A case of coarctation of the aorta: ECG,echo and treatment
A case of newly diagnosed coactation of the aorta. Discussion of the physical examination , ECG, echocardiogram and treatment. The video has sound (narration). For echo videos see also my channel in
you tube https://www.youtube.com/channel/UCRoOCgmBNnj1kjaemu8dhWw
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Adult with congenital heart defect (Part 1 of 2)
about 50 y old patient with septic shock. A genetic defect is known. There exists no documents of clinical history. In Part 1 you can see the transthoracal echocardiography: we could see an ASD, a
VSD. There is no sign of AV-canal or a stenosis of the pulmonary valve. Furthermore we see a distinct hypertrophy of the right cavum (about 14-15 mm; by comparison with the left ventricular: 12-13
Added: 2050 days ago
Adult with congenital heart defect (Part 2 of 2)
Patient with septic shock and congenital heart defect: in TEE we could see an ASD, a VSD and we had an idea, that there is a sinus venosus defect and a parietal thrombus in the right pulmonary artery
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BiV ICD: Can you see all three leads?
This loop shows the RV inflow view of a patient with a BiV ICD. There are three echodensities representing the three leads in the right side of the heart, can you identify them all?
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Bivalvular endocarditis TTE
about 50 y old patient was admitted to our hospital with weakness and indeterminate fever (> 38,9°C tympanal). Alkcohol addiction is known. We saw a tachypnoea, mild peripheral cyanosis and
tachykardia (atrial fibrillation with herat frequence of about 160 per minutes). We heard a loud diastolic heart murmur: decrescendo above 2. intercostal space right and holodiastolic murmur above 4.
intercostal space left).
Blood samples showed us severe infection with distinct elevated iinfammatory markers.
In TTE I saw the picture of aortic endocarditis with severe aortic insufficiency and a suspicion of mitral valve endocaditis.
Added: 1221 days ago
biventricular cardiomyopathy in sustained slow VT
about 75 y old patient with known dilatative cardiomyopathy. Condition after implantation of 2-chamber-ICD and several electrophysiological therapies/ ablations in context of recurrent VTs.
Actually the patient was admitted to our ICU with cardial decompensation. In ECG we found a slow VT (heart rate about 110 bpm; VT-detection range of ICD 133/min). The TTE you can see shows a
biventricular cardiomyopathie in context of continuous slow VT (this is NO sinus rhythm); beside we see a high-grad insufficiency of mitral valve with reflux into pulmonary veins and a liver
congestion. Despite of application of amiodarone and using the ICD (several application of bursts and 30-Joule-cardioversion-shocks via ICD) there was a severe deterioration of the clinical picture.
At last we couldn´t rescue the patient.
What do you think? Could it be any other options in this case?
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decompensation of DCM caused by failed CRT-D-system
about 50y old patient with known DCM for 5 years. Condition after CRT-D-implantation (indication: left-brandle block with QRS of 130-140 msec, LV-EF about 30-35%). Actually the patient was admitted to
our ER with clinical symptoms of cardial decompensation and a NEW right-brandle-block with QRS of 200 msec!!! So we suggest a failure of CRT-D-system.
In TTE we found a distinct LV-function (measured by Simpson about 20%), a high grade mitral insufficiency and a small AI and PI (probably underestimated in context of severe deceased LV-EF).
Approach to CO: about 3,0 l/min (Sorry not shown, because I couldn´t convert my pictures in avi-format: LVOT-diameter 2,0 cm, LVOT-VTI 14,1 cm, heart-rate 65/min)
Approach to LVEDP: E-velocity: 0,58 m/sec, E`-velocity: 0,03 m/sec; Vp 19 cm/s; E/E`19,3 as an approach of LVEDP).
pulmonal hypertension (postcapillar): PAPs about 40 mmHg, RAP 5-10 mmHg estimated by IVC-collapsity, PV-ATC 70 msec, PV-VTI 7 cm, PAPd about 23-25 mmHg estimated by pulmonary insufficiency).
