GROUP REVIEWER INSTRUCTIONS: 1.

1 Physiology of: ROBIN

1. STRICTLY A GROUP REVIEWER – DO NOT SHARE 1.1.1 Respiratory function (pulmonary ventilation, diffusion, transport
UNLESS AGREED UPON BY THE ENTIRE GROUP and cellular respiration.
2. THE ASSIGNMENT OF THE SOS DURING SYNTHESIS IS 1.1.2 Normal values of blood gases
AS FOLLOWS FOR THE REVIEWER 1.1.3 Oxygenation and ventilation
3. FOR FONT COLOR & REFERENCES 1.2 4 Types of respiratory failure based in pathophysiologic
● FROM THE BOOK = BLACK derangement in respiratory function: MARIEL
● IF BOTH FOUND IN BOOK & GUCCI = STILL 1.2.1 Type 1: Hypoperfusion of respiratory muscles
BLACK 1.2.2 Type 2: Ventilatory failure
● FROM GUCCI = BLUE 1.2.3 Type 3: Second degree to lung atelectasis
● ADDITIONAL FROM DOC = PURPLE 1.2.4 Type 4: Hypoperfusion of respiratory muscles
● OTHER INFO = BROWN 1.3 Causes and risk factors of respiratory failure- KRING
4. PLEASE USE THE LATEST VERSION OF HARRISON 1.3.1 Direct causes
21ST!!! 1.3.2 Indirect causes
5. PLEASE ADD ALL THE RELEVANT INFORMATION / 1.4 Clinical manifestations, to include clinical course and
DETAILS pathophysiology WITH Morphologic changes- KENNIE, DAWN
6. PLEASE INCLUDE ILLUSTRATIONS / TABLES FROM 1.6 Diagnostics work up to include:- NICO
THE BOOK INCLUDING THE DESCRIPTION OF THAT 1.6.1 ABG
ILLUSTRATION (sometimes they get the questions there 1.6.2 PIF ratio
lmao) 1.6.3 Diagnostic criteria
7. 1.7 Management -
The two failures - Minimizing Venticular Induced Lung Injury- MARIEL
CASE 2: - Minimizing Atelectrauma by Prevention of Alveolar Collapse
SPECIFIC OBJECTIVES: CASE 2 - Prone Positioning- ROBIN
When given a theoretical case scenario illustrating as adult patient - FLUID MANAGEMENT
with clinical - NEUROMUSCULAR BLOCKADE- KENNIE
manifestations of acute respiratory failure and hypoxemia, the - GLUCOCORTICOIDS
student should be - OTHER THERAPIES & OTHER STRATEGIES IN
able to: MECHANICAL VENTILATION- DAWN
1.8 Prognosis- KRING
1.9 Complications- NICO

1. Discuss acute respiratory failure, to include:

 Acute Respiratory Failure

PHYSIOLOGY TYPES based CAUSES CLINICAL MORPHOLOGI DIAGNOSTI MANAGEMENT COMPLICATIONS &
on MANIFESTATI C CHANGES C WORK-UP PROGNOSIS
Pathophysiolo ONS
gy

Respiratory function Type 1: Direct Causes Minimizing

(pulmonary Hypoperfusion Venticular Induced
ventilation, diffusion, of respiratory Lung Injury-
transport muscles
MARIEL
and cellular
respiration: Minimizing
Atelectrauma by
Normal values of Type 2: Prevention of
blood gases vs 2 px. Ventilatory Alveolar Collapse
failure
Prone Positioning-
Oxygenation and Type 3: Indirect
ROBIN
ventilation Second Causes
degree to lung FLUID
atelectasis MANAGEMENT

Type 4: NEUROMUSCULA
Hypoperfusion R BLOCKADE-
of respiratory
KENNIE
muscles
GLUCOCORTICOI
DS

