Step 2 CK · Internal Medicine · Pulmonology

Critical Care Respiratory Failure & ARDS

Name: Critical Care Respiratory Failure & ARDS
Creator: Veli Bakalov, MD

Sorting hypoxemic from hypercapnic failure, then mastering ARDS ventilation

Pulmonology·Critical Care & Respiratory Failure·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Type 1 (hypoxemic) failure = PaO2 under 60 with normal or low CO2; type 2 (hypercapnic) = PaCO2 over 45–50 from hypoventilation (won't breathe, can't breathe, or COPD dead space).
The A–a gradient (normal ~5–15, upper limit ≈ age/4 + 4) is elevated in V/Q mismatch, shunt, and diffusion limitation but normal in pure hypoventilation or low inspired O2.
Shunt (ARDS, pneumonia, edema, atelectasis) causes hypoxemia refractory to 100% O2; V/Q mismatch, the most common cause, corrects with oxygen.
Nasal cannula adds ~4% FiO2 per L/min (about 44% at 6 L), a Venturi mask gives a precise FiO2, a non-rebreather ~90%, and high-flow nasal cannula is favored for acute hypoxemic failure.
NIV is first-line for COPD with hypercapnic acidosis and for cardiogenic pulmonary edema; it is contraindicated with altered mentation, an unprotected airway, instability, vomiting, or facial trauma.
Berlin ARDS: onset within 1 week, bilateral opacities, not explained by cardiac failure or overload, P/F on PEEP ≥5: mild 200–300, moderate 100–200, severe ≤100.
Lung-protective ventilation (6 mL/kg predicted body weight, plateau under 30 cmH2O, permissive hypercapnia) lowered ARDS mortality from ~40% to ~31%.
Severe ARDS (P/F under 150): prone positioning ≥16 h/day lowers mortality (PROSEVA); use a conservative fluid strategy after shock, and VV-ECMO for refractory hypoxemia; sepsis is the most common cause.
Wean with a daily sedation holiday plus a spontaneous breathing trial; an RSBI (RR/Vt) under 105 predicts successful extubation.

Hypoxemic vs hypercapnic respiratory failure

Two types. Type 1 (hypoxemic) failure is a PaO2 <60 mmHg with a normal or low PaCO2. It is an oxygenation problem caused by V/Q mismatch, shunt, or diffusion limitation. Type 2 (hypercapnic) failure is a PaCO2 >45–50 mmHg from alveolar hypoventilation, which is a ventilation problem. Hypoventilation has three patterns:

"Won't breathe": CNS depression, opioids
"Can't breathe": neuromuscular or chest-wall disease
COPD: wasted dead-space ventilation

The A–a gradient. The alveolar–arterial gradient is normally about 5–15 mmHg and rises with age. A rough upper limit of normal is (age/4) + 4. The gradient is elevated when the lung itself is abnormal (V/Q mismatch, shunt, diffusion limitation). It is normal in pure hypoventilation and when inspired O2 is low, as at altitude.

Mechanisms of hypoxemia

Mechanism	A–a gradient	Corrects with 100% O2?	Examples
Hypoventilation	Normal	Yes (PaCO2 is high)	Opioid overdose, neuromuscular weakness
Low inspired O2	Normal	Yes	High altitude
V/Q mismatch (most common)	Elevated	Yes	COPD, asthma, pulmonary embolism
Right-to-left shunt	Elevated	No: refractory	ARDS, pneumonia, pulmonary edema, atelectasis
Diffusion limitation	Elevated	Yes	Interstitial lung disease

In a shunt, blood passes alveoli that are filled or collapsed and never meets the extra oxygen, so hypoxemia persists even on a 100% non-rebreather.

Oxygen delivery and noninvasive ventilation

Oxygen devices

Device	FiO2	Use
Nasal cannula	Adds ~4% per L/min, up to ~44% at 6 L	Mild hypoxemia
Venturi mask	Precise, fixed FiO2	When exact FiO2 matters, e.g., CO2 retainers
Non-rebreather	~90%	Short-term high-FiO2 rescue
High-flow nasal cannula	High FiO2, heated and humidified, with some PEEP	Favored in acute hypoxemic failure

Noninvasive ventilation (NIV). BiPAP or CPAP is first-line for two conditions, where it reduces both intubation and mortality:

COPD exacerbation with hypercapnic acidosis
Cardiogenic pulmonary edema

CPAP alone treats cardiogenic edema by recruiting alveoli and reducing preload and afterload. BiPAP adds inspiratory pressure support, which increases tidal volume to clear CO2 in COPD.

