Respiratory Critical Care
Mechanical ventilation, ARDS, severe asthma, COPD exacerbation, and acute respiratory failure.
Core Topics
15 topicsAcute Respiratory Distress Syndrome
Acute, diffuse inflammatory lung injury causing hypoxemia and bilateral infiltrates not fully explained by cardiac failure or fluid overload.
Respiratory Failure: Basic Principles
Core taxonomy (Types I–IV), alveolar gas exchange physiology, work-of-breathing mechanics, and escalation thresholds in acute respiratory failure.
Invasive Mechanical Ventilation
Complete clinical topic overview. For the full 10-level interactive course, visit Master MV. Covers core ventilator modes, respiratory mechanics (Cstat, Raw, driving pressure), waveform dyssynchrony analysis, VILI prevention, and liberation protocols.
Pneumothorax & Barotrauma in Critical Care
Tension physiology, point-of-care ultrasound diagnosis, needle/finger/tube thoracostomy, and management of bronchopleural fistulas on mechanical ventilation.
Hypoxemic Respiratory Failure
Pathophysiologic mechanisms (shunt vs V/Q mismatch), dynamic ROX index trajectories, P-SILI prevention, and evidence-based oxygen escalation ladders.
Hypercapnic Respiratory Failure
Mechanism-based diagnosis of acute and acute-on-chronic hypercapnia, controlled oxygen, NIV, invasive ventilation, auto-PEEP troubleshooting, neuromuscular monitoring, and post-acute planning.
COPD Exacerbation (Acute & Severe)
Pathophysiology of acute-on-chronic hypercapnia, controlled oxygen targets (88–92%), evidence-based NIV, and auto-PEEP matching mechanics.
Asthma (Severe & Near-Fatal Exacerbation)
Pathophysiology of dynamic hyperinflation, auto-PEEP hemodynamics, stepped acute pharmacotherapy, and ventilator mechanics in status asthmaticus.
Severe Community-Acquired Pneumonia (Severe CAP)
IDSA/ATS severe CAP criteria, rapid microbiology, targeted empiric antimicrobial regimens, and landmark adjunctive hydrocortisone evidence (CAPE COD).
Acute Pulmonary Embolism
Pulmonary vascular occlusion, acute RV pressure overload, ESC/AHA risk stratification, systemic thrombolysis, catheter-directed therapies, and hemodynamic support.
Interstitial Lung Disease (ILD) in the ICU
Acute exacerbation and decompensated ILD: differential diagnosis, HRCT patterns, oxygen/NIV/HFNC, ventilation strategy, immunosuppression limits, and transplant decisions.
Pneumonia Variants in the ICU
Pattern-based ICU pneumonia approach: severe CAP, HAP/VAP, aspiration, viral, necrotizing, immunocompromised and nonresolving pneumonia.
Life-Threatening Hemoptysis
Airway-first management of clinically significant hemoptysis with localization, bronchoscopy and bronchial artery embolization
Pleural Infection / Empyema
Diagnosis and source control of complicated parapneumonic effusion and empyema with drainage, tPA/DNase and surgical escalation
Bronchoscopy in the ICU
Safe diagnostic and therapeutic bronchoscopy in hypoxemic, mechanically ventilated and bleeding ICU patients
Clinical Problems & Bedside Triage
19 guidesSudden Hypoxemia
Bedside triage of acute desaturation: signal verification, immediate danger screening (DOPE / tension pneumothorax), oxygen escalation ladder, and mechanism-based differential.
Acute Hypercapnia & Ventilatory Failure
Triaging rising PaCO2: distinguishing acute uncompensated acidemia from chronic compensation, identifying central vs pump vs dead-space failure, and titrating noninvasive ventilation.
Sudden Ventilator Deterioration & High Airway Pressures
Algorithmic troubleshooting of acute patient-ventilator collapse: the DOPE framework, peak vs plateau pressure differentiation, auto-PEEP evaluation, and manual bagging separation.
Acute Severe Respiratory Distress
Bedside management of the gasping, tachypneic patient: work-of-breathing assessment, accessory muscle use, P-SILI prevention, and timely intubation vs noninvasive support.
New or Massive Hemoptysis
Airway preservation and bleeding localization: non-massive vs massive hemoptysis (> 100–200 mL/hr), lateral decubitus positioning, isolation of the bleeding lung, and endovascular/bronchoscopic intervention.
