Cardiac anesthesiologist | Intensivist • Founder, Africa’s first Hypoxia Lab • Scalable ICU systems in Africa • Global Health • Medical Simulationist
kampala, Uganda
Joined November 2012
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Cornelius Sendagire, MD retweeted
🫁 Pendelluft in ARDS: when spontaneous breathing may injure the lung despite protective tidal volumes
In mechanical ventilation, we often focus on tidal volume, plateau pressure and driving pressure to prevent ventilator-induced lung injury. However, these global measurements may fail to reveal important regional mechanical phenomena.
One of them is pendelluft, the redistribution of gas between lung regions without a corresponding change in the total tidal volume delivered by the ventilator.
In ARDS, heterogeneous lung injury creates regional differences in compliance and pleural pressure. During inspiratory effort, dependent lung regions may experience greater negative pleural pressure, drawing gas from nondependent regions.
This internal redistribution can produce regional overdistension even when global ventilatory parameters appear protective.
Using electrical impedance tomography (EIT) and esophageal pressure monitoring, they analyzed 1,135 patient-triggered breaths and 807 reverse-triggered breaths.
Three findings deserve particular attention.
First, pendelluft was significantly greater during patient-triggered breaths than during reverse triggering.
Mean pendelluft volume was 3.9 ± 6.8 mL during triggered breaths versus 1.9 ± 2.8 mL during reverse triggering, compared with 0.5 ± 0.8 mL at rest.
Second, greater inspiratory effort increased dependent lung ventilation and pendelluft, but the response varied considerably between patients.
Interestingly, patients with greater effort-related pendelluft during triggered breaths had lower respiratory system and lung elastance, lower airway pressures and predominantly focal radiological involvement.
Lower airway pressures did not necessarily indicate lower regional mechanical risk.
Third, esophageal pressure swings alone were poor positive predictors of substantial pendelluft.
This suggests that respiratory effort and regional gas redistribution are related but not interchangeable measurements.
What does this mean at the bedside?
Spontaneous breathing is not inherently protective or harmful. Its effects depend on respiratory drive, regional lung mechanics, patient-ventilator interaction and the distribution of transpulmonary pressures.
During the transition from controlled to assisted ventilation, acceptable tidal volumes and airway pressures should not automatically reassure us that regional ventilation is homogeneous.
EIT may provide additional physiological information, particularly when respiratory effort or patient–ventilator asynchrony raises concern for patient self-inflicted lung injury.
Nevertheless, this was a small observational study restricted to volume-controlled ventilation. It did not demonstrate that pendelluft caused lung injury or that suppressing it improves clinical outcomes.
Reference 📚
Lin WC, et al. 2023. Scientific Reports, 13:22143.
doi.org/10.1038/s41598-023-4…
#ARDS #CriticalCare #MechanicalVentilation #RespiratoryPhysiology #Pendelluft
Cornelius Sendagire, MD retweeted
#ICU Evidence #002:
Earlier vasopressin in septic shock (VASSPR trial): are we treating the patient or the norepinephrine dose?
Add vasopressin at a norepinephrine-equivalent dose of 0.1 or 0.4 µg/kg/min? VASSPR tested these strategies across 13 US hospitals and nearly 4,000 patients. It changed practice, but not outcomes. I think it also raises a more interesting question:
Should vasopressor dose alone tell us when to add another hemodynamic intervention?
This was a pragmatic cluster-crossover trial. Hospitals alternated monthly between recommending fixed-dose vasopressin at a norepinephrine-equivalent dose ≥0.1 µg/kg/min (0.1 arm) or ≥0.4 (0.4 arm). Clinicians retained discretion, so this was not vasopressin vs placebo or a protocol that overrode clinical judgment.
Among patients reaching the relevant vasopressor range, vasopressin was used in 68.0% in the 0.1 arm vs 42.7% in the 0.4 arm. But 28-day mortality was 31.8% vs 33.0%, 90-day mortality 37.9% vs 38.4%, and clinically significant arrhythmias 18.4% vs 18.1%. None of the other secondary clinical outcomes materially differed either.
Here is what bothers me. Two patients on exactly the same norepinephrine dose may have profoundly different circulations: vasoplegia with preserved cardiac output, septic cardiomyopathy with impaired forward flow, RV dysfunction, persistent tissue hypoperfusion despite acceptable macrohemodynamics, or some combination.
A norepinephrine dose tells us how much drug we are giving, not WHY the patient remains in shock.
So I struggle with using a drug-dose threshold to trigger another major hemodynamic intervention. Starting vasopressin changes vascular tone and therefore the loading conditions under which the heart and circulation operate. Before treating the blood pressure, I want to understand the circulation.
POCUS is an excellent bedside tool here: LV and RV function, chamber size, important valvular or pericardial pathology, and clues about filling and forward flow, integrated with examination, perfusion, lactate trajectory, and other hemodynamic data.
