Inability of the respiratory system to provide oxygenation and/or remove carbon dioxide from the body. The most common admitting diagnosis in critical care units. Mortality of 20-50%. What are the two types?
Acute respiratory failure.
Type 1: oxygenation failure, hypoxemic ARF
Type 2: Ventilation failure, hypercapnia ARF
What is Type 1 ARF, hypoxemic ARF?
What is Type 2 ARF, hypercapnic?
1: Oxygenation failure. A partial pressure of arterial oxygen (PaO2) lower than 60 mmHg with normal to decreased levels of carbon dioxide. Most commonly occurring type.
2: Ventilation failure. A PaCO2 greater than 50 mmHg with a pH less than 7.30.
Values are based on arterial blood values with pt breathing room air.
How does ARF differ from chronic respiratory failure?
ARF evolves rapidly over minutes to hours, providing little time for physiological compensation. Chronic respiratory failure develops over time and allows the body’s compensatory mechanisms to activate.
ARF and chronic failure are not mutually exclusive. Explain?
ARF may occur when a pt with chronic failure develops a respiratory infection or is exposed to other kinds of stressors, creating an increased demand or decreased supply of O2 that overwhelms the already compromised respiratory system. Acute-on-chronic respiratory failure.
What are five generally accepted mechanisms that reduce PaO2 and create a state of hypoxemia?
Hypoventilation, intrapulmonary shunting, ventilation-perfusion mismatching, diffusion deficits, and decreased barometric pressure.
The amount of gas that enters the alveoli per minute.
Alveolar ventilation. In the normal lung, the partial pressure of alveolar oxygen (PAO2) is about equal to the PaO2. If alveolar ventilation is reduced because of hypoventilation, the PAO2 and PaO2 are both reduced.
What are some factors that can lead to hypoventilation?
Drug overdose that leads to CNS depression, neuro disorders that cause decreased RR, abdominal or thoracic surgery leading to shallow breathing patterns secondary to pain on inspiration.
Physiological shunt: In normally functioning lungs, a small amount of blood returns to the left side of the heart without engaging in alveolar gas exchange. What is a pathological shunt?
A larger amount of blood returns to the left side of the heart without participating in gas exchange, resulting in a decrease in PaO2. Exists when areas of the lung that are inadequately ventilated are adequately perfused, causing the blood to shunt past the lung and return unoxygentated to the left side of the heart. Atelectasis, pneumonia, pulmonary edema.
What is the tx for a pathological shunt that involves the alveoli?
The cause of hypoxemia cannot be effectively treated solely by increasing the fraction of inspired oxygen (FiO2) because the increased O2 is unable to reach the alveoli. Tx is directed at opening the alveoli and improving ventilation.
The rate of pulmonary ventilation (V) usually equals the rate of perfusion (Q), resulting in a ventilation-to-perfusion ratio (V/Q) of 1.0. Mismatches?
If V exceeds blood flow, the V/Q ratio is greater than 1.0.
If V is less than blood flow, the V/Q ratio is less than 1.0.
Can occur when obstructed airways inhibit ventilation (and perfusion is normal), or when a clot in pulmonary circulation obstructs perfusion.
The alveolar-capillary membrane has what six barriers to the diffusion (the movement of gas from an area of a higher concentration to an area of lower concentration) of O2 and CO2? How long does diffusion take?
Surfactant, alveolar epithelium, interstitial fluid, capillary endothelium, plasma, red blood cell membrane
Under normal circumstances, O2 and CO2 diffuse across the membrane in 0.25 seconds.
Physiological changes in respiratory failure?
Distance between alveoli and capillaries may increase cause accumulation of fluid in the interstitial space. Changes in capillary perfusion pressure, leakage of plasma protein into interstitial space, and destruction of the capillary membrane contribute to fluid buildup. Fibrotic changes in lung tissue that may be there (COPD) reduce diffusion.
As diffusion capacity in the alveoli is reduced, what changes occur in PaO2 and CO2?
Reductions in PaO2 occur first, resulting in hypoxemia. Cause CO2 is more readily diffusible than O2, hypercapnia is a late sign of diffusion defects.
A normal cardiac output results in the delivery of how much O2 per minute?
600-1000 mL/min of O2, which generally exceeds the normal amount of O2 needed by the tissues.
How does the body compensate when CO decreases, meaning less oxygenated blood is delivered?
To maintain normal aerobic metabolism in low CO states, tissues extract increasing amounts of O2 from the blood. When this increase can’t compensate anymore for the lower CO, cells convert to anaerobic metabolism. Results in the production of lactic acid, which depresses function of the myocardium and further lowers CO.
Between 96-100% of body’s O2 is transported to the tissues bound to hemoglobin. Each gram of hgb can carry 1.34mL of O2 when all of its O2 binding sites are filled. Arterial saturation and hgb?
Arterial O2 saturation (SaO2) refers to the percentage of O2 binding sites on each hgb molecule that are filled with O2. If hgb is low, O2 to tissues impaired, leads to tissue hypoxia. Alteration in hgb function can also decrease O2 delivery.
Hypercapnia effects on neuro?
Significantly increases cerebral blood flow, causing the pt to appear restless and anxious. As ICP rises, LOC decreases, progressing to coma if effective treatment doesn’t occur.
What are some causes of hypoventilation?
CNS abnormalities, neuromuscular disorders, drug overdoses, and chest wall abnormalities. Respiratory acidosis occurs rapidly, before renal compensation can catch up.
The upper and lower airways do not participate in gas exchange, therefore the volume of inspired gas that fills these structures is known as what?
Dead space. Accounts for 25-30% of inspired volume. A major mechanism for elevation of PaCO2 is an increase in the volume of dead space in relation to the total tidal volume. Dead space increases when an area that is well ventilated has reduced perfusion and no longer participates in gas exchange.
Changes in mental status resulting from hypoxemia and hypercapnia?
Begin with anxiety, restlessness, and confusion, and may deteriorate to leathery, severe somnolence, and coma.
What compensatory mechanisms may be seen during an assessment on a pt with hypoxemia?
Tachypnea and an increase in tidal volume (hyperventilation). As compensatory mechanisms fail, respirations become shallow, bradypnea is seen. Use of accessory muscles and intercostal retractions indicate respiratory muscle fatigue.
Acute respiratory distress syndrome is the most severe form of ARF. What are the criteria for diagnosis according to the Berlin criteria (2012)?
Acute onset within 1 week of clinical insult. Bilateral pulmonary opacities not explained by other conditions. Altered PaO2/FiO2 ratio.
Severity is determined by the PaO2/FiO2 ratio when the pt is treated with PEEP or CPAP of 5cm H2O or higher.
Ranges for mild to severe ARDS?
Mild: 200-300 mmHg
Moderate: 100-200 mmHg
Severe: less than 100mmHg
Possible causes of ARDS? Direct and indirect
Direct: Aspiration of gastric contents, fat embolism, inhalation of toxic gases, multi system trauma (chest and/or lung injury), near-drowning, pneumonia
Indirect: Burns, cardiopulmonary bypass, drug overdose, fractures (esp of pelvis or long bones), multiple transfusions, multi system trauma (w/out chest and/or lung injury), pancreatitis, sepsis
