Introduction: The Complex Role of Protein in ICU Patients

For decades, ICU nutrition guidelines emphasized high protein intake (≥1.5 g/kg/day) to combat muscle wasting, malnutrition, and immune dysfunction in critically ill patients. However, recent landmark RCTs and meta-analyses have challenged the belief that “more protein is always better.”

Definition of Sarcopenia

• Consensus Definitions:

Major working groups such as the European Working Group on Sarcopenia in Older People (EWGSOP) and the Asian Working Group for Sarcopenia (AWGS) define sarcopenia as a condition involving both low muscle quantity and low muscle function (either strength or performance).

• Probable Sarcopenia: Identified by low muscle strength (commonly measured by handgrip strength).

• Confirmed Sarcopenia: When low muscle mass is also present.

• Severe Sarcopenia: When there is low muscle mass, low muscle strength, and poor physical performance (e.g., slow gait speed).

Methods to Measure Sarcopenia

1. Imaging Techniques for Muscle Mass

• Dual-Energy X-ray Absorptiometry (DXA):

• Pros: Widely used; provides detailed body composition analysis.

• Cons: Requires patient transfer and specialized equipment; less practical in critically ill patients.

• Computed Tomography (CT) and Magnetic Resonance Imaging (MRI):

• Pros: Considered gold standards for measuring muscle cross-sectional area; excellent image quality.

• Cons: Exposure to radiation (CT), high cost, and impractical for repeated bedside evaluations.

• Ultrasound:

• Pros: Non-invasive, portable, and repeatable at the bedside.

• How It’s Done:

• Site: The rectus femoris muscle of the thigh is commonly used.

• Technique:

• Patient Positioning: Patient is in a supine position with the knee extended and relaxed.

• Landmarks: Measure at the midpoint between the anterior superior iliac spine (ASIS) and the patella.

• Probe: A high-frequency linear probe (7–12 MHz) is used.

• Measurements:

• Muscle Thickness (RF-MLT): Distance between the superficial and deep fascia layers of the muscle.

• Cross-Sectional Area (RF-CSA): Outline the muscle boundary to calculate area.

• Interpretation: A reduction of more than 10% in muscle thickness over 7 days is often considered indicative of significant muscle wasting, which correlates with sarcopenia and poorer outcomes.

• Bioelectrical Impedance Analysis (BIA):

• Pros: Quick and easy; provides estimates of fat-free mass.

• Cons: Accuracy can be affected by fluid shifts common in critically ill patients.

2. Functional Measures

• Handgrip Strength:

• Method: Use a dynamometer to measure the maximum voluntary contraction of the hand.

• Thresholds (EWGSOP2): Common cutoffs are <27 kg for men and <16 kg for women in older adults, though ICU-specific thresholds might differ.

• Significance: Reduced grip strength is a strong predictor of sarcopenia and overall functional decline.

• Physical Performance Tests:

• Tests such as gait speed or the Short Physical Performance Battery (SPPB) are used in ambulatory patients but are often not feasible in critically ill, immobilized patients.

Because sarcopenia encompasses both muscle mass and muscle function, the diagnosis is typically made by combining measurements:

• Step 1: Screening for low muscle strength (e.g., low handgrip strength).

• Step 2: Confirming low muscle mass through imaging (ultrasound, DXA, CT) or body composition analysis (BIA).

• Step 3: Assessing physical performance (if possible), to gauge the severity.

Integration with Nutritional Assessments:

Tools like GLIM, NRS-2002, and mNUTRIC incorporate various parameters (e.g., weight loss, BMI, decreased food intake, severity of illness) to assess nutritional risk. Although these tools have limitations in the ICU (due to fluid shifts and rapid metabolic changes), they can be complemented by direct muscle measurements to provide a fuller picture of a patient’s nutritional and functional status.

• Implications for Treatment:

Early identification of sarcopenia through ultrasound and functional tests can lead to timely interventions, such as adjusting protein intake, initiating early mobilization, and using anabolic agents or nutritional supplements (e.g., HMB) to preserve muscle mass.

This article will cover:

✅ What does the latest research say about protein intake in ICU patients?

✅ How does malnutrition impact ICU outcomes, and how can we assess it?

✅ Why might excessive protein be harmful in conditions like AKI?

✅ What are the molecular mechanisms of muscle wasting in ICU patients?

✅ How can bedside ultrasound help monitor muscle loss?

✅ What is the optimal protein dosing strategy for different ICU populations?

By the end, we’ll establish a personalized, evidence-based approach to ICU protein nutrition.

1. The Burden of Malnutrition in ICU Patients

Malnutrition is common in ICU patients due to:

🔹 Hypermetabolism & catabolic stress (sepsis, trauma, burns)

🔹 Reduced oral/enteral intake (NPO status, GI dysfunction)

🔹 Muscle breakdown from immobilization & inflammation

📊 Key Facts:

• Up to 60% of ICU patients develop malnutrition within 48 hours of admission

• Malnourished ICU patients have:

🚨 Higher mortality (30–50%)

🚨 Longer mechanical ventilation & ICU stay

🚨 Greater risk of ICU-acquired weakness (ICUAW)

How Do We Assess Malnutrition in ICU Patients?

🔹 1. GLIM Criteria (Global Leadership Initiative on Malnutrition)

📌 Two-Step Diagnosis:

1️⃣ Phenotypic Criteria (Need at least 1)

• Weight loss (>5% in 6 months or >10% in 1 year)

• Low BMI (<20 if <70 years, <22 if >70 years)

• Reduced muscle mass (via ultrasound, CT, bioimpedance)

2️⃣ Etiologic Criteria (Need at least 1)

• Reduced food intake/absorption (>50% of needs for >1 week)

• Systemic inflammation (sepsis, burns, major surgery)

🚀 Patients meeting 1 phenotypic + 1 etiologic criterion = Malnutrition diagnosis

🔹 2. NRS-2002 (Nutritional Risk Screening – 2002)

📌 Used in ICU to screen for malnutrition risk

🔹 Scoring System (0–6 points):

✔ Nutritional Status (0-3 points) → Weight loss, BMI, intake reduction

✔ Disease Severity (0-3 points) → Sepsis, major surgery, ICU stay

✔ Age ≥70 years → Add +1 point

📌 Scores ≥3 indicate malnutrition risk → Early nutrition therapy needed

🔹 3. mNUTRIC Score (Modified Nutrition Risk in Critically Ill)

📌 Designed for ICU patients to predict mortality risk

🔹 Includes:

✔ APACHE II / SOFA score

✔ Age, BMI, number of comorbidities

✔ Days from ICU admission to nutrition initiation

🚀 mNUTRIC ≥5 = High risk → Early aggressive nutrition needed

2. ICU-Acquired Weakness (ICUAW): Causes & Prevention

What Causes ICUAW?