This also brings to mind the four-hemodynamic-interface model proposed by @ThinkingCC and colleagues. Increasing vascular tone may be exactly what a profoundly vasoplegic patient needs. In another phenotype, excessive vasoconstriction could adversely affect ventricular-arterial coupling (Interface I, the heart pumping into the arterial system) and potentially arterial-to-microcirculatory coupling (Interface II, translating arterial pressure and flow into tissue perfusion). A higher MAP is not necessarily better hemodynamics.
And we should look again after starting vasopressin. Did MAP rise? Fine. But what happened to cardiac function, forward flow and tissue perfusion? Is the RV tolerating the new loading conditions? Can catecholamines actually be reduced? Otherwise, hemodynamic management risks becoming “set it and forget it”: reach a norepinephrine threshold → add vasopressin → celebrate the MAP → move on.
One safety finding caught my attention. Clinically diagnosed cardiogenic shock occurred in 7.4% in the 0.1 arm vs 6.3% in the 0.4 arm (adjusted OR 1.19, 95% CI 0.93–1.54). This was an exploratory endpoint and the difference was not statistically significant, so I would not interpret it as evidence that earlier vasopressin causes cardiogenic shock.
I do question the endpoint itself. Cardiogenic shock was captured as a clinical diagnosis rather than defined by a pre-specified objective hemodynamic phenotype. I appreciate that systematically phenotyping cardiac function in a pragmatic 4,000-patient trial is not trivial. I’d still want something more objective than a clinical diagnosis, especially with echo this accessible.
There’s some irony here: we study when to alter vascular tone, see a hint of a cardiac signal, and still know little about what the heart and circulation were actually doing.
My criticism is of the paradigm, not the investigators. Running a cluster-crossover trial across 13 hospitals and actually changing bedside vasopressin use is an impressive accomplishment. VASSPR answers the pragmatic policy question it was designed to answer.
What it cannot tell us is whether earlier vasopressin might benefit one hemodynamic phenotype while being unhelpful, or potentially disadvantageous, in another.
Perhaps our next trials should ask less “What norepinephrine dose have we reached?” and more:
“Why does this patient still need norepinephrine, and what happened after we intervened?”
“Pragmatic” explains the design. It does not replace physiology.
#JAMA #FOAMcc #FOAMed
Cornelius Sendagire, MD retweeted
🫁 Gas exchange in ARDS: why oxygenation is not simply a pulmonary problem
In ARDS, we frequently interpret PaO₂/FiO₂ as a measure of lung injury and PaCO₂ as an indicator of ventilation. Yet neither parameter can be understood independently of pulmonary perfusion, cardiac output and ventilation-perfusion relationships.
Collino, Camporota and Pinsky revisit these principles in an excellent 2026 physiological review, a must read!
1. Hypoxemia is predominantly a shunt problem.
Perfusion of nonventilated or poorly ventilated alveoli produces venous admixture, reducing arterial oxygenation.
Increasing FiO₂ may improve oxygenation in low V̇A/Q̇ regions, but has limited effectiveness in true shunt.
Moreover, excessive FiO₂ may promote absorption atelectasis and attenuate hypoxic pulmonary vasoconstriction, potentially worsening shunt.
2. Cardiac output changes PaO₂ even when pulmonary pathology remains unchanged.
This is particularly important in septic shock and ARDS.
According to the Fick principle, reduced cardiac output lowers mixed venous oxygen content when oxygen consumption remains constant.
With a fixed shunt fraction, lower mixed venous oxygenation produces lower PaO₂.
The authors illustrate that with a 20% shunt and FiO₂ 1.0, PaO₂ may exceed 400 mmHg at normal cardiac output but fall below 150 mmHg when cardiac output decreases.
Therefore, deteriorating oxygenation does not necessarily indicate worsening lung injury.
3. PaO₂/FiO₂ is not a fixed characteristic of the lung.
It changes with FiO₂, PEEP and cardiac output.
The same patient may move between ARDS severity categories without a proportional change in underlying pulmonary injury.
Standardizing ventilator conditions improves interpretation.
4. Hypercapnia is frequently a dead space problem.
Increased alveolar dead space reduces effective alveolar ventilation, requiring greater minute ventilation to maintain PaCO₂.
However, not all dead space indices measure the same physiology.
The Bohr equation estimates true physiological dead space, whereas the Enghoff modification incorporates the effects of shunt and V̇A/Q̇ heterogeneity.
Consequently, elevated Enghoff VD/VT does not necessarily mean increased anatomical or alveolar dead space alone.
The ventilatory ratio and EtCO₂/PaCO₂ provide practical bedside information, although neither replaces direct physiological assessment.
The clinical implication is fundamental.
When PaO₂ decreases, investigate not only recruitment and shunt, but also cardiac output and mixed venous oxygenation.
When PaCO₂ increases, assess dead space, CO₂ production and effective alveolar ventilation before simply increasing respiratory rate.
