Always need to learn🧑⚕️ Cardiology Fellow / ECG / ETT/Interventional Cardiology /Internal Medecine /
Joined January 2024
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FLUTTER retweeted
The L-wave has a new cut-off. 👀
The updated ASE Guideline 2025 on LV Diastolic Function changes the number - and potentially how we read the signal.
FLUTTER retweeted
AS 🆚 MR 🆚 LVOTO?
Read the ECG. Read the Doppler.
The ECG is part of the echo exam.
AS 🆚 LVOTO 👀 CWform + timing
AS 🆚 MR 👀 CWform + timing
MR 🆚 LVOTO 👀 CWform + timing
#echofirst
@NMerke @Irina67790690
This echo for 30 age male , recently Diagnosed with HOCM
Is this LVOT gradient real or contataminated with MR ? Third image .. is there MCO ? Comments on 2nd image ?
@alex1708ander @argulian @iamritu @Irina67790690 @DrRajeshG1
FLUTTER retweeted
High-output heart failure associated with arteriovenous fistula remains an underrecognized, albeit well-described, clinical entity. This is a nice case with illustrative images - doi: 10.1016/j.jaccas.2026.107193. PMID: 41770183
#POCUS #Nephpearls
FLUTTER retweeted
Most echocardiography laboratories have adopted the 2016 diastolic guidelines. With the release of the 2025 update, an important question arises:
What are the key conceptual differences between the 2016 and 2025 approaches to diagnosing diastolic dysfunction?
academic.oup.com/ehjcimaging…
@JGrapsa
FLUTTER retweeted
#ASEchoJC The Pickelhaube sign: Lateral annular S′ ≥16 cm/s associated with ventricular arrhythmias in MVP ⚡️
#EPeeps
👉jacc.org/doi/epdf/10.1016/j.…
FLUTTER retweeted
#POCUS #echofirst #Nephpearls
RVOT pulse-wave Doppler can provide useful clues about pulmonary vascular resistance.
In normal individuals (A), the waveform has a smooth, dome-shaped appearance, with peak velocity occurring in mid-systole, reflecting a compliant, low-resistance pulmonary circulation.
As RV afterload increases, the waveform gradually becomes more triangular. The RVOT acceleration time shortens, and the peak velocity shifts earlier into systole (B).
With further increases in pulmonary vascular impedance and reduced arterial compliance, a characteristic mid-systolic notch may appear (C), creating the classic "W sign."
In advanced pulmonary hypertension with RV failure, the Doppler envelope becomes smaller and more abbreviated, with a very short and steep AccT (D). This reflects rapid equilibration of RVOT and proximal pulmonary artery pressures due to severe afterload elevation.
Like most POCUS findings, RVOT Doppler should be interpreted in the context of the overall echocardiographic picture rather than in isolation.
#POCUS #Nephpearls #FOAMed
The RV should normally appear smaller than the LV in the apical 4-chamber view and should not exceed about two-thirds of the LV size. If the RV appears equal to or larger than the LV, significant RV dilation should be suspected.
Another helpful visual clue is when the RV becomes the apex-forming ventricle instead of LV. While this finding has not been formally validated with quantitative thresholds, it generally suggests at least moderate RV dilation.
If you remember just one measurement, remember this: the upper limit of normal RV basal diameter is 4.2 cm, measured at end-diastole in an RV-focused apical 4-chamber view.
Also assess RV wall thickness. An RV end-diastolic free wall thickness >5 mm (typically measured in the subcostal view) indicates RV hypertrophy, which often accompanies chronic pressure overload and RV dilation.
Finally, don’t forget to look for interventricular septal flattening on the parasternal short-axis view. Septal flattening (“D-shaped” LV) is another important clue to RV pressure and/or volume overload.
FLUTTER retweeted
#CardioNuggets™
The Pickelhaube sign is a sharp, spiked high-velocity systolic tissue Doppler signal of the lateral mitral annulus seen in arrhythmic mitral valve prolapse.
It’s named after the old German “Pickelhaube” helmet because the Doppler waveform resembles the helmet’s pointed spike.
Why it happens:
Prolapsing mitral leaflets cause abrupt systolic tugging of the papillary muscles/mitral annulus → creating a tall systolic velocity spike on TDI.