🚨 Critical illness leads to a combination of:

• Inflammation-induced muscle breakdown (TNF-α, IL-6, IL-1β)

• Corticosteroid-induced myopathy

• Mitochondrial dysfunction

• Insulin resistance & anabolic resistance

• Disuse atrophy from bed rest

📊 Up to 50% of ventilated ICU patients develop ICUAW, leading to:

🚨 Delayed ventilator weaning

🚨 Longer ICU stay

🚨 Increased 1-year mortality

3. Molecular Mechanisms of Muscle Loss in ICU Patients

✅ Muscle protein synthesis is impaired due to:

• mTOR inhibition by inflammatory cytokines

• Suppression of IGF-1 (growth factor needed for muscle regeneration)

🚨 Muscle breakdown is accelerated due to:

• Activation of Ubiquitin-Proteasome System (UPS)

• Mitochondrial dysfunction leading to oxidative stress

🔬 Anabolic resistance → Even with high protein intake, ICU patients fail to utilize amino acids efficiently.

4. What Do Major Clinical Trials Say About ICU Protein Needs?

Major Clinical Trials: The High-Protein Controversy

🔹 EFFORT Trial (2023, The Lancet)

“More Protein Didn’t Improve Outcomes—And May Have Harmed Some Patients.”

• Study Design: Large multicenter RCT (85 ICUs, 1,301 patients)

• Intervention: High protein (2.2 g/kg/day) vs. Standard protein (1.2 g/kg/day)

• Primary Outcome: No difference in time-to-discharge-alive (p=0.27)

🔍 Key Findings:

🚨 High protein worsened outcomes in AKI patients (HR 1.12, 95% CI: 1.02–1.27)

🚨 No benefit in mortality, ventilator-free days, or infections

📌 Takeaway: Very high protein (>2.2 g/kg/day) might be harmful, especially in AKI & multi-organ failure patients.

🔹 TARGET Trial (2018, NEJM)

“More Calories Did Not Improve Survival.”

• Study Design: Multicenter RCT (3,957 ICU patients)

• Intervention: High-energy EN (1.5 kcal/ml) vs. Standard EN (1 kcal/ml)

• Primary Outcome: No difference in 90-day mortality

🔍 Key Findings:

❌ Higher calorie intake did not reduce ICU mortality or ventilator duration

❌ No reduction in infections or complications

📌 Takeaway: Caloric overfeeding is ineffective—protein needs should be separately optimized.

🔹 NUTRIREA-2 Trial (2018, JAMA)

“Route of Feeding Matters More Than the Protein Dose.”

• Study Design: Multicenter RCT (2,400 ICU patients)

• Intervention: Early Enteral Nutrition (EN) vs. Early Parenteral Nutrition (PN)

• Primary Outcome: No difference in 28-day mortality

🔍 Key Findings:

🚨 EN group had more GI complications (vomiting, diarrhea, aspiration pneumonia)

🚨 PN group had more bloodstream infections

📌 Takeaway: EN remains the preferred route, but careful monitoring for GI intolerance is needed.

🔹 2024 Meta-Analysis (Lee et al.)

“High Protein Increased Mortality in AKI Patients.”

• Data: 23 RCTs, 3,303 ICU patients

• Primary Outcome: No mortality benefit of high protein overall

🔍 Key Findings:

🚨 Increased mortality in AKI patients (42% higher risk, NNH = 7)

✅ High protein preserved muscle mass but increased nitrogen waste

📌 Takeaway: Moderate protein (~1.2–1.5 g/kg/day) is safest, while AKI patients should receive ≤1.2 g/kg/day.

However, excessive protein intake may:

❌ Increase metabolic waste (urea, nitrogen load), worsening AKI

❌ Cause unintended hyperglycemia (via gluconeogenesis)

❌ Fail to translate into better survival outcomes (as seen in recent trials)

Study

Protein Intake

Key Findings

EFFORT (2023, Lancet)

2.2 g/kg/day vs. 1.2 g/kg/day

Higher protein increased mortality in AKI patients (p=0.005) 🚨 No benefit in ICU/hospital stay ❌

TARGET (2018, NEJM)

High-calorie EN (1.5 kcal/ml) vs. Standard EN (1 kcal/ml)

No survival benefit of increased calorie intake ❌

NUTRIREA-2 (2018, JAMA)

Early EN vs. Early PN

No difference in mortality, but EN caused more GI issues ❌

Meta-Analysis (2024, Lee et al.)

1.5 g/kg/day vs. 0.92 g/kg/day

🚨 High protein increased AKI mortality by 42% (NNH = 7) ❌ No mortality benefit overall

📌 Takeaway: Moderate protein (1.2–1.5 g/kg/day) is safest, while AKI patients should receive ≤1.2 g/kg/day.

5. Bedside Ultrasound for Muscle Monitoring in ICU

✅ Rectus Femoris ultrasound (RF-US) is the best tool for real-time muscle loss assessment.

📊 How to interpret:

📉 >10% muscle loss in 7 days → ICUAW risk

📉 >15% loss over ICU stay → Long-term disability risk

🔬 Combining nutrition + rehab (electrical stimulation, resistance exercise) improves muscle preservation.

6. Practical ICU Protein Guidelines Based on Current Evidence

Patient Type

Protein Intake

General ICU Patients

1.2–1.5 g/kg/day

Sepsis, Trauma, Burns

1.5–2.5 g/kg/day

AKI (No CRRT)

≤1.2 g/kg/day

CRRT (Dialysis Patients)

2.0–2.5 g/kg/day

The ESPEN guidelines on clinical nutrition in the ICU provide several key recommendations on protein intake, timing, and considerations for different patient groups. Here are the most relevant points extracted from the document:

Protein Intake Recommendations

• General ICU Patients: ESPEN recommends 1.3 g/kg protein equivalents per day during critical illness, delivered progressively .

• Sepsis & Septic Shock: ESPEN does not provide a single definitive target but suggests avoiding overfeeding, as septic patients may not benefit from increased protein intake (1.2 g/kg/d) compared to non-septic patients, though no harm was reported either .

• Acute Kidney Injury (AKI): Traditional recommendations suggest 1.2-1.5 g/kg/d, but some studies indicate that higher protein intake might be associated with worse outcomes in AKI patients not receiving renal replacement therapy .