Reference 📚
Collino F, et al. Intensive Care Medicine. 2026.
doi.org/10.1007/s00134-026-0…
#ARDS #CriticalCare #RespiratoryPhysiology #MechanicalVentilation #Hemodynamics #GasExchange
Cornelius Sendagire, MD retweeted
🫁ARDS beyond the guidelines: lung protection is not a ventilator setting
We often describe ARDS ventilation with numbers: VT 6 mL/kg PBW, plateau pressure <30 cmH₂O, driving pressure <15 cmH₂O, adequate PEEP.
Necessary? Yes. Sufficient? Probably not.
This excellent 2026 review by Wongtirawit, Menga, Brochard and colleagues makes an important point: ARDS is not a single physiological phenotype. Recruitability, respiratory drive, chest wall mechanics and cardiovascular interaction differ substantially between patients. The same ventilator setting may therefore protect one lung and injure another.
Driving pressure is not just a target. It is a diagnostic signal.
When ΔP is high, simply reducing tidal volume misses the question: why is it high?
Airway closure can falsely elevate apparent ΔP. A recruitable lung may need more PEEP. An overdistended lung may need less. Increased chest wall load may produce high airway pressures without equivalent transpulmonary stress.
This changes the meaning of PEEP.
PEEP should not be titrated only according to oxygenation. In recruitable lungs it can increase functional lung size and reduce cyclic opening and closing. In poorly recruitable lungs, the same PEEP may predominantly overdistend already aerated units.
And here is a particularly important bedside warning:
Better PaO₂ does not necessarily mean better physiology.
PEEP induced overdistension can decrease cardiac output and shunt fraction, paradoxically improving PaO₂ while actually reducing oxygen delivery. Oxygenation therefore needs to be interpreted together with ΔP and hemodynamics.
This is why the right ventricle belongs inside the ARDS ventilatory strategy. Both collapse and overdistension can increase pulmonary vascular resistance. Worsening oxygenation, hypercapnia, increasing PEEP or rising vasopressor requirements should lower our threshold for echocardiographic assessment.
Then spontaneous breathing adds another dimension.
Airway pressure no longer tells us the whole story because part of the transpulmonary pressure is generated by the patient. P0.1, ΔPocc, waveforms and synchrony can reveal excessive respiratory drive and potentially injurious effort invisible on the usual ventilator numbers.
Guidelines define the safe starting point. Physiology tells us where the individual patient needs to go.
Reference 📚
Wongtirawit N, Menga LS, Brito R, et al. 2026. Intensive Care Medicine.
doi.org/10.1007/s00134-026-0…
#ARDS #CriticalCare #MechanicalVentilation #RespiratoryPhysiology #Hemodynamics #POCUS #IntensiveCare
ALT
Cornelius Sendagire, MD retweeted
🫀Septic shock: are we treating hypoperfusion or STILL treating the MAP?
Norepinephrine remains the first line vasopressor in septic shock. But increasing evidence is shifting the question from how high we can push the dose to how much adrenergic exposure the patient actually needs.
This new review explores the concept of catecholamine sparing resuscitation.
This does not mean delaying norepinephrine. Early norepinephrine can shorten hypotension, accelerate shock control and reduce fluid requirements. In CENSER, early treatment increased shock control at 6 hours from 48% to 76%.
The problem comes when MAP becomes the therapeutic endpoint rather than tissue perfusion.
Norepinephrine increases arterial tone, but microcirculatory flow depends on more than MAP. Critical closing pressure, mean systemic filling pressure, venous congestion and microvascular alterations determine whether increasing arterial pressure actually improves tissue perfusion.
This explains an important concept:
MAP restoration ≠ microcirculatory restoration.
Once an adequate perfusion pressure is reached, escalating vasopressors simply to achieve a higher MAP may increase adrenergic exposure without improving outcomes. The review emphasizes individualization using capillary refill time, fluid responsiveness, diastolic pressure and bedside echocardiography.
Catecholamine sparing therefore becomes multimodal.
Vasopressin provides non adrenergic vasoconstriction and reduces AF risk. Angiotensin II may eventually have a role in selected RAAS dysfunctional phenotypes, potentially identified by renin. Corticosteroids can restore vasopressor sensitivity and accelerate weaning. β1 blockade remains intriguing but inconsistent, reinforcing that tachycardia may be pathological in one patient and compensatory in another.
The future may therefore be less about choosing the “best vasopressor” and more about identifying which cardiovascular regulatory pathway is failing.
The objective is not the lowest norepinephrine dose.
It is the lowest adrenergic exposure compatible with adequate tissue perfusion.