Why it matters:
Suggests arrhythmic MVP
Associated with ventricular arrhythmias/SCD risk
Often seen with bileaflet MVP and mitral annular disjunction (MAD)
Image from @drahmedmohsen85
#CardioNuggets #MedEd #EchoFirst
FLUTTER retweeted
🚨 HOT OFF THE PRESS! 🚨
New guidance from the American Society of Echocardiography @ASE360 for Cardiac Ultrasound Artifacts 🫀📡
➡️bit.ly/4tKDSvf
👉 A must-read for everyone in #EchoFirst!
🔍 What is an artifact?
➡️ An imaging feature that does NOT reflect true anatomy/pathology
➡️ Common, expected, and rooted in ultrasound physics ⚙️
💡 Why this matters
⚠️ Artifacts can mimic disease → misdiagnosis → inappropriate management
⚠️ Present across ALL modalities:
• 2D 🖥️
• Spectral Doppler 📈
• Color Doppler
• 3D echo 🧊
📘 What this guideline delivers
✅ Standardized, structured approach to artifacts
✅ Clear explanation of:
• Appearance 👁️
• Mechanism ⚙️
• Clinical impact 🏥
• Real-world cases 🧾
• Mitigation strategies 🛠️
🧠 Also covers
🔹 “Artifact-like” phenomena
🔹 Interference from external devices & equipment 📡
🎯 Key takeaway
👉 Artifacts are inevitable—but misinterpretation is not
👉 Mastering them = safer, smarter echo practice
👩⚕️👨⚕️ Who should read this?
➡️ Sonographers
➡️ Cardiologists
➡️ Trainees
➡️ Anyone interpreting cardiac ultrasound
📢 Elevate your imaging game. Recognize. Understand. Mitigate.
#CardioX #Cardiotwitter @JournalASEcho #ACCFIT
FLUTTER retweeted
Dagger-shaped LVOT Doppler - classic in HOCM, but increasingly relevant in #CriticalCare #Nephrology #POCUS
• What you see
Late-peaking, “dagger” CW Doppler profile
Slow rise → abrupt mid–late systolic peak
• Why it matters
Distinguishes dynamic LVOT obstruction from fixed AS (which peaks early)
• Mechanism
Systolic anterior motion (SAM) of mitral valve
→ leaflet pulled into LVOT during ejection
→ obstruction worsens as systole progresses
• Hemodynamics
Gradient = 4 × V²
≥30 mmHg → significant obstruction
Not just HCM — big ICU problem
Dynamic LVOTO can occur without structural HCM
Seen in septic shock, stress cardiomyopathy, hypovolemia
🚨 Can present as refractory hypotension
…and paradoxically worsens with inotropic vasoactive agents.
Triggers
• Hypovolemia
• Inotropes (dobutamine 👎)
• Low afterload (sepsis)
• Tachycardia, hypercontractility
• High sympathetic tone
Substrate
• LVH (common in #ESRD)
• Small LV cavity
• Sigmoid septum
• Elderly, often female
#POCUS clues (don’t miss this)
• Hyperdynamic, small LV
• SAM of mitral valve (use M-mode in PLAX)
• LVOT flow acceleration
• Dagger-shaped CW Doppler (key finding)
Management flips the script (“LVOTO bundle”)
❌ Stop harm
• Inotropes
• Diuretics
✅ Do the opposite
• Fluids → increase preload
• Afterload → switch norepinephrine to phenylephrine/vasopressin
• Beta-blockade → reduce contractility
• ↓ PEEP if too high
Bottom line
Not all hypotension needs more inotropy.
If you see a dagger, think LVOTO and reverse your reflexes.
FLUTTER retweeted
LBBB and AMI
1: Sensitivity is low with Sgarbossa, Smith, better with Barcelona Algorithm.
2: Don’t rely on ECG changes or troponins to activate Cath lab.
3: Rely on prolonged ischemic symptoms. If the story is good & reliable, don’t regret not calling the Cath lab in time.
FLUTTER retweeted
🫀Cardio DECISION-TRAP
The reflex is immediate:
Troponin up, even if mild = call it NSTEMI.
But every troponin rise is not plaque rupture.
What actually matters??
