Cornelius Sendagire, MD

Cardiac anesthesiologist | Intensivist • Founder, Africa’s first Hypoxia Lab • Scalable ICU systems in Africa • Global Health • Medical Simulationist

[Association of Anesthesiologists of Uganda @AnesthesiaUg]

LET US STAND WITH OUR JUNIOR COLLEAGUE, DR. KATENDE FREDRICK

The Association of Anesthesiologists of Uganda (AAU) calls upon colleagues, friends, partners and the general public to support Dr. Katende Fredrick in his urgent fight against end-stage kidney disease.

Our colleague urgently needs a kidney transplant, and every contribution brings him closer to receiving this life-saving treatment.

Please support him through the contribution channels provided on the flyer. Every amount counts. Every act of kindness matters.

Together, we can make a difference and help save a life.

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫁 PaO₂/FiO₂: are we measuring lung injury or ventilator settings?

Two patients with ARDS can have the same PaO₂/FiO₂ ratio and profoundly different lungs. One may have extensive shunt and poor compliance; the other, relatively preserved mechanics but substantial ventilation–perfusion mismatch. A single oxygenation number cannot identify which physiology dominates.

The central warning in this article is that oxygenation severity is not synonymous with lung injury severity.

PaO₂/FiO₂ depends on more than alveolar damage. Changing FiO₂ can alter the ratio nonlinearly, while PEEP, recruitment, airway pressure and ventilatory support modify gas exchange. An improving ratio after ventilator adjustment does not necessarily mean the underlying injury has resolved. Moreover, Berlin ARDS thresholds are practical categories, not distinct physiological boundaries. The review cites a meta-analysis of 28 trials involving 38,270 patients showing only modest mortality discrimination at common PaO₂/FiO₂ thresholds.

SpO₂/FiO₂ offers an accessible, noninvasive alternative, especially without arterial blood gases. But SpO₂ above 97% lies on the flat portion of the oxyhemoglobin dissociation curve, weakening estimation of PaO₂. Poor perfusion, motion, dyshemoglobinemias and skin pigmentation-related measurement bias add uncertainty. Misclassification becomes especially consequential near treatment thresholds.

What should complement these ratios? Respiratory mechanics, driving pressure, compliance, dead-space indices, shunt physiology and the pressure required to achieve oxygenation. Oxygenation index and PEEP-adjusted metrics incorporate some of this missing context. Serial changes over 24to48 hours may also offer more prognostic information than an admission snapshot.

This is a narrative synthesis, not proof that any composite metric improves outcomes or should replace established ARDS criteria.

A better PaO₂/FiO₂ tells us oxygenation changed. It does not, by itself, tell us why.

Reference 📚
Nasa et al. 2026. Journal of Intensive Medicine. https://t.co/IpZkkL234A

#ARDS #MechanicalVentilation #CriticalCare #RespiratoryPhysiology #Oxygenation

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫁ARDS is not only a disease of the alveoli but also a disease of the pulmonary circulation.

Sixty years after its original description, our understanding of ARDS continues to evolve.

In this article Vieillard-Baron, Chew, and Pinsky revisit a fundamental concept: pulmonary vascular dysfunction is both a consequence and an amplifier of lung injury.

The pulmonary circulation normally accommodates large variations in cardiac output through vascular recruitment and distension, maintaining low pulmonary vascular resistance (PVR).

During ARDS, endothelial injury, inflammation, alveolar hypoxia, and mechanical ventilation disrupt this adaptation.

The consequences extend beyond impaired oxygenation.

Increased PVR raises right ventricular (RV) afterload, potentially causing RV dilation, septal displacement, reduced left ventricular filling, and circulatory failure.

The ventilator can either protect or compromise the pulmonary circulation.

The relationship between lung volume and PVR follows a U-shaped curve.

At low lung volumes, alveolar collapse and hypoxic pulmonary vasoconstriction increase vascular resistance. Recruitment may reduce PVR by restoring aeration and vascular flow.

However, excessive lung inflation compresses alveolar capillaries, increases RV afterload, and may worsen cardiac output.

Therefore, higher PEEP is not necessarily better or worse. Its cardiovascular effect depends on recruitment versus overdistension.

