Everything she covered, taught rather than listed.

1.1 The Normal Gas Exchange Unit

She opens the entire module here, and she opens it by walking the blood through. Deoxygenated blood arrives from the right heart through the pulmonary artery and enters the pulmonary capillary that wraps the alveolus. At the capillary, carbon dioxide leaves the blood and enters the alveolus to be exhaled, and oxygen leaves the alveolus and enters the blood. Newly oxygenated blood returns to the left heart through the pulmonary vein.

The thin white space between the alveolus and the capillary is the alveolar-capillary membrane. Every respiratory problem in this module is, at bottom, a problem with that membrane or with what is on either side of it: fluid in the alveolus, a clot in the capillary, a membrane that has grown too thick, or a set of alveoli that have collapsed.

1.2 Oxygenation Is Blood Flow; Ventilation Is Airflow

This is her organizing frame for the whole module, and it is worth more than it looks. Oxygenation is the process of delivering oxygen to the body's tissues — think of it as blood flow. Ventilation is the process of moving air in and out of the lungs — think of it as airflow.

1.3 SaO2 and PaO2 — Two Different Measurements

The curve only makes sense once these two are separate in your head, and she takes real time to separate them.

• Oxygen saturation (SaO2 / SpO2) — the amount of oxygen bound to hemoglobin and being carried to the tissues. This is what the pulse oximeter on the finger reads. It is a percentage.
• Partial pressure of oxygen (PaO2) — the oxygen not bound to hemoglobin, dissolved and available in the plasma. It tells you how much oxygen is actually available for binding. Normal 80–100 mm Hg.

She adds a point the slide leaves out: PaO2 can only be measured with an arterial blood gas. A pulse oximeter cannot give it to you. That is why the diagnostic workup for respiratory failure always includes ABGs and not just continuous pulse oximetry — the oximeter tells you about the hemoglobin, the ABG tells you about the blood.

Each hemoglobin molecule has four binding sites for oxygen. Her arithmetic, spoken and not on the slide: if three of the four sites are occupied, that hemoglobin is 75% saturated. Saturation is simply the fraction of available sites that are filled, averaged across all the hemoglobin in the sample.

1.4 Cooperativity and Affinity

Cooperativity is the reason the curve is S-shaped rather than straight. When one oxygen molecule binds to a hemoglobin, the molecule changes shape slightly and the remaining sites become easier to fill. More oxygen is attracted and wants to bind. Her image for it: think of the additional oxygen molecules as followers — one binds and the others want to follow.

Affinity is the word for how tightly hemoglobin holds oxygen. High affinity means hemoglobin grabs oxygen readily and is reluctant to let go. Low affinity means it binds less eagerly and releases more easily. Every shift in the curve is a change in affinity, and every consequence follows from whether the change makes loading or unloading easier.

1.5 Left Shift and Right Shift

Hold one idea steady and the rest follows: the shift is named for which way the curve moves, and what matters clinically is what happens at the tissues.

• Left shift — hemoglobin has increased affinity for oxygen. It binds oxygen more avidly, so unloading at the tissue is harder. Less oxygen is released for use. Loading in the lung is easy; delivery is the problem.
• Right shift — hemoglobin has decreased affinity for oxygen. It holds oxygen more loosely, so unloading is easier and more oxygen becomes available to the tissues.

She also points students to a video she uploaded to the Canvas module site for this curve, saying it can be confusing. If the shift logic does not settle from the slide alone, that video is her own recommended route.

1.6 What Causes a Shift

Her slide gives four factors for the right shift and then says the left shift is a decrease in all of the same four. That symmetry is the efficient way to learn it — memorize one column and invert.

2,3-DPG is a molecule inside the red blood cell that regulates how readily hemoglobin releases oxygen to the tissues. Her definition is the one to use: it does not carry oxygen, it governs the handoff.

2.1 What Acute Respiratory Failure Is

Acute respiratory failure occurs when oxygenation, ventilation, or both are inadequate. Not enough oxygen is transferred into the blood, or not enough CO2 is removed from the lungs, or both at once.

Two definitions carry the rest of the unit:

• Hypoxemia — a decrease in arterial oxygen: a fall in PaO2 and in SaO2. It results from conditions that interfere with the diffusion of oxygen.
• Hypercapnia — an increase in arterial CO2 (PaCO2). It results from insufficient CO2 removal.

She stops on these two words and says outright that these are two definitions to know, because they are what the two classifications of respiratory failure are named after. Get the vocabulary exactly right before going further — hypoxemia and hypoxia are different words for different things (§2.9), and hypercapnia is a synonym for neither.

2.2 The Two Classifications

Her classification slide is the single most testable slide in deck one, because everything downstream sorts into these two columns. Learn the numbers first — the numbers are the definitions.

Each type further divides into acute and chronic. Her flowchart slide is that whole structure on one page, and it is worth reproducing from memory.

2.3 Acute, Chronic, and Acute-on-Chronic

Chronic respiratory failure develops over days to weeks. The patient is usually more stable, because time has let the body compensate for small, subtle changes. It is usually not immediately life-threatening. The classic example is COPD — a patient who has lived with chronic respiratory failure for years, managed with medications.

Acute failure, by contrast, develops over minutes to hours or a day or two, and the compensation has not had time to build. The chapter adds the clinical texture her slides do not: in acute failure expect hemodynamic instability (tachycardia, hypotension), increased respiratory effort, and a decreased level of consciousness, and expect that urgent intervention is needed.

2.4 Hypoxemic Mechanism 1 — V/Q Mismatch

Four mechanisms can cause hypoxemic respiratory failure. She teaches them in order and the order is worth keeping: V/Q mismatch, shunt, diffusion impairment, alveolar hypoventilation.

In normal lungs the amount of blood perfusing the lungs and the amount of gas reaching the alveoli are almost identical. Her regional detail, which is on the slide and is examable: the base of the lungs has less ventilation than perfusion, and the apex has more ventilation than perfusion. Those two regional imbalances offset each other, so the net effect across the whole lung is close to a match.

A mismatch happens when one side of that pairing is disturbed. Her causes: increased secretions in the alveoli or the airways, or bronchospasm — so COPD, pneumonia, and asthma. She then splits the concept into its two directions using the picture:

• A ventilation problem. Something fills or blocks the alveolus — pus, blood, fluid, or a mucus plug. Perfusion through the capillary underneath is still fine, but the gas exchange cannot happen because the air side is blocked.
• A perfusion problem. The alveolus is normal and ventilating well, but a clot in the capillary — a pulmonary embolism — prevents blood from reaching it. Gas exchange happens for whatever blood arrives, but not enough blood arrives.

Treatment of V/Q mismatch: treat the cause. If it is a pulmonary embolism, treat the embolism; if it is secretions from pneumonia, treat the pneumonia. Add oxygen therapy, frequent ABGs, and continuous assessment of the patient's status including pulse oximetry.

2.5 Hypoxemic Mechanism 2 — Shunt

A shunt occurs when blood exits the heart without participating in gas exchange. The blood bypasses the exchange process entirely. There are two types.

Treatment: oxygen therapy alone is not effective at increasing PaO2 when the hypoxemia is due to shunt. These patients often need mechanical ventilation with a high FiO2.

2.6 Hypoxemic Mechanism 3 — Diffusion Impairment

Gas exchange is impaired by any process that damages the alveolar membrane or affects blood flow through the capillaries. Two routes to it:

• The membrane thickens. Pulmonary fibrosis, ARDS, and interstitial lung disease make the alveolar-capillary membrane thicker and fibrotic, which slows gas transport.
• The alveolus fills. Pulmonary edema — accumulation of fluid, white blood cells, or protein in the alveoli — decreases gas exchange.

The classic sign is hypoxemia that worsens with activity and is better with rest. Her explanation of why is the part the slide leaves out, and it is the part that makes the sign answerable in any wording.

2.7 Hypoxemic Mechanism 4 — Alveolar Hypoventilation

Alveolar hypoventilation is a decrease in ventilation that increases the PaCO2. Her causes: CNS problems, chest wall dysfunction, acute asthma, and restrictive lung disease.

This is mainly a mechanism of hypercapnic failure — it is the one item that appears on both lists — but it contributes to hypoxemia as well, which is why it sits fourth on the hypoxemic list.

2.8 The Mechanisms Rarely Act Alone

Her slide ends the four mechanisms with one line: it is rare that respiratory failure is caused by a single mechanism. She then works a full example that the slide does not contain.

2.9 From Hypoxemia to Hypoxia

Hypoxemia can lead to hypoxia, and the two words are not interchangeable.

When hypoxia becomes severe, cells shift from aerobic to anaerobic metabolism. That shift produces lactic acid, which is harder to remove from the body than CO2 because it must be buffered with sodium bicarbonate. If the body runs out of bicarbonate buffer, metabolic acidosis develops, and left uncorrected it causes cell dysfunction and cell death.

2.10 The Four Causes of Hypercapnic Failure

Hypercapnic failure — ventilatory failure — means the respiratory system cannot maintain a normal CO2 level, either from increased CO2 production or from decreased alveolar ventilation. Her slide gives four categories of cause. This is the mirror of the four hypoxemic mechanisms and should be learned as a matched pair with them.

Work of breathing (WOB) is the effort the respiratory muscles must make to inhale air into the lungs. In category 4 it is the whole story: the patient has to push air against increased resistance and against air already trapped in the alveoli, the muscles fatigue, and ventilatory failure follows.

She explains air trapping in a way the slide does not. Normally exhalation empties the lungs; in air trapping some air is left behind after each breath. That makes the next breath harder to take deeply, and over time the lungs become overinflated, which further limits ventilation.

2.11 Why the Body Tolerates CO2 Better Than Low Oxygen

Her slide ends the hypercapnia section with a comparison that explains a great deal of COPD management: the body will tolerate increased CO2 better than decreased oxygen.

3.1 What Determines the Clinical Picture

Her slide gives three variables, and they explain why two patients with identical ABGs can look completely different. The signs of respiratory failure are related to:

• the extent of the change in PaO2 and PaCO2,
• the speed of that change, and
• the patient's ability to compensate for it.

When compensatory mechanisms fail, respiratory failure occurs. Everything you assess is really an assessment of where the patient is on that compensation curve.

3.2 Mental Status Changes Come First

One of the first signs of hypoxemic acute respiratory failure is a change in mental status. Restlessness, confusion, and agitation suggest inadequate oxygen delivery to the brain.

3.3 Hypoxemia and Hypercapnia — Manifestations Side by Side

Her slide separates the two lists, and side by side is the way to hold them. Notice that the mental-status column is shared but arrives by different routes.

Her one-line rule for the hypercapnic column: a morning headache and a low respiratory rate with a decreased level of consciousness may indicate problems with CO2 removal. That triad is the signature of a patient retaining CO2 overnight.

She explains pursed-lip breathing beyond the slide, which lists only the words. Patients with COPD do it because it slows the respiratory rate, increases the time available for expiration, and prevents the smaller bronchioles from collapsing. It is a self-taught form of positive expiratory pressure, and the reason it raises saturation is that a longer expiration empties trapped air.

3.4 Reading the Patient — Position and Speech

Her slide turns assessment into three quick observations that cost nothing and grade severity before any equipment is involved.

3.5 Diagnostic Studies

Her list, with what each one is actually for:

3.6 Nursing Management by Severity

She adds a practical layer: respiratory therapy manages the ventilators at most sites, so nursing's job is to notice change and communicate it. Her instruction is to remain alert to subtle changes and communicate effectively with the care team — the provider and the respiratory therapist both.

3.7 Patient Goals and Prevention

Her five patient goals, which double as the evaluation criteria:

• Independently maintain a patent airway.
• Absence of dyspnea, or recovery to the baseline breathing pattern.
• Effective cough, able to clear secretions.
• Normal ABG values, or values within the patient's own baseline.
• Breath sounds within the patient's baseline.

Notice that three of the five are written as within the patient's baseline rather than as normal values. For a COPD patient a "normal" ABG is neither achievable nor the target.

Prevention is where nursing has the most leverage. Her targets are atelectasis, pneumonia, and the complications of immobility, and her interventions are deep breathing, incentive spirometry, and early ambulation, plus optimizing hydration and nutrition. Her at-risk examples: the elderly patient sitting in bed most of the day, and the postoperative patient who is neither breathing deeply nor walking.

3.8 Oxygen Therapy — Goal and the Lowest Effective Dose

The goal of oxygen therapy is to correct hypoxemia. The rule that governs how you do it: administer oxygen at the lowest possible FiO2 that achieves an acceptable saturation.

FiO2 is the fraction of inspired oxygen — the percentage of the air the patient is breathing that is oxygen. Her reference point: a normally breathing person on room air is at about 21% FiO2.

Monitor the response through mental status, ABGs, and respiratory rate. The chapter adds the interpretive rule: a trend toward a normal PaO2 tells you the patient is responding to oxygen.

3.9 Complications of Prolonged High-Concentration Oxygen

Oxygen is a drug, and her slide treats it as one. Three mechanisms to be able to explain, not just name:

Oxygen toxicity

High oxygen levels generate oxygen free radicals, which cause inflammation and cell death by disrupting the alveolar-capillary membrane. She adds the downstream consequence: this produces pulmonary edema and hypoxemia — the treatment starts causing the disease.

Absorption atelectasis

Alveoli normally contain oxygen, CO2, and nitrogen. Nitrogen is inert — it does not get absorbed, and its bulk is what holds the alveolus open. When a patient breathes very high concentrations of oxygen, oxygen replaces the nitrogen in the alveolus. The oxygen is then absorbed into the blood, and with no nitrogen left to hold the shape, the alveolus collapses. That collapse worsens the hypoxemia you were treating.

The other effects of prolonged exposure

• Increased pulmonary capillary permeability.
• Decreased surfactant production, and surfactant inactivation.
• Fibrotic changes in the alveoli.

She defines surfactant here rather than waiting for ARDS: it is a lubricating substance in the alveoli that lets them open and close smoothly. Losing it stiffens the lung. That definition carries straight into Unit 4.

3.10 COPD and the Oxygen Target

This is her most fully developed clinical teaching point in the ARF section, and the numbers are examable in both directions.

The reason is CO2 narcosis. Chronic hypercapnia blunts the response of the chemoreceptors to high CO2 as a respiratory stimulant. Give a chronic retainer a lot of supplemental oxygen and the drive to breathe falls further, so CO2 accumulates beyond even their usual baseline, and respiratory failure follows.

3.11 Mobilizing Secretions

Retained secretions can worsen or cause acute respiratory failure, because they limit the movement of oxygen into the alveoli and the removal of CO2. Her methods:

• Proper positioning — position the patient with ARF upright, with the head of the bed elevated at least 30 degrees.
• Effective coughing.
• Chest physiotherapy. She describes what she has seen: the respiratory therapist percusses areas of the chest, or applies a vest that vibrates to break secretions loose.
• Suctioning — covered in detail with the ventilated patient.
• Humidification, which makes secretions less thick and easier to remove.
• Hydration.
• Early ambulation when possible, which opens the lungs and helps the patient cough secretions up.

3.12 Drug Therapy

Her four goals of drug therapy: reduce airway inflammation and bronchospasm, relieve pulmonary congestion, treat infection, and reduce anxiety, pain, and restlessness.

Her last item is nutrition therapy. Nutrition depletion causes loss of muscle mass — and that includes the respiratory muscles, which delays recovery. This same reasoning reappears in §10.4 as a reason ventilated patients are fed early.

