NURS 471 Week 4: Care of the Patient with Acute Respiratory Failure

Two Main Functions of the Respiratory System

Ventilation = mechanical act of moving air into and out of respiratory tree; involves musculoskeletal and nervous systems.

Respiration = transport/diffusion of O2 and CO2 between alveoli and pulmonary capillaries.

Disruption of either (ventilation or respiration) can cause respiratory failure.

Mechanics of Ventilation and Compliance

Inspiration: diaphragm contracts & flattens → ↑ thoracic volume → negative intrapulmonary pressure; intercostals assist; in distress, accessory muscles (scalenes, SCM) recruited → ↑ work of breathing (WOB).

Compliance = ability of lungs/thorax to stretch and expand given a change in pressure.

Decreased Compliance

pulmonary fibrosis; stiff lungs → higher pressures needed, ↑ WOB.

Increased Compliance

emphysema/COPD → lungs overexpand, but poor recoil.

Types of Respiratory Failure

Acute respiratory failure (ARF): pulmonary system cannot adequately exchange O2 or remove CO2.

Type I respiratory failure (hypoxemic)

Type II respiratory failure (hypoxemic hypercapnic)

Type I Respiratory Failure

Impaired Gas Exchange: Hypoxemic

Related to:

-Alterations in alveolar capillary membrane.

-Disruption of O2 transport from alveolus to arterial flow.

Excessive Secretions.

-V/Q mismatch

Hypoxemia: PaO2 ≤ 60 mmHg on ≥ 60% FiO2.

Causes: pneumonia, cardiogenic pulmonary edema, ARDS, aspiration, atelectasis.

Nursing diagnosis: Impaired gas exchange.

Type I Respiratory Failure Desired Outcomes

PaO₂ > 80 mmHgon room air

SaO₂ > 90% on room air

Type I Respiratory Failure Interventions

Provide supplemental O2

Optimal positioning

Maintaining airway patency

Treat underlying causes of Alveolar Capillary Membrane alterations, V/Q mismatches

Type II Respiratory Failure

Ineffective Breathing Pattern: hypoxemic hypercapnic

Ventilation insufficient; failure to blow off CO2 and take in enough O2.

PaCO2 > 45 mmHg with pH < 7.35.

Hypercapnia: ↑PaCO₂, ↓pH, ↓SaO₂/PaO₂ is a hypercapnic patter of this type of ventilatory failure.

Nursing diagnoses: Impaired spontaneous ventilation, Ineffective breathing pattern.

Type II Respiratory Failure: Causes

Alveolar Hypoventilation

Musculoskeletal Dysfunction

Anatomical lung dysfunction: COPD.

CNS depression: narcotic overdose, head injury.

Neuromuscular: muscular dystrophy, ALS, Guillain-Barré (ascending paralysis → diaphragmatic failure).

Musculoskeletal/structural: kyphosis, multiple rib fractures (flail chest)

Mixed failure can occur (e.g., COPD with acute pneumonia).

Type II Respiratory Failure Desired Outcomes

PaCO₂ 35-45 mmHg with spontaneous breathing

Spontaneous tidal volume of 7mL/kg

Type II Respiratory Failure Interventions

Provide mechanical ventilation as needed

Treat causes of alveolar hypoventilation

Optimize musculoskeletal dysfunctions

Optimize neurological deficits

Ventilation-Perfusion (V/Q)

Normal ratio ≈ 1:1 (ventilation matches perfusion).

Mismatch: Imbalance between the amount of oxygen reaching the alveoli (ventilation) and the blood flowing to the lungs ( perfusion).

Dead Space Unit

Normal Ventilation, No perfusion

Potential Cause - pulmonary artery blood clot blocking flow to an area completely

Key point: This is physiologic dead space: air is getting there, but there is no blood to pick up oxygen or drop off CO₂.

Ventilation partially compromised

Ventilation to that unit is reduced but not zero (e.g., narrowing/partial blockage from mucus, bronchospasm).

