Acute Respiratory Distress Syndrom (ARDS) is a sudden and progressive form of acute respiratory failure in which the alveolar capillary membrane becomes damaged and more permeable to intravascular fluid
Here is an ARDS awareness video
(ARZ, 2009)
And here is a small demonstration of how ARDS effects the lungs
(Zobeck, 2008)
Wednesday, January 27, 2010
Pathopyhsiology of ARDS
Most common cause of ARDS is sepsis.
Direct lung injury may cause ARDS or ARDS may develop as a consequence of the systemic inflammatory response syndrome or multiple organ dysfunction syndrome.
An exact cause for the damage to the alveolar-capillary membrane is not known.
The pathophysiological changes of ARDS are thought to be due to stimulation of the inflammatory and immune systems which causes an attraction of neutrophils to the pulmonary interstitium. The neutrophils cause a release of biochemical, humoral and cellular mediators that produce changes in the lung.
The pathophysiological changes in ARDS are divided into three phases:
1. Injury or Exudative Phase
2. Reparative or Proliferative Phase
3. Fibrotic Phase
(Lewis, et. al 2007 pg 1812- 1813)
Direct lung injury may cause ARDS or ARDS may develop as a consequence of the systemic inflammatory response syndrome or multiple organ dysfunction syndrome.
An exact cause for the damage to the alveolar-capillary membrane is not known.
The pathophysiological changes of ARDS are thought to be due to stimulation of the inflammatory and immune systems which causes an attraction of neutrophils to the pulmonary interstitium. The neutrophils cause a release of biochemical, humoral and cellular mediators that produce changes in the lung.
The pathophysiological changes in ARDS are divided into three phases:
1. Injury or Exudative Phase
2. Reparative or Proliferative Phase
3. Fibrotic Phase
(Lewis, et. al 2007 pg 1812- 1813)
Three Phases of ARDS
Injury or Exudative Phase
Occurs approximately 1 to 7 days (usually 24 to 48 hours) after the direct lung injury or host insult.
The primary pathophysiological changes that characterize this phase are interstitial and alveolar edema (noncardiogenic pulmonary edema) and atelectasis.
Severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia unresponsive to increasing concentrations of O2 termed refractory hypoxemia.
Hypoxemia and the stimulation of juxtacapillary receptors in the stiff lung parenchyma (J reflex) initially cause an increase in respiratory rate, decrease in tidal volume, respiratory alkalosis and an increase in cardiac output.
Reparative or Proliferative Phase
Begins 1 to 2 weeks after the initial lung injury.
During this phase there is an influx of neutrophils, monocytes, lymphocytes and fibroblast proliferation as part of the inflammatory response.
The proliferative phase is complete when the diseased lung becomes characterized by dense, fibrous tissue.
Increased pulmonary vascular resistance and pulmonary hypertension may occur in this stage because fibroblasts and inflammatory cells destroy the pulmonary vasculature.
Lung compliance continues to decrease as a result of interstitial fibrosis and hypoxemia.
Hypoxemia worsens because of the thickened alveolar membrane causing diffusion limitation and shunting.
If the reparative phase persists widespread fibrosis results, if it is arrested the lesions resolve.
Fibrotic or Chronic Phase
Occurs approximately 2 to 3 weeks after the initial lung injury.
By this time the lung is completely molded by sparsely collagenous and fibrous tissues.
There is diffuse scarring and fibrosis resulting in decreased lung compliance.
The surface area for gas exchange is significantly reduced because the interstitium is fibrotic and therefore hypoxemia continues.
Pulmonary hypertension results from pulmonary vascular destruction and fibrosis.
(Lewis, et. al 2007 pg 1812)
Occurs approximately 1 to 7 days (usually 24 to 48 hours) after the direct lung injury or host insult.
The primary pathophysiological changes that characterize this phase are interstitial and alveolar edema (noncardiogenic pulmonary edema) and atelectasis.
Severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia unresponsive to increasing concentrations of O2 termed refractory hypoxemia.
Hypoxemia and the stimulation of juxtacapillary receptors in the stiff lung parenchyma (J reflex) initially cause an increase in respiratory rate, decrease in tidal volume, respiratory alkalosis and an increase in cardiac output.
Reparative or Proliferative Phase
Begins 1 to 2 weeks after the initial lung injury.
During this phase there is an influx of neutrophils, monocytes, lymphocytes and fibroblast proliferation as part of the inflammatory response.
The proliferative phase is complete when the diseased lung becomes characterized by dense, fibrous tissue.