4.1 What ARDS Is

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. Go back to the gas exchange unit in §1.1: the membrane between alveolus and capillary starts leaking, so fluid crosses into the alveolar space, and gas exchange fails.

The most common cause is sepsis. Another cause is multisystem organ dysfunction syndrome (MODS).

4.2 Phase 1 — The Injury or Exudative Phase

Three phases, and she says outright that the three phases are something to know. Learn each one by its timing and its defining process.

What happens, in her order:

• Engorgement of the peribronchial and perivascular interstitial space produces interstitial edema.
• Fluid crosses into the alveolar space. As the alveoli fill, V/Q mismatch and shunt both develop — the same two mechanisms from §2.4 and §2.5, now occurring together.
• The membrane damage is thought to come from stimulation of the inflammatory and immune systems, which draws neutrophils into the pulmonary interstitium.
• The neutrophils release biochemical, humoral, and cellular mediators, which increase pulmonary capillary permeability, destroy collagen, form pulmonary microemboli, and cause pulmonary artery vasoconstriction.
• Respiratory rate rises and tidal volume falls.
• Cardiac output increases in response to the hypoxemia, as the body tries to raise pulmonary blood flow.
• Eventually compensation fails, and hypoventilation, decreased cardiac output, and decreased tissue oxygen perfusion occur.

4.3 Surfactant, Atelectasis, and the Hyaline Membrane

This is the chain that turns a leaky membrane into a stiff lung, and it is the highest-value mechanism in the unit because so many later facts hang off it.

• Alveolar type I and type II cells make surfactant. Surfactant maintains alveolar stability and prevents alveolar collapse.
• In ARDS these cells are damaged, so surfactant production falls and existing surfactant is inactivated — surfactant dysfunction.
• Without surfactant the alveoli become unstable and collapse — atelectasis.
• Widespread atelectasis decreases lung compliance, compromises gas exchange, and contributes to hypoxemia.
• A hyaline membrane — made of necrotic cells, protein, and fibrin — forms and thickens on the inside of the alveolus, further impairing gas exchange and lung compliance.
• The patient must generate higher airway pressures to inflate the stiff lungs, so the work of breathing rises — and at that point mechanical ventilation is needed.

4.4 Refractory Hypoxemia — the Hallmark

Refractory hypoxemia is the classic sign and the hallmark of ARDS: despite higher and higher oxygen concentrations, the patient's condition may still get worse.

4.5 Phase 2 — The Proliferative Phase

• The inflammatory response is still going.
• There is damage to the pulmonary vasculature, and lung compliance continues to fall because of interstitial fibrosis.
• Hypoxemia continues because of the thickened alveolar membrane — producing V/Q mismatch, diffusion limitation, and shunting all at once.
• The phase ends when dense, fibrous tissue replaces the diseased lung.
• If this phase stops, the lesions often resolve. That is the good outcome.

4.6 Phase 3 — The Fibrotic Phase

• Lung remodeling occurs: diffuse scarring, interstitial fibrosis, and alveolar duct fibrosis.
• All of that decreases lung compliance.
• The surface area available for gas exchange is reduced, so hypoxemia continues.

4.7 The Three Phases Side by Side

4.8 Clinical Progression and the Chest X-Ray

ARDS is dangerous partly because it starts quietly.

That 72-hour film is the one she calls the "whiteout." Her explanation of the term is the useful part: on a normal chest x-ray the air-filled spaces read black. In ARDS those spaces fill with fluid and consolidated infiltrate, so they turn white — widespread, throughout the lung, where there should be black.

She also flags the long view: patients with ARDS may need several weeks of mechanical ventilation, which is why she raises advance directives here and tells you to talk with patients and families about their wishes before a crisis.

4.9 The P/F Ratio

The PaO2/FiO2 ratio — the P/F ratio — evaluates the severity of hypoxemia. It is the patient's PaO2 divided by the FiO2 they are receiving, with FiO2 expressed as a decimal.

The P/F ratio returns in §10.9 as a weaning criterion. She makes that link herself in the ventilator lecture, telling students to remember the ARDS ratios when they see PaO2/FiO2 >300 on the readiness-to-wean list.

4.10 Complications of ARDS

She explains CRRT in the ARDS lecture rather than waiting: continuous renal replacement therapy is a slower form of dialysis run over 24 hours, pulling toxins out of the blood and returning it. The chapter adds why the slow version is used: ARDS patients are often hemodynamically unstable, may be on vasopressors, and cannot tolerate the large fluid shifts of conventional hemodialysis.

4.11 Nursing Management — the Seven Best Practices

The overall goal is a PaO2 of 60 mm Hg or higher and adequate lung ventilation to help with acid-base balance. Her slide then lists seven best practices, numbered, and the list is worth memorizing as a list.

Low tidal volume ventilation

4 to 8 mL/kg. Her reasoning: delivering a large volume into stiff lungs causes volutrauma or barotrauma, damaging the alveoli. A stiff lung cannot accept a normal breath without being injured by it.

Permissive hypercapnia

Permissive hypercapnia is the PaCO2 slowly rising above normal limits as a result of delivering a lower than normal tidal volume. It is a consequence of the low-volume strategy, not a goal in itself — you accept the rising CO2 as the price of not injuring the lung.

PEEP

Positive end-expiratory pressure increases the volume of air left in the lungs at the end of a normal expiration, which helps open collapsed alveoli and may let you lower the FiO2. Patients with ARDS may need higher levels of PEEP — and her reason is the surfactant chain from §4.3: if the surfactant that normally holds alveoli open is gone, external pressure has to do that job instead. Full treatment of PEEP is in §9.14.

Prone positioning

Turning the patient onto the stomach, which may help with lung expansion. The chapter gives the mechanism she does not: proning better matches perfusion to ventilation — anterior alveoli become dependent and stop being overdistended, while posterior alveoli are recruited and re-expand. It is used for refractory hypoxemia not responding to other strategies, needs at least 3 nurses plus an intensivist and respiratory therapist, and patients may stay prone up to 16 hours a day.

ECMO

She keeps this brief and says she posted a video. Her description: blood leaves the body, is oxygenated in the machine, and is returned — the machine does the job of the lungs. The chapter adds that it requires large-bore vascular access and systemic anticoagulation, so bleeding risk is weighed before starting.

Analgesia, sedation, perfusion and fluids

Her closing items. Analgesia and sedation matter because the tube is uncomfortable, because sedation reduces the work of breathing, and because it prevents the patient from breathing against the ventilator — ventilator dyssynchrony. Then promote tissue perfusion, and maintain fluid balance and nutrition.

5.1 What NIV Is and Who Gets It

Noninvasive ventilation uses a mask instead of an invasive endotracheal tube. It is ideal for the patient who needs a high level of ventilatory support but whose condition is not bad enough to require mechanical ventilation. Her framing is that NIV is what you try first, before intubating.

5.2 Mode 1 — CPAP

• Continuous positive airway pressure provides one level of pressure continuously, during both inspiration and expiration.
• Delivered through a tight-fitting mask.
• It increases the work of breathing, because the patient must forcibly exhale against the CPAP.
• Use with caution in patients with heart problems.

5.3 Mode 2 — BiPAP

• Bilevel positive airway pressure provides two levels of positive pressure support — one for inhaling, a different one for exhaling.
• IPAP — inspiratory positive airway pressure. It is the higher of the two, and it helps with CO2 removal.
• EPAP — expiratory positive airway pressure. The lower level; it helps keep the alveoli open at end expiration.
• The patient must be awake, alert, and able to breathe spontaneously to use it.

5.4 CPAP versus BiPAP

5.5 Nursing Management of the Patient on NIV

Her slide is a list of assessments; the reasons are hers, spoken.

5.6 When NIV Is Not Enough

If the patient cannot tolerate noninvasive ventilation, or their respiratory status declines on it, they move to mechanical ventilation. Her indications for mechanical ventilation, which close deck one and open deck two:

• Acute respiratory failure
• Apnea
• Inability to breathe or to protect the airway
• Acute respiratory distress
• Severe hypoxemia and/or hypercapnia
• Respiratory muscle fatigue

A ventilator delivers oxygen to the lungs and supports the patient until they can breathe spontaneously again. Her recurring point, made in both lectures: encourage patients and families to discuss mechanical ventilation before a crisis occurs, because some people do not want to be ventilated and some want noninvasive treatment only. Advance directives belong in this conversation.

6.1 Why a Chest Tube — the Pressure Physiology

Her slide gives one line of physiology. She gives the whole system, and the whole system is what makes every later chest tube rule reasonable.

Now the pathology follows. If enough fluid or air accumulates in the pleural space, the normally negative pressure becomes positive, and the lung collapses. A chest tube drains the pleural space, re-establishes negative pressure, and lets the lung re-expand.

6.2 Indications and Sizes

Chest tube sizes run 12F to 40F, and the size chosen depends on what is being drained.

The chapter adds one size class her slide omits: pigtail catheters, 10F–14F — very small tubes with a curled end that holds them in place, sometimes a safe and effective alternative to a larger-bore tube for a pneumothorax.

6.3 Insertion

6.4 The Three Chambers

6.5 Suction Control — Wet and Dry

6.6 Bubbling and Tidaling

This is the assessment section, and it is the one she repeats most often in the lecture. Four findings, and each has an action attached.

One practical point on her slide that is easy to miss: tidaling is not seen when the chest tube is connected to suction. You have to disconnect the tube from suction momentarily to evaluate tidaling. If a question describes "no tidaling" in a patient on wall suction, that may simply be the suction, not an occlusion.

6.7 The Heimlich (Flutter) Valve

• A flutter valve used to remove air from the pleural space.
• Attached to the external end of the chest tube.
• Used for a small to moderate-sized pneumothorax.
• Allows better patient mobility.

She adds the quality-of-life reason: it is far more comfortable than carrying the big tube and the large suction chamber unit, and patients can sometimes go home with it. She also says fluid can be removed with it as well as air — that goes beyond the slide, which says air only, so if a question is written from the slide, air is the keyed answer.

6.8 Nursing Management

She develops subcutaneous emphysema well beyond the slide's single word:

• It feels like a crackling sensation when you palpate the skin — her comparison is popcorn.
• There will probably be pain on palpation of that area, and you may see swelling around it.
• Palpating for it is part of the routine chest tube assessment, not something you do only when suspicious.
• If it is small it may resolve on its own.
• If it starts to move up toward the neck or head, the swelling can put pressure on the trachea and cause airway compromise.

6.9 The Four Chest Tube Emergencies

These are the items most likely to be written as a "what do you do first" question, and two of them look alike on purpose.

6.10 Chest Tube Removal

7.1 Oxygen Therapy — Goals and Orders

• Oxygen is the most common therapy for hypoxemia and hypoxia.
• It requires a provider order.
• The dose of oxygen administered is the fraction of inspired oxygen (FiO2).
• Goal for most patients: SaO2 >92% or PaO2 >60 mm Hg.
• Patients with COPD may be acceptable at SpO2 >88%.

These are the same targets she taught with the mechanism in §3.10. Seeing them a second time in a different lecture is itself the signal — the numbers appear in both decks.

7.2 Low-Flow versus High-Flow Systems

7.3 Complications of Oxygen Therapy

She gives the mechanism of oxygen toxicity beyond the slide: it is due to oxygen free radicals that damage the alveolar-capillary membrane, which causes pulmonary edema and hypoxemia.

7.4 ABG Normal Values

7.5 The Method — Four Steps

Her interpretation procedure, in her order. Work every gas the same way and the hard ones stop being hard.

Steps 2 and 3 are really one question: which value matches the direction of the pH? Whichever one agrees with the pH is the cause; the other one, if it has moved, is the compensation.

7.6 ROME

Her second memory aid, for remembering which value is which: CO2 is what we breathe out in our lungs, so CO2 is respiratory. CO2 is lungs. Bicarbonate, by elimination, is the metabolic one.

7.7 Compensation

Her decision rule, stated as a procedure and present on no slide:

A fully compensated gas still has a direction. If the pH lands at 7.36, it is on the acidotic side of the midpoint, so the underlying disorder was an acidosis. Read which half of the normal range the pH sits in.

7.8 Worked Example 1

Her first example, solved aloud in full. The slide shows the three numbers and no answer — the whole solution is hers.

• Step 1 — pH. 7.29 is below 7.35, so the patient is acidotic.
• Step 2 — PaCO2. 47 is above 45, and a high CO2 is acidotic. So the CO2 is also acidotic. Her observation: the pH is low and the PaCO2 is high — these are opposite, which by ROME means respiratory. Respiratory acidosis.
• Step 3 — HCO3. 24 is within the normal range of 22–26. The bicarbonate has not moved.
• Step 4 — Compensation. Because the bicarbonate is normal, the body has not begun compensating. Not compensated.

7.9 Worked Example 2

• Step 1 — pH. 7.31 is below 7.35, so acidotic.
• Step 2 — PaCO2. 49 is above 45, so also acidotic. pH and CO2 are opposite. Respiratory acidosis.
• Step 3 — HCO3. 30 is above 26, so it is higher than normal — more alkaline. Her interpretation: this tells you the body is trying to compensate, because the base is rising to offset the acid.
• Step 4 — Compensation. The pH is still abnormal, and the bicarbonate has moved abnormal in the opposite direction. Nothing here is normal. Partially compensated.

7.10 The Four Patterns, Assembled

Everything above collapses into one table. Build it once from her method and it covers any uncompensated gas.

8.1 Nasopharyngeal Airway (NPA)

• Can be placed in a conscious OR unconscious patient.
• Measuring length: hold the NPA to the side of the patient's face and choose the one that measures correctly from the tip of the nose to the tip of the ear.
• Diameter: choose a tube slightly smaller than the patient's nostrils.
• Choose the nostril with the best airflow.
• Lubricate and insert gently while rotating the tube toward the patient's ear.
• Stop if you encounter obstruction or difficulty.

8.2 Oropharyngeal Airway (OPA)

• A smaller, shorter tube of firm, hard plastic.
• Do not insert in a conscious patient.
• Measuring length: hold it against the side of the face and measure from the corner of the mouth to the angle of the jaw or the earlobe.
• Insertion: lubricate, insert with the bevel pointed toward the roof of the mouth, and as the flange reaches the lips, rotate the OPA 90 degrees so its curve fits the natural curve of the upper airway.
• The flange should sit comfortably against the lips.

8.3 NPA versus OPA

8.4 The Endotracheal (ET) Tube

A long, flexible plastic tube that secures the airway when a patient needs mechanical ventilation. Intubation is the process of securing the airway with an oral or nasal ET tube. The tube passes through the mouth and through the vocal cords.

The most common sizes are 7F and 8F, referring to the internal diameter. The chapter adds the typical assignment: 7F for females, 8F for males.

8.5 The Nasotracheal (NT) Tube and the GlideScope

• Used when oral intubation is not possible — her slide's examples are unstable cervical spine injury, dental abscess, and epiglottitis.
• Slightly longer than an ET tube.
• Inserted through the nostril and placed blindly, without seeing the larynx.
• Attaches to the ventilator via an adaptor at the end.

She adds two intubation risks that are on no slide, and one decision that follows from them. Limited neck mobility or a spinal cord injury makes an oral tube very difficult to place, and in that situation you may need a nasotracheal tube instead. And teeth can be chipped or removed during the procedure. She also names who performs intubation: the health care provider or a respiratory therapist.