Perfusion is relatively normal → V/Q < 1, but not zero.

Key point: This is low V/Q (poor ventilation relative to perfusion), which is a common form of V/Q mismatch seen in diseases like COPD, asthma, or areas with mucus plugging.

Think:

Shunt = no ventilation

Low V/Q = decreased ventilation

Perfusion partially compromised

Ventilation is normal, but blood flow is reduced (partial obstruction, e.g., smaller pulmonary emboli).

So ventilation > perfusion → V/Q > 1, but not infinite

Key point: This is high V/Q (good air, not enough blood), another type of V/Q mismatch.

Absolute Shunt Unit

No ventilation, normal perfusion

Potential Causes: pneumonia, tumor, fluid, not breathing, anything blocking ventilation (e.g., pneumonia, atelectasis).

Silent Unit

Absence of both ventilation and perfusion (severe ARDS, Large Pneumothorax).

Oxyhemoglobin dissociation curve

97% of O2 carried on Hgb (SaO2), ~3% dissolved (PaO2).

Right shift = ↓ Hgb affinity for O2 → easier O2 release to tissues; Caused by ↑ temp, acidosis, ↑ CO2, ↑ 2,3-DPG.

Left shift = ↑ affinity → O2 held tightly, ↓ tissue delivery; Caused by hypothermia, alkalosis, ↓ CO2, ↓ 2,3-DPG.

SaO2 < 90% corresponds to rapid PaO2 drop → unsafe; monitor closely and intervene.

Systematic ABG interpretation

Assess oxygenation: PaO2 and SaO2 relative to FiO2.

Assess pH (acidosis vs alkalosis), then PaCO2 (respiratory) and HCO3 (metabolic).

Respiratory acidosis: ↑ PaCO2 + ↓ pH; respiratory alkalosis: ↓ PaCO2 + ↑ pH.

Metabolic acidosis: ↓ HCO3 + ↓ pH; metabolic alkalosis: ↑ HCO3 + ↑ pH.

Compensation:

-Acute metabolic acidosis → respiratory compensation (↑ RR, "blow off" CO2).

-Acute respiratory acidosis → metabolic compensation (kidneys ↑ HCO3 over days).

-Normal pH with abnormal PaCO2/HCO3 suggests compensated state.

A-a gradient & P/F ratio

Alveolar O2 (PAO2) calculation and A–a gradient: normal < 20 mmHg, ↑ gradient = impaired gas exchange (e.g., shunt/VQ mismatch).

Helps figure out why a patient is hypoxemic (normal vs high A–a → hypoventilation vs V/Q mismatch/shunt/diffusion).

P/F ratio = PaO2 / FiO2 (FiO2 as decimal); normal 400–500; lower values indicate worse shunt (ARDS severity metric)

Quickly quantifies how severe the oxygenation problem is and is used to classify ARDS.

A-a gradient

What it is:

is the difference between the alveolar partial pressure of oxygen (PAO₂, from the alveolar gas equation) and the arterial partial pressure of oxygen (PaO₂, from an ABG); it tells you how efficiently oxygen is crossing the alveolar–capillary membrane into the blood.

A–a gradient=PA​O2​−Pa​O2​​: the difference between alveolar oxygen (PAO₂) and arterial oxygen (PaO₂).

It tells you how well oxygen is moving from alveoli into the blood (i.e., the efficiency of gas exchange).ncbi.nlm.nih+1

In a perfect lung with no diffusion barrier or V/Q mismatch, PAO₂ and PaO₂ would be equal and the A–a gradient would be zero; in reality there is a small normal gradient due to minor physiologic shunt and V/Q variability.

What an increased A-a gradient means

Elevated A–a gradient = oxygen can’t get from alveoli to blood efficiently.

Causes include:

V/Q mismatch (low V/Q, shunt-like states)

Right-to-left shunt (anatomic or intrapulmonary)

Diffusion problems (e.g., severe interstitial lung disease).