OTHER
THERAPIES &
OTHER
STRATEGIES IN
MECHANICAL
VENTILATION-
DAWN
■■TYPE I: ACUTE HYPOXEMIC RESPIRATORY FAILURE
This type of respiratory failure occurs with alveolar flooding and subsequent ventilation-perfusion mismatch and intrapulmonary shunt physiology.
Alveolar flooding may be a consequence of pulmonary edema, lung injury, pneumonia, or alveolar hemorrhage. Pulmonary edema
can be further categorized as occurring due to elevated pulmonary microvascular pressures, as seen in heart failure and intravascular volume
overload or ARDS (“low-pressure pulmonary edema,” Chap. 301). This syndrome is defined by acute onset (≤1 week) of bilateral opacities on
chest imaging that are not fully explained by cardiac failure or fluid overload and of ventilation-perfusion mismatch, and shunt physiology
requiring positive end-expiratory pressure (PEEP). Type I respiratory failure occurs in clinical settings such as sepsis, gastric aspiration,
pneumonia, COVID-19 (Chap. 199), near-drowning, multiple blood transfusions, and pancreatitis. The mortality rate among patients with
ARDS was traditionally very high (50–70%), although changes in patient care have led to mortality rates closer to 30% (see below). The
COVID-19 pandemic has resulted in a substantially increased incidence of viral-mediated ARDS, and studies are ongoing to determine
whether management of COVID-19 ARDS should fully mirror that of non-COVID ARDS. The established mechanical ventilation practices
for non-COVID-19 ARDS have been largely applied to the support of COVID-19 ARDS patients (Chap. 199).
It is well established that mechanical ventilation of patients with ARDS may propagate lung injury. As seen in Fig. 300-5, the pressurevolume
relationship of the lung in ARDS is not linear. Alveoli may collapse at very low lung volumes. Animal studies have
suggested that repeated stretching and overdistention of injured alveoli during mechanical ventilation can further injure the lung. Concern over this
alveolar overdistention, termed ventilator-induced “volutrauma,” led to a multicenter, randomized,
prospective trial comparing traditional ventilator strategies for ARDS (large tidal volume: 12 mL/kg of ideal
body weight) with a low tidal volume (6 mL/kg of ideal body weight). This study showed a dramatic reduction in mortality rate in the low-tidalvolume
group from that in the high-tidal-volume group (31% vs 39.8%). Other studies have suggested that large tidal volumes may lead
to ARDS in patients who initially do not have this problem. Prone positioning has been shown to improve survival in those with severe ARDS
and has been more broadly applied in many centers in COVID-19 ARDS. Select patients may benefit from neuromuscular blockade in
ARDS. In addition, a “fluid-conservative” management strategy (maintaining a low central venous pressure [CVP] or pulmonary capillary
wedge pressure [PCWP]) is associated with fewer days of mechanical ventilation than a “fluid-liberal” strategy (maintaining a relatively high
CVP or PCWP) in ARDS in those patients who have been resuscitated from shock. There is growing interest in avoiding intubation in patients
with ARDS by the use of a variety of devices, such as masks, high-flow oxygen delivery systems, and helmets for respiratory support; however,
this is tempered by concern that higher tidal volumes during spontaneous breathing with these devices could result in progression of
preexisting lung injury.

■■TYPE II RESPIRATORY FAILURE: HYPERCAPNEIC RESPIRATORY FAILURE

This type of respiratory failure is a consequence of alveolar hypoventilation and results from the inability to eliminate carbon dioxide effectively.
Mechanisms are categorized by impaired central nervous system (CNS) drive to breathe (colloquially termed, “won’t breathe”), impaired
strength with failure of neuromuscular function in the respiratory system, and increased load(s) on the respiratory system (with the latter two
colloquially termed, “can’t breathe”). Reasons for diminished CNS drive to breathe include drug overdose, brainstem injury, sleep-disordered
breathing, and severe hypothyroidism. Reduced strength can be due to impaired neuromuscular transmission (e.g., myasthenia gravis,
Guillain-Barre syndrome, amyotrophic lateral sclerosis) or respiratory muscle weakness (e.g., myopathy, electrolyte derangements, fatigue).
The overall load on the respiratory system can be subclassified into resistive loads (e.g., bronchospasm), loads due to reduced lung compliance
(e.g., alveolar edema, atelectasis, intrinsic positive end-expiratory pressure [auto-PEEP]—see below), loads due to reduced chest wall
compliance (e.g., pneumothorax, pleural effusion, abdominal distention), and loads due to increased minute ventilation requirements (e.g.,
pulmonary embolus with increased dead-space fraction, sepsis).
The mainstays of therapy for hypercapnic respiratory failure are directed at reversing the underlying cause(s) of ventilatory failure.
Noninvasive positive-pressure ventilation with a tight-fitting facial or nasal mask, with avoidance of endotracheal intubation, may stabilize
these patients in certain circumstances. This approach has been shown to be beneficial in treating patients with exacerbations of chronic
obstructive pulmonary disease; it has been tested less extensively in other kinds of respiratory failure but may be attempted nonetheless
with close monitoring in the absence of contraindications (hemodynamic instability, inability to protect the airway, respiratory arrest, significant
airway secretions, significant aspiration risk). There has been reticence in some centers to use noninvasive ventilation in COVID-19
patients due to increased risk of virus aerosolization and transmission to health care workers.