New Tachycardia & Tachyarrhythmias
Algorithmic triage of acute heart rates > 100–150 bpm: stability screen (immediate cardioversion if unstable), narrow vs wide QRS differentiation, Brugada VT rules, and sinus tachycardia etiology search.
Rapidly Progressive Weakness / Impending Ventilatory Failure
Bedside assessment and airway decision-making in rapidly ascending or fatiguable weakness risking ventilatory pump failure.
Severe Metabolic Alkalosis
Bedside evaluation of severe alkalemia (pH > 7.55, HCO3 > 35 mEq/L): assessing chloride responsiveness (urine chloride), diuretic-induced contraction alkalosis, nasogastric suction loss, hypokalemia, and acetazolamide/CRRT rescue.
Immunocompromised Patient with Fever + Organ Failure
Bedside diagnostic framing and emergency management of acute fever, sepsis, respiratory failure, or oncologic emergency in an immunocompromised host.
Critically Ill Pregnant or Postpartum Patient
Maternal-first stabilization with rapid differentiation of hypertensive, hemorrhagic, thromboembolic, septic, hepatic and cardiac obstetric emergencies.
Progressive Weakness with Impending Respiratory Failure
Use trajectory, bulbar function and respiratory mechanics to intubate before arrest and choose disease-specific therapy.
Acute Deterioration in Fibrotic ILD
Separate exacerbation from infection, edema, PE and pneumothorax; choose support according to recruitability and reversibility.
Deterioration After Central/Arterial Line Placement
Acute hypoxemia, hypotension, bleeding, arrhythmia, limb ischemia or line malfunction after vascular access.
Life-Threatening Hemoptysis — Bedside Problem
Airway-first management of clinically significant hemoptysis with localization, bronchoscopy and bronchial artery embolization
Pleural Infection / Empyema — Bedside Problem
Diagnosis and source control of complicated parapneumonic effusion and empyema with drainage, tPA/DNase and surgical escalation
Bronchoscopy in the ICU — Bedside Problem
Safe diagnostic and therapeutic bronchoscopy in hypoxemic, mechanically ventilated and bleeding ICU patients
Pneumonia Not Improving in the ICU
A progressive bedside problem for apparent pneumonia with persistent hypoxemia, fever or shock despite initial therapy.
High-Risk PE, Acute RV Failure & Obstructive Shock
Shock or peri-arrest physiology with suspected pulmonary embolism or acute RV failure requiring RV-protective resuscitation and immediate reperfusion planning.
Difficult Airway & Failed Intubation
Oxygenation-first rescue after difficult or failed intubation: optimized attempts, supraglottic rescue, deliberate wake-up decisions, and immediate front-of-neck access for CICO.
Physiology Modules & Waveforms
24 conceptsPlateau Pressure
During active inspiratory flow, airway pressure includes both the resistive pressure needed to drive gas through the airways and the elastic pressure needed to inflate the lung. Pausing flow removes the resistive component, leaving only elastic recoil — Pplat. A gap between peak pressure and Pplat therefore reflects resistance, while Pplat itself reflects compliance and how much lung is available to be inflated at the set tidal volume.
Driving Pressure
A fixed tidal volume set to a 'safe' 6 mL/kg predicted body weight can still overstress the lung if the aerated lung volume is small, because that volume is then distributed into a smaller functional space — the same tidal volume produces a larger driving pressure in a stiffer, more diseased lung. Driving pressure captures this in a single number, unlike tidal volume alone, which doesn't account for how much lung is actually available to be inflated.
Compliance
A compliant lung expands easily for a small pressure change; a stiff lung requires a large pressure change to achieve the same volume. In ARDS, inflammation, edema, and loss of aerated lung units reduce the number of alveoli available to receive a tidal volume, so the same breath is distributed into a smaller 'baby lung' — measured compliance falls even though the aerated units themselves may be relatively normal. Compliance is calculated from tidal volume divided by driving pressure (Vt / (Pplat − PEEP)) during a no-flow condition.
Resistance
Peak pressure reflects the pressure needed to overcome both airway resistance (to generate flow) and elastic recoil (to achieve volume); plateau pressure, measured during a brief no-flow pause, reflects elastic recoil alone. A widening gap between peak and plateau pressure at constant flow indicates rising resistance — from bronchospasm, secretions, a kinked or obstructed endotracheal tube, or a small-bore airway — rather than a change in lung or chest wall stiffness.