Added: 1918 days ago
Do you know what prosthesis it is?
about 80 y old patient, condition after heart surgery with aortic valve replacement (in the early 80´s) and implantation of DDD-pacemaker in context of intermittent sinu-atriale blockade, long
AV-Block 1° (above 300 msec) and chronotropic incompetence. In TEE we could see the aortic valve prosthesis, but what kind of prosthesis it is? It looks like a tilting-disk-valve like medtronic-hall
or bjork-shiley-valve (but this would be very unlikely). Unfortunately I couldn´t see the pivot struts and I couldn´t better focalize the regurgitation-flow. It exists no documents about this aortic
prosthesis (in cw: mean pressure gradient is about 20 mmHg, Vmax about 2,4 m/s).
What does the community think about? Please comment!
Added: 2003 days ago
Endocarditis of aortic prosthesis with dehiscence
about 75 y old patient with tachycardia, dyspnoea, new heart murmur and elevated inflammatory markers; a condition after implantation of aortic prosthesis is known because of multiple abscesses in
spleen and liver. The patient was admitted to our ER from another hospital. In TTE we could see a dehiszence of aortic prosthesis and high grade insufficiency. In TEE we saw a typical picture of
endocarditis of aortic prosthesis with dehiszence and paravalvulare abscess.
Added: 1589 days ago
Endocarditis of aortic valve
about 70 y old patient with prolonged subfebrile fever, new heart murmur and weakness. In TTE we assume a floatting structure on aortic valve. In TEE I could see a endocarditis vegetation on
non-coronary aortic cup.
Added: 1537 days ago
endokarditis of aortic valve prosthesis
about 70 y old patient with intermitted fever, high inflammatory markers in blood, prolonged weakness and a new diastolic murmur of heart in Erb-position. In clinical history there was an implantation
of aortic bio-prosthesis about 6 month ago. In TTE we could find a very high transprosthetic gradient and an aortic insufficiency. In TEE you can see a typical endocarditic vegetation of aortic valve
prosthesis. In this case we decided to send that patient to cardiac surgery, because of that large vegetation. Do you agree? Or do you prefer a conservative/ nonsurgical therapy?
Added: 1609 days ago
floating structure on posterior mitral leaf
about 80 y old patient with congestive heart failure and sepsis with pulmonary focus (gram-stain: gram-positive cluster coccal).
In TEE we found a floating structure an posterior leaf of mital valve. not typical for active endocarditis. What could it be? We thought it could be a residual of a former endocarditis or a calcified
residual of tendon of papillary muscle.
What do you think?
Added: 1945 days ago
giant myxoma of LA
young patients with paroxysmale tachycardia and diastolic heart murmur.
In TTE we could see a giant space-occupying lesion.
In TEE I could demonstrate the typical finding of a myxoma in LA with partial prolaps in mitral valve with beginning obstruction (PG mean of cw in mitral position about 5-7 mmHg).
In cardiac catheter I could demonstrate an intense perfusion by an atypical ramus of RCX.
Cardiac surgery is necessary.
Added: 1350 days ago
Haemodynamic monitoring using echocardiography: a trial 1
This is a trial: haemodynamic measurements/ results by echocardiography in comparison with PA-cath-results.
about 75 y old patient with cardiogenic shock by occlusion of RCA.
1. contractility by mv-insufficiency: dp/dt about 320 mmHg/s (this shows a distinct impairment of left ventricle).
