Airway & Respiratory Failure study guide previews.

An acute worsening of respiratory symptoms (dyspnea, cough, sputum) beyond baseline that requires a change in therapy. Baseline physiology is characterized by Chronic inflammation leading to fixed airflow obstruction, Loss of elastic recoil leading to air trapping, and increased airway resistance leading to prolonged expiration.

Exhalation of anatomical dead space (trachea, bronchi, oropharynx). Then inspiration resumes leading to waveform drops back to ~0 and cycle repeats. When there is airflow obstruction, the capnographic waveform takes on a characteristic slanted, triangular shape. Compared to normal include Phase 2 (mixed air) is no longer a sharp vertical rise, Phase 3 (alveolar plateau) slants upward instead of staying flat, and The whole expiratory portion looks like a shark fin.

It reflects include How well it diffuses into alveoli (lung perfusion) and How effectively it is exhaled (ventilation). You can measure EtCO₂ via include Nasal cannula (capnography prongs for non-intubated patients). Moves CO₂-laden blood from tissues leading to lungs. Washes CO₂ out of alveoli and out the airway. In a perfect world (normal physiology) include PvCO₂ / PaCO₂ ≈ EtCO₂ (with small 3-5 mmHg gradient). Normal ventilation (no hypoventilation, no huge dead space).

If any of these are abnormal, EtCO₂ and blood CO₂ can diverge Cardiac output leading to less CO₂ delivered to lungs leading to low EtCO₂, even if blood CO₂ is high, Lung perfusion (e.g., PE) leading to less CO₂ reaches alveoli leading to low EtCO₂, and Ventilation leading to CO₂ retained in blood leading to EtCO₂ may be lower than PaCO₂ and pattern gives diagnostic clues.

Low EtCO₂ (< ~10 mmHg) during CPR Persistently low EtCO₂ after prolonged, high-quality CPR is a poor prognostic sign for ROSC.

Unlike conventional nasal cannula systems, HFNC can deliver flow rates that meet or exceed a patient's inspiratory demand. The nasopharynx functions as an anatomic dead space reservoir. HFNC continuously flushes exhaled carbon dioxide from the upper airway. This mechanism is particularly important in patients with tachypnea and respiratory distress. Although HFNC is not a form of noninvasive ventilation, high flow rates generate a modest amount of positive end-expiratory pressure. Approximate effect include cm H₂O pressure for every 10 L/min of flow (with mouth closed) and Actual pressure varies substantially.

It is important to recognize that not all oxygen delivery devices are equivalent. Some primarily improve oxygenation, while others also provide ventilatory support. A useful way to think about respiratory support is Conventional Oxygen leading to High-Flow Oxygen leading to Noninvasive Ventilation leading to Mechanical Ventilation. Less effective in patients with significant respiratory distress. Stable patients requiring low levels of supplemental oxygen.

V/Q mismatch is one of the most important mechanisms of hypoxemia in emergency and critical care. Ventilation and perfusion are both present, but they are not matched well enough for efficient gas exchange. This guide explains why that mismatch lowers arterial oxygen content and why it remains one of the most common causes of low oxygen levels at the bedside.

The preview walks through normal V/Q relationships, regional differences from apex to base, low V/Q physiology, high V/Q physiology, and why supplemental oxygen usually improves V/Q mismatch. It also helps separate V/Q mismatch from pure hypoventilation and true shunt physiology.

Clinically, the guide is useful for thinking through pneumonia, COPD exacerbation, pulmonary embolism, atelectasis, pulmonary edema, and other common causes of hypoxemia. The emphasis is practical: identify the mechanism, predict oxygen response, and connect the physiology to bedside management.

Pneumonia Basics: Overview, Symptoms, Etiology, Diagnosis, Treatment, Prognosis introduces the clinical pattern, physiology, and bedside decisions that matter for emergency and critical care practice.

Pneumonia is an infection of the lung parenchyma, typically caused by bacteria, viruses, or fungi, resulting in inflammation and alveolar consolidation. Prevalence includes one of the most common infectious causes of hospitalization and death worldwide. Those with chronic diseases (e.g., COPD, heart failure, diabetes). Hospital-acquired pneumonia (HAP): Develops ≥48 hours after hospital admission. Ventilator-associated pneumonia (VAP): Occurs ≥48 hours after endotracheal intubation. Associated with contaminated water, high fever, GI symptoms.

Pulmonary shunt is a severe form of gas exchange failure where blood reaches lung units that receive little or no useful ventilation. In V/Q language, shunt is V/Q = 0. Blood moves through the pulmonary circulation without picking up oxygen, then mixes with oxygenated blood from healthier lung regions.