■■TYPE III RESPIRATORY FAILURE: LUNG ATELECTASIS

This form of respiratory failure results from lung atelectasis. Because atelectasis occurs so commonly in the perioperative period, this form
is also called perioperative respiratory failure. After general anesthesia, decreases in functional residual capacity lead to collapse of dependent
lung units. Such atelectasis can be treated by frequent changes in position, chest physiotherapy, upright positioning, and control of incisional
and/or abdominal pain. Noninvasive positive-pressure ventilation may also be used to reverse regional atelectasis.

■■TYPE IV RESPIRATORY FAILURE: METABOLIC DEMANDS

This form most often results from hypoperfusion of respiratory muscles in patients in shock. Normally, respiratory muscles consume <5%
of total cardiac output and oxygen delivery. Patients in shock often experience respiratory distress due to pulmonary edema (e.g., in cardiogenic
shock), lactic acidosis, and anemia. In this setting, up to 40% of cardiac output may be distributed to the respiratory muscles. Intubation
and mechanical ventilation can allow redistribution of the cardiac output away from the respiratory muscles and back to vital organs
while the shock is treated. In addition, other causes of significant metabolic acidosis might require ventilatory support while reversal of the
underlying cause of the acidosis is addressed

GENERAL PRINCIPLES
Recent reductions in ARDS mortality rates are largely the result of general advances in the care of critically ill patients (Chap. 300).
Thus, caring for these patients requires close attention to (1) the recognition and treatment of underlying medical and surgical disorders (e.g.,
pneumonia, sepsis, aspiration, trauma); (2) the minimization of unnecessary procedures and their complications; (3)
standardized “bundled care” approaches for ICU patients, including prophylaxis against venous thromboembolism, gastrointestinal
bleeding, aspiration, excessive sedation, prolonged mechanical ventilation, and central venous catheter infections; (4) prompt
recognition of nosocomial infections; and (5) provision of adequate nutrition via the enteral route when feasible.
MANAGEMENT OF MECHANICAL VENTILATION
(See also Chap. 302) Patients meeting clinical criteria for ARDS frequently become fatigued from increased work of breathing
and progressive hypoxemia, requiring mechanical ventilation for support.
Minimizing Ventilator-Induced Lung Injury Despite its lifesaving potential, mechanical ventilation can aggravate lung injury.
Experimental models have demonstrated that ventilator-induced\lung injury can arise from at least two principal mechanisms:
“volutrauma” from repeated alveolar overdistention from excess tidal volume (that might also coincide with increased alveolar pressures,
or “barotrauma”) and “atelectrauma” from recurrent alveolar collapse. As is evident from chest CT (Fig. 301-4), ARDS is a heterogeneous
disorder, principally involving dependent portions of the lung with relative sparing of other regions. Because compliance
differs in affected versus more “normal” areas of the lung, attempts to fully inflate the consolidated lung may lead to overdistention of
and injury to the more normal areas. Ventilator-induced injury can be demonstrated in experimental models of acute lung injury, in
particular with high-tidal-volume (VT) ventilation. A large-scale, randomized controlled trial sponsored by the National Institutes of Health and
conducted by the ARDS Network compared low VT ventilation (6 mL/kg of predicted body weight) to conventional VT ventilation (12 mL/kg
predicted body weight).
Lower airway pressures were also targeted in the low-tidal-volume group (i.e., plateau pressure measured on the ventilator after a 0.5-s
pause after inspiration), with pressures targeted at ≤30 cm H2O in the low-tidal-volume group versus ≤50 cm H2O in the hightidal-
volume group. The mortality rate was significantly lower in the low VT patients (31%) than in the conventional VT patients
(40%). This improvement in survival represents a substantial ARDS mortality benefit.