Auto-PEEP
Every exhalation needs enough time to let alveolar pressure equilibrate back to baseline. High respiratory rates, prolonged inspiratory times, and especially high airway resistance (bronchospasm, secretions, small endotracheal tubes) all shorten the effective time available to exhale or slow the rate of exhalation, so the next breath stacks on top of residual volume that hasn't left the lung. The result is progressively rising alveolar pressure and volume — breath stacking — that the ventilator's airway pressure gauge alone does not reveal, since it's normally measured at the mouth, not the alveolus.
Transpulmonary Pressure
Plateau pressure alone doesn't distinguish how much of the applied airway pressure is spent distending the lung versus moving a stiff chest wall or a distended abdomen. In a patient with a very compliant chest wall, a given Pplat corresponds to a higher transpulmonary pressure (more of it reaches the lung); in a patient with a stiff chest wall or high intra-abdominal pressure, the same Pplat corresponds to a lower transpulmonary pressure, because more of the applied pressure is absorbed by the chest wall itself. Estimating pleural pressure (commonly with an esophageal balloon) allows transpulmonary pressure to be calculated directly rather than inferred from Pplat alone.
Dead Space
Every breath must first fill the anatomic dead space before any of it reaches gas-exchanging alveoli, so a portion of each tidal volume is 'wasted' by design. Alveolar dead space increases pathologically when perfusion to ventilated units falls — from pulmonary embolism, hypovolemia, or overdistended alveoli compressing adjacent capillaries at high PEEP. The dead-space fraction (Vd/Vt) rises accordingly, and more minute ventilation is needed to clear the same amount of CO2.
Shunt
Because shunted blood bypasses ventilated alveoli, increasing FiO2 has a limited effect when the shunt fraction is large; oxygenation often plateaus compared with low-V/Q hypoxemia. Management therefore focuses on treating the cause and improving the proportion of perfusion reaching ventilated lung (for example recruitment/PEEP when recruitable, prone positioning in appropriate ARDS, secretion clearance, drainage of compressive processes, or selected pulmonary vasodilator rescue), while also optimizing hemoglobin, cardiac output, and systemic oxygen delivery.
Work of Breathing
Anything that raises resistance (bronchospasm, secretions, a narrow endotracheal tube) or lowers compliance (pulmonary edema, ARDS, a stiff chest wall) increases the pressure the muscles must generate for a given tidal volume, raising work of breathing. Auto-PEEP compounds this further by requiring the muscles to first overcome the trapped alveolar pressure before inspiratory flow can even begin. Sustained high work of breathing eventually outpaces respiratory muscle endurance, leading to fatigue and, if unaddressed, ventilatory failure.
Ventilation-Perfusion Mismatch
When alveoli are perfused but inadequately ventilated — filled with inflammatory exudate, as in ARDS, or collapsed, as in atelectasis — blood passes through without picking up oxygen, producing low-V/Q physiology. At the extreme, when ventilation is essentially zero, this becomes true shunt. Low-V/Q hypoxemia still improves somewhat with supplemental oxygen because some ventilation is still reaching the unit; true shunt does not improve, because the shunted blood never contacts a ventilated alveolus regardless of the inspired oxygen fraction.
Oxygen Delivery
Arterial oxygen content is dominated by hemoglobin-bound oxygen (1.34 mL O2/g Hb × Hb[g/dL] × SaO2[fraction]), with dissolved oxygen (0.003 mL O2/dL/mmHg × PaO2[mmHg]) contributing very little at normal atmospheric pressure. Because hemoglobin saturation dominates the equation, the clinically important drop in CaO2 only becomes steep once SaO2 falls below roughly 90% — the shoulder of the oxyhemoglobin dissociation curve. DO2 then scales linearly with cardiac output, so a fall in either CO or CaO2 alone can be compensated by a rise in the other, up to a point.
Cardiac Output
Because CO is a product of rate and volume, the body can maintain it in more than one way — a fall in stroke volume can be partly compensated by a rise in heart rate, which is why early compensated shock often presents with tachycardia and a preserved blood pressure before stroke volume failure becomes clinically obvious. Beyond a certain heart rate, however, shortened diastolic filling time reduces stroke volume enough that further tachycardia no longer helps, and can even reduce CO.