• Sarcopenic ICU Patients: Those with muscle loss may benefit more from >1.2 g/kg/day protein intake .

• Parenteral Nutrition (PN): ESPEN suggests that PN should be used if enteral nutrition (EN) is insufficient after three days. Overfeeding should be avoided in the first days of ICU admission 

1. Acute Phase of Sepsis:

During the initial acute phase (first 24–96 hours), it’s recommended to provide a protein intake of approximately 1.0 g/kg/day. This approach aims to balance the need for protein while avoiding potential adverse effects associated with higher protein delivery during this critical period. 

2. Post-Acute Phase of Sepsis:

After the acute phase, as the patient stabilizes, increasing protein intake becomes crucial to minimize muscle loss and support recovery. Guidelines suggest aiming for a protein intake of 1.2–2.0 g/kg/day during this period. 

3. Recovery Phase:

In the recovery phase, particularly for patients engaging in rehabilitation and physical therapy, protein requirements may further increase. Some recommendations advocate for protein intakes up to 2.0 g/kg/day to support muscle rebuilding and overall recovery. 

Clinical Evidence Supporting Higher Protein Intake:

• A retrospective study observed that patients with sepsis who received higher protein intake during the first week had a lower in-hospital mortality rate. Specifically, an average daily protein intake was associated with a reduced risk of in-hospital death. 

• The ESPEN guidelines on clinical nutrition in the ICU highlight that protein intakes greater than 1.2 g/kg/day are associated with improved outcomes in critically ill patients, including those with sepsis. 

It’s important to note that while higher protein intake is beneficial during the post-acute and recovery phases, individual patient factors such as kidney function, metabolic status, and overall clinical condition should guide specific protein targets. Close monitoring and adjustment of nutritional strategies are essential to optimize outcomes in septic patients.

🚀 The future isn’t “more protein” but “right protein, right patient, right time.”

📌 Final Thought: ICU nutrition must be tailored—not just based on general guidelines, but on real-time patient responses.

Extras

Detailed Overview of HMB (β-Hydroxy β-Methylbutyrate) in ICU Patients

HMB (β-Hydroxy β-Methylbutyrate) is a metabolite of leucine that has been widely studied for its muscle-preserving and anabolic effects in critically ill patients. Below is a comprehensive review of its mechanism of action, clinical benefits, side effects, and landmark studies supporting its use.

1. Mechanism of Action: How HMB Works in ICU Patients

HMB exerts multiple beneficial effects in critically ill, immobilized, and muscle-wasting patients through the following mechanisms:

(A) Stimulation of Muscle Protein Synthesis (mTOR Activation)

✅ HMB activates the mTOR pathway, which is the key regulator of muscle growth.

✅ This leads to increased muscle protein synthesis (MPS) → Helps maintain lean body mass.

✅ Unlike leucine, HMB is more potent in stimulating MPS because it bypasses certain metabolic steps.

📌 Supporting Study:

• Eley et al. (2008): HMB increased muscle protein synthesis by 30% in septic rats.

(B) Inhibition of Muscle Protein Breakdown (Ubiquitin-Proteasome Pathway Suppression)

✅ Critical illness activates the Ubiquitin-Proteasome System (UPS) → leading to muscle proteolysis (breakdown).

✅ HMB directly inhibits UPS, preventing excessive protein degradation.

✅ This helps preserve muscle mass even during immobilization or sepsis.

📌 Supporting Study:

• Smith et al. (2005): HMB reduced muscle protein breakdown by 50% in cachectic cancer patients.

(C) Anti-Inflammatory Effects (↓ TNF-α, IL-6, IL-1β)

✅ Critical illness triggers systemic inflammation (sepsis, trauma, burns), leading to muscle wasting.

✅ HMB reduces pro-inflammatory cytokines (IL-6, TNF-α, IL-1β) → Improves muscle retention.

✅ HMB also preserves mitochondrial function, reducing oxidative stress.

📌 Supporting Study:

• Hsieh et al. (2006): ICU patients receiving HMB-enriched nutrition had a 59% reduction in CRP (inflammatory marker).

(D) Enhancing Immune Function & Wound Healing

✅ HMB supports immune cell function by maintaining glutathione levels.

✅ Stimulates collagen synthesis → Improves wound healing in post-surgical ICU patients.

📌 Supporting Study:

• Clark et al. (2000): HMB improved wound healing & reduced hospital stay in elderly ICU patients.

2. Clinical Benefits of HMB in ICU Patients

HMB is particularly useful in catabolic ICU conditions where muscle loss is rapid and severe.

✅ Preserves Muscle Mass & Strength

• ICU patients lose 2-4% of muscle mass per day due to immobilization.

• HMB supplementation slows down this muscle loss by inhibiting protein breakdown.

• Deutz et al. (2013): HMB prevented significant muscle atrophy in ICU patients receiving high-protein enteral nutrition.

✅ Reduces ICU-Acquired Weakness (ICU-AW)

• ICU-AW affects 40-50% of critically ill patients, leading to long-term disability.

• HMB supplementation improves functional outcomes (grip strength, mobility).

• NOURISH Trial (2016): ICU patients receiving HMB-enriched oral nutrition supplements (ONS) had a 50% lower 90-day mortality.

✅ Supports Recovery Post-ICU (Rehabilitation Phase)

• Post-ICU patients continue losing muscle for weeks to months after discharge.

• HMB combined with physiotherapy accelerates muscle recovery & reduces re-hospitalization.

• Deutz et al. (2021): ICU patients receiving HMB showed improved physical function at 30 days post-discharge.

3. Landmark Studies Supporting HMB Use in ICU

Study

Key Findings

Clinical Impact

Deutz et al. (2013)

HMB preserved muscle mass in ICU patients receiving high-protein EN.

Supports HMB in ICU nutrition.

NOURISH Trial (2016)

HMB-enriched ONS reduced 90-day mortality by 50%.

Strong evidence for HMB in ICU recovery.

Hsieh et al. (2006)

CRP reduced by 59% in ICU patients receiving HMB.

HMB has anti-inflammatory benefits.

Eley et al. (2008)

HMB increased muscle protein synthesis by 30% in sepsis.

Supports HMB in ICU-acquired weakness.

Clark et al. (2000)

HMB improved wound healing & recovery in ICU.

Useful in post-surgical patients.

📌 Takeaway:

HMB has well-documented benefits for ICU patients, including muscle preservation, inflammation reduction, and improved recovery.