Normal A–a in a hypoxemic patient → think hypoventilation or low FiO2 (high altitude, etc.).

High A–a in a hypoxemic patient → think shunt, V/Q mismatch, or diffusion defect.

P/F ratio (PaO₂/FiO₂)

What it is:

P/F ratio = PaO₂ / FiO₂, where FiO₂ is written as a decimal (e.g., 21% = 0.21, 40% = 0.40).

It’s also called the PaO₂/FiO₂ ratio, P/F, or Horowitz index.

It measures overall oxygenation efficiency for a given FiO₂ and is used as a surrogate for shunt fraction and to grade ARDS severity.

ARDS severity (Berlin definition)

lower values indicate worse shunt

Mild ARDS: PaO₂/FiO₂ 200–300 mmHg.

Moderate ARDS: PaO₂/FiO₂ 100–200 mmHg.

Severe ARDS: PaO₂/FiO₂ ≤ 100 mmHg.

How to think about it clinically:

Start with an ABG: say PaO₂ = 60 mmHg on FiO₂ 0.5 (50% O₂).

P/F = 60 / 0.5 = 120 → moderate ARDS–range oxygenation.

Clinical Manifestations of Respiratory Decompensation

*Inadequate Airway

*Inadequate ventilation

*Inadequate gas exchange

Inadequate Airway

Stridor (high-pitched, upper airway obstruction; e.g., epiglottitis, croup, foreign body, anaphylaxis, post-extubation edema).

Noisy respirations.

Supraclavicular/intercostal retractions, nasal flaring.

Labored breathing with accessory muscle use.

Inadequate Ventilation

Absence of air exchange at nose/mouth; minimal/absent chest wall motion.

Manifestations of obstructed airway

Paradoxical chest movement (flail chest) from multiple rib fractures.

Decreased/absent breath sounds on affected side.

Restlessness, anxiety, confusion.

ABGs: ↓ PaO2, ↑ PaCO2, ↓ pH.

Inadequate Gas Exchange

Tachypnea, hypoxemia.

Decreased PaO2

Chest infiltrates on CXR (e.g., pneumonia, ARDS).

Early: dyspnea, rapid shallow breathing, use of accessory muscles, dry cough, abnormal breath sounds, tachycardia, fever, mental status changes.

Diagnostic Tests

History and physical (focus on respiratory history, exposures, comorbidities).

Pulse oximetry; ABG analysis (gold standard for respiratory status).

Chest X-ray; CT for detailed assessment and ARDS severity/response monitoring (balance benefit vs transport risk).

Labs: CBC, sputum and blood cultures, electrolytes.

ECG.

V/Q scan if PE suspected.

Treatment Type I

(hypoxemic): treat underlying cause (e.g., pneumonia, pulmonary edema, ARDS, aspiration, atelectasis) + oxygen therapy; may need mechanical ventilation.

Treatment Type II

(hypoxemic/hypercapnic): treat underlying cause (e.g., COPD, neuromuscular, CNS depression, chest wall trauma) + support ventilation (NIV or invasive ventilation).

Oxygen Therapy

Indications and goals

Indicated for hypoxia: ↓ PaO2, SaO2, or SpO2 plus clinical signs (tachypnea, tachycardia, SOB, ↑ WOB, restlessness, HTN, confusion, dysrhythmias).

Goal: correct alveolar and tissue hypoxia (↑ PaO2 to acceptable level, ↓ RR and WOB).

Low-flow devices

Nasal cannula

Simple mask

Partial rebreather mask

Non-rebreather mask

Venturi mask

Nasal cannula

up to 6 L/min

FiO2 approx 25-45%

Simple mask

~8-12 L/min

FiO2 ~35-60%.

Partial rebreather mask

reservoir bag with vents; FiO2 40-60%.

Non-rebreather mask

10-15 L/min

one-way valves prevent room air entrainment; FiO2 up to ~100%.