Reference 📚
Dubech A, et al. 2026. Critical Care.
doi.org/10.1186/s13054-026-0…
#CriticalCare #SepticShock #Hemodynamics #Sepsis #Vasopressors #Norepinephrine #Perfusion #POCUS
ALT
Cornelius Sendagire, MD retweeted
Today's Paper of the Day is:
Bedside assessment of the respiratory system during invasive mechanical ventilation
criticalcarereviews.com/late…
Join us to read 1 paper per day and stay up-to-date as we cover the spectrum of critical care across 2026
Cornelius Sendagire, MD retweeted
💧 Fluid Management in Heart Failure and Cardiogenic Shock
Preload vs Congestion
This chapter explains that in acute and chronic heart failure, the challenge is not simply “giving or withholding fluids” but balancing preload to support cardiac output against the risk of venous congestion and pulmonary edema. Conventional preload markers (CVP, PAOP) are often misleading in dilated, stiff or ischemic ventricles, so the authors emphasize integrated assessment using echo, blood pressure, urine output and clinical signs of congestion.
Cardiogenic Shock Strategy
In cardiogenic shock, small, carefully tested fluid challenges may be justified early, but ongoing hypotension is usually better addressed with inotropes, vasopressors and mechanical support rather than repetitive fluid boluses. The chapter highlights how positive fluid balance worsens outcomes in decompensated heart failure and advocates early decongestive therapy and, when needed, ultrafiltration as part of a broader deresuscitation plan.
📘 Full chapter in Rational Use of Intravenous Fluids in Critically Ill Patients:
👉 link.springer.com/book/10.10…
🔵 Discussed in depth at IFAD 2026 in Antwerp.
👉Registration: fluidacademy.org/ifad-2026-r…
#HeartFailure #CardiogenicShock #FluidManagement #VEXUS #ICU
Cornelius Sendagire, MD retweeted
My two preferred papers of life are “the holistic view..(COCC 2012) and the recent “25 years of septic shock resuscitation…(CCF 2026). Science, soul, heart. The first was after 15 years of research in perfusion that started with gut tonometry. The last one “what have we learnt!”
Cornelius Sendagire, MD retweeted
🔥 Congratulations to Dr Sendagire on this great achievement!
Aba critical care tubalaba mutandise!
We see you!
@Internist_02
@ErasmusMD
Congratulations, Dr. Cornelius Sendagire, on Your Successful PhD Defence!
The Association of Anesthesiologists of Uganda warmly congratulates Dr. Cornelius Sendagire on the successful defence of his PhD at the D’Or Institute for Research and Education in 2026.
Dr. Sendagire successfully defended his PhD thesis, MOTIVATE-ICU, and passed with no changes required to the thesis, a remarkable achievement.
We celebrate this significant milestone and commend Dr. Sendagire for his dedication, excellence, and contribution to anaesthesia and critical care research.
Congratulations, Dr. Cornelius Sendagire, PhD! 🎓👏
Cornelius Sendagire, MD retweeted
❤️ Shock resuscitation: physiologically attractive does not always mean clinically useful
The venoarterial CO2 gap, Pv-aCO2, and the Pv-aCO2/Ca-vO2 ratio are elegant physiological variables. They attempt to integrate blood flow, oxygen extraction and CO2 production, potentially identifying situations in which apparently acceptable macrohemodynamics coexist with inadequate tissue perfusion.
But should we routinely use them to guide shock resuscitation?
A recent correspondence in Intensive Care Medicine raises an important point: the physiological rationale is stronger than the clinical outcome evidence.
In a multicenter trial of 228 patients with severe sepsis or septic shock, targeting Pv-aCO2/Ca-vO2 achieved the physiological target more frequently, but did not reduce 28-day mortality compared with an ScvO2-guided strategy.
Similarly, the Lactel randomized trial found no significant improvement in lactate clearance or 28-day mortality when resuscitation was guided by CO2/O2-derived indices.
This does not make these variables useless, but it changes how we should use them.
A Pv-aCO2 abnormality may provide additional physiological information when the clinical picture remains unclear. But it should probably be interpreted as one component of a multimodal assessment rather than as another isolated resuscitation target.
And this becomes particularly relevant in resource-limited ICUs. Serial calculation requires arterial and central venous blood gases, often repeated several times, while capillary refill time provides immediate information about peripheral perfusion essentially without additional cost.
The broader lesson extends beyond these specific variables:
Hemodynamic monitoring should answer a clinical question, not simply generate another number.
Macrohemodynamics, peripheral perfusion, lactate kinetics, cardiac function, fluid responsiveness and selected advanced variables should complement each other according to the patient's phenotype and the resources available.
The most sophisticated monitoring strategy is not necessarily the one measuring the most variables. It is the one that obtains enough physiological information to make the next therapeutic decision.
Reference 📚
Pérez-Nieto, O. R., Deloya-Tomas, E., & Reyes-Monge, R. A. (2025). Pv-aCO2 and Pv-aCO2/Ca-vO2 in shock resuscitation: physiologically appealing, but challenging in resource-limited ICUs. Intensive Care Medicine.
doi.org/10.1007/s00134-025-0…
ALT
Cornelius Sendagire, MD retweeted
🫀Septic shock resuscitation is entering a new era. Physiology is replacing protocols.