Minimizing Atelectrauma by Prevention of Alveolar Collapse In

ARDS, the presence of alveolar and interstitial fluid and the loss of surfactant can lead to a marked reduction of lung compliance.
Without an increase in end-expiratory pressure, significant alveolar collapse can occur at end-expiration, with consequent impairment
of oxygenation. In most clinical settings, positive end-expiratory pressure (PEEP) is adjusted to minimize Fio2 (inspired O2 percentage)
and provide adequate Pao2 (arterial partial pressure of O2) without causing alveolar overdistention. Currently, there is no
consensus on the optimal method to set PEEP, because numerous trials have proved inconclusive. Possible approaches include using
the table of PEEP-Fio2 combinations from the ARDS Network trial group, generating a static pressure-volume curve for the respiratory
system and setting PEEP just above the lower inflection point on this curve to maximize respiratory system compliance,
and measuring esophageal pressures to estimate transpulmonary pressure (which may be particularly helpful in patients with a
stiff chest wall). Of note, a recent phase 2 trial in patients with moderate-to-severe ARDS demonstrated no benefit of routine use
of esophageal pressure-guided PEEP titration over empirical high PEEP-Fio2 titration. Until more data become available on how
best to optimize PEEP settings in ARDS, clinicians can use these options or a practical approach to empirically measure “best PEEP”
at the bedside to determine the optimal settings that best promote alveolar recruitment, minimize alveolar overdistention and hemodynamic
instability, and provide adequate Pao2 while minimizing Fio2 (Chap. 302).

Respiratory failure can indeed be classified into four types based on oxygenation status and carbon dioxide levels. Here they are, along with their
pathophysiology, morphology, and clinical manifestations:

1. **Type 1 Respiratory Failure (Hypoxemic Respiratory Failure):**

- **Pathophysiology:** Type 1 respiratory failure is primarily characterized by inadequate oxygenation of arterial blood (hypoxemia). This can
result from conditions that impair gas exchange in the lungs, such as ventilation-perfusion (V/Q) mismatch, shunt, or diffusion impairment.
- **Morphology:** In conditions like acute respiratory distress syndrome (ARDS), there can be diffuse alveolar damage, leading to alveolar
collapse, interstitial and alveolar edema, and inflammatory cell infiltration.
 - **Clinical Manifestations:** Patients typically present with symptoms of hypoxemia, such as dyspnea, tachypnea, cyanosis, and confusion.
They may also exhibit signs of the underlying condition causing the respiratory failure, such as pulmonary edema or pneumonia.

2. **Type 2 Respiratory Failure (Hypercapnic Respiratory Failure):**

- **Pathophysiology:** Type 2 respiratory failure is characterized by inadequate alveolar ventilation leading to hypercapnia (elevated arterial
carbon dioxide levels). This can result from conditions that depress the respiratory drive, impair neuromuscular function, or cause airway
obstruction.
- **Morphology:** In chronic conditions like severe COPD, there may be airway inflammation, mucous plugging, and destruction of alveolar walls
leading to air trapping (hyperinflation) and loss of elastic recoil.
- **Clinical Manifestations:** Patients may exhibit signs of hypercapnia, such as headache, confusion, lethargy, and eventually coma. They may
also present with symptoms of the underlying condition, such as chronic cough, wheezing, or decreased exercise tolerance.

3. **Type 3 Respiratory Failure (Combined Hypoxemic and Hypercapnic Respiratory Failure):**

- **Pathophysiology:** Type 3 respiratory failure involves both hypoxemia and hypercapnia. This can occur in conditions where there is a severe
compromise in both gas exchange and alveolar ventilation, such as severe exacerbations of COPD or neuromuscular diseases affecting
respiratory muscles.
- **Morphology:** Morphological changes depend on the underlying condition, but they may include features of both hypoxemic and hypercapnic
respiratory failure.
- **Clinical Manifestations:** Patients present with a combination of symptoms seen in both hypoxemic and hypercapnic respiratory failure,
including dyspnea, tachypnea, cyanosis, altered mental status, and signs of respiratory distress.

4. **Type 4 Respiratory Failure (Respiratory Failure with Normal Arterial Oxygen Partial Pressure):**
- **Pathophysiology:** Type 4 respiratory failure occurs when the arterial oxygen partial pressure (PaO2) is normal, but the arterial carbon
dioxide partial pressure (PaCO2) is elevated. This can happen in situations where there is an increased metabolic rate or production of carbon
dioxide, such as in sepsis, fever, or excessive heat production.
- **Morphology:** There may not be specific morphological changes associated with type 4 respiratory failure, as it is often secondary to
systemic conditions.
- **Clinical Manifestations:** Patients may present with signs of hypercapnia, such as headache, confusion, and eventually coma. Other
symptoms depend on the underlying cause of the increased carbon dioxide production.