If patient removes NRB for water, SpO2 can drop sharply; sometimes NC is left on underneath to avoid going from 100% to 0%.

Venturi mask

precise FiO2 via adapters/dials; port must remain uncovered for accurate delivery.

High-flow oxygen therapy

High-flow nasal cannula/face mask delivers flows above patient's inspiratory flow (e.g., up to 60 L/min); provides a more reliable FiO2 and some positive pressure effect; heated and humidified.

Helps decrease WOB, may create oxygen reservoir in dead space, and improves comfort/secretions.

Clear condensation; keep collection chamber below face to avoid splashing.

Pharyngeal airways

(airway adjuncts)

Nasopharyngeal airway

Oropharyngeal airway

Nasopharyngeal airway

soft tube from nares to posterior pharynx; used even in conscious patients; size = earlobe to nose; lubricate before insertion.

Oropharyngeal airway

rigid; measure from corner of mouth to angle of jaw; contraindicated if alert with intact gag; inserted with distal end up then rotated 180°.

Noninvasive Ventilation (NIV)

ventilatory support without invasive airway (ETT/trach); interfaces: nasal pillows, oronasal/full-face mask, or helmet.

Types: CPAP and BIPAP

Indications: COPD exacerbation, obesity hypoventilation, cardiogenic pulmonary edema, lung contusions.

Contraindications: apnea, recent airway/GI surgery; caution in risk for aspiration, excessive secretions, poor airway protection, severe hypoxemia/acidosis, multi-organ failure, hemodynamic instability.

CPAP

continuous positive airway pressure (same pressure in inspiration and expiration, e.g., 5-15 cmH2O); recruits alveoli, prevents atelectasis, ↑ FRC, improves oxygen diffusion.

BiPAP

higher inspiratory pressure (IPAP) + lower expiratory pressure (EPAP), e.g., 15/5; reduces WOB more, increases comfort; may not significantly change mortality vs CPAP.

Oxygen Therapy Complications

Complications: hypotension in hypovolemia (↓ preload), aspiration, skin breakdown (bridge of nose), gastric insufflation, barotrauma, dryness, anxiety.

Oxygen Therapy Nursing Care

Monitor RR, depth, effort, SpO2/ABGs (effects evident within ~15 minutes).

Stay with patient during initiation; manage anxiety, give ordered anxiolytics.

Oral care, protect skin (gel pads under mask), periodic mask removal to offload pressure.

Ensure patient can remove mask if vomiting; restraints are generally inappropriate with NIV.

Elevate HOB ~45° to optimize ventilation and reduce aspiration risk.

During meals/hygiene: temporarily remove mask and use NC or high-flow O2 if tolerated; closely monitor SpO2 and respiratory status.

Invasive Mechanical Ventilation

Endotracheal tubes (ETT)

Nasotracheal tubes

Tracheostomy

Endotracheal tubes (ETT)

mouth → trachea; cuff seals trachea, secures depth, prevents aspiration

radiopaque line assists with CXR confirmation

some tubes have subglottic suction ports.

Nasotracheal tubes

nose → trachea when oral route not possible (trauma, surgery, anatomy).

Tracheostomy

indicated for long-term ventilation (>21 days), airway protection, or obstruction

can improve comfort, ADLs, may shorten ventilation time

single vs double lumen

complications: bleeding, infection, ulceration, dysphonia, obstruction, fistulas.

Rapid Sequence Intubation

Pre-intubation: explain to patient/family, ensure sedation/paralytic meds ready (etomidate, succinylcholine, rocuronium, propofol, midazolam). (PPT "Medications for intubation")

During procedure: monitor SpO2 and hemodynamics; if SaO2 < 90%, pause and manually ventilate with bag-valve-mask until > 90%.

Post-intubation checks:

-Auscultate lungs (apices and bases bilaterally).

-Use CO2 detector (esophageal placement will not show CO2).