For more than two decades, septic shock research has challenged one assumption after another. We targeted central venous oxygen saturation. We targeted lactate. We targeted mean arterial pressure. We restricted fluids. Yet despite these advances, improvements in patient-centered outcomes remained inconsistent.
This remarkable perspective from many of the world's leading experts argues that the problem was never the individual variables. The problem was expecting a single physiological target to represent an extraordinarily heterogeneous disease.
The evolution of septic shock management tells an important story. Early Goal Directed Therapy demonstrated that protocolized resuscitation could improve outcomes, but subsequent multicenter trials showed that fixed algorithms cannot account for the diversity of septic shock phenotypes. Lactate proved invaluable for risk stratification but increasingly unreliable as an isolated treatment target beyond the initial hours of resuscitation. Mean arterial pressure also evolved from a universal threshold to an individualized physiological variable whose optimal value depends on the patient's underlying cardiovascular state.
The most important conceptual shift has been moving from treating numbers to treating perfusion. Capillary refill time emerged as a rapidly responsive bedside marker that reflects the adequacy of tissue reperfusion. The ANDROMEDA-SHOCK program demonstrated that combining capillary refill time with systematic assessment of fluid responsiveness, focused critical care echocardiography, and sequential hemodynamic phenotyping allows clinicians to individualize therapy while reducing unnecessary interventions.
Another major lesson is that fluids are no longer considered inherently beneficial. Every fluid bolus should answer a physiological question. Is the patient fluid responsive? Will the patient tolerate additional volume? Is venous congestion already limiting organ perfusion? Fluid administration has evolved from a routine intervention into a reversible physiological test.
Perhaps the strongest message of this review is that hemodynamic resuscitation is no longer protocol driven but physiology guided. Septic shock should be understood as a dynamic process requiring repeated cycles of observation, bedside testing, intervention, and reassessment.
The future of resuscitation will not be defined by new numbers, but by a deeper understanding of physiology.
Reference 📚
Hernandez, G., Hunsicker, O., de Backer, D., Monnet, X., Pinsky, M. R., Teboul, J. L., et al. (2026). Twenty-five years of septic shock hemodynamic resuscitation trials: a conceptual perspective. Critical Care, 30, 400. doi.org/10.1186/s13054-026-0…
ALT
Cornelius Sendagire, MD retweeted
💧 Fluid Management in Heart Failure and Cardiogenic Shock
Preload vs Congestion
This chapter explains that in acute and chronic heart failure, the challenge is not simply “giving or withholding fluids” but balancing preload to support cardiac output against the risk of venous congestion and pulmonary edema. Conventional preload markers (CVP, PAOP) are often misleading in dilated, stiff or ischemic ventricles, so the authors emphasize integrated assessment using echo, blood pressure, urine output and clinical signs of congestion.
Cardiogenic Shock Strategy
In cardiogenic shock, small, carefully tested fluid challenges may be justified early, but ongoing hypotension is usually better addressed with inotropes, vasopressors and mechanical support rather than repetitive fluid boluses. The chapter highlights how positive fluid balance worsens outcomes in decompensated heart failure and advocates early decongestive therapy and, when needed, ultrafiltration as part of a broader deresuscitation plan.
📘 Full chapter in Rational Use of Intravenous Fluids in Critically Ill Patients:
👉 link.springer.com/book/10.10…
🔵 Discussed in depth at IFAD 2026 in Antwerp.
👉Registration: fluidacademy.org/ifad-2026-r…
#HeartFailure #CardiogenicShock #FluidManagement #VEXUS #ICU
Cornelius Sendagire, MD retweeted
🫁 Respiratory Medicine in the ICU 2026: From Physiology to Precision Care
Key Clinical Takeaways
1. ARDS is becoming a precision medicine disease
The future appears to lie in identifying physiological phenotypes that evolve over time rather than relying on a single diagnosis at ICU admission. Corticosteroid effects may vary according to both inflammatory phenotype and timing of administration.
2. Driving Pressure and Mechanical Power remain critical, but not treatment target
2025 strengthened evidence linking higher driving pressure (DP) and mechanical power (MP) with mortality and poorer ICU outcomes.
However, randomized trials failed to consistently demonstrate improved patient-centered outcomes when ventilation was adjusted solely to optimize DP.
Ventilation should integrate recruitability, spontaneous effort, and hemodynamic tolerance rather than focus on a single number.
3. Patient Self-Inflicted Lung Injury (P-SILI) moved to the bedside
One of the most important developments of was the operationalization of excessive inspiratory effort. This supports an emerging effort-guided ventilation strategy aimed at preventing P-SILI before irreversible injury develops.