8.6 Tracheostomy — Introduction

She introduces the tracheostomy briefly here and defers the detail to the end of the lecture (Unit 10). At this point:

• A small plastic tube consisting of a flange, pilot balloon, balloon inflation port, and a cuff.
• Placed into the trachea through a surgical incision on the anterior surface of the neck.
• Can be inserted urgently when other methods are not possible.

She explains the two cannulas, which the slide assumes you know: there is one cannula sitting in the tracheostomy site and another cannula on the inside that you can remove, clean, and put back. That inner cannula is the object of most trach care (§10.14). The tube is placed through the anterior surface of the neck.

8.7 Rapid Sequence Intubation

RSI is the rapid, concurrent administration of both a sedative and a paralytic during emergency airway management, to induce unconsciousness for intubation. Its purpose is to decrease injury and aspiration risk.

Immediately after the tube is placed: inflate the cuff, and continue to manually ventilate the patient with a bag-valve mask and 100% oxygen while placement is being confirmed.

8.8 Confirming Placement

Her confirmation sequence, in her order. The list is short enough to memorize whole, and the exam version of this question usually asks which finding confirms versus which merely suggests.

The chapter adds the rationale for the 2-to-3-cm position: it allows the patient to move their neck without moving the tube or letting it drop into the right mainstem bronchus.

8.9 Immediately After Intubation

9.1 The Ventilator Settings

Her two settings slides, combined. Learn the definition and the typical value together — a question can give you either one and ask for the other.

A notation point she makes: tidal volume is usually abbreviated with a capital V and a lowercase subscript t, and she notes she could not format it that way on the slide. Expect to see it as VT.

9.2 Peak Inspiratory Pressure and the Overflow Mechanism

PIP is a ceiling, not a target. The ventilator will build pressure to deliver the breath, but it is not permitted to exceed the PIP you set.

Her reason for setting a PIP at all: so the ventilator cannot over-pressurize the patient, which would cause volutrauma — damage to the alveoli.

9.3 Ventilator Alarms

9.4 The Mode Framework

A ventilator mode is the way the ventilator delivers effective ventilation, and it is chosen based on how much work of breathing the patient can perform. Her definition of WOB in this context: the inspiratory effort needed to overcome the elasticity and viscosity of the lungs, plus airway resistance.

She translates that into plain language: if the lungs are stiffer, the work of breathing is harder, because the patient has to push against a harder pressure.

9.5 Which Modes Matter

One footnote on the slide itself: it announces five most common modes and then lists six — assist control, pressure control, PRVC, SIMV, pressure support, and CPAP. If a question asks you to name them, name the six that are actually printed.

9.6 Assist-Control (AC)

• Also called volume control.
• A full support mode.
• A preset tidal volume is delivered at a preset respiratory rate — the patient will always get that preset rate no matter what.
• When the patient takes a spontaneous breath, the ventilator senses the change in airflow in the circuit and delivers the full preset tidal volume for that breath too.
• Used in postoperative patients, patients with neuromuscular disorders, and acute respiratory failure.
• Hyperventilation can occur.

She also names two clinical triggers for that hyperventilation, neither on the slide. A patient waking up from anesthesia starts taking more spontaneous breaths and gets each one at full tidal volume. And a patient in pain or anxious may start breathing fast spontaneously. Both are stems waiting to happen: the post-op patient whose ABG shows a rising pH and a falling CO2.

She adds one indication the slide does not list: AC is used for a patient who has just had CPR and needs help breathing, or someone in bad respiratory failure who cannot do any of the breathing on their own.

9.7 Synchronized Intermittent Mandatory Ventilation (SIMV)

• Both the patient and the ventilator do the work of breathing — a partial support mode.
• Delivers a preset tidal volume at a preset respiratory rate, in synchrony with the patient's own spontaneous breathing.
• In between the ventilator-delivered breaths, the patient breathes spontaneously and achieves whatever tidal volume they can achieve.
• Used when the patient's condition is too good for a full support mode, but they are not ready for a spontaneous mode.
• Benefits: improved patient-ventilator synchrony, lower mean airway pressures, and prevention of respiratory muscle atrophy as the patient takes on more of the work of breathing.

9.8 AC versus SIMV — the Discriminator

9.9 Pressure-Control (PC) Ventilation

• A full support mode that provides a pressure-limited breath.
• There is a set respiratory rate and a set peak inspiratory pressure.
• When the patient breathes, the ventilator delivers a volume of gas up to the PIP limit.
• The PIP limit is never exceeded, and there is NO set tidal volume.
• Useful for patients with decreased lung compliance and increased resistance — "stiff lungs".
• Gives control over the amount of pressure going into the lungs, which decreases the risk of volutrauma and barotrauma.
• Usually used for a trial before extubation.

Her stiff-lung indication connects straight back to ARDS. The chapter names the same example — pressure control for the ARDS patient with decreased compliance and increased resistance, because limiting pressure prevents alveolar overdistention and rupture.

9.10 Pressure-Regulated Volume Control (PRVC)

• A full support mode that combines features of both volume and pressure delivery.
• The ventilator attempts to deliver the targeted tidal volume with the least amount of pressure.
• It constantly analyzes each breath — resistance and compliance of the lungs, the exhaled tidal volume, and the PIP — and adjusts the delivery of each breath based on that feedback.

9.11 Pressure Support Ventilation (PSV)

• A spontaneous mode.
• Positive pressure is applied to the airway on inspiration only.
• The patient must be able to initiate their own breath.
• The preset positive airway pressure is set so the inspiratory flow rate of gas is greater than the patient's own inspiratory flow rate.
• When the patient starts a breath, the ventilator supplies a rapid flow of gas at initiation and then tapers the flow toward the end of inhalation.
• The patient determines their own inspiratory length, tidal volume, and respiratory rate.
• Purpose: to help facilitate weaning.
• Benefits: patient comfort, decreased work of breathing, and decreased oxygen consumption.

The chapter notes PSV is the most common spontaneous mode in North America, may be combined with SIMV during weaning when the respiratory drive is not yet stable, and that the nursing priority is to monitor for apnea and for rising work of breathing.

9.12 CPAP as a Ventilator Mode

• A spontaneous mode in which the ventilated patient controls almost all aspects of the breath.
• Not the same as the noninvasive CPAP used for sleep apnea — this is a mode on a ventilator, delivered through an artificial airway.
• Only FiO2 and PEEP are set. One level of pressure during both inspiration and expiration.
• The patient determines their own respiratory rate and tidal volume.
• Used to assess the patient's rate and rhythm, work of breathing, and hemodynamic status after a period of intubation.
• Usually used for only about 30 to 120 minutes — the patient may be extubated after this.

9.13 All Six Modes at Once

9.14 Positive End-Expiratory Pressure (PEEP)

• Positive pressure applied to the airway during exhalation.
• PEEP increases oxygenation by splinting open previously collapsed alveoli and preventing alveolar collapse throughout the respiratory cycle, which increases the opportunity for O2 and CO2 to diffuse across the alveolar-capillary membrane.
• Used in all patients who are mechanically ventilated.
• Optimal PEEP is PEEP titrated so oxygenation improves without compromising hemodynamics.
• FiO2 can usually be reduced when PEEP is used.
• Classic indication for PEEP: ARDS.
• Use with caution in traumatic brain injury, increased ICP, and low cardiac output. Her slide also lists hypovolemia.

She ties PEEP to ARDS with a callback to the previous week's images: patients with ARDS have those secretions in their alveoli, so they are going to need PEEP for sure. It is the same reasoning as §4.11 — if the surfactant that normally holds alveoli open has been lost, applied pressure has to do the job.

10.1 Maintaining Correct Tube Placement

Her four nursing responsibilities for the artificial airway: maintain correct tube placement, maintain proper cuff inflation, maintain tube patency, and maintain alarm systems. The first one is where the emergencies live.

How you confirm placement is still correct: observe for symmetric chest wall movement, auscultate and confirm bilateral breath sounds, and record and mark the position of the ET tube at the lip or teeth so the next shift can compare.

10.2 Maintaining Proper Cuff Inflation

• Maintain cuff pressure at 20 to 30 cm H2O.
• Measure and record cuff pressure routinely — she says usually every shift, or according to hospital policy.

10.3 Maintaining Tube Patency — Suctioning

Her procedure, in order:

10.4 Oral Care, Skin Integrity, and Nutrition

For feeding, an NG or OG tube is usually inserted. Her definitions, which the slide assumes: an NG tube goes in through the nose and down the back of the throat; an OG tube is the same concept but goes in through the mouth.

She also defines the two feeding routes, which the slide uses without explaining: enteral nutrition is feeding into the stomach — through a tube such as a PEG — and parenteral is intravenous, going directly to the bloodstream. Know which one your patient is on.

10.5 Prophylaxis and Early Mobility

• Venous thromboembolism prophylaxis. She names it concretely: SCDs, and if there are no contraindications, subcutaneous anticoagulants such as heparin.
• Stress ulcer prophylaxis with a PPI.
• Early mobility. Encourage most patients receiving invasive ventilation to exercise and mobilize as soon as possible unless contraindicated; collaborate with physical and occupational therapy.
• Proper positioning to prevent pressure injuries.

She describes the turning routine concretely: go in and turn the patient, position pillows, turn them onto the right side and onto the left, and elevate the heels so they do not develop pressure sores on the heels. She notes that hospitals watch pressure injuries closely because they are preventable.

10.6 Complications of Mechanical Ventilation

Her list, with the mechanism attached to each. Several have already appeared in other units, which is the point — this slide is a synthesis.

10.7 Ventilator-Associated Pneumonia

Her prevention guidelines, which double as the ventilator bundle:

The chapter adds the definition and the epidemiology her slides omit: VAP is pneumonia occurring 48 hours or more after intubation, it develops in as many as 40% of intubated patients, most cases appear within 96 hours, and the usual organisms are gram-negative bacteria. Signs suggesting VAP: fever, high WBC count, a change in the color or amount of sputum, crackles or wheezes, and new infiltrates on chest x-ray.

10.8 Unplanned Extubation

The chapter adds the recognition half. Unplanned extubation is not always obvious; sometimes the tip sits in the hypopharynx or esophagus. Its signs: the low-pressure ventilator alarm, decreased or absent breath sounds, respiratory distress, an audible cuff leak — and the clearest of all, the patient may be talking to you.

10.9 Weaning Readiness

Weaning is the process of gradually reducing ventilator support so the patient assumes greater responsibility for breathing. A formal readiness assessment is done first.

10.10 The Spontaneous Breathing Trial

10.11 Tracheostomy — Indications and Advantages

Advantages over an ET tube: more comfortable for the patient, easier to keep the tube clean, and less long-term risk to the vocal cords.

Post-procedure care: inflate the cuff immediately, confirm correct placement, and monitor vital signs. Her complications list: airway obstruction, bleeding, infection, and potential tube dislodgement.

10.12 Nursing Management of the Tracheostomy

She explains why mucus plugs matter, which the slide does not: a plug blocks the patient's airway, causing coughing and difficulty breathing. Humidification is not a comfort measure alone; it is plug prevention.

10.13 Accidental Decannulation

10.14 Stoma and Inner Cannula Care

Her procedure, which is the last content slide of the module:

• Open sterile equipment. Pour sterile water or normal saline into 2 compartments of a sterile container or 2 basins, then apply sterile gloves.
• If present, unlock and remove the inner cannula. Many tracheostomy tubes do not have inner cannulas; care for those includes every step except inner cannula care.
• Disposable inner cannula: replace with a new one.
• Non-disposable inner cannula: immerse in sterile solution and clean inside and outside with a tube brush or pipe cleaners; rinse in sterile solution; remove and shake to dry; insert into the outer cannula with the curved part downward and lock in place.
• Stoma care: remove dried secretions using a 4 × 4-inch gauze pad soaked in sterile water or saline; gently pat dry; and clean under the tracheostomy flange using cotton swabs.

She adds one instruction the slide does not: dry the inner cannula really well before reinserting it.

Where it comes from

This is the assigned reading for Module 2, worked through on its own terms — Lewis’s Medical-Surgical Nursing, 12th ed., Ch. 28 (airway management, ventilation and critical care) and Ch. 32 (respiratory failure and ARDS), plus the posted unit objectives.

Nothing here is attributed to the instructor, because none of it came from her. The boxes marked HIGH-YIELD are the textbook’s emphasis and this guide’s, which is why they are a different colour from the yellow instructor boxes in Lecture. There are no lecture play buttons in this view for the same reason.

1.1 Two Jobs, Not One: Ventilation and Oxygenation

The chapter opens with a sentence worth memorizing whole: exchange of O2 and CO2 is vital for life; without an optimal route for ventilation, O2 therapy will not benefit the patient; providing optimal ventilation is no guarantee that oxygenation improves — but without a patent airway, the patient will die. That sentence is the whole module in miniature. Airway first, then ventilation, then oxygenation, and the three are not interchangeable.

Ventilation is air movement: gas in and gas out. Oxygenation is gas transfer: O2 crossing from alveolus to capillary blood. A patient can ventilate beautifully and still be hypoxemic (fluid-filled alveoli), and can oxygenate acceptably on a high FIO2 while retaining CO2 to the point of narcosis. The exam separates them constantly, and each is measured by a different number.

1.2 The V/Q Ratio — Matching Air to Blood

Gas exchange only happens where ventilated alveoli sit against perfused capillaries. In normal lungs the two are nearly identical: alveolar ventilation 4–6 L/min against pulmonary blood flow 4–6 L/min, giving a V/Q ratio of 0.8 to 1.2. A perfect match is V/Q = 1 (1:1). Anything else is a V/Q mismatch.

Some mismatch is normal and regional, and knowing the pattern explains half the positioning questions in this module. The apex is relatively over-ventilated and under-perfused; the base is the reverse. Because apex and base changes balance each other, the blood leaving the lung is a mixture with a close overall match.

Push each side of that ratio to its extreme and you get the two named failures of matching. Dead space is ventilation without perfusion (V/Q approaching infinity) — the alveolus fills with air that never meets blood, as distal to a pulmonary embolus. Shunt is perfusion without ventilation (V/Q approaching zero) — blood flows past an alveolus filled with fluid and leaves the lung exactly as it arrived.

1.3 The Oxyhemoglobin Dissociation Curve

Nearly every threshold in these two chapters — PaO2 60 mm Hg, SaO2 90%, SpO2 92% — is a point on one curve. The oxyhemoglobin dissociation curve plots the partial pressure of oxygen dissolved in plasma (PaO2, on the horizontal axis) against the percentage of hemoglobin carrying oxygen (SaO2, on the vertical axis). It is S-shaped, and the shape is the point.

The curve can slide left or right, changing how tightly hemoglobin holds oxygen at any given PaO2. A right shift means decreased affinity — hemoglobin lets go of oxygen more readily, so tissues get more oxygen but the blood saturates less well in the lung. A left shift means increased affinity — hemoglobin binds oxygen more tightly, loading well in the lung but releasing poorly at the tissue.

1.4 Hypoxemia Versus Hypoxia

The two words are not synonyms and the chapters are careful with them. Hypoxemia is a laboratory finding: a decrease in arterial O2 (PaO2) and saturation (SaO2) below normal values. Hypoxia is a tissue event: a decrease in O2 supply at the cellular level, occurring when the PaO2 falls far enough to produce signs and symptoms of inadequate oxygenation. Hypoxemia is what the blood gas shows; hypoxia is what the patient is experiencing.