-Inflate cuff, secure tube; document cm at lip; order stat portable CXR to confirm tip ~2-3 cm above carina, below clavicles.

Medications for intubation

*Midazolam: Sedation or amnesic.

*Ketamine: Anesthetic sedative

*Propofol: Sedative, hypnotic.

*Etomidate: anesthetic, sedative/hypnotic agent

* Rocuronium: Rapid acting neuromuscular blocking agent

*Succinylcholine: Neuromuscular blocking agent that can cause major muscle fasciculations that can cause increased ICP, rhabdomyolysis, hyperkalemia and muscle pain.

Modes of Mechanical Ventilation

Controlled Mandatory Ventilation

Assist-Control Ventilation

Synchronized Intermittent Mandatory Ventilation

Continuous Positive Airway Pressure

Controlled Mandatory Ventilation

Preset volume delivered at a preset rate

Triggered by time only - Patient is "locked out" from triggering a breath

Cannot be used on spontaneously breathing patients or non-paralyzed patients

Target Population: apneaic pts or those with little to no respiratory drive.

Assist-Control Ventilation

Tidal volume delivered at a set rate in response to pts effort. If pt fails to breathe at redetermined time, ventilator will deliver a breath.

Target Population: pts able to breathe spontaneously with weak respiratory muscles.

Pt is able to hyperventilate if volume controlled or may become hypercapneic if pressure controlled.

Synchronized Intermittent Mandatory Ventilation

Tidal volume delivered at a low set rate in response to patient effort while allowing spontaneous breathes between.

Target Population: pts who cannot sustain spontaneous ventilation for extended periods.

Provides better synchrony and preserves some respiratory muscle function.

Continuous Positive Airway Pressure

Applies positive pressure during spontaneous breaths.

Target Population: effective as a weaning trial or training mode in pts capable of spontaneous ventilation.

Ventilator Settings

*FiO2: amount of oxygen in gas delivered to patient (21-100%)

*Tidal volume  (TV) volume of gas delivered in one cycle (6-8ml/kg)

*Rate:  minimal number of breaths per minute

*Pressure support:  positive pressure used to decrease patient’s work of breathing ( 5-20cmH20)

*PEEP  positive pressure left in alveoli at the end of expiration: prevents atelectasis and may enhance oxygenation at higher levels ( 5-10 cm H20)

*Peak inspiratory pressure (PIP ) highest proximal Pressure reached during inspiration <35

Nursing Care - Mechanically Ventilated Patient

Routine assessments & safety

Suctioning (airway maintenance)

Alarm safety

Communication & restraints

Nutrition

NC-MVP: Routine assessments & safety

Verify ET size, lip position; note any migration.

Monitor SpO2, RR, pattern, ventilator tolerance, LOC/sedation level, vitals, breath sounds bilaterally.

Confirm ventilator settings match orders; check circuit for kinks/disconnections; avoid unnecessary disconnections.

Ensure ambu bag with O2, suction, oral care supplies at bedside; connect ventilator to red emergency outlet.

Monitor secretions: color, amount, odor, consistency; document; assess mouth/nose for pressure ulcers from tubes.

Evaluate daily CXR for tube position and evolving complications if able.

NC-MVP: Suctioning (airway maintenance)

Indications: coarse crackles, ↑ PIP, ↓ VT, ↓ SpO2, visible secretions, ineffective cough, acute distress, suspected aspiration, need sputum sample.

Technique:

Assess q2-4h for need; not routine.

Pre/post hyperoxygenation with 100% FiO2 for 30-60 seconds.

Use lowest suction needed (80-100 mmHg); advance catheter until resistance then withdraw 1-2 cm; apply suction ≤15 seconds.

Avoid routine saline instillation.

NC-MVP: Alarm safety

Respond promptly to alarms; know unit-specific alarm priorities.

Joint Commission: hospitals must establish policies for alarm parameters, authority to change/disable, monitoring and response, and staff education.