Increased pulmonary vascular resistance and pulmonary hypertension may occur in this stage because fibroblasts and inflammatory cells destroy the pulmonary vasculature.
Lung compliance continues to decrease as a result of interstitial fibrosis and hypoxemia.
Hypoxemia worsens because of the thickened alveolar membrane causing diffusion limitation and shunting.
If the reparative phase persists widespread fibrosis results, if it is arrested the lesions resolve.
Fibrotic or Chronic Phase
Occurs approximately 2 to 3 weeks after the initial lung injury.
By this time the lung is completely molded by sparsely collagenous and fibrous tissues.
There is diffuse scarring and fibrosis resulting in decreased lung compliance.
The surface area for gas exchange is significantly reduced because the interstitium is fibrotic and therefore hypoxemia continues.
Pulmonary hypertension results from pulmonary vascular destruction and fibrosis.
(Lewis, et. al 2007 pg 1812)
Clincial Progression of ARDS
Progression of ARDS varies among patients and several factors determine the course of ARDS, including the nature of the initial injury, extent and severity of coexisting diseases and pulmonary complications.
(Lewis, et. al 2007 pg 1815)
(Lewis, et. al 2007 pg 1815)
Clinical Manifestations of ARDS
ARDS is considered to be present if the patient has
1. refractory hypoxemia
2. a chest x-ray with new bilateral interstitial or alveolar infiltrates
3. a pulmonary artery wedge pressure of 18mmHg or less and no
evidence of heart failure
4. a predisposing condition for ARDS within 48 hours of clinical
manifestations
At the time of the initial injury the patient may not experience respiratory symptoms or may exhibit only dyspnea, tachypnea, cough and restlessness.
Chest auscultation may be normal or reveal fine scattered crackles.
ABG’s usually indicate mild hypoxemia and respiratory alkalosis caused by hyperventilation.
Chest x-ray may be normal or exhibit evidence of minimal scattered interstitial infiltrates or demonstrate diffuse and extensive bilateral infiltrates termed whiteout or white lung.
As ARDS progresses, tachypnea and intercostal and suprasternal retractions may be present and pulmonary function tests reveal decreased compliance and decreased lung volumes.
Tachycardia, diaphoresis, changes in sensorium with decreased mentation, cyanosis and pallor may develop.
Pulmonary artery wedge pressure does not increases in ARDS because the cause of pulmonary edema is noncardiogenic.
Hypoxia and a PaO2/FIO2 ratio below 200 despite increase FIO2 are the hallmarks of ARDS.
(Lewis, et. al 2007 pg 1815)
1. refractory hypoxemia
2. a chest x-ray with new bilateral interstitial or alveolar infiltrates
3. a pulmonary artery wedge pressure of 18mmHg or less and no
evidence of heart failure
4. a predisposing condition for ARDS within 48 hours of clinical
manifestations
At the time of the initial injury the patient may not experience respiratory symptoms or may exhibit only dyspnea, tachypnea, cough and restlessness.
Chest auscultation may be normal or reveal fine scattered crackles.
ABG’s usually indicate mild hypoxemia and respiratory alkalosis caused by hyperventilation.
Chest x-ray may be normal or exhibit evidence of minimal scattered interstitial infiltrates or demonstrate diffuse and extensive bilateral infiltrates termed whiteout or white lung.
As ARDS progresses, tachypnea and intercostal and suprasternal retractions may be present and pulmonary function tests reveal decreased compliance and decreased lung volumes.
Tachycardia, diaphoresis, changes in sensorium with decreased mentation, cyanosis and pallor may develop.
Pulmonary artery wedge pressure does not increases in ARDS because the cause of pulmonary edema is noncardiogenic.
Hypoxia and a PaO2/FIO2 ratio below 200 despite increase FIO2 are the hallmarks of ARDS.
(Lewis, et. al 2007 pg 1815)
Complications of ARDS
Hospital Acquired Pneumonia
Occurs in 68% of patients with ARDS. Risk factors include impaired host defenses, contaminated medical equipment, invasive monitoring devices, aspiration of GI contents, and prolonged mechanical ventilation. Strategies for prevention are infection control measures (hand washing, sterile technique during endotracheal suctioning) elevating head of bed 30-40 degrees to prevent aspiration
Barotrauma
May result from rupture of over distended alveoli during mechanical ventilation, this can lead to pulmonary interstitial emphysema, pneumothorax, subcutaneous emphysema, and tension pneumonthorax. To avoid barotrauma and minimize risk associate with elevated plateau and peak inspiratory pressures, the patient with ARDS may be ventilated with smaller tidal volumes and varying amounts of positive end expiratory pressure (PEEP) in order to minimize oxygen requirements of intrathoracic pressures.