4. HMB Dosage & Administration in ICU

Route

Recommended Dose

Duration

Oral / Enteral (EN)

3 g/day (divided into 2-3 doses)

Minimum 7-14 days, ideally 4-6 weeks

Parenteral (IV HMB not widely available)

Not routinely used

–

📌 Best Administered With:

✔ High-protein EN (whey/casein) → Enhances muscle anabolism.

✔ Omega-3s (EPA/DHA) → Synergistic anti-inflammatory effect.

5. Potential Side Effects of HMB

HMB is very safe, but some mild side effects have been reported:

Side Effect

Frequency

Clinical Relevance

Mild GI Discomfort (bloating, diarrhea)

Rare (<5% of patients)

Dose-dependent, resolves with lower dose

Hypoglycemia Risk (in diabetics)

Low

Monitor blood sugar in insulin-dependent patients

No Liver/Kidney Toxicity

None reported

Safe for long-term ICU use

📌 Safety Summary:

✔ HMB has no major side effects.

✔ Safe in elderly, renal failure, and chronic ICU patients.

✔ Can be continued post-ICU to aid rehabilitation.

6. Final Takeaways

✔ HMB is a potent muscle-preserving agent, working via mTOR activation & protein breakdown inhibition.

✔ HMB reduces inflammation, improving ICU recovery.

✔ HMB supplementation (3 g/day) is recommended in critically ill patients at risk of muscle loss.

✔ Safe, with no major side effects (unlike anabolic steroids).

✔ HMB should be combined with high-protein nutrition + physiotherapy for best results.

Vanhorebeek I, et al. (2020) – ICU-Acquired Weakness Review

🔹 Objective:

• Comprehensive review of ICU-acquired weakness (ICU-AW), its mechanisms, and interventions.

🔹 Key Findings:

• ICU-AW is caused by sepsis, hyperglycemia, neuromuscular blockers, and prolonged immobility.

• 40% of ICU patients develop ICU-AW; in surgical ICUs, this rate is 56-74%.

🔹 Clinical Impact:

• Early mobilization, nutrition (≥1.5 g/kg protein/day), and glucose control are key to preventing ICU-AW.

📌 Reference: Vanhorebeek I, et al. Intensive Care Med. 2020;46(4):637-53 

Appleton RT, et al. (2015) – Incidence of ICU-AW

🔹 Objective:

• Systematic review analyzing the prevalence of ICU-AW in critically ill patients.

🔹 Key Findings:

• 4 out of 10 critically ill patients develop ICU-AW.

• ICU-AW significantly delays recovery and increases mortality.

🔹 Clinical Impact:

• ICU patients should undergo early screening for weakness & receive aggressive rehabilitation.

📌 Reference: Appleton RT, et al. J Intensive Care Soc. 2015;16(2):126-36 

Wang W, et al. (2020) – ICU-AW & Nutrition

🔹 Objective:

• Reviewed nutritional strategies for ICU-AW patients.

🔹 Key Findings:

• Early enteral nutrition (EN) is superior to PN unless contraindicated.

• Delaying PN for 7 days reduces infection risk (EPaNIC Trial).

🔹 Clinical Impact:

• Reinforces ESPEN guidelines recommending early EN over PN in critically ill patients.

📌 Reference: Wang W, et al. Front Med (Lausanne). 2020;7:559789 

Lees et al. (2024) – Muscle Loss in ICU Patients

🔹 Objective:

• Examined muscle wasting trends in critically ill patients across different conditions.

🔹 Key Findings:

• ICU patients lose ~2% of muscle mass per day in the first week.

• 15% muscle loss in 1 week → ICU-AW develops in ~50% of patients.

🔹 Clinical Impact:

• Supports high-protein feeding (1.5-2.0 g/kg/day) & resistance training in ICU.

📌 Reference: Lees et al. Crit Care Clin. 2024 

Yuan G, et al. (2021) – ICU-AW & Muscle Mass

🔹 Objective:

• Investigated erector spinae muscle cross-sectional area in ICU-AW patients.

🔹 Key Findings:

• Significant muscle atrophy seen as early as day 7 of ICU stay.

• Worse prognosis in ICU patients with severe muscle loss.

🔹 Clinical Impact:

• ICU teams should monitor muscle loss using imaging & functional assessments.

📌 Reference: Yuan G, et al. Medicine (Baltimore). 2021;100(47):e27806 

Prado CM, et al. (2023) – Muscle’s Role in Metabolism

🔹 Objective:

• Analyzed muscle’s role as a metabolic organ & its impact on ICU recovery.

🔹 Key Findings:

• Muscle regulates glycemic control, immune function, and inflammation.

• Severe muscle loss post-ICU increases mortality & disability.

🔹 Clinical Impact:

• ICU recovery strategies must include nutritional & resistance training approaches.

📌 Reference: Prado CM, et al. JPEN J Parenter Enteral Nutr. 2023 

He Y, et al. (2019) – ONS & Surgical Site Infection in Orthopedic Patients

🔹 Objective:

• Evaluated whether ONS can reduce postoperative infections and readmission rates in elderly orthopedic patients with hypoalbuminemia.

🔹 Key Findings:

• ONS reduced 30-day readmission risk by 78%.

• Lower incidence of prosthetic joint infection.

🔹 Clinical Impact:

• ONS should be routinely provided postoperatively to improve nutritional status and lower infection risks.

📌 Reference: He Y, et al. J Orthop Surg Res. 2019;14(1):292 

Deutz NE, et al. (2021) – ONS & Handgrip Strength

🔹 Objective:

• Studied the effect of ONS on muscle strength (handgrip) in ICU patients with chronic obstructive pulmonary disease (COPD).

🔹 Key Findings:

• ONS improved handgrip strength significantly at day 30 post-discharge.

• CRP (inflammatory marker) levels decreased by 59%, indicating reduced systemic inflammation.

🔹 Clinical Impact:

• Suggests ONS has both anabolic and anti-inflammatory benefits for critically ill patients.

📌 Reference: Deutz NE, et al. Clin Nutr. 2021;40(3):1388-95 

Deutz NE, et al. (2016) – NOURISH Trial: ONS & ICU Recovery

🔹 Objective:

• Evaluated the impact of specialized oral nutritional supplements (ONS) on mortality and readmission rates in malnourished hospitalized older adults.

🔹 Key Findings:

• ONS significantly reduced 90-day mortality.

• Improved handgrip strength & body weight at day 30.

• Reduced hospital readmission rates.

🔹 Clinical Impact:

• Supports the use of high-protein ONS in ICU recovery to reduce mortality and improve muscle strength.