NC-MVP: Communication & restraints

Prefer non-restraint strategies; evidence suggests restraints don't reliably prevent self-extubation and can be harmful.

Establish communication method (yes/no blinks, hand squeezes, boards, writing) and ensure all staff use it consistently.

NC-MVP: Nutrition

Early enteral nutrition via functioning GI tract preferred; reduces complications and mortality.

Routes: NG, ND, NJ; post-pyloric preferred in high aspiration risk (e.g., pancreatitis).

Confirm tube placement—radiography is gold standard; CO2 detector/air bolus not sufficient alone.

HOB ≥30°, stop feeds during turning, suctioning, extubation; monitor residuals, diarrhea, hyperosmolar dehydration.

Weaning and Extubation

Weaning = gradually reducing ventilator support; extubation = ETT removal.

Risks: prolonged ventilation ↑ morbidity/mortality; premature extubation ↑ failure and reintubation risk.

Predictors of extubation failure: poor neuro status, copious secretions, weak cough, Hgb <10, Rapid Shallow Breathing Index >105, advanced age, fluid overload, high APACHE II, chronic cardiac/resp disease.

RSBI = f / VT (L); <105 suggests higher chance of success; usually measured on CPAP 5 or T-piece.

Max inspiratory pressure < -30 cmH2O supports success; > -20 cmH2O suggests risk, but not perfectly reliable.

Daily readiness screens + spontaneous breathing trials (SBT) on CPAP or T-piece (~2 hours) used rather than slow SIMV weans.

Post-extubation: cool humidified O2; monitor for stridor (laryngeal edema), VS, respiratory distress.

Complications of Mechanical Ventilation

Ventilator-associated pneumonia (VAP)

Ventilator-induced lung injury (VILI)

Cardiovascular compromise

Ventilator-associated pneumonia (VAP)

Pneumonia that develops ≥48 hours after intubation and starting mechanical ventilation.

Caused by aspiration of secretions, biofilm in the ET tube, and bacterial colonization of the oropharynx and airway.

Ventilator-associated pneumonia (VAP) Prevention Bundle

HOB > 30–45°: reduces risk of aspiration of gastric contents/secretions.

Daily sedation vacation + readiness-to-extubate assessment: lowers time on the vent, which lowers VAP risk.

PUD prophylaxis and DVT prophylaxis: part of the standard “ventilator bundle” (they protect GI and prevent clots but don’t directly prevent VAP; still tested as part of ICU bundles).

Chlorhexidine oral care: decreases oral bacterial load and aspiration-related infection.pmc.ncbi.nlm.nih+2

Strict hand hygiene and aseptic suctioning: prevents introducing pathogens into the airway/circuit.

Ventilator-induced lung injury (VILI)

Damage to the lungs caused by the ventilator itself when settings aren’t “lung-protective.”

Includes multiple mechanisms: barotrauma, volutrauma, atelectrauma, biotrauma.

Barotrauma

Injury from high pressures (e.g., high peak inspiratory pressure, high PEEP) causing alveolar rupture → pneumothorax, subcutaneous emphysema, pneumomediastinum.

Volutrauma

Injury from overdistention: tidal volumes that are too large for the patient’s lung size (or high PEEP driving overexpansion), leading to alveolar stretch injury.

Cardiovascular compromise

Positive pressure ventilation and higher PEEP increase intrathoracic pressure.

Increased intrathoracic pressure compresses the vena cava → ↓ venous return (preload) to the right heart.

↓ preload → ↓ stroke volume → ↓ cardiac output → hypotension and tissue hypoperfusion, especially if the patient is already hypovolemic or vasodilated.

Acute Lung Injury & ARDS

*What is it?

*ALI  injury to the lungs begins with the inflammatory response.

*ARDS: an inflammatory disorder that damages the alveolar capillary membrane throughout the lung, interfering with gas exchange.

*High morbidity and mortality

Pa02/Fi02 Ratio: crude assessment of the severity of lung injury used in the definition of ARDS.

