid and inflammatory cells into air spaces
Dysfunction of surfactant

16. Inflammatory Alveolar Injury
Pro-inflmm cytokines (TNF, IL1,6,8)
Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells
Increased permeability of alveolar capillary membrane
Influx of protein rich edema fluid and inflammatory cells into air spaces
Dysfunction of surfactant

17. Inflammatory Alveolar Injury
Pro-inflmm cytokines (TNF, IL1,6,8)
Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium
Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells
Increased permeability of alveolar capillary membrane
Influx of protein rich edema fluid and inflammatory cells into air spaces
Dysfunction of surfactant

18. 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
Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells
Increased permeability of alveolar capillary membrane
Influx of protein rich edema fluid and inflammatory cells into air spaces
Dysfunction of surfactant
Fluid in interstitium and alveoli

19. 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
Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells
Increased permeability of alveolar capillary membrane
Influx of protein rich edema fluid and inflammatory cells into air spaces
Dysfunction of surfactant
Fluid in interstitium and alveoli
Impaired gas exchange
 Compliance
 PAP

20. Hypoxemic Respiratory Failure
Acute Respiratory Distress Syndrome
Direct Lung Injury:
a) PNA and aspiration of gastric contents
or other causes of chemical pneumonitis
b) pulmonary contusion, penetrating lung injury
c) fat emboli
d) near drowning
e) inhalation injury
f) reperfusion pulm edema after lung transplant
Indirect lung injury
a) sepsis
b) severe trauma w/ shock hypoperfusion
c) drug over dose
d) cardiopulmonary bypass
e) acute pancreatitis
f) transfusion of multp blood products
Exudative phase
Proliferative phase
Fibrotic phase
Diffuse alveolar damage

21. 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 - lung transplant
Indirect lung injury
a) sepsis
b) severe trauma w/ shock hypoperfusion
c) drug over dose
d) cardiopulmonary bypass
e) acute pancreatitis
f) transfusion of multp blood products

22. 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

23. Hypoxemic Respiratory Failure
Acute Respiratory Distress Syndrome
Complications
Barotrauma
Nosocomial pneumonia
Sedation and paralysis  persistent MS depression and neuromuscular weakness