• Troponin reflects myocardial injury not mechanism
• Type 2 MI and demand ischemia are common
• Sepsis, tachyarrhythmia, anemia, PE and shock can elevate troponin
• Chronic structural heart disease may produce baseline elevation
• Small dynamic changes matter more than isolated values
The physiology:
Troponin is released when myocytes are injured.
That injury can be due to:
• Acute coronary thrombosis
• Oxygen supply-demand mismatch
• Increased wall stress
• Inflammation
• Direct myocardial strain
The biomarker tells you damage occurred. It does not tell you why.
Why this matters on call??
Anchoring on “NSTEMI” can lead to:
• Unnecessary anticoagulation
• Delayed treatment of the real driver (sepsis, arrhythmia, hypoxia)
• Missed systemic instability
The question should not be:
“Is troponin elevated?”
The question should be:
“What is the physiology causing the injury?”
Action points to avoid this trap:
• Look for dynamic change, not a single value
• Correlate with symptoms and ECG
• Assess hemodynamics and systemic stress
• Treat the cause, not just the biomarker
Save for your calls.
What is the most common non-ACS cause of troponin elevation you see on call?
#CardioDecisionTraps #CardioEd #Cardiology @mmamas1973 @Hragy @APSIC6
FLUTTER retweeted
🟡 SA Wenckebach block 🟡
Diagnosis from resting ECG, 24-hour Holter recordings, external ECG event monitoring.
pubmed.ncbi.nlm.nih.gov/1865…
FLUTTER retweeted
🚨 Cardio pearls you should never miss part-3 ( 16-20)
🔴 1️⃣6️⃣ Electrical alternans + low voltage
Think Cardiac Tamponade
• Beat-to-beat QRS amplitude variation
• QRS <5 mm limb leads
• Sinus tachycardia common
• May see PR depression if pericarditis coexists
• Clinical: hypotension + JVP + muffled heart sounds
Large effusion until proven otherwise.
🔴 1️⃣7️⃣ Peaked T waves
Think Hyperkalemia
• Narrow, tall, symmetric T waves
• Shortened QT initially
• PR prolongation
• Loss of P waves
• QRS widening → sine wave pattern
• Bradycardia or arrest in late stage
Calcium first. Labs later.
🔴 1️⃣8️⃣ Short PR + delta wave
Think WPW (Pre-excitation)
• PR <120 ms
• Slurred upstroke of QRS
• Wide QRS
• Secondary ST-T changes
• Risk of AF with very rapid conduction
• Can degenerate into VT/VF
Not all delta waves are benign.
🔴 1️⃣9️⃣ Deep symmetric T inversion V2–V3 (pain-free presentation- Pseudo normalisation pattern pattern)
Think Wellens Syndrome
• Minimal or no ST elevation
• Normal or slightly elevated troponin
• Type A: biphasic T waves
• Type B: deep symmetric inversions
• Occurs after chest pain resolves
• Critical proximal LAD stenosis
• Stress testing can trigger massive MI
Cath not treadmill.
🔴 2️⃣0️⃣ Diffuse ST elevation + PR depression
Think Acute Pericarditis
• Concave (saddle-shaped) STE
• PR elevation in aVR
• No reciprocal ST depression (except aVR, V1)
• ST/T ratio in V6 >0.25
• Spodick’s sign (downsloping TP segment)
• Changes evolve through stages
ST elevation that doesn’t respect a coronary territory.
#MedTwitter #MedX #cardiology #ECG
@DrAkhilX @SameerYogi14 @DocPriyamMD @daoo100 @dr_manish_ydv @DrYdv_hitesh01 @khannaa @MedLearnHub @DrMedica_13 @hammerving @krish__murali @shakilED @ChShafiullah15 @fzn733 @MiguelP23970914 @FibrilloFlutter @Frances98392343 @Medzonetv @Radial2Medial @makkyecg
Cardio pearls you should never miss
Part- 2
🔴 1️⃣1️⃣ ST elevation in aVR + diffuse ST depression
Think Left Main / proximal LAD / severe triple vessel disease
• ST depression ≥1 mm in ≥6 leads
• ST elevation in aVR ≥ V1 strongly suggests LMCA
• Widespread horizontal/downsloping ST depression
• Often hemodynamic instability
• Represents global subendocardial ischemia
• High mortality pattern — activate cath lab
Not “just NSTEMI.”