Physiologic Stress Ulcers
Bleeding from stress ulcers occur in 30% of patients with ARDS who require PPV. Management strategies include correction of predisposing conditions such as hypotension, shock, acidosis. Prophylacitc management includes anti-ulcer agents, such as H2 histamine receptor antagonist, as well as proton pump inhibitors and mucosal protecting agents.
Renal Failure
Can occur from decreased renal tissue oxygenation as a result of hypotension, hypoxemia and hypercapnia.
(Lewis, et. al 2007 pg 1815-1816)
Occurs in 68% of patients with ARDS. Risk factors include impaired host defenses, contaminated medical equipment, invasive monitoring devices, aspiration of GI contents, and prolonged mechanical ventilation. Strategies for prevention are infection control measures (hand washing, sterile technique during endotracheal suctioning) elevating head of bed 30-40 degrees to prevent aspiration
Barotrauma
May result from rupture of over distended alveoli during mechanical ventilation, this can lead to pulmonary interstitial emphysema, pneumothorax, subcutaneous emphysema, and tension pneumonthorax. To avoid barotrauma and minimize risk associate with elevated plateau and peak inspiratory pressures, the patient with ARDS may be ventilated with smaller tidal volumes and varying amounts of positive end expiratory pressure (PEEP) in order to minimize oxygen requirements of intrathoracic pressures.
Physiologic Stress Ulcers
Bleeding from stress ulcers occur in 30% of patients with ARDS who require PPV. Management strategies include correction of predisposing conditions such as hypotension, shock, acidosis. Prophylacitc management includes anti-ulcer agents, such as H2 histamine receptor antagonist, as well as proton pump inhibitors and mucosal protecting agents.
Renal Failure
Can occur from decreased renal tissue oxygenation as a result of hypotension, hypoxemia and hypercapnia.
(Lewis, et. al 2007 pg 1815-1816)
Nursing Care for ARDS
Respiratory Therapy
O2 Administration
Prone Positioning
Lateral Rotation Therapy
Positive Pressure Ventilation with PEEP
Permissive Hypercapnia
Alternative modes of mechanical Ventilation which are: pressure support ventilation, pressure release ventilation, pressure control ventilation, Inverse Ratio ventilation, and high frequency ventilation
Supportive Therapy
Identification and treatment of underlying cause
Hemodynamic monitoring
Inotropic/vasopressor medications
Dopamine (Intropin)
Dobutamine (Dobutrex)
Norepinephrine (Levophed)
Diuretics
IV Fluid Administration
Sedation/anaglesia
Neuromuscular blockade
(Lewis, et. al 2007 pg 1812)
O2 Administration
Prone Positioning
Lateral Rotation Therapy
Positive Pressure Ventilation with PEEP
Permissive Hypercapnia
Alternative modes of mechanical Ventilation which are: pressure support ventilation, pressure release ventilation, pressure control ventilation, Inverse Ratio ventilation, and high frequency ventilation
Supportive Therapy
Identification and treatment of underlying cause
Hemodynamic monitoring
Inotropic/vasopressor medications
Dopamine (Intropin)
Dobutamine (Dobutrex)
Norepinephrine (Levophed)
Diuretics
IV Fluid Administration
Sedation/anaglesia
Neuromuscular blockade
(Lewis, et. al 2007 pg 1812)
Nursing Diagnosis for ARDS
• Ineffective airway clearance related to excessive secretions as evidence by innefective or absent cough
• Impaired gas exchange related alveolar hypoventilation as evidenced by hypoxemia an or hypercapnia
• Anxiety related to hypoxemia
• Risk for decreased cardiac output related to mechanical ventilation
• Risk for injury related to endotracheal intubation
(Lewis, et. al 2007 pg 1807-1809)
• Impaired gas exchange related alveolar hypoventilation as evidenced by hypoxemia an or hypercapnia
• Anxiety related to hypoxemia
• Risk for decreased cardiac output related to mechanical ventilation
• Risk for injury related to endotracheal intubation
(Lewis, et. al 2007 pg 1807-1809)
Wednesday, January 20, 2010
What is MODS?
MODS is the failure of two or more more organ systems in acutely ill patients so that homeostasis cannot be maintained without intervention.
It can be a result of primary injury (primary MODS) or secondary injury (secondary MODS)
MODS develops from SIRS (Systemic inflammatory response syndrome), which is a result of infection, ischemia, infarction, or injury.