NIV is contraindicated with altered mental status or inability to protect the airway, hemodynamic instability, vomiting, or facial trauma. These patients need intubation.

Intubation and ventilator basics

When to intubate. Intubate and ventilate for failed or contraindicated NIV, inability to protect the airway (falling GCS), refractory hypoxemia, or progressive hypercapnia with acidosis. Rapid-sequence intubation pairs a sedative with a paralytic. Avoid succinylcholine with hyperkalemia or in the days after major burns or crush injury, because it can cause dangerous hyperkalemia.

PEEP. Positive end-expiratory pressure keeps alveoli open at end-expiration and recruits atelectatic lung. This raises PaO2 and allows a lower FiO2. Too much PEEP overdistends alveoli, lowers preload and cardiac output, and risks barotrauma.

Airway pressures. A high peak pressure with a normal plateau pressure means high airway resistance, such as bronchospasm, a mucus plug, or a kinked or bitten tube. When both peak and plateau pressures are high, compliance is low: ARDS, pneumothorax, mainstem intubation, or abdominal distension.

ARDS: definition and causes

Berlin definition. ARDS requires all four of the following:

Onset within 1 week of an insult or of new or worsening symptoms
Bilateral opacities not fully explained by effusion or collapse
Respiratory failure not fully explained by cardiac failure or fluid overload
Hypoxemia graded by PaO2/FiO2 measured on PEEP ≥5

Berlin dropped the old wedge-pressure cutoff. Instead, a cardiac cause is excluded clinically, often with an echocardiogram.

MildP/F 200–300.
ModerateP/F 100–200.
SevereP/F ≤100.

Pathophysiology. Diffuse alveolar damage makes the capillaries leaky and floods the alveoli with protein-rich fluid (noncardiogenic pulmonary edema), leaving hyaline membranes. The result is stiff lungs and a large shunt.

Causes. Sepsis is the most common trigger. Others are aspiration, pneumonia, pancreatitis, massive transfusion (including TRALI), and trauma. Treating the cause is essential, for example antibiotics and source control in sepsis.

Managing ARDS

6 mL/kgtidal volume, by predicted body weight

<30cmH2O plateau pressure

≥16 h/dayprone positioning when P/F <150

Lung-protective ventilation. The ARDSnet (ARMA) strategy uses a tidal volume of 6 mL/kg predicted body weight, keeps plateau pressure <30 cmH2O, and accepts permissive hypercapnia. It cut mortality from about 40% to about 31% and is the foundation of ARDS care. PEEP and FiO2 are titrated together to the oxygenation target.

Predicted body weight is calculated from height and sex, not actual weight, so a large patient still gets small tidal volumes.

Severe or refractory ARDS.

Prone positioning ≥16 h/day lowered mortality in severe ARDS with P/F <150 (PROSEVA).
Early neuromuscular blockade (cisatracurium) can improve ventilator synchrony and oxygenation. Later trials did not show a consistent mortality benefit.
Conservative (dry) fluid strategy once shock resolves: it increases ventilator-free days (FACTT).
Veno-venous ECMO is reserved for hypoxemia that stays refractory despite these measures.

Liberation from the ventilator

Spontaneous awakening trialStop sedation daily.
Spontaneous breathing trialMinimal support, such as low pressure support or a T-piece, for 30–120 minutes.
RSBI <105Rapid shallow breathing index = respiratory rate ÷ tidal volume (in liters). A value <105 predicts success.
ExtubateIf oxygenation is adequate on modest FiO2 and PEEP, hemodynamics are stable, and the patient can protect the airway and clear secretions.

Pairing daily sedation interruption with a daily breathing trial shortens ventilation. Rapid, shallow breathing during the trial (a high RSBI) signals likely extubation failure.