That chain is why a patient in respiratory failure can arrive with a metabolic acidosis on top of a respiratory one, and why lactate is a severity marker rather than a lung number. It also explains the multi-system findings: the CNS loses consciousness without enough blood, O2, and glucose to the brain, with permanent brain damage if hypoxia is severe and prolonged; the gut develops tissue ischemia and increased intestinal wall permeability, letting bacteria migrate from the GI tract into the systemic circulation; and the kidneys respond with sodium retention, peripheral edema, and acute kidney injury.

1.5 Early Signs and Late Signs

This is the single most examined discrimination in the respiratory module, because the correct answer is almost always the early sign that a distracted nurse would dismiss.

1.6 Work of Breathing, and What Position Tells You

Work of breathing (WOB) is the inspiratory effort needed to overcome the elasticity and viscosity of the lungs plus airway resistance — the effort required by the respiratory muscles to move air in. You cannot measure it at the bedside, but the patient's posture grades it for you.

• Mild distress — the patient may still be able to lie down.
• Moderate distress — the patient prefers to sit.
• Severe distress — the patient cannot breathe unless sitting upright.
• Tripod position — sitting with the arms propped on an overbed table or on the knees. This decreases WOB in moderate to severe COPD and in ARF because propping the arms increases the anteroposterior diameter of the chest and changes pressure in the thorax, giving the accessory muscles a fixed point to pull against.

Pursed-lip breathing is the one patient-controlled manoeuvre the chapters credit with raising SaO2: it works by slowing respirations, increasing the time available for expiration, and preventing the small bronchioles from collapsing.

1.7 Reading the Lung Fields

Two palpation findings matter as much as the sounds. Crepitus (subcutaneous emphysema) is air in the tissue and points to an air leak — from a chest tube site, a ruptured alveolus, or a tracheostomy. A deviated trachea is a late sign and, in a patient on positive pressure, means tension pneumothorax until proven otherwise.

2.1 Why Secretions Cause Respiratory Failure

Retained pulmonary secretions may cause or worsen acute respiratory failure because the movement of O2 into the alveoli and the removal of CO2 from them is severely limited or blocked. Secretions in the airway are one of the most common causes of V/Q mismatch, and secretions in the alveoli — as in pneumonia — produce shunt. Airway clearance techniques (ACTs) loosen mucus and secretions so they can be cleared by coughing, maintaining a patent airway.

ACTs are for patients who retain secretions: COPD, cystic fibrosis (CF), and bronchiectasis. The order of operations matters — bronchodilator therapy first, then the airway clearance technique, then effective coughing (for example huff coughing). Opening the airway before you try to move mucus through it is the entire rationale.

2.2 Breathing Retraining

Diaphragmatic (abdominal) breathing

• Focuses on using the diaphragm instead of the accessory muscles of the chest to achieve maximum inhalation and slow the respiratory rate.
• Ideal candidates: thoracic and abdominal surgery patients.
• Caution: in COPD it may increase work of breathing and dyspnea. People with moderate to severe COPD and marked hyperinflation may not tolerate it at all — their diaphragms are already flattened and mechanically disadvantaged.

Pursed-lip breathing (PLB)

• Purpose: prolong exhalation, which prevents bronchiolar collapse and air trapping. The back-pressure created at the lips splints the small airways open long enough for trapped air to escape.
• Simple, easy to teach and learn; gives the patient more control over breathing, especially during exercise and periods of dyspnea. It slows the respiratory rate and is easier than diaphragmatic breathing.
• Teach "just enough" positive pressure — excessive resistance increases the work of breathing and defeats the purpose.
• In extreme acute dyspnea, the focus is helping the patient slow the respiratory rate using PLB.

2.3 Coughing Techniques

A cough only clears mucus if the airway stays open while the air moves. A hard conventional cough slams the glottis shut and collapses floppy airways in COPD, which is why the chapters teach three modified techniques instead.

Position the huff-coughing patient sitting, head slightly flexed, shoulders relaxed, knees flexed, forearms supported by a pillow, and if possible feet on the floor.

2.4 Chest Physical Therapy

Chest physical therapy (CPT) consists of postural drainage, percussion, and vibration. It can be done on spontaneously breathing patients and on those intubated and mechanically ventilated, and is used for patients with excessive bronchial secretions who have difficulty clearing them. It should be done by a physiotherapist or other trained person. Complications of improperly performed CPT: fractured ribs, bruising of the chest wall, hypoxemia, and discomfort.

Postural drainage

• Positioning techniques that drain secretions from specific lung segments into the trachea — each position drains one segment toward the larger airways, using gravity.
• Which position depends on the lung areas involved, determined by patient assessment, chest x-rays, chest auscultation, and where possible patient preference. Left lower lobe involvement means draining only that region; a CF patient may need all segments.
• A patient who cannot tolerate the head-down position may use a side-lying position instead.
• Give aerosolized bronchodilators and hydration therapy BEFORE postural drainage.
• The patient stays in each position about 5 minutes during percussion and vibration.
• Frequency: commonly 2–4 times a day; in acute situations as often as every 4 hours.
• Timing: at least 1 hour before meals or 3 hours after meals — the head-down position on a full stomach invites vomiting and aspiration.
• Best for: atelectasis, cystic fibrosis, COPD, pneumonia.

Percussion and vibration

• Percussion is done in the appropriate postural drainage position with the hands in a cuplike position, fingers and thumbs closed — as though scooping up water. The cupped hand creates an air pocket between chest and hand; both hands alternate rhythmically and a hollow sound confirms correct technique. The air-cushion impact promotes movement of thick mucus. Place a thin towel over the area for comfort.
• Vibration promotes movement of secretions to the larger airways. It is performed by tensing the hand and arm muscles repeatedly and pressing mildly with the flat of the hand on the affected area while the patient slowly exhales a deep breath. Mechanical vibrators exist for hospital and home use.

2.5 Airway Clearance Devices

These devices are often easier to tolerate than CPT and take less time, and most let the patient treat themselves.

2.6 Positioning

• Position the patient with ARF upright and elevate the head of the bed at least 30 degrees, or use a reclining chair or chair bed. This maximizes respiratory expansion, decreases dyspnea, and mobilizes secretions.
• Sitting improves pulmonary function by promoting the downward movement of the lungs. When the lungs are upright, ventilation and perfusion are best in the lung bases.
• If there is any chance of aspiration, position the patient side-lying.
• Patients with problems in both lungs — which is common in ARF — need repositioning at regular intervals on both sides.

2.7 Humidification and Hydration

• Thin secretions with aerosols of sterile normal saline or with mucolytic drugs (e.g., acetylcysteine mixed with a bronchodilator) given by nebulizer. O2 given by aerosol mask can also thin secretions.
• Caution: aerosol therapy may cause bronchospasm and severe coughing, which decreases PaO2. Frequent assessment of tolerance is critical — this is a therapy that can make the patient acutely worse.
• Unless contraindicated, adequate fluid intake of 2 to 3 L/day keeps secretions thin and easier to remove. A patient in ARF may not manage this orally and may need IV hydration.
• Assess cardiac and renal status before pushing fluids, to be sure the patient can tolerate the volume and to avoid precipitating heart failure and pulmonary edema.
• Regularly assess for fluid overload: crackles, dyspnea, weight gain, increased CVP.

2.8 Suctioning the Patient Without an Artificial Airway

• Suctioning is needed only if the patient cannot expectorate secretions on their own.
• In the awake, non-intubated patient, a soft-tip suction catheter passed through a nasopharyngeal tube can remove secretions at the back of the throat.
• Perform suctioning with caution — stimulating the gag reflex may induce vomiting, and a vomiting hypoxemic patient is now an aspiration problem as well.
• Suction through an artificial airway only as needed, never on a routine schedule.

3.1 Oxygen Is a Drug

O2 is a colorless, odorless, tasteless gas constituting 21% of the atmosphere. Supplemental O2 increases the partial pressure of O2 in inspired air, and that is the whole mechanism: raise the pressure gradient across the alveolar-capillary membrane and more O2 diffuses into blood. O2 therapy requires an order from the health care provider, and the dose of O2 is the fraction of inspired oxygen (FIO2).

3.2 Low-Flow Versus High-Flow Systems

The distinction is not about how many liters per minute; it is about whether the device can meet the patient's entire inspiratory demand. A low-flow device delivers less gas than the patient draws in, so the patient entrains room air along with it — and the resulting FIO2 is a range, not a number. A high-flow device delivers everything the patient needs and more, so the FIO2 is fixed regardless of how the patient breathes.

3.3 Low-Flow Delivery Devices

3.4 High-Flow Delivery Devices

3.5 Choosing a Device

Ch. 32 lists five factors, and a question that asks the "key consideration" in device selection is answered from this list, not from the device table: the patient's overall condition, the degree of respiratory failure, the ability to maintain a patent airway, the amount of FIO2 the device delivers, and the patient's ability to breathe spontaneously.

3.6 Humidification

• O2 from cylinders and wall systems is a dry gas; dry O2 irritates mucous membranes and dries secretions.
• Humidification adds sterile water to the delivery system — commonly the bubble-through humidifier, a small plastic jar of sterile water attached to the O2 source by a flowmeter.
• Many agencies have moved away from humidifying low-flow devices. Humidification with high-flow devices is important. Follow agency policy.

3.7 Complications of Oxygen Therapy

Combustion

O2 supports combustion and increases the rate of burning. Smoking must be prohibited in any patient care area where O2 is in use; post a "No Smoking" sign on the patient's door. A cannula in place can ignite easily and cause significant burns and life-threatening airway injury.

O2 toxicity

• Mechanism: prolonged exposure to a high FIO2 causes a severe inflammatory response because O2 free radicals damage the alveolar-capillary membrane → severe pulmonary edema, shunting of blood, and worsening hypoxemia. Ch. 32 adds increased pulmonary capillary permeability, decreased surfactant production, surfactant inactivation, and fibrotic changes in the alveoli.
• Manifestations to monitor for: blurred vision, coughing, chest pain, dyspnea, seizures.
• Prevention — the governing rule: provide the FIO2 at the lowest possible level that still maintains an acceptable SpO2 and PaO2 for that specific patient. Monitor ABGs often to guide tapering.

Absorption atelectasis

Alveoli normally contain O2, CO2, and nitrogen, and it is nitrogen that maintains the size, shape, and structure of the alveolus. Give a very high FIO2 and O2 replaces the nitrogen. If a bronchial tube then becomes obstructed — with mucus, for instance — gas exchange stops, the remaining O2 is absorbed into the bloodstream, nitrogen is no longer there to hold the alveolus open, and the alveolus collapses, worsening hypoxemia. Prevention: frequent chest x-rays for patients on higher levels of O2, ABG monitoring, suctioning the airway as needed, and the lowest possible FIO2.

CO2 narcosis

• Chemoreceptors control the drive to breathe, responding to CO2 and O2 concentrations in the blood. Normally, increased CO2 is the major stimulant of the respiratory center.
• Some patients — classically COPD — develop a tolerance for high CO2; the respiratory center loses sensitivity to it, and hypoxemia becomes the major drive to breathe. Ch. 32 phrases the same idea as chronic hypercapnia blunting the response of the chemoreceptors to CO2 as a respiratory stimulant.
• However: the hypoxic drive is complex and involves many other factors, and not all COPD patients retain CO2.
• Practical rule: give O2 to any patient likely to benefit from it. The danger of NOT giving O2 far outweighs the risk of giving it when it is not needed. Where chronic hypercapnia is known, start low: nasal cannula at 1–2 L/min or a Venturi mask at 24%–28%, and monitor.

Infection

A rare complication, related to the device and how often it is cleaned or changed. Heated nebulizers present the highest risk because constant humidity supports bacterial growth. Use disposable and single-patient equipment wherever possible.

3.8 Oxygen Therapy at Home

• Sources: a liquid O2 storage system, compressed O2 in tanks or cylinders, or an O2 concentrator/extractor. Choice depends on activity level, environment, insurance coverage, and proximity to a supply company.
• Patients usually rent home systems, and the company sends a respiratory therapist to the home to teach use, maintenance, troubleshooting, recognizing a low supply, and reordering.
• Some patients need O2 only during exercise and/or sleep — evaluated with a 6-minute walk test or overnight oximetry.
• Long-term therapy is reassessed every 30 to 90 days during the first year, then yearly if stable.
• Air travel: inform the airline when making reservations. O2 needs for flying are determined by pulmonary function test, 6-minute walk test, hypoxic challenge test, or a predictive formula. Portable O2 concentrators recharge at home or on DC (auto) power and several are airline-approved.

3.9 Nursing Management and Delegation

• Use pulse oximetry and/or ABGs to determine the FIO2 each patient needs; titrate with close monitoring of PaO2 and PaCO2.
• Evaluate the response to O2 therapy, especially whenever a change is made. A trend toward a normal PaO2 tells you the patient is responsive to O2 — and failure of the PaO2 to rise on increasing FIO2 is itself a diagnostic finding pointing toward shunt.
• Assistive personnel may use pulse oximetry and report the value to the RN, assist the patient with adjusting the delivery device, and report any change in condition.
• Collaborate with the respiratory therapist to choose the optimal device, keep equipment clean and replaced, check the accuracy of delivery, and assess the need for flow-rate adjustments.

4.1 The Five Artificial Airways

Inserting a tube into the nose, mouth, or trachea bypasses the upper airway and laryngeal structures and creates a route for ventilation. The chapter names five commonly used artificial airways, and they sort cleanly by how far down they go and by what the patient's level of consciousness allows.

4.2 Nasopharyngeal Airway

• A small, flexible plastic tube inserted into the nostril to maintain a route for ventilation. Can be placed in a conscious or an unconscious patient — its flexibility and position mean it does not reliably trigger the gag reflex.
• Sizing for length: hold the airway to the side of the face and measure from the tip of the nose to the tip of the ear.
• Sizing for diameter: choose a tube slightly smaller in diameter than the patient's nostril.
• Insertion: choose the nostril with the greatest airflow; lubricate; insert gently while rotating the tube toward the patient's ear; stop if you meet any obstruction or difficulty. Correctly placed, the flange rests comfortably against the nostril.

4.3 Oropharyngeal Airway

• A shorter tube of firm, hard plastic, curved, with a flange at one end and a blunt opening at the other.
• DO NOT insert an OPA in a conscious patient — it will induce vomiting and risk aspiration. Only insert into an UNCONSCIOUS patient.
• Sizing: measure the tube against the corner of the mouth to the angle of the jaw or the earlobe.
• Too short → it may push the tongue back into the oropharynx and occlude the airway — the exact problem it was inserted to fix.
• Too long → it may damage the posterior oropharynx.
• Insertion: lubricate with a water-soluble lubricant; insert with the bevel pointed toward the roof of the mouth; as the flange reaches the lips, rotate the airway 90 degrees so its curve follows the natural curve of the upper airway. The flange should then sit comfortably against the lips.