📌 Reference: Deutz NE, et al. Clin Nutr. 2016;35(1):18-26 

Percutaneous dilatational tracheostomy (PDT) has revolutionized airway management in intensive care units (ICUs). Its minimally invasive nature, ability to be performed bedside, and cost-effectiveness make it a preferred choice for patients requiring prolonged ventilation. However, as simple as it may seem, the success and safety of PDT hinge on one critical factor: the force applied during the procedure.

Emerging evidence highlights how excessive dilatational force can lead to catastrophic complications. Understanding this risk and adopting refined techniques such as controlled force application and pre-dilation dissection can significantly improve outcomes.

The Role of Dilatational Force

During PDT, the tracheal stoma is dilated to insert the tracheostomy tube. This process involves the application of force, often using instruments such as the Griggs forceps or Ciaglia Blue Rhino (CBR) dilator. While straightforward in concept, the force applied during dilation is a double-edged sword:
• Low Force: Ensures controlled dilation with minimal trauma to the tracheal rings and surrounding tissue.
• Excessive Force: Risks complications such as tracheal cartilage fractures, subcutaneous emphysema, pneumothorax, or even complete tracheal rupture.

A 2019 report highlighted two real-world cases of tracheal rupture during PDT, even when performed under bronchoscopic guidance. Excessive force or the operator’s inability to identify pre-rupture signs, such as anterior-posterior tracheal wall approximation, played a significant role in these complications.

What Research Reveals About Force Management

Recent studies have quantified the forces applied during PDT, providing insights into how experience and technique influence safety:
1. Force Profiles Differ by Expertise
• Experienced surgeons applied significantly lower forces, averaging 31.3 N (mean) compared to 48.8 N for less experienced operators.
• Procedures performed by experienced surgeons showed smoother and more consistent force curves, typically with a single peak indicating controlled dilation.
• In contrast, less experienced surgeons produced inconsistent force curves with multiple peaks, indicating poor positioning and increased tissue trauma risk.
2. Force Magnitude and Moments
• Axial force (P) was the dominant force during the procedure, but bending moments (Mx, My) and torque (Mz) were higher in less experienced operators, reflecting inefficient technique and potential for injury.
• The peak axial force reached up to 88.2 N in inexperienced hands, compared to 82.8 N in experienced ones—a critical difference when dealing with fragile tracheal structures.
3. Simulations Show the Path to Improvement
• Using a strain-gauge-equipped CBR dilator, researchers demonstrated that training and feedback could significantly reduce variability and improve procedural safety.

Why Some Dissection is Necessary

Pre-dilation dissection, though not always emphasized, can reduce the resistance faced during dilation:
• Clearing Tissue Resistance: Limited pre-tracheal dissection minimizes the force required to insert the dilator, reducing stress on tracheal rings.
• Avoiding Cartilage Damage: In cases of prolonged intubation or infection, tracheal rings may weaken or become flaccid, making them more susceptible to rupture even under normal force.

Both the 2018 experimental study and real-world cases from 2019 emphasize that minor preparatory dissection can make a substantial difference in procedural outcomes.

Training and Technology: The Future of Safer PDT

The studies also highlight the role of advanced tools and structured training in preventing complications:
1. Force-Sensing Dilators:
• Devices equipped with strain gauges provide real-time feedback on the forces applied, alerting operators when they exceed safe thresholds.
• Such tools can guide less experienced surgeons toward a safer, more consistent technique.
2. Simulation-Based Training:
• Using lifelike tracheostomy simulators, operators can practice applying optimal forces and refine their skills without putting patients at risk.
• Incorporating visual or auditory feedback during simulations can further enhance learning.
3. Standardized Techniques:
• Following well-defined procedural steps, including pre-dilation assessments and controlled force application, can minimize variability and ensure adherence to safety standards.

Takeaways for Clinicians
1. Excessive Dilatational Force Leads to Complications
• Tracheal rupture, cartilage damage, and post-procedure complications like tracheal stenosis are closely linked to higher force application.
2. Experience Matters
• Skilled operators use lower, more consistent forces, reducing procedural time and complication rates.
3. Pre-Dilation Dissection Improves Outcomes
• Small dissections before dilation reduce resistance and protect fragile tracheal structures.
4. Technology and Training Are Game-Changers
• Force-monitoring tools and simulation-based training can bridge the gap for less experienced practitioners, ensuring patient safety.

Conclusion

Percutaneous dilatational tracheostomy is a vital procedure in ICU care, but its success depends on precise execution. By understanding the risks of excessive force, embracing preparatory techniques like limited dissection, and leveraging modern training tools, clinicians can make PDT safer and more effective.

As research and technology continue to evolve, the future of PDT looks promising, offering new ways to standardize practices and reduce complications. Let’s work toward a safer, more consistent approach to this life-saving procedure.

International Congress on Human-Computer Interaction, Optimization and Robotic Applications (HORA) – Importance of Big Data in Precision and Personalized Medicine. , (), 1–6.doi:10.1109/HORA49412.2020.9152842

“One of the very few silver linings about me getting sick is that Reed’s gotten to spend a lot of time studying with some very good doctors… I think the biggest innovations of the twenty-first century will be the intersection of biology and technology. A new era is beginning, just like the digital one when I was his age.” –Steve Jobs (from his biography, Steve Jobs)

Introduction:
As aspiring medical professionals, the journey of becoming a healer is marked by endless learning and unwavering dedication to patient care. In the dynamic landscape of modern medicine, a revolutionary force is reshaping the way we approach healthcare – precision medicine. At the heart of this transformative approach lies the vast reservoir of information known as big data. In this blog, we will explore how big data is empowering medicine students like you, equipping you with the tools to provide personalized, targeted treatments, and revolutionizing patient care.