2. an approach to LVEDP by E/E`: about 12,7 mmHg
3. approach to CVP alternatively RAP: collapsibility of IVC: one can see, that there is no undulation/ collapsibility of IVC, diameter of IVC > 2 cm: RAP about 15-20 mmHg
4. approach to cardiac output: LVOT-VTI about 23,5 cm, LVOT-area 1,53 cm^2 (radius 0,7 cm) > stroke volume about 36 ml; heart rate: 110/min > cardiac aoutout about 3,9 l/min
5. tricupid valve (TV): Vmax: 3,4 m/sec, PAPs 35 mmHg + CVP; ATC of PV-flow 89 msec, PV-VTI 12,3 cm, one can calculates the PVR with two methods:
> a. PVR= TV-flow velocity/ VTI of RVOT x 10 + 0,16; in this case you can calculate: PVR= 3,4 m/s / 0,125 m x 10 + 0,16 = 276 dyn*s*cm^-5
> b. PVR= (PAPm-PCWP)/CO x 79,9; in this case I couldn´t measure the PAPm and PAPd because I couldn´t depict a PV-insufficiency-signal by echocardiography.
PCWP (LVEDP) 13-14 mmHg, CVP 19 mmHg, CO 4,3-4,5 l/min, PVR 285 dyn*s*cm^-5, SVR 890 dyn*s*cm^-5, cardiac power 0,71 W
In my opinion is echocardiographic measurements of a few parameters a good option to approach haemodynamic in patient and to make a fast decision of therapeutical treatment in ER or ICU. I´m lookinf
forward to any comment, hints, tipps and critic. That could help me to improve my skills in that kind of echocardiographic technique.
Added: 1944 days ago
haemodynamic monitoring using echocardiography: a trial 2
about 60 y old patient with condition after operation of carcinoma of pancreas and chemotherapy. Actually the patient was admitted to our ER with severe oedema of lower limbs: no thromboses of IVC or
deep lower veins of both legs or V. iliacae. We found a severe lack of proteins, especially of albumin.
The patient was hypoton, tachycardiac and weak. No fever, no new heart murmur.
in TTE I found a hyperdynamic heart. Approach to cardiac output demonstrated a cardiac output of about 11,2 l/min (LVOT-diameter 19 mm, LVOT-VTI 42 cm, LVOT-velocity 1,76 m/s, heart rate 96-110/min).
There was a increase of flow in aortic valve looking like low-grade aortic stenosis, but the dimensionsless index was near 1,0 (0,97) showing that there is no aortic stenosis (AV Vmax 2,2 m/s, PGmean
11,2 mmHg). There was also a midventricular gradient and distinct collaps of IVC;
LVOT-VTI-variation was > 13% (I used that variation instead of delta pulse pressure-variation, because I did that echocardiography before tapping an artery)
There wasn´t an incease of LVEDP (E/A 0,88, E/E`about 6 mmHg, velocitiy-prolongation about 0,37 - 0,42 m/s, E´-velocity 0,15 m/s).
No us-b-lines or effusion of pleura.
After fluid-challenge despite of the severe oedema there was a stabilisation of haemodynamic.
Added: 1924 days ago
about 60 y old patient was admitted to our icu with typical clinical afflictions of ACS. Condition after transaortale septal myectomy in the case of HOCM for years. Actually we saw a distinct
LV-hypertrophy with midventricular gradient dependent on heart rate. In LVOT we could found a notable acceleration of flow but NO SAM or midsystolic closure of aortic valve. Under the therapy with
volume and beta-blocker (esmolol) we could see a rapidly haemodynamic improvement.
DON´T give that patient inotropics in cases of haemodynamic instability!
What do you think about? Make it sense to implantate a DDD-pacemaker to reach an asynchronous stimulation of the heart (with asynchronous contraction behavour/ cycle of right and left ventricle) to
moderate the ventricular gradients?
Added: 1985 days ago
huge endocarditic vegetation on tricuspid valve
about 80 y old patient. In medical history, the patient had a metastasizing carcinoma; concition after surgery and chemotherapy. Now the patient was admitted to our ICU with fever and a new heart
murmur. In TEE we could found a huge endocarditic vegetation on the tricuspid valve, probably caused by an infected hickman-catheter.
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