Understanding Angiographic Views
Every angiographic image is named according to the path of the X-ray beam and the position of the image intensifier (II)/detector.
🟨 AP (Anterior–Posterior): The X-ray beam travels posterior ➡️ anterior, with the detector directly above the patient.
🟥 Lateral: Side view of the patient.
⬜ RAO (Right Anterior Oblique): The detector is on the patient's right. Think of the right shoulder turned toward the detector.
⬛ LAO (Left Anterior Oblique): The detector is on the patient's left. Think of the left shoulder turned toward the detector.
🟩 Cranial view: The detector is tilted toward the patient's head, angling the beam headward.
🟪 Caudal view: The detector is tilted toward the patient's feet, angling the beam footward.
💡 Easy memory trick:
RAO = Right shoulder forward
LAO = Left shoulder forward
Cranial = Head
Caudal = Feet
Mastering these projections is essential for accurately visualizing coronary arteries, reducing vessel overlap, and guiding safe catheter-based procedures.
【Splenic Abscess】
In addition to Staph/Strep, it is also important to consider other microorganisms!
Level: Intermediate to advanced
#IDMedEd#IDFellow#IMResident
Squatting position is a classic clinical sign in patients with which of the following conditions?
A) Asthma
B) Tetanus
C) Tetralogy of Fallot
D) Meningitis
An 81-year-old female presented complaining of dizziness, nausea and fatigue. She has a history of pulmonary hypertension and paroxysmal atrial fibrillation.
- What’s your interpretation ?
#medtwitter#foamed#ecg#cardioed
Journal of Clinical Ultrasound
Correlation Between RVOT VTI Measured via a Modified Subcostal View and LVOT VTI in Critically Ill Patients
DOI: 10.1002/jcu.70280
Shareable-link: https://t.co/KsKGfeETtj
#POCUS#VTI#Strokevolume#cardiacoutput#Echo
🫁COPD ventilation is not ARDS ventilation.
In acute COPD exacerbation, the enemy is often not alveolar collapse. It is expiratory flow limitation, dynamic hyperinflation, intrinsic PEEP, respiratory muscle overload, and CO₂ retention.
Recent PubMed indexed literature from 2023 to 2026 reinforces a practical message: in acute hypercapnic COPD exacerbation, NIV remains the first line ventilatory strategy when there is respiratory acidosis, increased work of breathing, and no immediate contraindication (Farmer et al., 2024; Mein & Ferrera, 2025). HFNC may be useful in selected patients, especially when NIV is not tolerated, but recent meta analysis suggests higher treatment failure and crossover to NIV, so it should not replace NIV as default support in acidotic AECOPD (Qin et al., 2025).
The invasive ventilation strategy is different from hypoxemic lung disease.
For the intubated COPD patient, the goal is not to normalize PaCO₂ quickly. The goal is to reduce dynamic hyperinflation.
That means:
Low respiratory rate
Long expiratory time
Modest tidal volume, usually around 6 to 8 mL/kg predicted body weight
Avoidance of excessive minute ventilation
Permissive hypercapnia when pH is acceptable
Monitoring plateau pressure, driving pressure, auto PEEP, expiratory flow, and hemodynamics
PEEP is the controversial part.
External PEEP can help when the patient is spontaneously triggering, because it reduces the inspiratory threshold load caused by intrinsic PEEP. In this context, carefully applied external PEEP may improve synchrony, reduce work of breathing, and facilitate assisted ventilation (Jubran, 2024).
But in controlled ventilation without spontaneous effort, excessive external PEEP may worsen hyperinflation, raise plateau pressure, reduce venous return, increase RV afterload, and precipitate hypotension. Here, low PEEP or minimal PEEP may be safer unless oxygenation requires more support.
A practical bedside rule:
If the COPD patient is triggering and fighting auto PEEP, external PEEP may help.
If the COPD patient is passive, hypotensive, hyperinflated, and not oxygenation limited, high PEEP may harm.
The ventilator question is not:
“How much PEEP does COPD need?”
It is:
Is PEEP unloading the patient, or inflating the trap?
#COPD #CriticalCare #ICU #MechanicalVentilation #NIV #AutoPEEP #Hypercapnia #RespiratoryFailure #VentilatorManagement #IntensiveCare
References📚
*Farmer, M. J. S. Chest, 165(6), 1473–1483. https://t.co/ZgblBs1ZZK
*Jubran, A. Current Opinion in Critical Care, 30(1), 89–96. https://t.co/JKkchvgKDj
*Mein, S. A. CHEST Critical Care, 3(1), 100107. https://t.co/tO69w9ahnl
*Qin, J., Annals of Intensive Care, 15, 64. https://t.co/ay4Wgxbpai
🫁One of the most underappreciated complications of mechanical ventilation may not be inside the lung.
It may be inside the kidney.