(Lewis, et. al 2007 pg 1794)
It can be a result of primary injury (primary MODS) or secondary injury (secondary MODS)
MODS develops from SIRS (Systemic inflammatory response syndrome), which is a result of infection, ischemia, infarction, or injury.
(Lewis, et. al 2007 pg 1794)
Different Responses to MODS
Vascular Response
In an uncontrolled inflammatory response, activation of inflammatory cells, release of mediators, damage to endothelium, and hypermetabolism occur.
Vasodilatation becomes excessive and leads to decreased SVR, hypotension, and an increase in vascular permeability allowing mediators and protein to leak out of the endothelium into the interstitial space.
Hypotension and decreased SVR causes compromised organ perfusion and microemboli.
Respiratory Problems
In MODS, the respiratory system is often the first system to show signs of dysfunction.
Inflammatory mediators and endothelial damage cause an increase in capillary permeability and movement of proteinaceous fluids into pulmonary interstitial spaces.
These fluids then move into the alveoli, causing edema and a decrease in surfactant production and alveolar collapse.
Ultimately the result is ARDS.
The Cardiac Response
Myocardial depression, massive vasodialation, decreased SVR, and decreased BP are factors that decrease the CO.
The baroreceptor reflex causes the release of inotropic and chronotropic factors and an increase in HR are factors that attempt to compensate for the low CO.
Capillary permeability causes a shift of albumin and fluid out of the vascular space, eventually leading to poor organ tissue perfusion from low CO.
Neurologic Response
Neurologic dysfunction is caused by hypoxia
Renal Problems
Acute renal failure is caused by hypoperfusion, and the effects of the mediators.
Decreased perfusion activates the renin angiotensin system, causing systemic vasoconstriction, release of aldosterone, and water resorbtion.
GI Dysfunction
Early in MODS blood is shuted away fro the GI tract making it susceptible to ischemic injury.
Decreased perfusion leads to the breakdown of the protective mucosal barrier leading to the risk of ulceration and GI bleeding.
Bacteremia can result from can translocate from the gut to the blood with the breakdown of the mucosal layer.
Liver Dysfunction
Hypermetabolism results in liver dysfunction.
Protein synthesis is impaired
Synthesis of albumin is impaired leading to decreased oncotic pressure of the plasma and fluid and protein leakage into the interstitial space.
Administration of albumin does not normalize oncotic pressure in these patients.
Electrolyte Imbalances
Electrolyte imbalances are common and are related to fluid shifts as well as metabolic and hormonal changes.
Decreased renal perfusion results in ADH and aldosterone release, resulting in Na and water retention, potassium loss, and metabolic acidosis
Hypocalcemia, hypomagnesemia, and hypophosphatemia are common
(Lewis, et. al 2007 pg 1794-1795)
In an uncontrolled inflammatory response, activation of inflammatory cells, release of mediators, damage to endothelium, and hypermetabolism occur.
Vasodilatation becomes excessive and leads to decreased SVR, hypotension, and an increase in vascular permeability allowing mediators and protein to leak out of the endothelium into the interstitial space.
Hypotension and decreased SVR causes compromised organ perfusion and microemboli.
Respiratory Problems
In MODS, the respiratory system is often the first system to show signs of dysfunction.
Inflammatory mediators and endothelial damage cause an increase in capillary permeability and movement of proteinaceous fluids into pulmonary interstitial spaces.
These fluids then move into the alveoli, causing edema and a decrease in surfactant production and alveolar collapse.
Ultimately the result is ARDS.
The Cardiac Response
Myocardial depression, massive vasodialation, decreased SVR, and decreased BP are factors that decrease the CO.
The baroreceptor reflex causes the release of inotropic and chronotropic factors and an increase in HR are factors that attempt to compensate for the low CO.
Capillary permeability causes a shift of albumin and fluid out of the vascular space, eventually leading to poor organ tissue perfusion from low CO.
Neurologic Response
Neurologic dysfunction is caused by hypoxia
Renal Problems
Acute renal failure is caused by hypoperfusion, and the effects of the mediators.
Decreased perfusion activates the renin angiotensin system, causing systemic vasoconstriction, release of aldosterone, and water resorbtion.
GI Dysfunction
Early in MODS blood is shuted away fro the GI tract making it susceptible to ischemic injury.
Decreased perfusion leads to the breakdown of the protective mucosal barrier leading to the risk of ulceration and GI bleeding.
Bacteremia can result from can translocate from the gut to the blood with the breakdown of the mucosal layer.
Liver Dysfunction
Hypermetabolism results in liver dysfunction.