RV Failure Physiology
A sudden rise in pulmonary vascular resistance — from hypoxia, hypercapnia, acidosis, high intrathoracic pressure (high PEEP, auto-PEEP), or pulmonary embolism — can acutely overwhelm the RV's limited ability to generate pressure. As the RV dilates to compensate, it shifts the interventricular septum leftward (ventricular interdependence), impairing left ventricular filling and reducing left-sided cardiac output even though the primary problem is right-sided. This creates a self-reinforcing cycle: falling systemic pressure reduces RV coronary perfusion (which occurs throughout the cardiac cycle, not just diastole), further impairing RV function.
RV Failure: Afterload, Interdependence, and Treatment Pitfalls
The normal RV operates at low pressure (~25/5 mmHg) and fills easily at low end-diastolic pressures. When PVR rises acutely — from massive PE, severe ARDS, acute hypoxia, hypercapnia, or acidosis — RV wall stress increases. The RV initially compensates by dilating (Frank-Starling) to maintain stroke volume, but in the non-hypertrophied RV, dilation quickly becomes maladaptive. RV dilation causes leftward displacement of the interventricular septum (ventricular interdependence), mechanically compressing the LV cavity. LV end-diastolic volume falls despite adequate systemic venous filling, reducing LV stroke volume and MAP — a paradox where the LV appears 'underfilled' even though the problem is entirely right-sided. The RV is uniquely vulnerable to coronary ischaemia during failure: unlike the LV, the RV receives coronary perfusion throughout the entire cardiac cycle (both systole and diastole). As RV pressure rises and MAP falls, the aorta-to-RV pressure gradient narrows in both phases, critically reducing RV coronary perfusion. This creates a vicious cycle: ischaemia → worse contractility → more dilation → more septal shift → lower MAP → worse ischaemia.
Positive-Pressure Ventilation: Cardiovascular Effects
During spontaneous inspiration, intrathoracic pressure falls below atmospheric, increasing the pressure gradient from the peripheral venous system to the right atrium. This augments venous return and RV filling — the natural respiratory 'bellows' effect on circulation. The LV simultaneously faces increased transmural pressure (intracavitary pressure minus intrathoracic pressure) because pleural pressure is sub-atmospheric; this functionally increases LV afterload. Positive-pressure ventilation reverses these relationships. Raised intrathoracic pressure narrows the venous return gradient (mean systemic filling pressure minus right atrial pressure), reducing RV preload. If tidal volumes are large enough to cause lung overdistension, alveolar capillaries are compressed and PVR rises, increasing RV afterload further. The consequences are most severe in hypovolaemic or RV-failure patients who are already near the limit of their RV reserve. However, PPV simultaneously helps the left ventricle. Positive pleural pressure raises the external pressure on the LV, reducing transmural pressure for the same intracavitary pressure — the LV effectively 'works less' against a lower afterload. For patients with severe LV failure, PPV can be dramatically beneficial: reducing LV afterload increases stroke volume and reduces pulmonary oedema. This is why non-invasive ventilation in acute cardiogenic pulmonary oedema improves haemodynamics within minutes.
Auto-PEEP: Air Trapping and Cardiovascular Collapse
When expiratory time is insufficient — due to high respiratory rate, prolonged inspiratory time, obstructive physiology (asthma, COPD), or secretion plugging — lungs do not fully empty before the next breath begins. Each successive breath adds residual volume, progressively increasing end-expiratory lung volume and intrinsic PEEP. The cardiovascular consequence follows directly from the physiology of venous return: venous blood flows from the peripheral venous system (mean systemic filling pressure, ~7 mmHg) to the right atrium (right atrial pressure). Anything that raises right atrial pressure narrows or eliminates this gradient. Elevated intrathoracic pressure from dynamic hyperinflation raises right atrial pressure — and if the raise is severe enough, the venous return gradient collapses. Right atrial filling falls, RV stroke volume falls, and ultimately cardiac output and MAP drop precipitously. This mechanism is separate from and additive to any hypoxic or hypercapnic effect on the pulmonary vasculature. In severe status asthmaticus or obstructive COPD exacerbations requiring mechanical ventilation, this cardiovascular collapse can be immediate and life-threatening — clinicians must recognise it rapidly.