4.4 The Endotracheal Tube

• Parts: a standard adaptor (the 15-mm connector that attaches a bag-valve mask or ventilator), the cuff, a pilot balloon with a spring-loaded inflation valve and inflation line, and radiopaque markings along the tube used to gauge the depth of insertion.
• Most common sizes: 7F and 8F — size refers to the internal diameter. Commonly 7F for females, 8F for males.
• Advantages of a larger-diameter tube: it reduces work of breathing (less airway resistance — resistance rises steeply as radius falls), makes it easier to suction and remove secretions, and makes bronchoscopy possible if it is needed.
• Oral intubation is preferred because the airway can be secured rapidly, with a laryngoscope or bronchoscope passing the tube through the vocal cords.

Nasotracheal tube

Used when oral intubation is not possible — for example with an unstable cervical spine injury, a dental abscess, or epiglottitis. It is slightly longer than an oral ET tube and is placed blindly, without seeing the larynx. Mark the position of a nasotracheal tube at the nare rather than at the lip or teeth.

4.5 Indications for Intubation

Notice how many of these are airway-protection problems rather than oxygenation problems. A patient with a normal SpO2 who cannot clear secretions or protect their airway is still an intubation candidate — which is why a declining level of consciousness on noninvasive ventilation is such an ominous finding.

4.6 The Intubation Procedure

Preparation

• Unless the situation is emergent, consent is obtained. Tell the patient and caregiver the reason and the steps, and explain that the patient will not be able to speak while intubated but that other means of communication will be provided. Warn them the hands may have removable mitts or the wrists soft restraints as a reminder not to touch the tube.
• Have a self-inflating bag-valve mask (BVM) attached to O2 and suction equipment ready at the bedside. The BVM has a reservoir filled with O2 so it can deliver up to 100%.
• A patent IV is needed to give pre-intubation drugs. Remove dentures or partial plates. Premedication varies with the patient's level of consciousness, the urgency, and provider preference.

Positioning

• Oral intubation: supine with the head slightly extended and the neck flexed — the "sniffing" position. Rationale: it aligns the axes of the mouth, pharynx, and larynx so the vocal cords can be seen.
• Nasal intubation: spray the nasal passages with a local anesthetic and vasoconstrictor (e.g., lidocaine with epinephrine) to reduce trauma and bleeding.

Timing rules

4.7 Rapid Sequence Intubation

• RSI is the rapid, concurrent administration of a sedative and a paralytic during emergency airway management to induce unconsciousness for intubation. It decreases the risks of aspiration and injury — the patient is deeply unconscious and completely still, so the attempt is fast and the airway reflexes that would provoke vomiting are abolished.
• Drugs: a sedative-hypnotic-amnesic (e.g., propofol, etomidate) to induce unconsciousness; a rapid-onset opioid (e.g., fentanyl) to blunt the pain of the procedure; then a drug producing skeletal muscle paralysis (e.g., rocuronium).
• RSI is NOT indicated in patients in cardiac arrest or with a known difficult airway. In arrest there is no need to induce unconsciousness; with a known difficult airway, paralyzing a patient you may not be able to intubate removes their own respiratory effort as a fallback.

4.8 Confirming Tube Placement

Immediately after the tube passes, placement is confirmed by a sequence of checks — no single one is sufficient on its own, and the definitive check is radiographic.

4.9 Risks Specific to Oral Intubation

• Hard to place with limited head and neck mobility (e.g., spinal cord injury) — this is when nasotracheal intubation is chosen instead.
• Teeth can be chipped or accidentally removed.
• Patients can obstruct the tube by biting down; sedation plus a bite block or oropharyngeal airway prevents it.
• Salivation increases and swallowing is difficult — suction the mouth often with a Yankauer.
• Mouth care is a challenge because of limited space; use smaller or pediatric-sized oral products.

5.1 The Physiology a Chest Tube Restores

The pleural space normally holds a negative, subatmospheric pressure, and that negative pressure is what keeps the lung expanded against the chest wall. If enough fluid or air accumulates in the space, the negative pressure becomes positive and the lung collapses. A chest tube re-establishes negative pressure, drains the pleural space, and allows the lung to re-expand. Every rule that follows — why you never clamp, why the drainage unit stays below the chest, why a disconnection is an emergency — comes back to protecting that pressure gradient.

5.2 Sizes and What Each Drains

Chest tubes are about 20 inches (51 cm) long and range from 12F to 40F. Size is chosen by what has to move through the tube: blood is viscous and clots, so it needs the widest bore; air needs the least.

5.3 Insertion

• May be done in the ED, the operating room, or at the bedside. Time permitting, a chest x-ray confirms the affected side first.
• Positioning: raise the arm above the head on the affected side to expose the midaxillary area, the standard insertion site. Elevate the head up to 45 degrees when possible to lower the diaphragm and reduce the risk of injuring it.
• After antiseptic prep and local anesthetic (1% lidocaine), a small incision is made over a rib and the tube is advanced up and over the TOP of the rib. Rationale: the intercostal nerves and blood vessels run along the inferior border of each rib, so going over the top avoids them.
• The tube is sutured in place, connected to the drainage system, and covered with an occlusive dressing; most providers seal around the tube with petroleum (airtight) gauze.
• Placement is confirmed by chest x-ray.
• Chest tube insertion is painful — monitor comfort frequently and medicate.

5.4 The Three Chambers

Most disposable drainage units hold 2000 mL and contain three compartments in series. Understanding what each one does converts every chest-tube question into a reasoning problem instead of a memory problem.

5.5 Tidaling and Bubbling — Reading the System

These two observations are the water-seal chamber's entire vocabulary, and nearly every chest-tube exam question turns on telling them apart.

5.6 Wet Versus Dry Suction

5.7 The Flutter (Heimlich) Valve

• A one-way rubber valve inside a rigid plastic tube, attached to the external end of the chest tube and used to remove air from the pleural space.
• Mechanism: during inspiration, when pressure in the chest falls, the valve closes, preventing air from re-entering the chest; during expiration, when intrathoracic pressure rises, the valve opens and air escapes.
• Used for a small to moderate-sized pneumothorax. It allows patient mobility — the small drainage bag can be hidden under clothing, and patients may go home with a flutter valve in place.

5.8 Nursing Management and Emergencies

• Immediately after insertion, monitor closely for complications — vital signs including respiratory rate and rhythm — and monitor the color and amount of drainage HOURLY for the first few hours.
• Report at once: drainage greater than 200 mL in the first hour, development of subcutaneous emphysema, or any signs of respiratory distress. Ongoing, notify the HCP for drainage greater than 100 mL/hr, and report any change in the character of drainage (clear yellow turning bloody).
• If 1 to 1.5 L of fluid or blood is removed rapidly, re-expansion pulmonary edema or severe symptomatic hypotension may occur. Ask the HCP how much drainage to expect.
• Subcutaneous emphysema is air leaking into the tissue around the site — you feel a "crackling" sensation when palpating the skin. A small amount is harmless and reabsorbs; severe subcutaneous emphysema around the head and neck can cause swelling with airway compromise.
• Keep all connections tight and taped. Keep tubing loosely coiled below chest level so drainage flows freely, and never raise the drainage system to the level of the chest — fluid can drain back into the lungs.
• Change the unit when the collection chamber is full. Do NOT try to empty it.
• Encourage coughing, deep breathing, incentive spirometry every hour while awake, and range-of-motion exercises to the shoulder on the affected side to prevent atelectasis and shoulder stiffness. Use sterile technique for dressing changes.

5.9 Chest Tube Removal

• Removed when the lung is re-expanded and drainage has ceased or is minimal. Sometimes suction is discontinued and the tube drains by gravity for 24 hours first.
• Give pain medication about 30 to 60 minutes before removal.
• The HCP or advanced practice nurse cuts the suture and removes the tube while the patient holds their breath or bears down (Valsalva maneuver) — raising intrathoracic pressure so air cannot be drawn in through the tract as the tube leaves.
• The site is IMMEDIATELY covered with an airtight, occlusive dressing (petroleum gauze) with dry gauze over it, to prevent air entering the pleural space. The pleura seals and the wound heals in a few days.
• A chest x-ray is done 30 to 60 minutes after removal to check for pneumothorax or fluid reaccumulation.
• Assess for respiratory distress afterward — it may signal recurrence of the original problem. Notify the HCP at once.

5.10 Thoracentesis

Thoracentesis drains air or excess fluid from the pleural space with a needle rather than an indwelling tube. Usually no more than 1000 to 1200 mL of fluid is removed at one time. Rationale: rapid removal of a large volume of pleural fluid can cause hypotension, hypoxemia, or re-expansion pulmonary edema — the same physiology behind the 1 to 1.5 L chest-drainage warning. Bronchoscopy, by contrast, is both diagnostic and therapeutic: it removes mucous plugs and foreign bodies and can restore patency to an airway partly obstructed by tumor.

5.11 Chest Surgery

Approaches

• Thoracotomy is a surgical incision into the chest to reach the heart, lungs, esophagus, thoracic aorta, or anterior spine.
• Median sternotomy splits the sternum and is used mainly for surgery involving the heart.
• Posterolateral thoracotomy is used for most lung surgery, made front to back at the level of the 4th, 5th, or 6th intercostal space, with mechanical retractors separating the ribs.
• Anterolateral thoracotomy is made in the 4th or 5th intercostal space from the sternal border to the midaxillary line — used for trauma, mediastinal operations, and wedge resections of the upper and middle lobes.
• Video-assisted thoracoscopic surgery (VATS) is a minimally invasive approach giving a real-time video image of the chest cavity through small incisions. Advantages: less pain, faster return to activity, shorter stay, lower postoperative morbidity — valuable for patients with low respiratory reserve. A chest tube is placed through one of the incisions at the end.

Perioperative care

• Preoperative evaluation may include chest x-ray, ECG, ABGs, pulmonary function studies, CT or MRI, and laboratory studies (CBC, glucose, electrolytes, BUN, creatinine, PT/INR, aPTT).
• Preoperative teaching should ALWAYS include deep breathing and incentive spirometry. Rationale: practicing before surgery makes them far easier to perform afterward, when the incision hurts. Teach splinting the incision with a pillow and have the patient teach back ROM exercises on the affected side.
• Reassure the patient that the lungs have a large functional reserve — even after removal of one lung there is enough tissue to maintain adequate oxygenation.
• The thoracotomy incision is the MOST PAINFUL surgical incision, because respiratory muscles are cut during surgery.
• Pain management is a priority to prevent respiratory compromise. A multimodal approach is best: oral, subcutaneous, and/or IV opioids, PCA, epidural infusions, and/or intercostal nerve blocks. Rationale: effective analgesia is what allows the patient to breathe deeply, cough, move the arm and shoulder, and mobilize — every one of which prevents a pulmonary complication.
• Postoperative priorities: assess respiratory rate and effort, breath sounds, and sputum volume and color; monitor chest tube drainage and function; expect daily chest x-rays; assess pain; monitor temperature; observe the surgical site.

6.1 Noninvasive Ventilation

Noninvasive ventilation (NIV, also called NIPPV) uses a mask instead of an ET tube — nasal, full face, or nasal pillows — to help oxygenate and ventilate. It is ideal for the patient who needs a higher level of ventilatory support but whose condition is not bad enough to require mechanical ventilation. It provides O2, decreases work of breathing, reduces respiratory muscle fatigue, helps open collapsed airways, decreases shunt, and avoids the need for intubation altogether.

Nursing management of the patient on NIV

• Patients need constant assessment of level of consciousness, hemodynamic stability, and work of breathing.
• Elevate the head of the bed 30 to 45 degrees.
• The patient MUST be able to remove the mask independently, because of the risk of vomiting.
• Provide mouth, nare, and eye care.
• Protect the skin — ANY degree of redness constitutes a Stage I pressure injury. Alleviate pressure from the tight mask by alternating the length of time it is on, trying different sizes and styles, and collaborating with the respiratory therapist.

6.2 Indications for Mechanical Ventilation

Mechanical ventilation is the process by which a ventilator delivers O2 to the lungs, supporting the patient until they recover the ability to breathe independently. It may be a bridge to long-term ventilation or to a decision to stop support. Mechanical ventilation is not curative — it buys time for the underlying problem to be treated.

Other patients who commonly receive it: hemorrhage, trauma, neuromuscular problems, drug overdose, burns, and shock. The chapter also raises an ethical point worth carrying: patients with chronic lung disease and their caregivers should discuss mechanical ventilation before a health crisis, and wishes about end-of-life treatment should be recorded in an advance directive. Where team, patient, and caregiver disagree, care conferences are essential and an ethics committee may be consulted.

6.3 Negative Versus Positive Pressure Ventilation

6.4 Volume Versus Pressure Ventilation

Every positive-pressure breath is delivered by guaranteeing one variable and letting the other float. That is the entire distinction, and it determines what you monitor.

6.5 Ventilator Settings

Settings are based on the patient's condition, level of consciousness, respiratory muscle strength, chest x-ray, and ABGs, and manipulating them corrects hypoxemia and hypercarbia. In most settings, changing ventilator settings is the responsibility of the HCP or respiratory therapist — but always assess the patient's response to any setting change.

6.6 PEEP

• Definition: positive pressure applied to the airway during exhalation. Normally airway pressure falls to near zero during passive exhalation; with PEEP, exhalation is still passive but pressure only falls to the preset level — often 5 to 10 cm H2O.
• Effect: PEEP increases functional residual capacity and often improves oxygenation, by restoring the lung volume that should remain at end expiration.
• Two mechanisms: (1) splinting open previously collapsed alveoli, increasing the surface available for O2 and CO2 to diffuse across the alveolar-capillary membrane; (2) preventing alveolar collapse throughout the respiratory cycle, so the alveolus does not have to be re-opened with every breath.
• Physiologic PEEP is 5 cm H2O, used to replace the glottic mechanism, which is bypassed once an ET tube is in place. The glottis normally provides a small back-pressure at end expiration; the tube removes it, so the ventilator supplies it.
• PEEP is indicated in ALL mechanically ventilated patients. An intubated patient would NEVER be placed on zero PEEP.
• Optimal PEEP is PEEP titrated to the point where oxygenation improves without compromising hemodynamics. FIO2 can often be reduced once PEEP is applied, which is how PEEP protects against O2 toxicity.
• The classic indication for PEEP therapy is ARDS, where levels of 10 to 20 cm H2O may be needed.
• During weaning, PEEP improves gas exchange, vital capacity, and inspiratory force.

6.7 Modes — the Framework

The ventilator mode is the way the ventilator delivers ventilation, and it is selected based on how much work of breathing the patient can perform. Mode is mainly determined by level of consciousness, respiratory drive, work of breathing, and ABGs. Terminology varies among manufacturers, so the chapter tells you to hold on to two questions: how much work is the ventilator doing (full support, partial support, or spontaneous), and how is the breath delivered (by volume or by pressure).

The five most common modes in North America are assist control, pressure control, synchronized intermittent mandatory ventilation, pressure support, and CPAP.

6.8 Assist-Control (AC)

• Settings: respiratory rate, VT, inspiratory time, and PEEP. The ventilator delivers a preset number of breaths at a designated VT.
• If the patient initiates a spontaneous breath, a FULL breath with the designated VT is delivered. The ventilator senses the change in airflow in the circuit and responds with a whole machine breath.
• The patient's respiratory rate on AC will never be below the set rate, and the patient may breathe over it whenever they want.
• AC is the most common full-support mode when a patient is first intubated: new postoperative patients, neuromuscular disorders, and ARF.
• Nursing focus: VT is consistent, so trend the PIP.