-Pa02 85 on 5L (40%) = 85/.40 = 212 P/F Ration

-Values:

<300 = ALI

<200 = ARDS

Acute Respiratory Distress Syndrome (ARDS)

inflammatory disorder damaging alveolar–capillary membrane → noncardiogenic pulmonary edema and refractory hypoxemia; high morbidity and mortality.

Sepsis is the most common cause.

Berlin definition:

-Acute onset, bilateral opacities on CXR, not fully explained by heart failure/volume overload.

-Hypoxemia severity by P/F ratio with PEEP ≥5 cmH2O:

Mild: P/F >200–≤300.

Moderate: P/F >100–≤200.

Severe: P/F ≤100.

Direct vs indirect injury

Direct: chest trauma, pneumonia, aspiration, pulmonary contusion, inhalation injury, near drowning, radiation, PE, eclampsia.

Indirect: sepsis, burns, multiple transfusions, drug overdose, cardiopulmonary bypass, acute pancreatitis, intracranial HTN.

Phases of ARDS

Exudative (first 2-4 days): capillary leak → protein-rich fluid in alveoli, bilateral infiltrates, neutrophil infiltration, hyaline membrane formation, severe V/Q mismatch and hypoxemia.

Fibroproliferative: type II pneumocyte injury, reduced surfactant, atelectasis, decreased Functional Residual Capacity and compliance, pulmonary hypertension → R Ventrical strain.

Recovery/fibrotic: variable; reorganization and fibrosis of Alveolar Capillary Membrane; degree of type II cell recovery influences outcome.

ARDS Clinical signs

Early: dyspnea, tachypnea, shallow breathing, accessory muscle use, dry cough, abnormal breath sounds, mottling/cyanosis, tachycardia, fever, mental status changes.

ABGs: hypoxemia despite supplemental O2; evolving mixed acid-base disturbances.

P/F ratio used to trend severity.

Imaging: CXR—progression to diffuse bilateral infiltrates; CT increasingly used to assess severity and response.

Collaborative Care ARDS

*Mechanical ventilation with PEEP

*Prone positioning

*Neuroblocking agents, steroids, nitrous oxide, surfactant tx., V-V ECMO, PUD, sedation, pain management

*Nutritional support

*Family / SO support

*Prevention: VAP, pressure ulcers, infections

The 5 " P's" ARDS Management

*Perfusion adequate MAP

*Positioning prone

*Protective lung ventilation low TV 4-6mL/kg (baraotrauma)

*PEEP

*Paralysis maybe needed short term 48 hrs. avoids ventilator dyssynchrony & optimizes oxygenation

Mechanical ventilation strategies in ARDS

Lung-protective ventilation: VT 4-6 mL/kg Ideal Body Weight and maintain plateau pressure ≤ ~30; reduces mortality and ventilator days.

PEEP titration: improve oxygenation and limit FiO2 <60%; avoid overdistention and hemodynamic compromise; ideal PEEP uncertain.

Permissive hypercapnia: accepted consequence of low VT; avoid in elevated ICP or severe metabolic issues; aim to prevent VILI rather than normalize PaCO2.

Prone positioning In ARDS

improves oxygenation and may ↓ mortality in severe ARDS (P/F<150, FiO2>60%, PEEP≥5); contraindicated in spinal injury, ↑ ICP, abdominal compartment syndrome, unstable hemodynamics.

Neuromuscular blocking agents in ARDS

short-term (first 48 hours) in severe ARDS may improve oxygenation and outcomes; risk of ICU weakness; must ensure deep sedation.

ECLS (VV-ECMO) in ARDS

rescue therapy for refractory hypoxemia or hypercapnia (pH<7.15; very high plateau pressures) despite optimal conventional measures; evidence limited and risk significant.

Pharmacologic adjuncts in ARDS

(limited/controversial evidence): statins, corticosteroids (low-dose), inhaled NO, epoprostenol, surfactant, β-agonists (not recommended due to harm in adults), fluid strategies, nutrition modulation.