ARDS: Alveolar-Capillary Permeability, Shunt, and PEEP Mechanics
The hallmark of ARDS is disruption of both the microvascular endothelium and the alveolar epithelium by direct (pneumonia, aspiration) or indirect (sepsis, pancreatitis, trauma) insults. Activated neutrophils and alveolar macrophages release proteases, reactive oxygen species, and pro-inflammatory cytokines (IL-1, IL-6, TNF-alpha), degrading the alveolar-capillary membrane. Protein-rich fluid floods the alveoli, inactivating pulmonary surfactant and causing widespread microatelectasis. This creates a massive intrapulmonary right-to-left shunt (perfusion without ventilation), meaning deoxygenated mixed venous blood traverses non-aerated alveolar capillary beds unchanged. Applying Positive End-Expiratory Pressure (PEEP) counteracts cyclic end-expiratory alveolar collapse (atelectrauma), recruits instable alveoli, increases functional residual capacity (FRC), and decreases intrapulmonary shunt, improving PaO2 while distributing tidal volume more homogeneously across the aerated 'baby lung'.
Obstructive Shock: Massive Pulmonary Embolism & Acute Cor Pulmonale
The normal right ventricle is a thin-walled, compliant volume pump unaccustomed to acute pressure overloads. When acute mechanical obstruction and neurohumoral vasoconstrictors (thromboxane A2, serotonin) double or triple pulmonary vascular resistance, RV systolic pressure cannot exceed 50–60 mmHg. The RV acutely dilates and its wall tension spikes (Laplace's Law), dramatically increasing RV myocardial oxygen consumption while compressing right coronary artery capillary perfusion in the wall. As the RV dilates within the non-compliant pericardial sac, ventricular interdependence causes the interventricular septum to shift leftward ('D-shaped LV'), restricting left ventricular diastolic filling. LV stroke volume collapses, MAP plummets, and systemic hypotension extinguishes aortic root driving pressure to the right coronary artery, completing a fatal ischemic spiral.
Oxygen Delivery (DO2): The 3 Pillars & Failure Modes
Arterial oxygen content (CaO2) is determined overwhelmingly by hemoglobin-bound oxygen; dissolved oxygen in plasma (0.003 × PaO2) contributes less than 2% of total content under normobaric conditions. Oxygen Delivery can fail through three distinct physiological mechanisms: 1. Flow Failure (Cardiogenic/Hypovolemic Shock): Cardiac output collapses, but hemoglobin and arterial oxygen saturation are normal. (Treated with inotropes, vasopressors, or fluids). 2. Anemic Failure (Severe Hemorrhage / Critical Anemia): Hemoglobin drops below critical thresholds, halving CaO2 despite hyperdynamic cardiac output. (Treated with red blood cell transfusion). 3. Hypoxic Failure (Severe ARDS / Shunt / Hypoventilation): SaO2 plummets due to severe alveolar gas exchange impairment, desaturating available hemoglobin. (Treated with PEEP, recruitment, FiO2, prone positioning). When DO2 drops below the critical oxygen delivery threshold (DO2crit), tissue oxygen consumption (VO2) becomes supply-dependent, forcing cells into anaerobic glycolysis with lactate generation and cellular death.
RV-PA Coupling & Acute Afterload Mismatch
The right ventricle is thin-walled, compliant, and adapted to low afterload (PVR is ~1/10th of SVR). In acute massive PE, ARDS, or high-PEEP ventilation, sudden afterload spikes uncouple the RV from the pulmonary artery (Ees/Ea < 0.8). The RV dilates acutely to preserve stroke volume via heterometric autoregulation. However, excessive dilation increases RV wall stress, shifts the interventricular septum leftward (D-sign), compresses the LV, and impairs LV filling. Critically, the right coronary artery (RCA) supplies the RV during both systole and diastole under normal conditions because aortic root pressure far exceeds RV intracavitary pressure. When RV cavity pressure rises and systemic aortic MAP drops, RV coronary perfusion pressure (MAP - RVSP) collapses, inducing RV ischemia and precipitating acute circulatory arrest.
Peak vs Plateau Airway Pressure Differentiation
By the Equation of Motion: Pvent = Flow × Raw + (Vt / Crs) + PEEP. When flow drops to zero during an inspiratory hold, the resistive component (Flow × Raw) disappears, isolating the static elastic pressure (Pplat = Vt / Crs + PEEP). - If Ppeak is high but Pplat is normal (elevated transairway pressure gradient, Ppeak - Pplat > 5–10 cmH2O): the problem is elevated airway resistance (bronchospasm, secretions, endotracheal tube obstruction, biting, kinking). - If both Ppeak and Pplat are elevated (Ppeak - Pplat gradient normal): the problem is reduced respiratory system compliance (ARDS, pulmonary edema, tension pneumothorax, abdominal compartment syndrome, severe chest wall stiffness).