1. Embracing the Age of Information:
   In the era of big data, the sheer volume of medical information available can be overwhelming. However, for medical students, it presents an unprecedented opportunity to deepen your understanding of diseases, treatments, and patient outcomes. By leveraging big data analytics, you can explore intricate patterns and correlations that would have been impossible to grasp using traditional methods.
2. Personalizing Patient Care:
   As medicine students, you have probably witnessed how patients respond differently to treatments. Precision medicine, fueled by big data, seeks to unravel the molecular and genetic underpinnings of these variations. Armed with this knowledge, you will be able to design personalized treatment plans, optimizing efficacy while minimizing adverse effects.
3. Advancing Diagnostic Precision:
   One of the pillars of precision medicine is early and accurate diagnosis. With the vast array of data at your disposal, you can delve deeper into the intricacies of diseases, identifying subtle biomarkers and genetic signatures. This level of diagnostic precision holds the potential to revolutionize patient outcomes and save lives.
4. Unlocking the Secrets of Complex Diseases:
   As future medical professionals, you are no strangers to the challenges posed by complex diseases like cancer and neurological disorders. Big data offers a key to unlocking their secrets. By harnessing this data, you can explore the multifactorial nature of these conditions, paving the way for targeted therapies and groundbreaking research.
5. Bridging the Gap Between Research and Practice:
   The integration of big data into precision medicine bridges the gap between research and clinical practice. As medicine students, you can actively contribute to this vital process by engaging in data-driven research, translating cutting-edge discoveries into tangible improvements in patient care.
6. Ethical Considerations and Patient Privacy:
   With the immense power of big data comes an equal responsibility to uphold ethical standards and protect patient privacy. As you navigate the world of precision medicine, it is essential to prioritize the ethical use and handling of patient information, ensuring that the potential benefits outweigh any potential risks.

Conclusion:
As medicine students, you are poised to embark on a transformative journey, shaping the future of healthcare through the lens of precision medicine and big data. The wealth of information at your disposal holds the promise of personalized patient care, diagnostic accuracy, and breakthroughs in understanding complex diseases. Embrace the opportunities presented by big data, and let it be a guiding light in your pursuit of becoming tomorrow’s compassionate and data-savvy healers. Together, we can revolutionize patient care and create a healthier and more resilient world.

“Time constant, the silent conductor of the cosmic orchestra, conducting the symphony of life’s harmonies, bridging the past and future, as each note of the present moment unfurls into the eternal melody of existence.” ⌛🎵

In physics and engineering, the time constant, usually denoted by the Greek letter τ (tau), is the parameter characterizing the response to a step input of a first-order, linear time-invariant (LTI) system. The time constant is the main characteristic unit of a first-order LTI system.

If, instead of curving exponentially and slowing its rate of decay, the function continued to decay at the same rate as it had at Time Zero, it would obviously reach the bottom rather quickly. The time it would take to reach the bottom is one time constant. Because this happens to be an exponential curve (using the base of natural logarithms, e), after one time constant the function has decreased to 37% of its initial value (i.e. it has decreased by 63%). Thus, one might say that the time constant is

“A time which represents the speed with which a particular system can respond to change, typically equal to the time taken for a specified parameter to vary by a factor of 1− 1/ e “

Concept:

• The time constant is defined as the measure of time required for certain changes in voltages and currents in RC and RL circuits.
• The elapsed time exceeds five-time constants (5τ) after switching has occurred, the currents and voltages have reached their final value, which is also called steady-state response
• A Pulse is a voltage or current that changes from one level to another and back again. If a waveform’s high time equals its low time it is called a square wave. The length of each cycle of a pulse is its period 
• A short time constant is defined as no more than one-fifth the pulse width, in time, for the applied voltage.

Example 1: Imagine you have a toy car that can go faster or slower when you press a button. The time constant is like how quickly the toy car gets to the right speed after you press the button. If it takes a long time, it’s slow. If it happens quickly, it’s fast. So, time constant tells us how fast or slow something happens in a special way! 🚗⏱️

Example 2: Imagine you have a magic potion that you use to grow a plant. The time constant is like how quickly the plant grows after you pour the potion on it. If it takes a long time, the plant grows slowly, and if it happens quickly, the plant grows fast. So, the time constant helps us understand how fast or slow things change or develop in a special way! 🌱⏱️

Example 3: Imagine you have a smart home with a thermostat that adjusts the room temperature. The time constant is like the speed at which the thermostat reaches the desired temperature after you change it. If it takes a long time, the temperature changes slowly, and if it happens quickly, the temperature changes fast. So, the time constant gives you an idea of how responsive the system is to changes, whether it’s in a technical circuit or any other dynamic system! 🏠🌡️⏱️

Example 4: When you have a dynamic system, like an electronic circuit or a chemical reaction, the time constant measures how quickly it responds to changes. It’s like a special “reaction speed” parameter. For instance, in an RC circuit, it’s determined by multiplying the resistance and capacitance values. A larger time constant means the system responds slowly to changes, and a smaller time constant means it reacts quickly. Understanding the time constant helps engineers and scientists predict and control how systems behave in real-world situations. 📊⏱️🔌

Example 5: The time constant is a significant concept used in physics and engineering to analyze dynamic systems. It represents the time it takes for a system to reach approximately 63.2% of its final or steady-state value after a sudden change in input.

In various applications, such as electrical circuits, mechanical systems, and chemical processes, understanding the time constant is essential for predicting the system’s response to changes and disturbances. A higher time constant implies a slower response, while a lower time constant indicates a quicker response.

By knowing the time constant, engineers and scientists can optimize and control system behavior, ensuring stability and efficiency in a wide range of real-world situations. 🕰️⏱️🔌🚀

The defining properties of any LTI system are linearity and time invariance.

• Linearity means that the relationship between the input x(t) and the output y(t), both being regarded as functions, is a linear mapping: If a is a constant then the system output to ax(t)is ay(t); if x′(t) is a further input with system output y′(t)then the output of the system to x(t)+x′(t) is y(t)+y′(t), this applying for all choices of a,x(t), x′(t). The latter condition is often referred to as the superposition principle.
• Time invariance means that whether we apply an input to the system now or T seconds from now, the output will be identical except for a time delay of Tseconds. That is, if the output due to input x(t) is y(t), then the output due to input x(t−T) is y(t−T). Hence, the system is time invariant because the output does not depend on the particular time the input is applied.

Physically, the time constant represents the elapsed time required for the system response to decay to zero if the system had continued to decay at the initial rate, because of the progressive change in the rate of decay the response will have actually decreased in value to 1 /e ≈ 36.8%in this time (say from a step decrease). In an increasing system, the time constant is the time for the system’s step response to reach 1 − 1 /e ≈ 63.2%of its final (asymptotic) value (say from a step increase). In radioactive decay the time constant is related to the decay constant (λ), and it represents both the mean lifetime of a decaying system (such as an atom) before it decays, or the time it takes for all but 36.8% of the atoms to decay. For this reason, the time constant is longer than the half-life, which is the time for only 50% of the atoms to decay.