🔴 1️⃣2️⃣ Tall R in V1 + ST depression V1–V3
Think Posterior MI (posterior STEMI equivalent)
• R/S ratio >1 in V1
• Upright T waves in V1–V3
• Horizontal ST depression
• Mirror image of posterior STE
• Confirm with V7–V9 (≥0.5 mm STE)
• Often associated with inferior or lateral MI
Hidden STEMI.
🔴 1️⃣3️⃣ Regular narrow tachycardia ~150 bpm
Think 2:1 Atrial Flutter until proven otherwise
• Ventricular rate ~150 (atrial ~300)
• Sawtooth flutter waves in II, III, aVF
• Flutter waves may be buried in QRS/T
• Vagal maneuvers or adenosine unmask flutter waves
• Pseudo r’ in V1 may be seen
Don’t label as “SVT” casually.
🔴 1️⃣4️⃣ Irregular wide QRS tachycardia
Think AF with WPW until proven otherwise
• Very fast rates (>200 bpm)
• Beat-to-beat QRS morphology variation
• No consistent P waves
• Delta waves may be visible in sinus rhythm history
• Avoid AV nodal blockers (beta blockers, CCB, digoxin, adenosine)
• Use procainamide or cardiovert
High VF risk.
🔴 1️⃣5️⃣ Coved ST elevation V1–V3 + syncope
Think Brugada pattern (Type 1)
• ≥2 mm coved STE in V1–V2
• T wave inversion following STE
• Incomplete/complete RBBB morphology
• Often normal echo
• Fever can unmask pattern
• Young patient + syncope = high sudden death risk
Not “early repolarization.”
#MedTwitter #MedX #cardiology
@DrAkhilX @albertoortegana @dr_manish_ydv @daoo100 @SameerYogi14 @DocPriyamMD @shakilED @MiguelP23970914 @DrYdv_hitesh01 @TrackYourHeart @MedLearnHub @Frances98392343
FLUTTER retweeted
Cardio pearls you should never miss
Part- 2
🔴 1️⃣1️⃣ ST elevation in aVR + diffuse ST depression
Think Left Main / proximal LAD / severe triple vessel disease
• ST depression ≥1 mm in ≥6 leads
• ST elevation in aVR ≥ V1 strongly suggests LMCA
• Widespread horizontal/downsloping ST depression
• Often hemodynamic instability
• Represents global subendocardial ischemia
• High mortality pattern — activate cath lab
Not “just NSTEMI.”
🔴 1️⃣2️⃣ Tall R in V1 + ST depression V1–V3
Think Posterior MI (posterior STEMI equivalent)
• R/S ratio >1 in V1
• Upright T waves in V1–V3
• Horizontal ST depression
• Mirror image of posterior STE
• Confirm with V7–V9 (≥0.5 mm STE)
• Often associated with inferior or lateral MI
Hidden STEMI.
🔴 1️⃣3️⃣ Regular narrow tachycardia ~150 bpm
Think 2:1 Atrial Flutter until proven otherwise
• Ventricular rate ~150 (atrial ~300)
• Sawtooth flutter waves in II, III, aVF
• Flutter waves may be buried in QRS/T
• Vagal maneuvers or adenosine unmask flutter waves
• Pseudo r’ in V1 may be seen
Don’t label as “SVT” casually.
🔴 1️⃣4️⃣ Irregular wide QRS tachycardia
Think AF with WPW until proven otherwise
• Very fast rates (>200 bpm)
• Beat-to-beat QRS morphology variation
• No consistent P waves
• Delta waves may be visible in sinus rhythm history
• Avoid AV nodal blockers (beta blockers, CCB, digoxin, adenosine)
• Use procainamide or cardiovert
High VF risk.
🔴 1️⃣5️⃣ Coved ST elevation V1–V3 + syncope
Think Brugada pattern (Type 1)
• ≥2 mm coved STE in V1–V2
• T wave inversion following STE
• Incomplete/complete RBBB morphology
• Often normal echo
• Fever can unmask pattern
• Young patient + syncope = high sudden death risk
Not “early repolarization.”