4. Ventilator mode matters less than execution
Several major trials demonstrated that under appropriate lung-protective ventilation any mode produced similar patient-centered outcomes.
The quality of execution appears more important than the choice of ventilator mode itself.
5. Noninvasive respiratory support continues to expand
New evidence supports:
✓ Prophylactic NIV after extubation in selected obese patients
✓ HFNO as a valid alternative to NIV in many acute respiratory failure patients
✓ Early recognition of respiratory support trajectories rather than focusing exclusively on device selection
✓ HFNO during bronchoscopy in COPD to reduce procedural hypoxemia.
6. A major setback for inhaled volatile sedation in ARDS
The SESAR trial found that prolonged inhaled sevoflurane sedation in moderate-to-severe ARDS resulted in:
• Fewer ventilator-free days
• Increased 90-day mortality compared with intravenous propofol.
7. EIT continues its march toward routine clinical practice
Electrical Impedance Tomography (EIT) is evolving from a research tool into a practical bedside monitoring technology. EIT is increasingly becoming a cornerstone of precision respiratory care.
8. AI is entering respiratory critical care
The most realistic near-term role is not replacing clinicians but acting as an evidence-based clinical copilot that improves consistency while preserving physician accountability.
Reference 📚
Xia J, Wu Z, Zhang H. Respiratory medicine in the ICU 2026: From physiology to precision care. Journal of Intensive Medicine. 2026. DOI: 10.1016/j.jointm.2026.04.002.
ALT
Cornelius Sendagire, MD retweeted
Part 4 - Heart Surgery in Uganda @HeartUganda
What happens after the heart-lung machine is turned off?
The heart begins beating again, but recovery varies from patient to patient. How long it takes depends on the operation done, the condition of the patient, and a number of other factors. Among them are the type of heart defect and the other diseases the patient has been presenting.
▶️ Watch the full video: youtu.be/avjIMxhskPM?si=O2ee…
#OpenHeartSurgery #UgandaHeartInstitute #DontMissABeat
Cornelius Sendagire, MD retweeted
❤️ Venous Return vs Cardiac Function: Who Really Drives the Circulation?
For decades, intensivists have debated whether cardiac output (CO) is determined primarily by the heart or by venous return (VR). The answer is that both are inseparable components of the same system. At steady state, the heart can only pump the blood that returns to it.
Key physiological concepts:
🔹 Venous return is driven by the gradient between mean systemic filling pressure (Pmsf) and right atrial pressure (RAP).
🔹 Pmsf depends on stressed blood volume and venous tone.
🔹 Cardiac output equals venous return at equilibrium.
🔹 The operating point of the circulation is where the cardiac function curve intersects the venous return curve.
Clinical implications:
✅ In septic shock, vasodilation reduces effective circulating volume and venous return. Fluids increase stressed volume, while vasopressors recruit blood from the unstressed to the stressed compartment, restoring venous return and cardiac output.
✅ In cardiogenic shock, the failing heart becomes the major limitation. Increasing venous return often raises filling pressures more than cardiac output, worsening congestion and pulmonary edema.
✅ Venous congestion itself may impair organ perfusion even when cardiac output appears preserved.
The practical message is simple:
📌 Low cardiac output is not always a pump problem.
📌 Low venous return is not always a volume problem.
📌 Effective hemodynamic management requires identifying whether the primary limitation is venous return, cardiac performance, or both.
Understanding the interaction between Guyton physiology and Frank-Starling physiology remains essential for fluid therapy, vasopressor selection, and shock management in the ICU.
#CriticalCare #Hemodynamics #Shock #SepticShock #CardiogenicShock #ICU #POCUS #FluidResponsiveness #CardiacOutput #IntensiveCare
Reference 📚
Cecconi M, Ostermann M, Pinsky MR. Venous return versus cardiac function: who drives the circulation? Intensive Care Medicine. 2026. DOI: 10.1007/s00134-026-08499-y.
ALT
Cornelius Sendagire, MD retweeted
🫀 Septic Shock Is Not Just About Blood Pressure: It Is About Ventriculo-Arterial Coupling
For years, septic shock resuscitation has focused on restoring MAP, increasing cardiac output, and normalizing lactate.
But what if the real problem is not flow alone?
What if the heart and arterial system are no longer working together?
This is the concept of ventriculo-arterial coupling (VAC): the dynamic interaction between ventricular contractility (Ees) and arterial load (Ea). When coupling is preserved, the cardiovascular system operates efficiently, maximizing stroke work while minimizing myocardial energy expenditure.
Why VAC Matters in Septic Shock
Sepsis causes profound vasoplegia, myocardial depression, and alterations in vascular tone.
As a result, many patients develop ventriculo-arterial uncoupling, where ventricular contractility and arterial load become mismatched. This leads to:
✅ Reduced cardiovascular efficiency
✅ Increased myocardial energetic cost
✅ Impaired tissue perfusion despite apparently adequate cardiac output
✅ Variable responses to fluids, vasopressors, and inotropes
In other words:
Two patients may have the same MAP and cardiac output but completely different cardiovascular efficiency and energetic burden.