The Time Constant of the lung (TC) is a concept borrowed from electrical engineering (as explained above) which describes the phenomenon whereby a given percentage of a passively exhaled breath of air will require a constant amount of time to be exhaled regardless of the starting volume given constant lung mechanics. That’s quite a mouth-full of a definition but consider what determines how long it takes to exhale a tidal breath passively. At the start of exhalation, the initial flow of gas out of the lung depends upon the driving pressure (i.e. alveolar pressure – mouth pressure) and it depends on the airway resistance. For any given volume of gas, the alveolar pressure at the start of exhalation is only dependent upon the lung compliance. Mathematically, the time constant is defined as compliance multiplied by the airway resistance and the resulting value has units of seconds of time.

• Time constant (τ) is the time required for inflation up to 63% of the final volume, or deflation by 63% 
• It is the product of resistance and compliance
• For a normal set of lungs as a whole, the time constant is 0.1-0.2 seconds

The time constant determines the length of time needed for a passive exhalation and that the time constant is the product of airway resistance and lung compliance. The lower the compliance, the higher the driving pressure pushing gas out of the lungs during exhalation; the lower the resistance, the higher the expiratory flow rate can be when driven by the alveolar pressure. If the time constant is known (or can be estimated) then the maximum mechanical respiratory rate that can be used before Auto PEEP results can be estimated. Consider that at least 3 time constants are required to exhale passively any volume of gas. The combination of inspiratory and expiratory time leads to a give respiratory rate such that:

Total Breath Time = Insp time + Exp time

Respiratory Rate = 60 / Total Breath Time

Maximum Rate = 60 / (Insp time + 3 x TC)

A patient with a compliance of 0.05 L/cm H20 and an airway resistance of 30 cm H20/L/sec. This would give a time constant of 1.5 seconds. A complete exhalation would take around 4.5 seconds. If inspiratory time is 1 second then total breath time is 5.5 seconds and the maximum respiratory rate without gas trapping would be 11 breaths per minute. When gas trapping occurs, the functional residual capacity (FRC) is increased. As the FRC increases, the alveolar pressure increases by an amount of pressure determined by the patient’s lung compliance. As the FRC rises in relation to the total lung capacity (TLC), the lung compliance will decrease. This decrease in lung compliance shortens the time constant for the next breath and thus shortens the time required to exhale the next breath and lessens the amount of trapping that will occur with each subsequent breath until the time constant shortens enough that gas trapping no longer occurs. When this steady state is reached, the FRC is at its maximum and the auto-PEEP is also at its maximum. This fact gives us a way to measure how much auto-PEEP exists since we can serially measure exhaled tidal volumes and then interrupt ventilation (by turning the respiratory rate to zero for several seconds) and measuring how much gas the patient exhales as the patient exhales back to the FRC level that existed prior to ventilation. If we take the difference between the exhaled volume during ventilation and the exhaled volume after interrupting ventilation then we have the amount of gas that was trapped. If we divide this volume by the lung compliance we will have calculated the amount of auto-PEEP applied to the alveoli during ventilation. Normally we are more interested in avoiding auto-PEEP than in measuring it though there are many patients in whom it cannot be avoided so it is useful to be able to quantitate it. Another way to detect auto-PEEP is to watch a patient’s chest movement and/or breath sounds during exhalation to see if exhalation stops prior to initiation of inspiration by the ventilator. If exhalation doesn’t finish then auto-PEEP is occurring. When exhaled tidal volumes cannot be measured (which is seldom with modern ventilators) the level of auto-PEEP can be very roughly estimated by interrupting exhalation just prior to initiation of inspiration and watching to see if there is a pressure increase at the airway as exhalation continues into the circuit between the patient and the point of your interruption. This is not an accurate measurement since the interruption necessarily cuts exhalation shorter than it would normally be and because the circuit volume dampens the pressure measurement but this technique can be useful if you are unable to use the more reliable methods outlined above.

In the presence of constant flow,

• Poor compliance units will have a shortened or normal time constant, and will fill rapidly but incompletely
• High resistance units will have a long time constant, and will fill slowly 
• When flow ceases, gas may flow from lung units with poor compliance into lung units with high resistance
• Exchange of gas between lung units with different time constants is called pendelluft

This has implications for dynamic compliance:

• With decreased inspiratory time, the fraction of the tidal volume delivered to lung units with long time constants will decrease (i.e. all the tidal volume will go to “faster” lung units)
• This will have the effect of decreasing dynamic compliance
• In addition to airway resistance, this factor contibutes to the frequency dependence of dynamic compliance (i.e. dynamic compliance becomes lower with increasing respiratory rates)

For normal lungs, the value for an expiratory time constant is usually given as approximately 100-200 millseconds, i.e over 0.6 seconds 95% of the total lung volume should be emptied. Obviously in states of extreme ICU-level illness, thing may be a little different; especially where airway resistance is increased. For example, Karagiannidis et al (2018) demonstrated time constants around 2500 milliseconds in patients intubated for severe COPD. Interestingly, in ARDS patients, Guttman et al (1995) found expiratory time constants in the range of 600-700 milliseconds, but these were mainly due to the mechanical properties of the endotracheal tube (and the lung itself was not to blame), which supports the concept of a normal but small “baby lung” in ARDS.

Basically, the implication of all these diagrams are that lung units with different time constants will fill at different rates and potentially also up to different final volumes. Then, when the inspiratory flow stops, the lung units with longer time constants (usually described as “slow alveoli”) will continue to fill with “borrowed” gas which redistributes from faster alveoli. This exchange of gas is usually given the term pendelluft, which seems to be the go-to German word to describe any gas movement between different lung units. 

Practically, this can be demonstrated by performing an inspiratory hold manoeuvre on a mechanical ventilator. When one’s mechanical breath has been delivered and the flow stops, the airway pressure first falls abruptly because resistance no longer contributes to it. That part is irrelevant. Then, as one holds the pause for longer, one may be able to see a gradual downward drift of the plateau pressure, as gas is exchanged between lung units with different time constants. This pendellufting of the tidal volume is one of the reasons the recommended duration of an inspiratory hold is about 2 seconds (the other reason for this phenomenon is the relaxation of the lung and chest wall tissues, which contributes to the total airway resistanceand is discussed elsewhere).But how much pendelluftis there in a normal respiratory system? Probably very little. Otis et al (1956) measured time constants from each of the main bronchi belonging to a Dr. Bruce Armstrong, according to the footnote. As one can see from their data (below), “flows in the two bronchi were roughly equal and exactly in phase with each other”. Only when some added resistance was introduced was there a change in the flow timing, seen in the diagram on the right.