6.9 Pressure Control (PC)

• Settings: respiratory rate, PIP, inspiratory time, and PEEP. The ventilator delivers a preset number of breaths up to a specific PIP. Patient-initiated breaths are also delivered up to that PIP.
• The PIP limit is never exceeded, and there is no set VT.
• Best for patients with decreased compliance and increased resistance — "stiff lungs." Rationale: controlling the amount of pressure entering the patient decreases the risk of volutrauma and barotrauma.
• The classic example is ARDS. Ch. 32 adds that pressure control keeps inspiratory and plateau pressures from becoming too high, preventing alveolar overdistention and rupture — though no mode of mechanical ventilation is superior to the others.
• Nursing focus: PIP is fixed, so trend the VT, which will be variable. A falling exhaled VT at an unchanged pressure means the lungs are getting stiffer.

6.10 Synchronized Intermittent Mandatory Ventilation

• Settings: respiratory rate and VT for the ventilator breaths, plus inspiratory time, sensitivity, and PEEP.
• The ventilator delivers its preset breaths in synchrony with the patient's own inspirations. Between ventilator breaths the patient breathes at their own rate and achieves whatever VT they can — those spontaneous tidal volumes are variable.
• Both patient and ventilator do the work of breathing, which is what makes it partial support.
• Used when the patient's condition is too good for a full support mode but not ready for a spontaneous mode. Sometimes combined with pressure support.
• Benefits: improved patient-ventilator synchrony, lower mean airway pressures, and prevention of respiratory muscle atrophy as the patient takes on more work.
• Risk: muscle fatigue from the increased work of breathing. The same feature that prevents atrophy can exhaust a patient who is not ready.

6.11 Pressure Support Ventilation

• Positive pressure is applied to the airway ONLY during inspiration. The patient must be able to initiate a breath.
• Settings: inspiratory pressure level, PEEP, and sensitivity. When the patient triggers a breath, a high flow of gas is delivered to the preselected pressure level and held there through inspiration, then tapers toward the end of inhalation.
• The patient determines their own inspiratory length, tidal volume, and respiratory rate.
• PSV is the most common spontaneous mode in North America, and its purpose is to facilitate WEANING. It may be combined with SIMV when the respiratory drive is less than stable.
• Advantages, each with its reason: increased comfort; decreased work of breathing because inspiratory efforts are augmented; decreased O2 consumption because inspiratory work is reduced; and increased endurance conditioning, because the patient is genuinely exercising the respiratory muscles.
• Monitor for apnea — there is no backup rate in a purely spontaneous mode.

6.12 CPAP as a Ventilator Mode

• A spontaneous mode in which the ventilated patient controls almost all aspects of the breath. Do not confuse it with noninvasive CPAP for sleep apnea — same pressure principle, different clinical setting.
• Only FIO2 and PEEP are set. One level of pressure on both inspiration and expiration. No set respiratory rate, no set VT, no set PIP.
• Used to assess the patient's respiratory rate and rhythm, work of breathing, and hemodynamic status after a period of intubation — in other words, as an extubation readiness test.
• Usually used for a short period, around 30 to 120 minutes. If the patient stays stable, assessment parameters remain within normal limits, and there is no increased work of breathing or desaturation, the patient is often extubated.
• Monitor for increased work of breathing and for apnea. The patient must be awake, alert, and breathing spontaneously.

6.13 The Newer Modes

Pressure-regulated volume control (PRVC)

A full support mode combining volume and pressure. Settings: respiratory rate, VT, PIP, PEEP, and sensitivity. There is a target VT and a PIP limit, and the ventilator attempts to deliver the desired VT with the LEAST amount of pressure, analyzing resistance and compliance breath by breath and adjusting continuously. Nursing: trend both VT and PIP, and monitor for increased work of breathing.

Airway pressure release ventilation (APRV)

• Can be a full support OR a spontaneous mode. Set two pressures (P-high, P-low) and two times (T-high, T-low).
• Most of the breath is spent at P-high and T-high — for example a pressure of 30 cm H2O for around 6 to 8 seconds — which holds collapsed alveoli open. A quick timed release to P-low for a very short T-low (about 0.8 second) allows CO2 elimination.
• VT is not a set variable; it varies with the pressure levels, compliance, resistance, and spontaneous effort.
• Adjust the pressure levels to meet OXYGENATION goals; adjust the timed releases to meet VENTILATION goals.
• Permits spontaneous breathing at any point during the inspiratory cycle, which may reduce the need for deep sedation or paralysis. APRV increases venous return to the heart and hemodynamic improvement may occur. Trend ABGs and acid-base balance.

Proportional assist ventilation (PAV)

The ventilator generates and adjusts inspiratory pressure in proportion to the patient's own respiratory effort — support is given as a percentage of patient effort (e.g., 80%), so the harder the patient works to initiate a breath, the more support arrives. The patient determines their own inspiratory flow rate and volume. Decreased work of breathing and less dyssynchrony result. PAV is of no use in a patient who is not breathing spontaneously — it will give no support at all, because there is no effort to be proportional to.

6.14 All Modes Side by Side

7.1 Four Airway Responsibilities

Artificial airway management is often shared with the respiratory therapist, and agency policy dictates who does what. The chapter frames the nurse's share as four responsibilities, and they make a usable mental checklist at the start of every shift.

7.2 Maintaining Correct Tube Placement

• Continuously monitor placement: note the exit point at the mouth or nare, assess the integrity of the tape or securement device, observe for symmetric chest wall movement, and auscultate to confirm bilateral breath sounds.
• Record and mark the position of the tube at the lip or teeth — for example 21 cm at the teeth, 23 cm at the lips.
• Assess tube position at least once per shift, and with any change in patient position, with early mobility, and before and after transport.

The chapter also names the practical safeguards. When the ET tube is repositioned or re-taped, two staff members should ALWAYS perform it — one maintaining tube position while the other works — and the tube is moved to the opposite side of the mouth, after which cuff inflation and tube placement are reconfirmed. Always assess the skin under the tube, including the upper and lower lips and chin, and under any securement device; some commercial devices increase the risk of breakdown compared with tape.

7.3 Maintaining Proper Cuff Inflation

The cuff is an inflatable sleeve encircling the lower outer wall of the tube. It stabilizes and seals the tube in the trachea, prevents escape of ventilating gases, helps maintain tube position, and seals off the lower airway to protect against aspiration. Too little air and the seal fails; too much and the tracheal mucosa is damaged.

7.4 Maintaining Tube Patency — Suctioning

Do not suction routinely. Suction when the patient needs it, and assess the need hourly.

Neurologic patients may show no signs at all that they need suctioning — suctioning at minimum once per shift is recommended in that group. Always note the color, character, consistency, and amount of sputum.

Closed versus open technique

• Closed-suction technique (CST) — the catheter is enclosed in a plastic sleeve connected directly into the patient-ventilator circuit. It reduces exposure to secretions and infection risk for both patient and staff, and it keeps the circuit closed so PEEP and oxygenation are not lost. CST is how most intubated patients are suctioned.
• Open-suction technique (OST) — used when a sterile sputum sample is needed or CST is unavailable. Best performed with 2 people: one removes the patient from the ventilator and bags, the second suctions using sterile technique with one hand designated contaminated.

Complications of suctioning

• Potential complications: hypoxemia, bronchospasm, increased intracranial pressure, dysrhythmias, hypertension, hypotension, airway trauma, pulmonary bleeding, pain, and infection.
• Three causes of dysrhythmias during suctioning: (1) hypoxemia leading to myocardial ischemia; (2) vagal stimulation from tracheal irritation — this is the bradycardia and hypotension route; (3) sympathetic stimulation from anxiety, discomfort, or pain — this is the tachycardia and hypertension route.
• STOP AT ONCE and remove the catheter if the patient becomes bradycardic or hypotensive — a vagal response has occurred. Stop if any new dysrhythmia develops, if the SpO2 falls, or if coughing is sustained. Reassess until stability returns before trying again.
• Tracheal mucosal damage comes from suction pressures greater than 120 mm Hg, overly vigorous insertion, and the catheter itself. Blood streaks or tissue shreds in the aspirate indicate mucosal damage and raise the risk of infection and bleeding — especially on anticoagulants.
• Thick, hard-to-suction secretions are caused by inadequate hydration or humidification, or by infection. Treat the cause: hydrate, humidify inspired gases through the ventilator, turn every 2 hours and mobilize early, and give antibiotics if infection is the cause.

7.5 Ventilator Alarms

Ensure that ALL ventilator alarms are ALWAYS on. They alert you to patient-ventilator dyssynchrony, ventilator disconnection or malfunction, and unplanned extubation. Alarms may be silenced or suspended for up to 2 minutes for suctioning, after which they turn back on automatically — pause, never turn off, and reactivate all alarms before leaving the patient.

7.6 Analgesia, Sedation, and Neuromuscular Blockade

• Patients on PPV may need analgesia (fentanyl, hydromorphone) and/or sedation (propofol).
• Before giving either, try to identify the CAUSE of the distress. Common causes: PPV itself, hypoxemia, hypercapnia, drugs, environmental stressors (fear, sleep deprivation), and discomfort from the tube.
• Assess effectiveness with a valid pain scale and a sedation scale — the Richmond Agitation and Sedation Scale (RASS) or Sedation Agitation Scale (SAS) — and a delirium scale. Consider relaxation techniques such as music therapy alongside drugs.
• GOAL: a patient who is awake, interacting with their environment, breathing comfortably and in synchrony with the ventilator — not a snowed one.

Neuromuscular blocking agents

• NMBAs paralyze skeletal muscles, including the diaphragm. Purpose: decrease work of breathing and provide effective synchrony with the ventilator, improving both oxygenation and ventilation. Ch. 32 names vecuronium and pancuronium.
• The paralyzed patient CAN HEAR, SEE, AND FEEL. It is essential to give IV sedation and analgesia CONCURRENTLY. Always address the patient as if they were awake and alert.
• Assess the depth of paralysis with train-of-four (TOF) peripheral nerve stimulation: four successive stimulating currents delivered along the ulnar nerve to elicit muscle twitches. The number of twitches falls as blockade deepens. Usual goal: 1 or 2 twitches out of 4.
• Also monitor for signs of pain or anxiety (changes in heart rate and BP) and for ventilator dyssynchrony; bispectral index (BIS) monitoring can help guide therapy.
• Never give an NMBA to a patient with a cholinesterase deficiency. Excess administration may cause prolonged paralysis and muscle weakness even after the drugs are stopped, so use the shortest duration and lowest dose possible.

7.7 Oral Care and VAP Prevention

Ventilator-associated pneumonia (VAP) is pneumonia occurring 48 hours or more after endotracheal intubation. It occurs in as many as 40% of all intubated patients, most often within 96 hours of starting ventilation, and it produces significantly longer ventilator days, longer hospital stays, and higher mortality.

• Most common organisms are gram-negative: Escherichia coli, Klebsiella, Streptococcus pneumoniae, Haemophilus influenzae; also antibiotic-resistant Pseudomonas aeruginosa and oxacillin-resistant Staphylococcus aureus. Colonization of the oropharynx by gram-negative organisms predisposes to gram-negative pneumonia — which is exactly why oral care is an infection-control intervention.
• Spread by: contaminated respiratory equipment, inadequate hand washing, poor room ventilation and high traffic, and the patient's decreased ability to cough and clear secretions.
• Signs suggesting VAP: fever, high WBC count, change in the color and/or amount of sputum, crackles or wheezes, and new infiltrates on chest x-ray. Management: obtain sputum cultures and start broad-spectrum antibiotics.

• Perform oral care every 2–4 hours using toothettes or a suction toothbrush, a Yankauer suction device, and toothpaste or mouthwash; use 0.12% chlorhexidine oral rinse twice daily (the narrative supports chlorhexidine at least 3 times a day to decrease oral contamination and VAP).
• Provide oral care for 1–2 minutes, suctioning often, and apply a mouth moisturizer to the oral mucosa and lips with each cleaning. With an oral ET tube the mouth is always open and the mucosa dries.
• Change all oral suction equipment and suction tubing every 24 hours. Use smaller or pediatric-sized products if space in the mouth is limited.

7.8 Nutrition

• Why it is aggressive: nutrition problems make the patient prone to poor O2 transport from anemia, delay weaning, decrease resistance to infection, and slow extubation and recovery. Nutrition depletion causes loss of muscle mass including the respiratory muscles.
• The ET tube eliminates the normal route for eating; an NG or OG tube is inserted and connected to low intermittent suction.
• Enteral nutrition is preferred because it preserves the structure and function of the gut mucosa and stops the movement of gut bacteria across the intestinal wall into the bloodstream. If EN is not possible, parenteral nutrition is used.
• Patients likely to remain intubated for 3 to 5 days should have a nutrition assessment on admission and enteral nutrition started within 24 hours (Ch. 32 states within 24 to 48 hours for ARF and ARDS). Consult the dietitian.

7.9 Prophylaxis, Mobility, and the ABCDEF Bundle

• VTE: the intubated patient is immobile, blood stases in the lower extremities, and VTE risk rises. Start VTE prophylaxis as ordered and assist the patient to sit in a chair at the bedside.
• GI/stress ulcers: serious illness, immobility, and ventilator discomfort raise the risk, and any circulatory compromise — including the reduced cardiac output caused by PPV — causes ischemia of gastric and intestinal mucosa and increases bacterial translocation. Higher risk with a pre-existing ulcer or corticosteroids. Prophylaxis: H2 blockers (e.g., ranitidine, famotidine), proton pump inhibitors (e.g., esomeprazole, pantoprazole), or enteral nutrition itself.
• Constipation: immobility, sedation, impaired circulation, decreased oral intake, opioids, and stress all decrease peristalsis, and the patient cannot exhale against a closed glottis, which makes defecation difficult. Start a bowel regimen.
• Early mobility: encourage most ventilated patients to exercise and mobilize as soon as possible. Exceptions: hemodynamic instability, patients receiving NMBAs, unstable cervical or thoracic spine fractures, and other medically contraindicated conditions. Use a portable ventilator or manual ventilation with a BVM and 100% O2 when ambulating.

7.10 Communication and Psychosocial Care

• Intubated patients are stressed by not being able to talk or communicate their needs. Methods: paper and pencil, a white board, a cellphone for texting, a communication board with pictures of common needs (convenient for patients who speak other languages), a visual alphabet for spelling (useful for patients who are weak or cannot write), picture boards, notepads, and computers.
• Explain what will happen as part of every procedure. Look directly at the patient and use hand gestures.
• The ICU has high levels of procedure-related touch and low levels of comfort-related touch; tolerance for touch varies with culture and personal history, so use comforting touch with ongoing evaluation of the response.
• Encourage the caregiver to talk to the patient even if intubated, sedated, or apparently comatose — hearing is often the last sense to decrease.
• Feeling safe is an overpowering need. Reduce anxiety by including patients and caregivers in conversations, explaining equipment and procedures, encouraging expression of concerns, and structuring the environment (photographs, personal items). Relaxation techniques and antianxiety drugs (e.g., lorazepam) may reduce the stress response.