The Norepinephrine Paradox
One of the most interesting concepts highlighted by Pinsky and Guarracino is that increasing blood pressure does not always improve cardiovascular performance.
In some septic shock patients with depressed contractility:
🔹 Norepinephrine increases arterial elastance (Ea)
🔹 MAP rises
🔹 Left ventricular afterload increases
🔹 Stroke volume may fall
🔹 VAC worsens
🔹 Cardiac output may remain unchanged or even decrease
The monitor shows a better blood pressure.
The ventricle may actually be working less efficiently.
Why Some Patients Respond and Others Do Not
The review provides a physiological explanation for the heterogeneity we see every day in the ICU.
Patients with preserved contractile reserve may tolerate increased afterload and maintain efficient coupling.
Patients with septic cardiomyopathy may not.
This may explain why identical norepinephrine doses can produce dramatically different hemodynamic responses among seemingly similar septic shock patients.
Beyond Left Ventricular Function
The same principles apply to the right ventricle.
In septic patients with ARDS:
🔹 Pulmonary vascular resistance rises
🔹 RV afterload increases
🔹 RV-pulmonary artery coupling deteriorates
🔹 Venous congestion develops
🔹 Organ perfusion worsens despite acceptable systemic pressures
This reminds us that shock physiology extends far beyond MAP alone.
Clinical Takeaway
Perhaps the next evolution of septic shock management is not simply asking: "Did cardiovascular efficiency improve?"
Reference 📚
Pinsky MR, Guarracino F. Pathophysiological implications of ventriculoarterial coupling in septic shock. Intensive Care Medicine Experimental. 2023;11:87.
doi.org/10.1186/s40635-023-0…
ALT
Cornelius Sendagire, MD retweeted
🫁 Persistent Air Leak in the ICU: Are We Treating the Fistula or Feeding It?
Few complications are as frustrating in critical care as a persistent air leak (PAL).
The patient remains hypoxemic, the chest drain keeps bubbling, the pneumothorax refuses to resolve, and every ventilator adjustment feels like a compromise.
A recent review in BJA Education provides a physiology-based framework for approaching this challenging problem.
The first key concept is understanding that not all persistent air leaks are the same.
🔹 Bronchopleural fistula (BPF): communication between a proximal airway and pleural space.
🔹 Alveolopleural fistula (APF): communication originating from distal airways or alveoli, often associated with pneumonia, ARDS, trauma, or diffuse lung injury.
The article emphasizes a principle that every intensivist should remember:
Air leak flow is largely driven by mean airway pressure (Pmean/Pmaw).
The higher the mean airway pressure, the greater the airflow through the fistula and the harder it becomes for the defect to heal.
This creates a therapeutic dilemma:
We need sufficient airway pressure to maintain oxygenation, but excessive pressure may perpetuate the air leak.
The recommended ventilatory strategy therefore focuses on:
✅ Lowest feasible PEEP
✅ Lowest feasible tidal volume and inspiratory pressure
✅ Short inspiratory time
✅ Lower respiratory rate when tolerated
✅ Permissive hypercapnia when appropriate
✅ Early transition to spontaneous breathing and extubation whenever possible
Interestingly, the authors challenge a common reflex in ICU practice:
Routine chest tube suction may not always help.
Although suction can maintain lung expansion in large leaks, excessive suction may increase the pressure gradient across the fistula and potentially delay healing. When suction is required, the lowest effective level should be used.
For refractory cases, modern management extends beyond conventional drainage:
🔹 Endobronchial valves
🔹 Bronchoscopic mechanical occlusion
🔹 Lung or lobar isolation with bronchial blockers or double-lumen tubes
🔹 VV-ECMO allowing ultra-protective ventilation or even temporary apnea to facilitate fistula healing
Perhaps the most important message is that persistent air leak is not merely a chest drain problem.
It is fundamentally a problem of respiratory physiology, pleural mechanics, and multidisciplinary decision-making, requiring close collaboration between intensivists, respiratory physicians, interventional pulmonologists, thoracic surgeons, and anesthesiologists.
Reference 📚
Mackintosh D, Whebell S, Saxena P, Senthuran S. Persistent air leak in the critically ill. BJA Education. 2026;26(3):101–110. DOI: 10.1016/j.bjae.2025.12.001.
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Cornelius Sendagire, MD retweeted
Haemodynamic equations are useful. But they also mislead.
Take:
CO = HR × SV
CO ≈ (MAP − RAP) / SVR
Both are mathematically true. But they can make the variables they contain look like the controllers of output.
Often they are not.
In the intact circulation, these equations describe the resolved state of the system. They do not, by themselves, tell you what is supplying energy, what is constraining flow, or what is actually limiting output.