Another important observation concerns acute cor pulmonale.

In moderate to severe ARDS, pneumonia, driving pressure ≥18 cmH₂O, PaO₂/FiO₂ <150 mmHg, and PaCO₂ ≥48 mmHg are associated with increased risk of RV dysfunction.

This reinforces the importance of monitoring respiratory mechanics together with echocardiographic RV assessment.

Prone positioning offers benefits beyond oxygenation. By improving aeration, reducing regional collapse, and preserving pulmonary perfusion, it may decrease PVR and improve RV performance.

In refractory cases, VV ECMO may facilitate RV unloading by improving gas exchange and reducing pulmonary vascular stress.

Lung-protective ventilation should also be right-ventricle-protective ventilation.

Optimizing oxygenation while ignoring pulmonary vascular resistance, RV function, and venous return may improve blood gases without improving the patient’s circulation.

Reference 📚
Vieillard-Baron A, 2026. Intensive Care Medicine. https://t.co/eALXvO4r4R

#ARDS #CriticalCare #Hemodynamics #MechanicalVentilation #RightVentricle

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫀Cardiogenic shock may begin long before hypotension appears.

In acute decompensated heart failure (ADHF), the transition toward cardiogenic shock is frequently gradual, concealed by compensatory mechanisms that preserve arterial pressure while tissue perfusion deteriorates.

Ris and colleagues describe this hypoperfusion-shock continuum, challenging the traditional interpretation of shock as predominantly low cardiac output and hypotension.

The physiological problem is more complex.

Tissue perfusion depends on arterial inflow, venous backpressure, and microcirculatory function.

Neurohormonal activation initially preserves arterial pressure through vasoconstriction and recruitment of stressed blood volume. However, increasing venous pressures progressively impair organ perfusion.

The kidney illustrates this mechanism particularly well. Elevated renal venous and interstitial pressures reduce the effective filtration gradient, promoting sodium retention, diuretic resistance, and worsening congestion.

Consequently, a patient may develop renal dysfunction and tissue hypoperfusion despite apparently acceptable blood pressure and cardiac output.

This explains why MAP alone is insufficient to assess perfusion. The difference between MAP and central venous pressure provides additional information about the pressure available for organ perfusion, although it remains an imperfect surrogate.

Another important concept is hemodynamic incoherence.

Prolonged congestion, endothelial dysfunction, inflammation, and altered microvascular autoregulation may uncouple macrocirculation from microcirculation. Restoring cardiac output or arterial pressure may then fail to normalize tissue oxygenation.

The clinical implications are substantial.

Capillary refill time, urine output, lactate trends, venous oxygen saturation, and the venous-to-arterial CO₂ difference provide complementary information. Importantly, normal lactate does not exclude early hypoperfusion.

Echocardiography and pulmonary artery catheterization can further distinguish predominant left ventricular, right ventricular, and biventricular failure, helping identify whether the principal problem is insufficient forward flow, excessive venous congestion, or both.

The therapeutic objective should not be normalization of isolated hemodynamic numbers, but restoration of effective tissue perfusion.

This is a pathophysiological review proposing an integrated monitoring approach, but not a validated treatment algorithm.

Reference 📚
Ris TH, 2026. Circ Heart Fail. https://t.co/d5A1hGst53

#CardiogenicShock #HeartFailure #Hemodynamics #CriticalCare #Microcirculation

[Dr. Chacón-Lozsán F .'. @franciscojlk]

💉Starting hemodialysis: the first sessions should define more than kidney replacement

Initiating hemodialysis is one of the most vulnerable transitions in chronic kidney disease. Early cardiovascular events, functional decline, psychological distress, and mortality remain major concerns.

This review from the European Renal Association's EuDial Working Group proposes ten practical considerations for the first hemodialysis sessions.

Its central message is that a successful dialysis initiation requires more than adequate solute clearance.

Patients should understand what dialysis means, how it will affect their lives, and which alternatives exist. Shared decision-making, including discussion of transplantation and conservative care, should begin early.

From a physiological perspective, volume management deserves particular attention.