Protein synthesis is impaired
Synthesis of albumin is impaired leading to decreased oncotic pressure of the plasma and fluid and protein leakage into the interstitial space.
Administration of albumin does not normalize oncotic pressure in these patients.
Electrolyte Imbalances
Electrolyte imbalances are common and are related to fluid shifts as well as metabolic and hormonal changes.
Decreased renal perfusion results in ADH and aldosterone release, resulting in Na and water retention, potassium loss, and metabolic acidosis
Hypocalcemia, hypomagnesemia, and hypophosphatemia are common
(Lewis, et. al 2007 pg 1794-1795)
Nursing Care for Patients with MODS
Prevention and Treatment of Infection
Prevention and treatment of infections important in MODS.
Minimize risks of nosocomial infections.
Early surgery to remove necrotic tissue that may provide a medium for bacterial growth.
Once a specific organism is identified, therapy should be modified.
Aggressive pulmonary management is indicated to avoid respiratory infections.
Strict asepsis is indicated for all patients with MODS.
Maintenance of Tissue Oxygenation
Maintaining adequate oxygenation is important.
Interventions that decrease O2 demand and increase O2 delivery are essential.
Sedation, mechanical ventilation, analgesia, paralysis, and rest decrease O2 need.
Appropriate Support of Individual Failing Organs
The patient with ARDS needs aggressive oxygen herapy and mechanical ventilation.
Nutritional and Metabolic Support
Providing adequate nutrition is important.
The total energy expenditure is 1.5 to 2 times normal and protein calorie malnutrition is common
Enteral nutrition is preferred because of a decreased risk of bacterial translocation
TPN is indicated if the enteral route is unavailable or insufficient.
(Lewis, et. al 2007 pg 1795-1796)
Prevention and treatment of infections important in MODS.
Minimize risks of nosocomial infections.
Early surgery to remove necrotic tissue that may provide a medium for bacterial growth.
Once a specific organism is identified, therapy should be modified.
Aggressive pulmonary management is indicated to avoid respiratory infections.
Strict asepsis is indicated for all patients with MODS.
Maintenance of Tissue Oxygenation
Maintaining adequate oxygenation is important.
Interventions that decrease O2 demand and increase O2 delivery are essential.
Sedation, mechanical ventilation, analgesia, paralysis, and rest decrease O2 need.
Appropriate Support of Individual Failing Organs
The patient with ARDS needs aggressive oxygen herapy and mechanical ventilation.
Nutritional and Metabolic Support
Providing adequate nutrition is important.
The total energy expenditure is 1.5 to 2 times normal and protein calorie malnutrition is common
Enteral nutrition is preferred because of a decreased risk of bacterial translocation
TPN is indicated if the enteral route is unavailable or insufficient.
(Lewis, et. al 2007 pg 1795-1796)
Clinical and Laboratory Markers for Organ Dysfunction
There is a website with a great chart, it divides the body up into systems and tells what signs and symptoms will be seen with MODS. We hope you find this helpful, please follow the link provided below
http://www.frca.co.uk/article.aspx?articleid=100855
Griffiths, J. (2007, May 5). Pathophysiology and management. Retrieved from http://www.frca.co.uk/article.aspx?articleid=100855
http://www.frca.co.uk/article.aspx?articleid=100855
Griffiths, J. (2007, May 5). Pathophysiology and management. Retrieved from http://www.frca.co.uk/article.aspx?articleid=100855
Works Cited
Arz, C. (Producer). (2009). Ards awareness. [Web]. Retrieved from http://www.youtube.com/watch?v=aXjaxvL6y7I&feature=related
Griffiths, J. (2007, May 5). Pathophysiology and management. Retrieved from http://www.frca.co.uk/article.aspx?articleid=100855
Lewis, S.L., Heitkemper, M.M. , Dirksen , S.R. O’Brien P.G., & Bucher, L. (2007). Medical-surgical nursing. St. Louis, Missouri: Elsevier Inc.
Zobeck, D. (Producer). (2008). Respiratory care: ards. [Web]. Retrieved from http://www.youtube.com/watch?v=SPWAR0bqMkM&feature=related
Griffiths, J. (2007, May 5). Pathophysiology and management. Retrieved from http://www.frca.co.uk/article.aspx?articleid=100855
Lewis, S.L., Heitkemper, M.M. , Dirksen , S.R. O’Brien P.G., & Bucher, L. (2007). Medical-surgical nursing. St. Louis, Missouri: Elsevier Inc.
Zobeck, D. (Producer). (2008). Respiratory care: ards. [Web]. Retrieved from http://www.youtube.com/watch?v=SPWAR0bqMkM&feature=related
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