#MedTwitter #MedX #cardiology
@DrAkhilX @albertoortegana @dr_manish_ydv @daoo100 @SameerYogi14 @DocPriyamMD @shakilED @MiguelP23970914 @DrYdv_hitesh01 @TrackYourHeart @MedLearnHub @Frances98392343
Cardio pearls you should never miss
🔴 1️⃣ Wide QRS tachycardia in age >35?
Treat as VT unless proven otherwise. Don’t fall for “SVT with aberrancy.”
🔴 2️⃣ Inferior MI + hypotension + clear lungs?
Think RV infarct. Give fluids, NOT nitrates.
🔴 3️⃣ New systolic murmur 3–5 days after MI?
Think papillary muscle rupture 👉🏻acute MR.
🔴 4️⃣ Sudden hypotension + JVP rise + muffled sounds post-MI?
Free wall rupture 👉🏻 Tamponade.
🔴 5️⃣ Atrial fibrillation + instability?
Immediate synchronized cardioversion. Don’t waste time with rate control.
🔴 6️⃣ Chest pain better on leaning forward + diffuse ST elevation + PR depression?
Acute pericarditis, not STEMI.
🔴 7️⃣ Syncope during exertion in young athlete?
Think HOCM first.
🔴 8️⃣ LBBB + chest pain?
Use modified Sgarbossa criteria, don’t ignore MI.
🔴 9️⃣ Hypertension + hypokalemia?
Primary hyperaldosteronism until proven otherwise.
🔴 🔟 Post-MI day 2–3 fever + pericardial rub?
Early fibrinous pericarditis (not Dressler that’s weeks later)
#MedTwitter #MedX #NEETPG
@SameerYogi14 @dr_manish_ydv @daoo100 @DrYdv_hitesh01 @DocPriyamMD @DrAkhilX @albertoortegana
FLUTTER retweeted
Cardio pearls you should never miss
🔴 1️⃣ Wide QRS tachycardia in age >35?
Treat as VT unless proven otherwise. Don’t fall for “SVT with aberrancy.”
🔴 2️⃣ Inferior MI + hypotension + clear lungs?
Think RV infarct. Give fluids, NOT nitrates.
🔴 3️⃣ New systolic murmur 3–5 days after MI?
Think papillary muscle rupture 👉🏻acute MR.
🔴 4️⃣ Sudden hypotension + JVP rise + muffled sounds post-MI?
Free wall rupture 👉🏻 Tamponade.
🔴 5️⃣ Atrial fibrillation + instability?
Immediate synchronized cardioversion. Don’t waste time with rate control.
🔴 6️⃣ Chest pain better on leaning forward + diffuse ST elevation + PR depression?
Acute pericarditis, not STEMI.
🔴 7️⃣ Syncope during exertion in young athlete?
Think HOCM first.
🔴 8️⃣ LBBB + chest pain?
Use modified Sgarbossa criteria, don’t ignore MI.
🔴 9️⃣ Hypertension + hypokalemia?
Primary hyperaldosteronism until proven otherwise.
🔴 🔟 Post-MI day 2–3 fever + pericardial rub?
Early fibrinous pericarditis (not Dressler that’s weeks later)
#MedTwitter #MedX #NEETPG
@SameerYogi14 @dr_manish_ydv @daoo100 @DrYdv_hitesh01 @DocPriyamMD @DrAkhilX @albertoortegana
FLUTTER retweeted
Compensatory (PVC) vs Non-Compensatory (PAC) pause
🔹 Compensatory Pause
▪︎Seen after: PVCs
▪︎Mechanism: The SA node is NOT RESET by the PVC, so it continues to fire on its normal schedule.
▪︎ECG finding: The interval between the two sinus beats surrounding the PVC equals 2× the normal R–R interval.
Example:
Normal R–R = 800 ms
R–PVC–R interval = ~1600 ms
🔹 Non-Compensatory Pause
▪︎Seen after: PACs
▪︎Mechanism: The SA node is RESET (or discharged early) by the PAC, which alters its timing.
▪︎ECG finding: The interval between the two sinus beats surrounding the PAC is less than 2× the normal R–R interval.
Example
Normal R–R = 800 ms
R–PAC–R interval < 1600 ms