Treatment for each type of respiratory failure aims to correct the underlying cause and restore adequate oxygenation and ventilation. This may
involve supplemental oxygen therapy, mechanical ventilation, bronchodilators, corticosteroids, or treating the underlying condition.
Acidosis refers to a condition in which the blood pH drops below the normal range (7.35-7.45), resulting in increased acidity. Acidosis can occur
due to various causes, including respiratory acidosis (caused by inadequate removal of carbon dioxide), metabolic acidosis (caused by increased
production or decreased elimination of acids), or a combination of both.
Altered mental status (AMS) is a broad term used to describe changes in cognitive function, consciousness, or behavior. Acidosis, especially
severe or prolonged metabolic acidosis, can lead to alterations in mental status. Here's how acidosis can cause AMS:

1. **Effect on Central Nervous System (CNS):** Acidosis affects the central nervous system directly by altering neuronal function and
neurotransmitter activity. The acidic environment interferes with the normal functioning of neurons, impairing their ability to transmit signals
efficiently. This disruption in neuronal function can lead to various neurological symptoms, including altered mental status.

2. **Cerebral Blood Flow:** Acidosis can also affect cerebral blood flow. Severe acidosis may lead to cerebral vasoconstriction, reducing blood
flow to the brain. Decreased cerebral perfusion can result in hypoxia and ischemia, further exacerbating neurological dysfunction and contributing
to altered mental status.

3. **Electrolyte Imbalance:** Acidosis is often associated with electrolyte disturbances, such as hyperkalemia (high potassium levels) in metabolic
acidosis. Electrolyte imbalances can have profound effects on neuronal excitability and function. Hyperkalemia, for example, can lead to
depolarization of cell membranes and interfere with neurotransmitter release, potentially contributing to altered mental status.

4. **Impaired Respiratory Drive:** In cases of severe acidosis, particularly respiratory acidosis, the body's compensatory mechanisms may be
overwhelmed. This can lead to respiratory depression or failure, resulting in hypoxemia and hypercapnia. Hypoxemia deprives the brain of oxygen,
impairing neuronal function and contributing to altered mental status. Additionally, hypercapnia can further exacerbate acidosis and cerebral
vasoconstriction, worsening neurological symptoms.

5. **Associated Conditions:** Acidosis often occurs secondary to underlying medical conditions such as diabetic ketoacidosis, lactic acidosis, renal
failure, or severe infections. These underlying conditions can themselves contribute to altered mental status through various mechanisms,
including direct effects on the CNS, systemic inflammation, or metabolic derangements.

In summary, acidosis can cause altered mental status through its direct effects on neuronal function, cerebral blood flow, electrolyte balance,
respiratory drive, and associated systemic conditions. Prompt identification and correction of the underlying acidosis are essential to prevent
further neurological deterioration and improve patient outcomes.

ARDS, or Acute Respiratory Distress Syndrome, is a severe lung condition that can be caused by various factors, including drowning. When a
person drowns, they inhale water into their lungs. This water can damage the delicate tissues of the lungs and interfere with their ability to
exchange oxygen and carbon dioxide effectively. This leads to a cascade of inflammatory responses and damage to the alveoli, the tiny air sacs in
the lungs where gas exchange occurs.
The process of drowning can lead to a lack of oxygen (hypoxemia) and an increase in carbon dioxide levels (hypercapnia) in the bloodstream. This
triggers a systemic inflammatory response, causing further damage to the lungs and leading to the development of ARDS.

In ARDS, the lungs become stiff and lose their ability to expand and contract properly, which severely impairs oxygen uptake and delivery to the
body's tissues. This can result in respiratory failure and, if not treated promptly and effectively, can be life-threatening.

In summary, drowning can cause ARDS through the inhalation of water, which damages lung tissue and triggers an inflammatory response,
ultimately leading to impaired lung function and respiratory failure.

Falling from a height, such as off a building, can lead to several injuries, including traumatic injuries to the chest and lungs, which can
subsequently result in Acute Respiratory Distress Syndrome (ARDS). When a person falls from a significant height, they may sustain multiple
injuries upon impact, including fractures of the ribs and other bones in the chest, as well as damage to the lungs themselves.

Here's how falling off a building can lead to ARDS:

1. **Thoracic Trauma:** The impact of the fall can cause severe chest trauma, including rib fractures, lung contusions (bruising of the lung tissue),
and pneumothorax (collapsed lung). These injuries can disrupt the normal functioning of the lungs and compromise their ability to exchange
oxygen and carbon dioxide efficiently.

2. **Pulmonary Contusion:** When the chest strikes a hard surface upon landing, it can result in pulmonary contusion, which is a bruising of the
lung tissue. This can lead to inflammation and impaired gas exchange, contributing to the development of ARDS.