This excellent review revisits a question many intensivists intuitively suspect at the bedside:
📌 can PEEP itself contribute to acute kidney injury?
The article moves beyond the simplistic “high vs low PEEP” debate and reframes the problem through physiology.
Not every kidney injury associated with ventilation is simply “shock related.”
The review proposes that:
🫁 lung recruitability
🫀 right ventricular loading
🩸 venous congestion
🧠 neurohormonal activation
🫁 transpulmonary pressure transmission
🩺 abdominal venous stasis
may all interact dynamically during mechanical ventilation.
One particularly important concept:
PEEP may impair renal function not only through reduced cardiac output, but also through venous congestion.
That changes the way we think about ventilator associated AKI.
The review highlights two distinct physiological scenarios:
1️⃣ Highly recruitable lungs
Higher PEEP increases lung volume and pleural pressure, potentially compressing the vena cava and impairing venous return.
2️⃣ Poorly recruitable lungs
Higher PEEP produces overdistension, elevated pulmonary vascular resistance, RV stress, and systemic venous congestion.
Different lungs.
Different mechanisms.
Potentially similar renal consequences.
Another major strength of this paper is the integration of:
• VExUS physiology
• renal venous Doppler
• abdominal congestion
• cardiorenal interactions
• Guytonian hemodynamics
• pulmonary vascular physiology
The figures are particularly educational for ICU clinicians trying to understand how intrathoracic pressure may propagate into systemic venous circulation and renal perfusion.
Importantly, the review does not conclude that “high PEEP is bad.”
Instead, it argues something much more nuanced:
📌 inappropriate PEEP for the individual lung may be harmful.
That distinction matters enormously.
The future probably lies in truly personalized PEEP:
🫁 recruitability based
🫀 RV aware
🩺 congestion monitored
🧠 physiology driven
rather than protocolized fixed tables alone.
For intensivists, this review is also a reminder that: oxygenation improvement does not automatically mean systemic benefit.
Sometimes the kidney is paying the hidden price for a “better” PaO₂.
📖 Benites et al. Critical Care (2025) 29:130 https://t.co/6XP5hYp45T
🧠🫁 In neurocritical care, extubation is not simply a respiratory decision.
It is a brain protection strategy.
The article proposes an important shift:
Weaning in neurocritical patients should not only evaluate:
✅ oxygenation
✅ ventilation
✅ secretion management
but also:
��� neurological stability
🧠 intracranial pressure dynamics
🧠 cerebral perfusion
🧠 delirium prevention
🧠 neuroinflammatory risk
One of the strongest messages of this review is that: Mechanical ventilation is not biologically neutral for the brain.
The review summarizes emerging evidence showing that ventilator induced lung injury (VILI) may trigger systemic cytokine cascades involving:
⚠️ IL 1
⚠️ IL 6
⚠️ TNF α
⚠️ NF κB activation
with potential downstream neuroinflammation and secondary brain injury.
Particularly interesting is the discussion around: 🧠 IL 6 mediated neuroinflammation 🧠 microglial activation 🧠 post extubation delirium 🧠 long term cognitive impairment after prolonged ventilation
The review also highlights an uncomfortable clinical reality:
📌 Failed extubation in neurocritical patients is not a benign event.
It is associated with:
• increased mortality
• longer ICU stay
• higher pneumonia rates
• prolonged mechanical ventilation
• higher tracheostomy rates
One of the most valuable contributions is the proposed CAPREVI algorithm.
Rather than asking: “Can this patient breathe?”
the algorithm asks: 🧠 “Is the brain stable enough to tolerate extubation?”
That distinction is fundamental.
The proposed framework integrates:
• neurological stability
• ICP considerations
• airway secretion control
• hemodynamic status
• delirium prevention
• sedation optimization
• respiratory muscle strength
• spontaneous breathing trials
• multimodal neuromonitoring
Another highly important point:
⚠️ traditional ICU weaning protocols may inadequately account for cerebral vulnerability.
This is particularly relevant in:
• severe TBI
• SAH
• ICH
• neuro postoperative patients
• prolonged neuro ICU admissions
The review also appropriately emphasizes resource limited settings.
Advanced multimodal neuromonitoring is ideal, but neuroprotection can still be approached systematically using:
📌 bedside clinical examination
📌 airway evaluation
📌 ultrasound
📌 CT imaging
📌 structured neurological assessment
Perhaps the most important conceptual takeaway is this:
🧠 Extubation failure in neurocritical care may itself constitute a form of secondary brain injury.
And that changes how we should think about ventilator liberation in this population.
Modern neurocritical care increasingly requires us to stop separating:
🫁 lung physiology
from
🧠 brain physiology
because critically ill patients experience both simultaneously.
📖 Zarra F,. Brain Circulation. 2026. DOI: 10.4103/bc.bc_10_26