7.11 Complications of Mechanical Ventilation

Ventilator disconnection and unplanned extubation

• Most disconnections are discovered by the LOW-PRESSURE alarm, and the most frequent site is between the tracheal tube and the adapter — push connections together firmly.
• Signs of unplanned extubation: the low-pressure alarm, decreased or absent breath sounds, respiratory distress, an audible cuff leak — and the patient may be talking to you. It is not always obvious: the tip may be sitting in the hypopharynx or esophagus.
• Response: stay with the patient and call for help; support oxygenation with a nasal cannula or manual ventilation with BVM and 100% O2; notify the HCP and RT immediately; assess for respiratory distress and the need for reintubation; if the patient cannot protect the airway or is in distress, prepare for immediate reintubation; provide emotional support.
• Prevention: ensure the tube is secured; support it during repositioning, procedures, and transfers; give adequate sedation and analgesia; follow weaning protocols, which decrease the incidence of self-extubation. Restraints deter self-extubation — explain their short-term use to patient and caregiver, discuss alternatives, and reassess the continued need.

7.12 Rescue Therapies

Rescue therapies alleviate hypoxemia in patients who cannot maintain reasonable oxygenation despite appropriate mechanical ventilation, high FIO2, and PEEP.

7.13 Weaning — Prerequisites and Trials

Weaning is the process of gradually reducing ventilator support and allowing the patient to assume greater responsibility for breathing spontaneously. Preparation begins almost as soon as the patient is intubated. Short-term ventilation (3 to 5 days) — after heart surgery, for example — usually means a straightforward wean. Long-term ventilation (longer than 5 days) tends to consist of alternating gains and losses.

Nonrespiratory factors matter as much: neurologic status, hemodynamic stability, acid-base balance, nutrition status, fluid and electrolyte balance, and hemoglobin. The ideal candidate is alert, well-rested, well-informed, and relatively free of pain and anxiety. This does not mean complete withdrawal of sedatives or analgesics — the drugs should be titrated to achieve comfort without excessive drowsiness.

Conducting the trial

• There is no "right" way to wean. Most providers attempt it early in the morning after a good night's rest, with the patient hemodynamically stable and comfortable, in a semi-recumbent position in bed or sitting in a chair. Obtain baseline vital signs and respiratory parameters, and make sure the whole team knows the plan.
• Approaches: decreasing the number of ventilator-delivered breaths in SIMV, or gradually decreasing the degree of pressure support daily. PSV provides gentle, slow respiratory muscle conditioning and may benefit deconditioned patients or those with heart problems.
• END the trial for: tachypnea, dyspnea, tachycardia, dysrhythmias, sustained desaturation (SpO2 less than 92%), hypertension or hypotension, agitation, diaphoresis, anxiety, and changes in mental status.
• If the trial fails, let the respiratory muscles REST between trials — once fatigued, they may need 12 to 24 hours to recover. Pushing a fatigued patient into another trial guarantees another failure.

7.14 Weaning Readiness — the Numbers

7.15 Extubation

• Assess muscle strength (negative inspiratory force) and endurance (spontaneous VT, vital capacity, minute ventilation, RSBI). There should be minimal secretions and an intact ability to cough and gag.
• Procedure: (1) hyperoxygenate and suction; (2) have an alternative O2 delivery device (e.g., nasal prongs) set up before you start; (3) loosen the tapes or holder; (4) have the patient take a deep breath and, AT THE PEAK OF INSPIRATION, deflate the cuff and remove the tube in one smooth motion. Rationale: the airway is at its widest at peak inspiration, and the patient exhales or coughs as the tube leaves, expelling secretions rather than inhaling them.
• After removal: encourage deep breathing and coughing; suction the oropharynx as needed; assess the ability to speak; give supplemental O2 and provide oral care.
• Monitor vital signs, respiratory status, and oxygenation closely immediately after extubation and for the first 2 to 3 hours.
• Signs of NOT tolerating extubation: decreased SpO2, tachypnea or bradypnea, tachycardia, decreased LOC, a decrease in PaO2 and an increase in PaCO2. Immediate reintubation, or a trial of noninvasive ventilation, may be needed.

8.1 Indications and Advantages

A tracheostomy is a surgically created stoma in the anterior part of the trachea. Where the ET tube is the emergency answer, the tracheostomy is the durable one.

• Early tracheotomy — done within 10 to 14 days — appears to have advantages over delayed tracheotomy when a prolonged artificial airway is expected: fewer ventilator-dependent days, reduced length of stay, decreased pain, and improved communication.
• Compared with an ET tube, the tracheostomy tube is shorter and slightly wider, which makes it easier to keep clean and promotes better oral and bronchial hygiene; it may increase comfort because no tube sits in the mouth; and there is less risk of long-term damage to the vocal cords.

8.2 Tube Anatomy and Types

• All tracheostomy tubes have a faceplate (flange) resting against the neck and an obturator used to insert the tube. Many have an outer cannula (keeps the airway patent) and an inner cannula (disposable or reusable, removed for cleaning). Others parts: 15-mm adapter, cuff, pilot balloon, inflation tube, one-way valve, rounded tip, and tie strings.
• Cuffed tubes are used most, especially if the patient needs mechanical ventilation. The cuff ensures the patient receives the volume of air delivered by the ventilator and decreases the risk of aspiration. A properly inflated low-pressure, high-volume cuff distributes pressure over a large area, minimizing pressure on the tracheal wall.
• Cuffless tubes are used for longer-term tracheostomies, when mechanical ventilation is not needed and aspiration risk has decreased; talking and eating may be possible.
• A fenestrated tube has an opening (a hole) on its dorsal surface, which promotes spontaneous breathing. With a cuffed fenestrated tube, when the cuff is DEFLATED and the inner cannula REMOVED, air can pass from the lungs up through the opening, through the vocal cords and into the upper airway — so the patient can breathe spontaneously and SPEAK. Reinflate the cuff and reinsert the inner cannula and air can no longer reach the cords.

8.3 Insertion Techniques

• Most patients who need mechanical ventilation get an oral ET tube first, because it can be inserted quickly in an emergency.
• When swelling, trauma, or upper airway obstruction prevents oral intubation, an emergent surgical CRICOTHYROIDOTOMY is needed — an incision through the skin and cricothyroid membrane on the anterior neck, completed in minutes.
• Surgical tracheostomy is usually done in the operating room under general anesthesia, often electively on an already intubated patient expected to need prolonged ventilation. A horizontal incision is made, the tube inserted, the incision sutured, and a sterile dressing applied.
• Percutaneous tracheostomy uses local anesthesia, sedation, and video guidance: the ET tube is withdrawn to the glottis, a needle is placed between the SECOND and THIRD tracheal rings, and the opening is progressively enlarged with dilators. Advantages: less risk of bleeding and fewer postoperative complications.
• Both approaches may be done at the bedside in the ED or ICU.

8.4 Immediately Before, During, and After

• Before: explain the purpose to patient and caregiver; if done at the bedside, ensure appropriate personnel including RT are present, and that a BVM, suction, and emergency resuscitation equipment are at the bedside, functional and ready. Record baseline vital signs, ensure the IV is patent, position the patient SUPINE, and give analgesia and sedation as ordered.
• During: monitor hemodynamic status and the response to sedation. Observe the SpO2 and immediately notify the HCP if it falls below 92%.
• After: the cuff is inflated IMMEDIATELY. Confirm placement by one of four methods — auscultation of the chest for air entry, EtCO2 capnography, video-assisted confirmation (percutaneous), or passage of a suction catheter through the tube. Once placement is confirmed the ET tube is removed.
• Secure the tube with cotton ties, tapes, or Velcro straps. Monitor vital signs and SpO2, obtain a chest x-ray, and record ventilator settings including mode, FIO2, and PEEP.
• Observe the amount of blood on the dressing at the insertion site — bleeding is the immediate care priority in the first few hours. Notify the HCP if bleeding persists.

8.5 Ongoing Care in the First Days

8.6 Accidental Decannulation

If the tracheostomy tube is accidentally dislodged, IMMEDIATELY CALL FOR HELP. While waiting for the HCP or RT, the options depend on agency policy and scope of practice — and on one variable above all: how old the stoma is.

8.7 Speech and Swallowing

• The spontaneously breathing patient may be able to talk. If the patient is at low risk of aspiration: (1) remove the inner cannula if non-fenestrated, (2) DEFLATE the cuff, (3) place the cap on the tube. With the cuff deflated, exhaled air can flow upward over the vocal cords.
• Passy-Muir valve: a one-way valve attached to the hub of the tracheostomy tube, used with the cuff DEFLATED. On inspiration the valve OPENS, letting the patient inhale through the tube; on exhalation it CLOSES, so air is redirected upward around the tube and through the vocal cords — the patient exhales through the nose and mouth instead of the tracheostomy, which produces speech. Patients may tolerate only short periods at first. Remove the valve immediately at any sign of respiratory distress.
• An inflated cuff may cause swallowing problems by interfering with the normal function of the muscles used to swallow. A speech language therapist should assess swallowing, using thickened fluids of different consistencies to test for aspiration. If the patient can swallow without aspirating when the cuff is deflated, the cuff may be left deflated or a cuffless tube inserted, and varying levels of thickened fluids and soft foods become possible.

8.8 Planned Decannulation

• Decannulation is possible when the primary condition has resolved and the patient is hemodynamically stable, has a stable intact respiratory drive, can adequately exchange air, and can independently expectorate secretions.
• Procedure: explain what will happen; monitor vital signs; suction through the tracheostomy; clear the mouth of oral secretions; loosen or cut the tapes; remove visible sutures; deflate the cuff; and pull the tube outward in one smooth motion. STOP if you meet any resistance and notify the HCP immediately.
• After removal: apply a sterile occlusive dressing and monitor for bleeding; change the dressing if soiled; close the stoma with tape strips if needed. Monitor respiratory status and O2 saturation for airway compromise, and apply an alternate O2 device if needed.
• Teach the patient to splint the stoma with the fingers when coughing, swallowing, or speaking.
• Epithelial tissue begins to form in 24 to 48 hours and the opening closes within 4 or 5 days. Surgery to close the tracheostomy is usually not needed.

8.9 The Long-Term and Home Tracheostomy

• Care is the same as for a new tracheostomy — site observation, inner cannula cleaning, suctioning, tape changes.
• Tube change schedule: about 1 MONTH after the first tube change, then EVERY 1 TO 3 MONTHS. The rationale for changing it at all is that doing so permits assessment of the stoma and cleaning of the tube.
• Teach the patient signs and symptoms of infection and how to change the tube at home using CLEAN technique. Note the contrast: sterile technique in the hospital, clean technique at home. Engaging patients in their own care decreases complications and infection and promotes well-being.
• Home mechanical ventilation: chronically ill ventilated patients meeting specific criteria may go home. Both negative and positive pressure ventilators can be used; negative pressure ventilators need no artificial airway and are less complicated, while small portable positive pressure ventilators mount on a wheelchair or bedside table with simpler settings and alarms.
• Advantages: less strain on family dynamics than a hospital stay; more mobility and participation in ADLs on a personalized schedule. Disadvantages: equipment problems, reimbursement (disposables may not be covered), and caregiver stress and fatigue.
• Nursing actions: carefully assess financial resources, and hold a care conference BEFORE starting a discharge teaching plan. Caregivers may seem enthusiastic without understanding the financial and personal sacrifices ahead. Encourage respite care.

9.1 What Acute Respiratory Failure Is

ARF occurs when oxygenation, ventilation, or both are inadequate. The chapter is emphatic about one framing: ARF is not a disease — it is a symptom that reflects insufficient lung function. That matters clinically, because the primary aim of care is always to identify and treat the underlying cause; the ventilator only buys time. ARF occurs with problems involving the lungs or other body systems — a spinal cord injury and a drug overdose both produce it with structurally normal lungs.

9.2 Classification

Each type is further divided by speed: acute (minutes to hours) and chronic (several days or longer). Five conditions can produce either type and appear at the top of both columns of the causes table: ARDS, asthma, chronic bronchitis, emphysema, and pulmonary edema.

9.3 Acute Versus Chronic — and Acute-on-Chronic

9.4 The Four Mechanisms of Hypoxemia

Every hypoxemic patient in this module is hypoxemic by one or more of four mechanisms. Learn them as a set, because acute hypoxemic respiratory failure is rarely caused by a single factor — most often it is a combination of two or more, and the treatment differs by mechanism.

9.5 Mechanism 1 — V/Q Mismatch

• Most common causes: increased secretions in the airways (COPD), increased secretions in the alveoli (pneumonia), or bronchospasm (asthma). Also pain, alveolar collapse (atelectasis), and pulmonary emboli.
• Pulmonary emboli affect perfusion: they limit blood flow distal to the occlusion, so some areas remain normally ventilated while others lose perfusion. A large embolus blocking a major pulmonary artery can cause severe hemodynamic instability.
• Treatment: treat the cause. O2 therapy is an appropriate first step to reverse the hypoxemia. Monitor with frequent ABGs, pulse oximetry, continuous assessment of level of consciousness, respiratory rate and rhythm, and the response to O2.

9.6 Mechanism 2 — Shunt

• Anatomic shunt: blood passes through an anatomic channel in the heart — for example a ventricular septal defect — and bypasses the lungs entirely.
• Capillary shunt: blood flows through pulmonary capillaries without taking part in gas exchange, because the alveoli are filled with fluid (as in pneumonia, pulmonary edema, or ARDS).
• Patients with shunt are usually MORE hypoxemic than patients with V/Q mismatch and often need mechanical ventilation with a high FIO2.

9.7 Mechanism 3 — Diffusion Limitation

• Gas exchange across the alveolar-capillary membrane is compromised by a process that damages or destroys the membrane or affects blood flow through the capillaries.
• Conditions that thicken (fibrose) the membrane slow gas transport: pulmonary fibrosis, interstitial lung disease, ARDS. Accumulation of fluid, white blood cells, or protein in the alveoli — as in pulmonary edema — has the same effect.
• Classic sign: hypoxemia that worsens with exercise but not at rest. With exercise, blood moves quickly through the lungs, decreasing the time available for O2 to diffuse across the membrane.
• The same time problem occurs when cardiac output is markedly increased — high-output heart failure, for example — because blood circulates through the pulmonary capillary bed too fast for full equilibration.

9.8 Mechanism 4 — Alveolar Hypoventilation

A decrease in ventilation that increases the PaCO2. Common causes are CNS problems, chest wall dysfunction, acute asthma, and restrictive lung disease. It is mainly a mechanism of hypercapnic respiratory failure, but it contributes to hypoxemia as well — alveolar gas that is not refreshed accumulates CO2 and loses O2.

9.9 Hypercapnic Respiratory Failure

The respiratory system cannot keep CO2 within normal limits, from either an increase in CO2 production or a decrease in alveolar ventilation. The important structural point: hypercapnic ARF from CNS, neuromuscular, and/or chest wall causes can occur with completely normal lungs. The bellows fails, not the gas exchanger.

9.10 Manifestations Side by Side

9.11 Assessment and Diagnostics

• PRIORITY: immediately assess the patient's ability to maintain a patent airway and to breathe. Everything else follows that.
• Observe TRENDS in ABGs, pulse oximetry, and assessment findings, and remain alert to subtle changes. A thorough assessment may allow early detection of respiratory insufficiency and prevent progression to failure.
• Monitor patients with pre-existing cardiac and/or respiratory disease closely — any change in overall condition can cause significant respiratory and hemodynamic decompensation.
• Most common studies: chest x-ray and ABG analysis. The chest x-ray identifies causes (atelectasis, pneumonia); ABGs evaluate oxygenation, ventilation, and acid-base balance; pulse oximetry monitors oxygenation indirectly.
• Other studies: CBC, serum electrolytes, urinalysis, 12-lead ECG, blood and sputum cultures, CT or V/Q lung scan if pulmonary embolus is suspected, and EtCO2 for ventilation trends in severe ARF.
• Initially cardiac output may be INCREASED because of the stress response; as hypoxemia, hypercapnia, and acidosis become more severe, cardiac output FALLS. The same reversal appears in the vital signs — tachycardia progressing to bradycardia, hypertension progressing to hypotension.