3. **Fat Embolism:** In severe cases of trauma, such as from a fall from height, there is a risk of fat embolism syndrome. This occurs when fat
globules from broken bones or soft tissue enter the bloodstream and travel to the lungs, where they can cause inflammation and compromise lung
function, potentially leading to ARDS.

4. **Secondary Infections:** Following a traumatic injury like a fall from a building, there is a risk of developing secondary infections such as
pneumonia. These infections can further exacerbate lung inflammation and contribute to the development of ARDS.

In summary, falling from a building can cause severe chest trauma, lung contusions, fat embolism, and secondary infections, all of which can lead
to the development of ARDS due to the disruption of normal lung function and the inflammatory response triggered by these injuries.

A contusion at the level of C3, which refers to an injury to the cervical (neck) vertebra at the third level, wouldn't directly cause ARDS (Acute
Respiratory Distress Syndrome) as ARDS primarily involves damage to the lung tissue and impairment of gas exchange. However, a contusion at
the level of C3 could potentially lead to respiratory compromise, which, if severe and untreated, might contribute to the development of ARDS
through secondary mechanisms.

Here's how a C3 contusion could indirectly lead to ARDS:

1. **Spinal Cord Injury (SCI):** A contusion at the level of C3 could result in damage to the spinal cord. Depending on the severity of the injury, this
could lead to paralysis of the muscles involved in breathing, such as the diaphragm and intercostal muscles. Paralysis of these muscles can impair
the ability to breathe effectively, leading to respiratory insufficiency or failure.

2. **Ventilatory Failure:** If the respiratory muscles are paralyzed due to the spinal cord injury at C3, the individual may require mechanical
ventilation to support breathing. However, ventilatory support is not without risks, and complications such as ventilator-associated pneumonia or
barotrauma (lung injury due to mechanical ventilation) could occur, potentially leading to ARDS.

3. **Pulmonary Complications:** Individuals with spinal cord injuries are also at an increased risk of developing pulmonary complications such as
pneumonia or atelectasis (collapse of lung tissue), particularly if they are immobilized for extended periods. These complications can exacerbate
lung inflammation and contribute to the development of ARDS.

While a contusion at the level of C3 itself does not directly cause ARDS, it can lead to respiratory compromise and complications that may
ultimately contribute to the development of ARDS if not managed promptly and effectively.

ARDS, or Acute Respiratory Distress Syndrome, is a condition characterized by rapid onset of respiratory failure, severe hypoxemia (low oxygen
levels in the blood), and bilateral pulmonary infiltrates not due to heart failure. It can develop as a result of various direct or indirect insults to the
lungs.

Here's a brief overview of ARDS as described in "Harrison's Principles of Internal Medicine":

1. **Pathophysiology**: ARDS involves inflammation and increased permeability of the alveolar-capillary barrier, leading to leakage of protein-rich
fluid into the alveoli and impaired gas exchange. This results in widespread lung damage and decreased lung compliance.

2. **Etiology**: ARDS can be caused by direct lung injury (such as pneumonia, aspiration of gastric contents, inhalation injury) or indirect lung
injury (such as sepsis, trauma, pancreatitis, transfusion-related lung injury).

3. **Clinical Features**: Patients typically present with acute onset of dyspnea, tachypnea, and hypoxemia. The condition can rapidly progress to
respiratory failure requiring mechanical ventilation. Physical examination may reveal diffuse crackles on auscultation and signs of respiratory
distress.
4. **Diagnostic Evaluation**: Diagnosis is based on clinical presentation, characteristic radiographic findings (bilateral infiltrates on chest X-ray or
CT scan), and exclusion of other causes of respiratory failure. Arterial blood gas analysis typically shows severe hypoxemia with respiratory
alkalosis.

5. **Management**: Treatment involves supportive care with mechanical ventilation to maintain adequate oxygenation and ventilation. Lung-
protective ventilation strategies, such as low tidal volume ventilation, are essential to minimize further lung injury. Addressing the underlying cause
(if present) is also crucial. Other supportive measures may include prone positioning, neuromuscular blockade, and conservative fluid
management.

6. **Prognosis**: ARDS carries a high mortality rate, particularly in severe cases. Survivors may experience long-term pulmonary dysfunction and
impaired quality of life.

It's important to note that management strategies and recommendations for ARDS may evolve over time as new evidence emerges. Therefore,
consulting the most current medical literature and guidelines is essential for providing optimal care to patients with ARDS.