Extracoporeal Membrane Oxygenation as a Treatment Strategy for Acute Severe Respiratory Failure
Aliaa Esam Mahmoud Adam;
Abstract
SUMMARY
K
nowledge of the respiratory anatomy provides a good foundation for understanding the complex process of respiration. Gas exchange occurs at the alveolar-capillary membrane. Diffusion distance and time may be increased in alveolar congestion, interstitial or alveolar edema, or pulmonary fibrosis.
The principle muscle of respiration is the diaphragm. The diaphragm can adapt with time to high-resistance workloads placed on it by some disease states. Expiration during normal quiet ventilation is passive activity that occurs because of relaxation of the inspiratory muscles and recoil of the lung parenchyma. During forceful expiration the internal intercostal muscles contract, decreasing the anterior-posterior diameter of the thorax by pulling the ribs downward and inward.
The basic principle of the movement of gas is that it travels from an area of higher to lower pressure. Physiologic pressures related to the flow of gases into and out of the lung are atmospheric pressure, intrapulmonary (intraalveolar) pressure, and intrapleural (intrathoracic) pressure. The difference between two pressures is called a pressure gradient. The three important pressure gradients related to ventilation are transrespiratory, transpulmonary, and transthoracic pressure.
The ratio of alveolar ventilation (V) to pulmonary blood flow (Q) determines the composition of the gas leaving the lung. Ideally, each alveolus would be matched to well-perfused capillaries, leading to a V/Q ratio of 1.0; however, ventilation and perfusion are not equally distributed throughout the lung. Normally, alveolar ventilation is 4 L/min, whereas cardiac output is 5 L/min. The V/Q ratio for the whole lung, then, averages 4/5, or 0.8, despite regional differences.
Types of respiratory failure:
1- Type 1 (Hypoxemic) - PO2 < 50 mmHg on room air.
2- Type 2 (Hypercapnic/ Ventilatory) - PCO2 > 50 mmHg (if not a chronic CO2 retainer).
3- Type 3 (Peri-operative). This is generally a subset of type 1 failure but is sometimes considered separately because it is so common.
4- Type 4 (Shock) - secondary to cardiovascular instability
Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition that prevents enough oxygen from getting to the lungs and into the blood. ARDS leads to a buildup of fluid in the air sacs. This fluid prevents enough oxygen from passing into the bloodstream. The fluid buildup also makes the lungs heavy and stiff, and decreases the lungs' ability to expand. The level of oxygen in the blood can stay dangerously low.
A number of closely inter-related pathophysiologic mechanisms and systems contribute to the development of ALI and ARDS. Inflammatory cytokines, oxygen radicals, activation of coagulation and complement, platelet and immune cell activation, proteases, leukotrienes, and eicosanoids have been hypothesized to play a role in the early stages of ALI and ARDS. In addition to ongoing inflammation and oxidation, factors specific to apoptosis, edema fluid resolution, fibrosis, and repair are likely to be important in the resolving and late phases of ALI and ARDS.
Patients with ARDS require meticulous supportive care, including intelligent use of sedatives and neuromuscular blockade, hemodynamic management, nutritional support, control of blood glucose levels, expeditious evaluation and treatment of nosocomial pneumonia, and prophylaxis against deep venous thrombosis (DVT) and gastrointestinal (GI) bleeding.
Maintaining adequate arterial oxygenation. The hallmark respiratory abnormality of ALI and ARDS is hypoxemia that is resistant to oxygen therapy. This is due to the presence of a large right-to-left intrapulmonary shunt arising from fluid-filled and collapsed alveoli. Maintaining adequate arterial oxygenation is a goal given high priority by both traditional and more recent approaches to ventilator management. One should use sufficient PEEP to reduce the right-to-left shunt to oxygenate the patient & avoid prolonged exposure of such patients to potentially toxic concentrations of high inspired oxygen (e.g., Fio2 of 0.7 and above). PEEP improves arterial oxygenation, primarily by recruiting collapsed and partially fluid-filled alveoli and thereby increasing the functional residual capacity (FRC) at end expiration. PEEP also redistributes alveolar fluid into the interstitium, which should also improve oxygenation.
Extracorporeal membrane oxygenation (ECMO) is a temporary life support technique, used to treat respiratory failure (where the lungs do not work effectively) in critically ill patients. The aim is to increase oxygen levels in the blood. During the procedure, a tube carries blood from the right side of the heart then pumps it through an artificial lung where it picks up oxygen. This oxygen-rich blood is then passed back into the person’s blood system. The advent of H1N1 infection has focused attention on young critically ill patients with severe ARF. Data from Australia and Canada suggest that those who require intensive care develop severe refractory hypoxemia for which ECMO may prove to be highly effective. Evidence is now available to suggest that building capacity to provide such support is timely.
Conventional Ventilation or ECMO for Severe Adult Respiratory Failure (CESAR; trial) was the only controlled clinical trial using modern ECMO technology. The primary outcome, death or severe disability at 6 months, occurred in 37% of the patients referred for consideration for ECMO, as compare with 53% of those assigned to conventional management. This recent trial provides support for a strategy of transferring patients with severe ARDS to a center that is capable of providing ECMO. However, this study was not a randomized trial of ECMO as compared with standard-of-care mechanical ventilation. Substantial differences in overall care between the study groups may account for the beneficial effect that was associated with referral for consideration for ECMO.
For the most severe forms of acute respiratory failure, ECMO Replaces pulmonary function, allows ultraprotective MV settings, should allow facilitated lung healing. Only experienced centers should run these programs. With a mobile ECMO retrieval team available 24H/7D.
K
nowledge of the respiratory anatomy provides a good foundation for understanding the complex process of respiration. Gas exchange occurs at the alveolar-capillary membrane. Diffusion distance and time may be increased in alveolar congestion, interstitial or alveolar edema, or pulmonary fibrosis.