This guide explains why shunt physiology can cause profound hypoxemia and why supplemental oxygen may only partially correct it. Because oxygen cannot reach nonventilated alveoli, even high inspired oxygen cannot fully oxygenate the blood flowing through those units.

The clinical focus includes alveolar filling, atelectasis, pneumonia, ARDS, severe pulmonary edema, and other conditions where perfusion persists despite absent ventilation. The goal is to help clinicians recognize when low oxygen is not just an oxygen-delivery problem, but a lung-unit recruitment and shunt problem.

V/Q mismatch and pulmonary shunt are related causes of hypoxemia, but they are not the same. V/Q mismatch means ventilation and perfusion are both present but poorly matched. Pulmonary shunt means perfusion is present while ventilation is essentially absent.

The distinction matters because oxygen response differs. Low V/Q units often improve with supplemental oxygen because some ventilation still reaches the affected alveoli. True shunt responds poorly because oxygen cannot reach the nonventilated lung units that are still receiving blood flow.

This guide compares low V/Q, high V/Q, dead space, and shunt physiology in practical bedside language. It is built for clinicians trying to interpret hypoxemia, understand why a patient is not responding to oxygen as expected, and decide whether the problem is oxygen delivery, ventilation, recruitment, or perfusion.

Hemoptysis is coughing up blood from the lower respiratory tract, but the emergency is often not blood loss alone. In life-threatening hemoptysis, patients usually deteriorate because blood obstructs the airway, floods functional lung units, and causes worsening gas exchange.

This guide frames hemoptysis around the decisions that matter first: confirm true hemoptysis, assess severity, protect oxygenation, position the patient when the bleeding side is known, reverse major coagulopathy when appropriate, and involve bronchoscopy and interventional radiology early.

The preview also distinguishes small-volume hemoptysis from life-threatening hemoptysis, reviews common causes, and emphasizes why localization matters. The bedside goal is to prevent the nonbleeding lung from becoming contaminated while moving quickly toward definitive control of the source.

Pulmonary embolism (PE) is a potentially life-threatening condition caused by obstruction of the pulmonary arteries by thrombus. Risk stratification into low, intermediate, and high risk (also referred to as submassive and massive) guides management decisions. This guide summarizes the advanced management strategies based on risk category.

The severity of PE is determined by hemodynamic stability, right ventricular (RV) function, and biomarker elevation (troponin, BNP). RV dysfunction results from increased pulmonary vascular resistance leading to RV strain and potential right heart failure. Elevated biomarkers indicate myocardial injury. Together, these parameters form the basis of PE risk classification.

Anticoagulation alone (preferred agents are DOACs such as apixaban or rivaroxaban).• Outpatient treatment may be considered if patient has low PESI score, good support, and low bleeding risk.• Warfarin is less preferred; requires INR monitoring and bridging with heparin.

Pulmonary embolism (PE) is a blood clot in the pulmonary arteries that can be life‑threatening. This overview covers epidemiology, risk factors (Virchow’s triad), pathophysiology, clinical presentation, evaluation strategies (PERC, Wells, D‑dimer, CTA), core management, prognosis (PESI), and complications.

Common cardiovascular condition with substantial morbidity and mortality.• Public‑facing recognition is important due to potential severity and recurrence risk. Thrombus lodges in pulmonary arteries, blocking perfusion to lung parenchyma.• Consequences: lung tissue ischemia, ventilation‑perfusion (V/Q) mismatch, and strain on the right ventricle.

Virchow’s Triad: • Hypercoagulability (genetic or acquired states). • Venous stasis (immobility, hospitalization, prolonged travel). • Endothelial injury (surgery, trauma).• Most PEs arise from lower‑extremity or pelvic DVT.• Additional risks: recent surgery, cancer, pregnancy, older age, obesity, smoking, prior VTE, oral contraceptives.

Types 1 - 4 Respiratory Failure introduces the clinical pattern, physiology, and bedside decisions that matter for emergency and critical care practice.

We’re not just interpreting numbers-we’re interpreting how those numbers are generated. If you don’t know what’s measured vs calculated, you can misinterpret the entire gas.

These come from electrodes on the machine pH leading to measured via glass electrode, pCO₂ leading to measured via Severinghaus electrode, pO₂ (ABG only clinically useful) leading to measured via Clark electrode, and These are the true primary data.

Translation include If pH or pCO₂ is off leading to HCO₃⁻ is also off.

Core idea include Perfusion depends on whether blood pressure can overcome alveolar pressure. No blood flow leading to dead space ventilation. Key Pearl include Zone 1 = ventilated but NOT perfused and Zone 2 - Intermittent Flow (Waterfall Zone). Blood flows only when arterial pressure exceeds alveolar pressure.