Driving Pressure & Respiratory System Compliance
In ARDS, the lung is not stiff throughout; rather, it is functionally small ('baby lung') due to dependent alveolar collapse and flooding. Normalizing tidal volume to predicted body weight (PBW) does not account for the fraction of aerated lung remaining. Driving pressure indexes tidal volume to actual functional lung size (compliance). Amato et al. (NEJM 2015) demonstrated that changes in driving pressure—rather than tidal volume or PEEP in isolation—strongly predict mortality in ARDS. Reductions in ΔP (achieved by lowering Vt or finding optimal PEEP that recruits alveoli and improves compliance) reduce cyclic alveolar strain and prevent ventilator-induced lung injury (VILI).
V/Q Mismatch vs Shunt vs Dead Space Mechanics
In low V/Q mismatch (e.g. COPD, asthma, mild atelectasis), alveoli receive some ventilation; increasing inspired FiO2 usually improves arterial oxygenation, although the degree of correction depends on the severity and heterogeneity of the V/Q mismatch. In true intrapulmonary shunt (V/Q = 0, e.g. severe ARDS alveolar flooding, complete lobar atelectasis, pulmonary arteriovenous malformations), mixed venous blood traverses non-ventilated lung units without any gas exchange. Increasing FiO2 does not directly oxygenate blood traversing completely non-ventilated units, so a large shunt responds poorly to oxygen alone. Overall arterial oxygenation can still improve through ventilated lung units; treatment focuses on the cause and, when appropriate, recruitment strategies such as PEEP and prone positioning. In dead space (V/Q = ∞, e.g. pulmonary embolism, microvascular thrombosis, alveolar overdistension by excessive PEEP), ventilated gas never encounters perfusion. Ventilation to nonperfused units is wasted and can increase ventilatory requirements; PaCO2 rises when total effective alveolar ventilation cannot compensate, and the ventilatory ratio may increase.
Dynamic Hyperinflation & Auto-PEEP Control Mechanics
In acute severe asthma and COPD, airway narrowing and loss of elastic recoil drastically slow expiratory flow. If a new ventilator breath is delivered before the expiratory flow curve returns to zero, gas is trapped. Alveolar volume expands until higher elastic recoil pressures force air out through narrowed airways. Auto-PEEP increases mean intrathoracic pressure, compresses the vena cava, and drops venous return, precipitating profound hypotension and cardiac arrest upon intubation. Additionally, hyperinflated lungs operate on the flat, non-compliant upper portion of the pressure-volume curve, increasing work of breathing and risk of tension pneumothorax.
Clinical Reasoning Cases
15 casesSevere ARDS Ventilator Strategy
Lung-protective ventilation, prone positioning, PEEP, and selective neuromuscular blockade
Status Asthmaticus in the ICU
Refractory bronchospasm, impending ventilatory failure, and prevention of dynamic hyperinflation
High-Risk Pulmonary Embolism with Obstructive Shock
RV perfusion support, rapid reperfusion selection, and high-risk airway management
Sudden Ventilator Deterioration
Rapid DOPE-style troubleshooting of acute hypoxemia, high airway pressure and shock
Acute RV Failure After Intubation
Post-positive-pressure collapse in severe pulmonary arterial hypertension
Auto-PEEP & Dynamic Hyperinflation Shock
Post-intubation obstructive shock from severe gas trapping
Ventilator-Associated Pneumonia Due to DTR Pseudomonas
Susceptibility-directed treatment with newer antipseudomonal beta-lactams
Tension Pneumothorax on Mechanical Ventilation
Recognition, emergency decompression, definitive drainage, and persistent air-leak management
Acquired Methemoglobinemia
Recognition, co-oximetry confirmation, methylene blue safety, and rescue therapy
Abdominal Compartment Syndrome
Standardized IAP measurement and stepwise decompression of overt ACS
ARDS: Driving Pressure
Using respiratory-system mechanics without turning one marker into a rigid target
Refractory ARDS with Acute Cor Pulmonale
RV-protective rescue in severe ARDS with hypoxemia and right-ventricular failure
Severe Metabolic Acidosis & Peri-Intubation Collapse
Physiologically difficult airway management when compensatory ventilation is life-sustaining