Achieving euvolemia is not equivalent to aggressively removing fluid. Excessive ultrafiltration may precipitate intradialytic hypotension, while persistent congestion contributes to cardiovascular complications. Target weight should therefore be reassessed progressively, integrating objective measurements, residual diuresis, and treatment tolerance.

The authors also challenge the automatic prescription of three weekly sessions.

Incremental hemodialysis, once or twice weekly in appropriately selected patients, may help preserve residual kidney function. However, evidence remains largely observational, and this approach requires repeated assessment of residual clearance, biochemical control, and clear criteria for increasing dialysis intensity.

Another important consideration is modality selection.

High-volume hemodiafiltration may improve cardiovascular outcomes in selected patients, but the evidence is not uniformly robust. During initiation, hemodynamic stability and prevention of dialysis disequilibrium should take priority over technological complexity.

Anticoagulation also requires individualization. Patients already receiving systemic anticoagulants may not require conventional additional heparin doses, particularly during shorter sessions.

Beyond the dialysis prescription, the review emphasizes medication reconciliation, vaccination, physical activity, and nutritional assessment.

These are not secondary interventions.

Unnecessary medication exposure increases treatment burden, while excessive dietary restrictions may aggravate protein-energy wasting. Exercise should be encouraged according to individual tolerance rather than postponed automatically.

Remember, these ten tips represent expert clinical suggestions, not formal guideline recommendations.

The first hemodialysis sessions should establish a sustainable therapeutic strategy, not merely initiate an extracorporeal procedure.

Reference 📚
Hecking M, 2026. Clinical Kidney Journal. https://t.co/b7rxhUHjs4

#Nephrology #Hemodialysis #CriticalCare #KidneyFailure #PatientCenteredCare

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫁 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.
https://t.co/cytyCA8v9M

#ARDS #CriticalCare #MechanicalVentilation #RespiratoryPhysiology #Pendelluft

[IMCrit @IM_Crit_]

#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

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫁 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.
https://t.co/t3VkD84f2r

#ARDS #CriticalCare #RespiratoryPhysiology #MechanicalVentilation #Hemodynamics #GasExchange

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫁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.
https://t.co/ea8mIIlh6U

#ARDS #CriticalCare #MechanicalVentilation #RespiratoryPhysiology #Hemodynamics #POCUS #IntensiveCare

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫀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.
https://t.co/TkRiyIDIpS

#CriticalCare #SepticShock #Hemodynamics #Sepsis #Vasopressors #Norepinephrine #Perfusion #POCUS

[Critical Care Reviews @CritCareReviews]

Today's Paper of the Day is:

Bedside assessment of the respiratory system during invasive mechanical ventilation

https://t.co/JKgcYjlUQ5

Join us to read 1 paper per day and stay up-to-date as we cover the spectrum of critical care across 2026

[Fluid Academy @Fluid_Academy]

💧 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:
👉 https://t.co/7pvDxZGh4I

🔵 Discussed in depth at IFAD 2026 in Antwerp.
👉Registration: https://t.co/RF6JwoL40J

#HeartFailure #CardiogenicShock #FluidManagement #VEXUS #ICU

[ANDROMEDA-SHOCK @AndromedaShock]

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!”

[Robert Kalyesubula,MD, FISN(USA), PhD-FRCP(London) @rkalyes1]

🔥 Congratulations to Dr Sendagire on this great achievement!

Aba critical care tubalaba mutandise!
We see you!
@Internist_02
@ErasmusMD

[Dr. Chacón-Lozsán F .'. @franciscojlk]

❤️ 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.
https://t.co/RbD4yxF17m

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫀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. https://t.co/57pYcSZ5de

[Fluid Academy @Fluid_Academy]

💧 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:
👉 https://t.co/7pvDxZGOUg

🔵 Discussed in depth at IFAD 2026 in Antwerp.
👉Registration: https://t.co/wATwBWBg5M

#HeartFailure #CardiogenicShock #FluidManagement #VEXUS #ICU

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫁 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.

[Uganda Heart Institute @HeartUganda]

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: https://t.co/q1Iv07GsWD

#OpenHeartSurgery #UgandaHeartInstitute #DontMissABeat

[Dr. Chacón-Lozsán F .'. @franciscojlk]

❤️ 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.