That is one of the central themes of our review:
Energy, flow and pressure in the cardiovascular system: a narrative review of how the circulation works.
doi.org/10.1111/anae.70238
Cornelius Sendagire, MD retweeted
🫀📈 One of the most controversial debates in critical care may be shifting again.
This new 2026 systematic review and meta analysis in Annals of Intensive Care challenges that narrative directly.
The study analyzed:
📊 34 studies
📊 636,441 shock patients
📊 PAC, PiCCO and advanced hemodynamic monitoring guided resuscitation strategies
Main finding: ✅ significant reduction in in hospital mortality with advanced hemodynamic monitoring guided management (OR 0.66)
The strongest signal appeared in:
⚠️ cardiogenic shock particularly with pulmonary artery catheter guided therapy.
One of the most interesting physiological observations:
Patients monitored with advanced hemodynamic systems received:
• more vasopressors
• more inotropes
• more mechanical circulatory support
• more RRT
Yet mortality was LOWER.
That is extremely important.
This suggests the benefit may not come from the device itself, but from:
🧠 earlier recognition of instability
🧠 physiology informed escalation
🧠 more precise therapeutic targeting
In other words: better decision making.
The paper strongly supports a concept many intensivists intuitively recognize at bedside:
Not all shock is “vasoplegia plus fluids.”
Different hemodynamic phenotypes require:
• different vasoactive strategies
• different fluid approaches
• different escalation timing
• different mechanical support thresholds
Advanced monitoring may allow clinicians to move away from: “one size fits all resuscitation.”
Another important nuance:
The mortality benefit was strongest in cardiogenic shock.
The evidence in septic shock remains less definitive, although trends still favored advanced monitoring.
This may reflect an important reality: cardiogenic shock is fundamentally a hemodynamic disease.
One particularly valuable message from this paper:
The authors emphasize that modern AHDM is not simply “placing a Swan Ganz catheter.”
It is:
📌 integrating dynamic physiology
📌 interpreting perfusion targets
📌 understanding ventricular interactions
📌 identifying fluid responsiveness limitations
📌 tailoring escalation
Technology without physiology remains insufficient.
Interesting practical point:
The analysis did NOT show major increases in serious complications related to advanced monitoring devices.
That matters because procedural fear has been one of the strongest arguments against invasive monitoring.
My personal takeaway:
Critical care may be entering a new era where: precision hemodynamics returns to the center of shock resuscitation.
Not because catheters are fashionable again because modern shock management increasingly requires individualized physiology rather than protocolized averages.
📖 Reference
Nagy, L., Tóth, P. R., Turan, C., et al. (2026). Annals of Intensive Care, 16, 100071. doi.org/10.1016/j.aicoj.2026…
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Cornelius Sendagire, MD retweeted
🍽️ ICU nutrition: we’ve been doing it wrong for years?
More calories
More protein
Earlier feeding
Sounds logical
But physiology disagrees
⚠️ The key update
High-quality RCTs now show:
❌ Early full-dose nutrition
→ NO benefit
→ Potential harm
Especially in:
• Shock
• Multiorgan failure
• High metabolic stress
👉 This is not neutral
👉 This is dangerous practice
🧠 Critical illness is not static
It evolves through metabolic phases:
1. Acute catabolic phase
2. Stabilization phase
3. Recovery phase
👉 Feeding must follow physiology
Not protocols
🔥 Phase 1: Acute catabolic
• High inflammation
• Insulin resistance
• Endogenous substrate mobilization
👉 The body is NOT ready for full nutrition
💡 Strategy:
✔️ Permissive underfeeding
✔️ Low protein
Why?
Because early overload leads to:
• Hyperglycemia
• Hepatic dysfunction
• Renal stress
• Impaired autophagy
👉 You are feeding dysfunction, not recovery
⚖️ Phase 2: Stabilization
• Inflammation decreasing
• Organ function improving
👉 Now metabolism starts to tolerate nutrition
💡 Strategy:
✔️ Slow escalation
✔️ Daily reassessment
⚠️ Red flags:
• Hypophosphatemia
• Hyperglycemia
→ Patient is NOT ready
💪 Phase 3: Recovery
• Anabolism returns
• Mobility improves
👉 NOW nutrition matters most
💡 Strategy:
✔️ Higher calories
✔️ Higher protein
✔️ Combine with rehab
👉 This is where you rebuild muscle and function
📊 The real takeaway
Nutrition is NOT:
❌ A fixed prescription
❌ A calorie target
It is:
✔️ A dynamic therapy
✔️ A metabolic intervention
🎯 The new principle
“Start low
Advance judiciously
Individualize throughout”
👉 Precision ICU nutrition
⚠️ Final thought
Overfeeding early harms
Underfeeding late harms
👉 Timing is everything
📚 Stoppe C et al. Curr Opin Clin Nutr Metab Care 2026
DOI: 10.1097/MCO.0000000000001186
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