9.12 Management

• Prevention matters most in patients with neuromuscular, cardiac, or respiratory problems. Preventing atelectasis and pneumonia, preventing complications of immobility, and optimizing hydration and nutrition decreases the risk for ARF. Early teaching strategies: deep breathing and coughing, incentive spirometry, and early ambulation.
• Overall goals for the patient with ARF: independently maintain a patent airway; absence of dyspnea or a return to baseline breathing; effective cough with secretion clearance; normal ABGs or values within the patient's baseline; breath sounds within baseline.
• Nutrition: the hypermetabolic state of critical illness raises calorie needs, and nutrition depletion causes loss of muscle mass including the respiratory muscles, which delays recovery. Ideally start enteral nutrition within 24 to 48 hours.

9.13 Drug Therapy

9.14 Gerontologic Considerations

• The reduced ventilatory capacity that accompanies aging increases the risk for ARF.
• Physiologic changes: alveolar dilation, larger air spaces, loss of surface area for gas exchange, decreased elastic recoil, decreased chest wall compliance, and decreased respiratory muscle strength.
• In older adults the PaO2 falls further and the PaCO2 rises higher before the respiratory system is stimulated to change the rate and depth of breathing. That delayed response is itself a contributor to respiratory insufficiency — the warning system is slow, so the patient presents later and sicker.
• A history of tobacco use accelerates age-related respiratory changes, and poor nutrition status with less cardiopulmonary reserve increases the risk of further compromise.

10.1 Definition and Scale of the Problem

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. Hold that definition precisely: the injury is to the membrane, the consequence is that fluid crosses where it should not, and everything else — the shunt, the refractory hypoxemia, the stiff lungs — follows from that.

Next to septic shock, ARDS is one of the most common conditions seen in the adult ICU. Besides the lungs, the vital organs most often involved are the kidneys, liver, and heart.

10.2 Etiology — Direct and Indirect Lung Injury

The most common cause of ARDS is SEPSIS. It may also develop from multisystem organ dysfunction syndrome, and patients with multiple risk factors are 3 or 4 times more likely to develop ARDS.

10.3 Pathophysiology — the Chain

One injury to the alveolar-capillary membrane sets off the release of inflammatory mediators, and from there five parallel consequences converge on the same endpoint.

The neutrophil is the cell at the center of it. The exact cause of the membrane damage is unknown, but it is thought to be stimulation of the inflammatory and immune systems, which attracts neutrophils to the pulmonary interstitium. Those neutrophils release biochemical, humoral, and cellular mediators producing increased pulmonary capillary membrane permeability, destruction of collagen, formation of pulmonary microemboli, and pulmonary artery vasoconstriction.

10.4 Phase 1 — Injury or Exudative Phase

• Timing: usually 24 to 72 hours after the initial insult; generally lasts 7 to 10 days.
• Engorgement of the peribronchial and perivascular interstitial space causes interstitial edema; that fluid then crosses the alveolar membrane into the alveolar space.
• V/Q mismatch and shunt develop because the alveoli fill with fluid — blood in the capillary network cannot be oxygenated.
• The early breathing pattern is deceptive: hypoxemia and stimulation of juxtacapillary receptors in the stiff lung (the J reflex) cause an increased respiratory rate with a decreased tidal volume. More CO2 is blown off, producing respiratory alkalosis, and cardiac output increases as a compensatory response to hypoxemia.
• As atelectasis, pulmonary edema, and shunt increase, compensation FAILS → hypoventilation, decreased cardiac output, and decreased tissue O2 perfusion.
• As the lungs become less compliant, the patient must generate higher airway pressures to inflate stiff lungs; the work of breathing rises, and at this point the patient needs mechanical ventilation.

10.5 Phase 2 — Reparative or Proliferative Phase

• Timing: begins 1 to 2 weeks after the initial lung injury.
• Continued influx of neutrophils, monocytes, lymphocytes, and fibroblasts as part of the inflammatory response.
• Increased pulmonary vascular resistance and pulmonary hypertension occur because fibroblasts and inflammatory cells destroy the pulmonary vasculature.
• Lung compliance continues to decrease due to interstitial fibrosis, and hypoxemia continues because of the thickened alveolar membrane, causing V/Q mismatch, diffusion limitation, and shunting. Fluid in the lungs and secretions in the airways increase airway resistance.
• The phase is complete when dense, fibrous tissue replaces the diseased lung. If the reparative phase persists → widespread fibrosis. If it stops → the lesions often resolve.

10.6 Phase 3 — Fibrotic Phase

• Timing: may start as early as 24 hours after the initial injury. Note that the phases overlap rather than following one another cleanly.
• Not all patients who develop ARDS enter the fibrotic stage; for those who do, it carries a poorer prognosis and they may need several weeks of long-term mechanical ventilation.
• Collagenous and fibrous tissues remodel the lung: diffuse scarring, interstitial fibrosis, and alveolar duct fibrosis decrease lung compliance and reduce the surface area available for gas exchange, so hypoxemia continues.
• Varying degrees of pulmonary hypertension result from pulmonary vascular destruction and fibrosis.
• Factors determining the clinical course: the nature of the initial injury; the extent and severity of comorbidities; how quickly the patient received medical care; and additional pulmonary complications such as pneumothorax. Genetics may play a part. It is not known why injured lungs repair in some patients and worsen in others.

10.7 Clinical Manifestations as ARDS Evolves

10.8 The P/F Ratio

The PaO2/FIO2 (P/F) ratio is the patient's PaO2 divided by the FIO2 they are receiving, expressed as a decimal. It exists because a PaO2 means nothing without knowing what oxygen was needed to produce it: a PaO2 of 80 on room air is healthy, and a PaO2 of 80 on 100% oxygen is catastrophic.

10.9 Management — Seven Best Practices

Management of ARF applies to the patient with ARDS; the following is additional care. Patients with moderate to severe ARDS are cared for in an ICU, and all mechanically ventilated ARDS patients have continuous heart rate, respiratory rate, BP, and SpO2 monitoring, with EtCO2 monitoring as standard. Overall goals: a PaO2 of 60 mm Hg or higher and adequate ventilation to correct acid-base imbalance; longer-term, a PaO2 within normal limits for age on room air, SaO2 greater than 90%, resolution of the cause, and clear lungs on auscultation.

Oxygen administration

• Initially a high-flow system delivering higher concentrations may be all that is needed, with continuous SpO2 monitoring to assess effectiveness. For most patients with ARDS, high-flow O2 (including BiPAP) is temporary — as the failure worsens it cannot keep the PaO2 acceptable.
• Patients with moderate to severe ARDS and refractory hypoxemia need mechanical ventilation.
• Even on the ventilator, the patient may need an FIO2 of 70% or higher to keep the PaO2 at least 60 mm Hg, and most providers agree that in the injury and reparative phases they may have to accept a lower-than-normal PaO2 (55 to 80 mm Hg) and SpO2 (88% to 95%).

Mechanical ventilation and low tidal volumes

• Pressure-control ventilation helps keep inspiratory and plateau pressures from becoming too high, preventing alveolar overdistention and rupture — by reducing the pressure going into stiff, noncompliant lungs, further lung injury is prevented. However, no mode of mechanical ventilation is superior to the others.
• Patients with ARDS are ventilated with a low tidal volume of 4 to 8 mL/kg. Delivering a large VT into stiff lungs causes volutrauma and barotrauma; volutrauma causes alveolar fractures — damage or tears in the alveolar-capillary membrane — and the movement of fluids and protein into the alveolar spaces.
• Low VT ventilation reduces mortality and the risk of volutrauma. This is the single intervention most likely to be the correct answer to "which intervention prevents or limits volutrauma."

Permissive hypercapnia

• Definition: as a result of delivering a lower-than-normal tidal volume, the PaCO2 slowly rises above normal limits. It is a CONSEQUENCE of low VT ventilation, not a strategy in its own right.
• A PaCO2 of up to 60 mm Hg is acceptable in the early phase of ARDS, and the patient usually tolerates it if the rise is GRADUAL, allowing the brain and systemic circulation to compensate.
• Frequent ABGs are needed, with careful monitoring of pH, PaO2, and PaCO2. The pH is kept between 7.30 and 7.45.
• Because acidosis and rising CO2 are powerful stimulants to breathe, the patient receives continuous IV analgesia and sedation — otherwise they would fight the ventilator constantly.
• CONTRAINDICATED in pregnancy and in patients with traumatic brain injury or increased ICP, because a rising CO2 dilates cerebral vessels and raises intracranial pressure further.

PEEP in ARDS

• PEEP at 5 cm H2O is applied routinely to compensate for the loss of glottic function with an ET tube. It increases functional residual capacity — the volume of air remaining in the lungs at the end of a normal expiration — and helps open ("recruit") collapsed alveoli.
• Application: increments of 3 to 5 cm H2O until oxygenation is adequate, with an FIO2 of 60% or less if possible. PEEP allows the FIO2 to be lowered, which is how it protects against O2 toxicity.
• ARDS patients may need higher levels — 10 to 20 cm H2O. There is no identified optimal level of PEEP for ARDS.
• Complications, with the mechanism: added intrathoracic and intrapulmonic pressure is transmitted to surrounding structures — the inferior vena cava and the heart — at end expiration, which compromises venous return to both sides of the heart, producing dramatic reductions in preload, cardiac output, and BP. High PEEP or excess inspiratory pressures cause barotrauma and volutrauma.

10.10 Prone Positioning and Rotation Therapies

• Indication: patients with refractory hypoxemia and ARDS who do not respond to other strategies to increase the PaO2.
• Mechanism: turning the patient prone better matches perfusion to ventilation. Air-filled alveoli in the anterior (ventral) lung become dependent, so their overdistention decreases; alveoli in the posterior (dorsal) lung are recruited — given the chance to re-expand — so collapse decreases. Oxygenation improves.
• Staffing: an ICU intensivist, a respiratory therapist, and AT LEAST 3 NURSES. Special attention must be given to securing and maintaining the airway before, during, and after proning, and the patient is reattached to hemodynamic monitoring once positioned.
• Effects: some patients improve enough to allow a reduction in FIO2 or PEEP. Watch for hemodynamic instability (dysrhythmias, falling BP) from fluid shifts, and expect more need for suctioning as secretions mobilize.
• Timing: prone EARLY in the course of ARDS. Patients can stay prone for up to 16 hours per day (Ch. 28 states that patients with refractory hypoxemia and ARDS should remain prone at least 12 hours per day). The optimal length of time is not known.

For either therapy, obtain baseline pulmonary assessments — respiratory rate and rhythm, breath sounds, ABGs, SpO2 — and continue to monitor throughout.

10.11 ECMO

ECMO is used most often in specialized ICUs in major cities. A large blood vessel — most often the internal jugular, femoral artery, or femoral vein — is cannulated; blood exits the body into the ECMO unit where O2 is delivered and CO2 removed, and oxygenated blood is returned. ECCO2R is similar but does not require as high a blood flow rate. Both are expensive and require specially trained personnel, and ECMO requires systemic anticoagulation, so bleeding risk is weighed before starting.

10.12 Supportive Therapy

Analgesia, sedation, and neuromuscular blockade

• Essential, by direct IV push or continuous infusion, to decrease the discomfort of the ET tube, reduce work of breathing, and prevent ventilator dyssynchrony.
• Patients breathing asynchronously may benefit from adjusting ventilator inspiratory flow rates or other settings first.
• Those who remain asynchronous despite aggressive analgesia and sedation may need an NMBA (vecuronium, pancuronium) to relax skeletal muscle and promote synchrony.
• A patient receiving neuromuscular blockade can appear to be asleep but still be awake and in pain. ALWAYS give concurrent analgesia and sedation. Use the NMBA for the shortest duration and lowest dose possible.
• Monitoring sedation depth under blockade is difficult: assess the respiratory rate and whether the patient is taking breaths above the set rate, use EtCO2 monitoring, and use a peripheral nerve stimulator to assess the depth of paralysis.

Promoting tissue perfusion

• Patients with ARDS are at risk for hemodynamic compromise, and those on PPV and PEEP often have decreased cardiac output.
• Causes of the decreased cardiac output: decreased venous return from the PEEP-induced increase in intrathoracic pressure; dysrhythmias; decreased preload; and changes in intrathoracic or intrapulmonary pressures from PPV. Alveolar hyperinflation and increased right ventricular afterload limit blood flow from the right heart through the pulmonary vasculature to the left heart.
• BP and MAP are important indicators of the adequacy of cardiac output. Monitor ECG, arterial BP, and SpO2 continuously; CVP may be ordered; newer technologies allow noninvasive monitoring of stroke volume variation, cardiac output, and ScvO2/SvO2.
• Closely monitor BP and indicators of cardiac output and tissue perfusion with the START of, or CHANGES in, mechanical ventilation — that is when the pressure shift happens. Treat a decreased cardiac output with IV fluids, drugs, or both: norepinephrine, vasopressin, dopamine, dobutamine.

Fluid balance and nutrition

For nutrition, the reasoning is the same as in ARF: nutrition depletion causes loss of muscle mass including the respiratory muscles, which may prolong mechanical ventilation and delay recovery. Consult the dietitian and start enteral nutrition as soon as possible, ideally within 24 to 48 hours.

10.13 Complications

On long-term lung function: most patients recover from ARDS within a year, many with normal to near-normal lung function — but not all. Abnormal lung function can persist for years or for the rest of the patient's life, and the key factors are the severity of scarring and changes within the lungs, with contributions from mechanical ventilation, the duration of ventilation, and the use of extracorporeal life support. Survivors commonly report fatigue, chest pain, shortness of breath after minimal activity, and persistent dyspnea.

11.1 Why Both Chapters Depend on This

Ch. 32 defines both types of respiratory failure by blood gas values, and Ch. 28 uses the gas to set ventilator settings, to judge weaning readiness, and to detect the complications of ventilation. ABGs evaluate oxygenation (PaO2), ventilation (PaCO2), and acid-base balance (pH and bicarbonate); pulse oximetry monitors oxygenation only, and only indirectly.

11.2 A Four-Step Method

The direction rule in steps 2 and 3 has a physiologic reason. CO2 dissolves to form carbonic acid, so it behaves like an acid: more CO2 means a lower pH. Bicarbonate is a base, so it behaves like a base: more bicarbonate means a higher pH. Whichever value is moving with the acid-base disturbance is the cause; whichever is moving against it is compensating.

11.3 Worked Examples From the Chapters

11.4 Ventilator Changes and the Gas They Fix

A great many questions ask which setting to change given an ABG. The mapping is short, because CO2 is controlled by minute ventilation and O2 is controlled by FIO2 and PEEP.

13.1 Oxygenation and Failure Thresholds

13.2 Oxygen Delivery at a Glance

13.3 Airways, Intubation, and Chest Tubes

13.4 Ventilator Settings and Weaning

13.5 Prevention Bundles and Timings

13.6 Tracheostomy Numbers

13.7 ARF and ARDS Numbers

13.8 Discriminators — If You Remember Nothing Else