Something very similar was the result of some experiments by Bates et al (1988), although these investigators used mongrel dogs instead of healthy colleagues. Alveolar pressure was measured, rather than bronchial pressure, making this somewhat more convincing. There was minimal difference in expiratory flow rates between different lung units in these animals, prompting the authors to remark that “the lungs of these animals …behaved as if they contained a single large and uniform alveolus, with no regional differences in time constants of emptying”.

In summary, in the presence of constant flow,

• Poor compliance units will have a shortened or normal time constant, and will fill rapidly but incompletely
• High resistance units will have a long time constant, and will fill slowly 
• When flow ceases, gas may flow from lung units with poor compliance into lung units with high resistance

Q: Bias flow can be set at range settings in one of the given ventilators:

a) Maquet Servo-I

b) GE carescape R860

c) Puritan Bennett™ 840 Ventilator

d) None of the above

Ans is B (GE CARESCAPE R860 Ventilator)

Bias flow on a ventilator refers to the continuous flow of gas that is provided to the patient, even during the expiratory phase of the breathing cycle. During expiration, the ventilator continuously delivers a gas flow (bias flow), which is measured in the expiratory channel. In the Maquet Servo i ventilator, the bias flow is set at factory default values (2 L/min in adults and 0.5 l/min in infants and there is no range settings while in GE CARESCAPE R860 the bias flow can be set as Bias Flow from 2 to 10 l/min and on NIV from 8 to 20 l/min in adult settings .

Gas flow through the Patient unit
Refer to the Patient Unit gas flow diagram for the location of the following numbered components:

1. Gas inlet for O2
2. Gas inlet for air
3. The gas flow is regulated by the gas modules for Air and O2.
4. The gases are mixed in the inspiratory mixing section.
5. The Oxygen concentration can be measured with an O2 cell or O2 sensor.
   An O2 cell is shown here.
   The O2 cell is protected by a bacteria filter.
6. The pressure of the mixed gas delivered to the patient is measured by the Inspiratory pressure transducer.
   The transducer is protected by a bacterial filter.
7. The inspiratory channel delivers the mixed gas to the patient systems inspiratory tubing. The inspiratory channel also contains a safety valve.
8. The patient breathing systems expiratory tubing is connected to the expiratory inlet. The inlet also contains a moisture trap.
9. The gas flow through the expiratory channel is measured by ultrasonic transducers.
10. The expiratory pressure is measured by the expiratory pressure transducer (located inside the ventilator). The transducer is protected by a bacterial filter inside the expiratory cassette.
11. The pressure (PEEP) in the patient system is regulated by the expiratory valve.
12. Gas from the patient system leaves the ventilator via the expiratory outlet. The outlet contains a non-return valve.

In servo i ventilator , At a trigger sensitivity level above zero (0),The ventilator senses deviations in the bias flow delivered during expiration. These deviations are caused by the inspiratory efforts of the patient. The further to the right on the scale, the more sensitive is the trigger function.
At a trigger sensitivity level below zero (0), the ventilator senses deviations in the pressure below PEEP created by the patient. The pressure below PEEP required to initiate a breath is shown when the setting is made.The further to the left on the scale, the more effort is required to trigger.

Trigger sensitivity
a. Below zero: Trigger sensitivity is
pressure dependant. The pressure below PEEP which the patient must create to initiate an inspiration (cmH2O) is indicated.
b. Above zero: Trigger sensitivity is flow dependent. As the dial is advanced to the right (step wise from the green into the red area) the trigger sensitivity increases i.e the inhaled fraction of the bias flow leading to triggering is reduced.

In GE CARESCAPE R680 , The continuous flow that is circulated through the patient circuit during the expiratory phase of the breath cycle. The bias flow may be increased above this setting by the ventilator for some FiO2 settings.

The Bias Flow rate, set by the clinician will be used to maintain PEEP and for the inspiratory phase of the time cycled mechanical breaths. Insufficient setting of the Bias Flow rate may cause an inability to reach or maintain the set PEEP and or inspiratory pressure during the mechanical breaths.

Interestingly, the flow trigger setting should probably be in litres per minute (that, after all, is how we measure flow) but this is not viewed as mandatory by all ventilator manufacturers. For instance, the Puritan Bennett 840 allows the user to set a flow trigger directly, in L/min. In the case below the trigger is set to 3L/min.Thus, in the Puritan Bennett models, setting a lower value of flow trigger (eg. 2L/min or 1L/min) represents an increase in sensitivity, i.e. a lower flow required to trigger a mechanical breath. In contrast, in the Maquet SERVO-i model interface, a decreasing trigger value corresponds to a decrease in sensitivity. Their trigger variable is controlled by the twiddly dial on the ventilator and can be tuned to a range of settings from -20 to +10. This range represents an increasing sensitivity of the trigger, from least sensitive at -20 to most sensitive at 10.

How Bias Flow is used for Flow Triggering : When a patient takes a breath, some of the flow is directed into their lungs. The expiratory flow rate in the ventilator circuit is decreased by this, such that Vin – Vout = x, where x is some “missing” flow measured in L/min. Flow triggering occurs when this missing flow reaches some prescribed threshold value, which causes the ventilator to open the inspiratory valve and deliver a breath. The exact value is susceptible to manipulation via the settings, and the default setting differs between manufacturers, but generally it’s in the ballpark of 1-2 L/min.

For comparison, the normal
mean inspiratory flow rate at rest is probably about 15L/min, with a peak of around 30- 35L/min (Tobin et al, 1983) which makes this a relatively effortless goal to achieve.

To make things more confusing, the range between -20 and 0 actually represents a pressure trigger; the values in this range correspond to a negative pressure in cm H2O, such that a setting of -20 represents a pressure trigger of -20 cm H2O. The range between 0 and 10 represents a flow trigger, and corresponds to a percentage of the bias flow which needs to be “deflected” by the patient in order to trigger the mechanical breath.

A setting of 0 is the least sensitive flow trigger, and represents a 100% deflection (i.e. the patient must generate a flow equal to 100% of the bias flow though the circuit, or 2L/min). A trigger of 10 is the most sensitive, and represents a flow deflection close to 1% of the bias flow. The default setting of a recently reset/restarted SERVO-i ventilator is a flow trigger of 5, which corresponds to a bias flow change of 50%, or 1L/min.

Pressure triggering
Pressure triggering describes a method whereby a decrease in circuit pressure is detected by the ventilator pressure sensors and interpreted as patient effort. The patient inhales against a close inspiratory valve, producing a pressure drop by this effort, and in response, the ventilator delivers a mechanical breath by opening the inspiratory valve. Conventionally, where a pressure trigger is used for a prolonged period, a typical setting would be 1 cm H2O.

A film by Robyn Symon

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