Fluid & nutrition in ARDS

Conservative fluid strategy improves oxygenation and reduces vent days but must be individualized; avoid fluid overload; consider albumin + diuretics cautiously.

Early adequate enteral nutrition supports gut integrity and may reduce complications; specific immune-modulating formulas (omega-3s, trophic feeds) show mixed/inconsistent benefit.

Nursing actions in ARDS

Prevention: strict hand hygiene, line and oral care, VAP bundle, HOB elevation.

Sedation: minimize O2 demand and promote synchrony; use propofol, fentanyl, midazolam; consider paralysis if needed.

Positioning: ensure safe proning when indicated; protect eyes, secure tubes/lines, monitor for pressure injuries and edema.

Holistic care: coordinate team; support patient and family; explain therapies, involve spiritual/psychosocial support.

ARDS Summary

*Sudden progressive form of acute respiratory failure

*Results in NON-CARDIAC pulmonary edema & progressive refractory hypoxemia

*ARDS is not primary

*Most common cause is sepsis

COVID-associated ARDS

a systemic disease primarily injuring the vascular endothelium and pulmonary parenchyma, leading to severe respiratory failure.

Clinically, COVID ARDS behaves somewhat differently from “classic” ARDS but still follows the same general principles of lung-protective ventilation, PEEP, and supportive care.

Clinical Features of COVID ARDS

Respiratory distress similar to other ARDS patients (tachypnea, increased WOB, hypoxemia).

Typical chest X-ray finding: “ground-glass” pattern—bilateral, hazy, patchy opacities rather than discrete consolidation.

COVID ARDS Pathophysiologic Points

Disrupted vasoregulation: patients lose the ability to regulate lung perfusion and hypoxic vasoconstriction.

Predominantly interstitial rather than purely alveolar edema, affecting compliance and lung “stretchability.”

Variability in phenotypes (L-type vs H-type) with different compliance and recruitability characteristics.

High activation of coagulation cascade with widespread microthrombosis in pulmonary vessels and potentially other organs.

Ventilator Management - COVID ARDS

Overall strategy remains lung-protective: low VT (4-6 mL/kg IBW), appropriate PEEP, and careful monitoring of plateau pressures to avoid VILI.

Prone positioning (manual proning or roto beds) is heavily used, often for prolonged sessions (e.g., 16 hours prone, brief supine assessments), to improve oxygenation by recruiting dorsal lung units and reducing dependent atelectasis.

Application of the 5 P's or ARDS Management

Nursing considerations specific to CARDS

Anticipate prolonged mechanical ventilation course (often weeks); many patients required extended ICU stays.

Vigilant thrombosis monitoring: COVID ARDS patients have high risk of microthrombi and macrothrombotic events (e.g., PE), so nurses closely monitor for sudden hypoxemia, hemodynamic changes, and signs of clotting complications alongside anticoagulation protocols.

Proning logistics

Ongoing family support: high emotional burden and visitation restrictions during COVID surges made communication and psychosocial support critical; nurses often served as primary link between patient and family.

Proning logistics

For intubated patients: secure all lines, tubes, ETT, chest tubes; pad bony prominences; coordinate multiple staff members or use specialized roto beds.

For non-intubated patients: encourage self-proning or "taco" wrapping techniques to improve oxygenation and potentially avoid intubation; monitor tolerance and SpO2 response.

Why prone positioning is part of ARDS management

In ARDS, many dependent (posterior/dorsal) lung units collapse and fill with inflammatory fluid, while nondependent ventral units remain more open, creating severe V/Q mismatch and hypoxemia.

Prone positioning redistributes perfusion and ventilation so more functional lung tissue participates in gas exchange, often dramatically improving PaO2 and P/F ratio. This is why “Positioning prone” is one of the 5 Ps of ARDS management in your slides and reading.