The principle muscle of respiration is the diaphragm. The diaphragm can adapt with time to high-resistance workloads placed on it by some disease states. Expiration during normal quiet ventilation is passive activity that occurs because of relaxation of the inspiratory muscles and recoil of the lung parenchyma. During forceful expiration the internal intercostal muscles contract, decreasing the anterior-posterior diameter of the thorax by pulling the ribs downward and inward.
The basic principle of the movement of gas is that it travels from an area of higher to lower pressure. Physiologic pressures related to the flow of gases into and out of the lung are atmospheric pressure, intrapulmonary (intraalveolar) pressure, and intrapleural (intrathoracic) pressure. The difference between two pressures is called a pressure gradient. The three important pressure gradients related to ventilation are transrespiratory, transpulmonary, and transthoracic pressure.
The ratio of alveolar ventilation (V) to pulmonary blood flow (Q) determines the composition of the gas leaving the lung. Ideally, each alveolus would be matched to well-perfused capillaries, leading to a V/Q ratio of 1.0; however, ventilation and perfusion are not equally distributed throughout the lung. Normally, alveolar ventilation is 4 L/min, whereas cardiac output is 5 L/min. The V/Q ratio for the whole lung, then, averages 4/5, or 0.8, despite regional differences.
Types of respiratory failure:
1- Type 1 (Hypoxemic) - PO2 < 50 mmHg on room air.
2- Type 2 (Hypercapnic/ Ventilatory) - PCO2 > 50 mmHg (if not a chronic CO2 retainer).
3- Type 3 (Peri-operative). This is generally a subset of type 1 failure but is sometimes considered separately because it is so common.
4- Type 4 (Shock) - secondary to cardiovascular instability
Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition that prevents enough oxygen from getting to the lungs and into the blood. ARDS leads to a buildup of fluid in the air sacs. This fluid prevents enough oxygen from passing into the bloodstream. The fluid buildup also makes the lungs heavy and stiff, and decreases the lungs' ability to expand. The level of oxygen in the blood can stay dangerously low.
A number of closely inter-related pathophysiologic mechanisms and systems contribute to the development of ALI and ARDS. Inflammatory cytokines, oxygen radicals, activation of coagulation and complement, platelet and immune cell activation, proteases, leukotrienes, and eicosanoids have been hypothesized to play a role in the early stages of ALI and ARDS. In addition to ongoing inflammation and oxidation, factors specific to apoptosis, edema fluid resolution, fibrosis, and repair are likely to be important in the resolving and late phases of ALI and ARDS.
Patients with ARDS require meticulous supportive care, including intelligent use of sedatives and neuromuscular blockade, hemodynamic management, nutritional support, control of blood glucose levels, expeditious evaluation and treatment of nosocomial pneumonia, and prophylaxis against deep venous thrombosis (DVT) and gastrointestinal (GI) bleeding.
Maintaining adequate arterial oxygenation. The hallmark respiratory abnormality of ALI and ARDS is hypoxemia that is resistant to oxygen therapy. This is due to the presence of a large right-to-left intrapulmonary shunt arising from fluid-filled and collapsed alveoli. Maintaining adequate arterial oxygenation is a goal given high priority by both traditional and more recent approaches to ventilator management. One should use sufficient PEEP to reduce the right-to-left shunt to oxygenate the patient & avoid prolonged exposure of such patients to potentially toxic concentrations of high inspired oxygen (e.g., Fio2 of 0.7 and above). PEEP improves arterial oxygenation, primarily by recruiting collapsed and partially fluid-filled alveoli and thereby increasing the functional residual capacity (FRC) at end expiration. PEEP also redistributes alveolar fluid into the interstitium, which should also improve oxygenation.
Extracorporeal membrane oxygenation (ECMO) is a temporary life support technique, used to treat respiratory failure (where the lungs do not work effectively) in critically ill patients. The aim is to increase oxygen levels in the blood. During the procedure, a tube carries blood from the right side of the heart then pumps it through an artificial lung where it picks up oxygen. This oxygen-rich blood is then passed back into the person’s blood system. The advent of H1N1 infection has focused attention on young critically ill patients with severe ARF. Data from Australia and Canada suggest that those who require intensive care develop severe refractory hypoxemia for which ECMO may prove to be highly effective. Evidence is now available to suggest that building capacity to provide such support is timely.
Conventional Ventilation or ECMO for Severe Adult Respiratory Failure (CESAR; trial) was the only controlled clinical trial using modern ECMO technology. The primary outcome, death or severe disability at 6 months, occurred in 37% of the patients referred for consideration for ECMO, as compare with 53% of those assigned to conventional management. This recent trial provides support for a strategy of transferring patients with severe ARDS to a center that is capable of providing ECMO. However, this study was not a randomized trial of ECMO as compared with standard-of-care mechanical ventilation. Substantial differences in overall care between the study groups may account for the beneficial effect that was associated with referral for consideration for ECMO.
For the most severe forms of acute respiratory failure, ECMO Replaces pulmonary function, allows ultraprotective MV settings, should allow facilitated lung healing. Only experienced centers should run these programs. With a mobile ECMO retrieval team available 24H/7D.
Other data
| Title | Extracoporeal Membrane Oxygenation as a Treatment Strategy for Acute Severe Respiratory Failure | Other Titles | الاكسجة الغشائية خارج الجسم كاستراتيجية لعلاج فشل الجهاز التنفسى الحاد | Authors | Aliaa Esam Mahmoud Adam | Issue Date | 2015 |
Recommend this item
Similar Items from Core Recommender Database
Items in Ain Shams Scholar are protected by copyright, with all rights reserved, unless otherwise indicated.