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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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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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thrombus of left atrial auricle
about 85 y old patient with atrial fibrillation. in TEE we found a thrombus in LAA.
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about 85 y old patient with atrial fibrillation. in TEE we found a thrombus in LAA.
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common atrium
common atrium : absence of the interatrial septum with common atrioventricular valve and 2 av orifices.apical view.
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common atrium : absence of the interatrial septum with common atrioventricular valve and 2 av orifices.apical view.
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Normal mitral annuloplasty
In this transthoracic parasternal long axis clip, there is an echodense structure at the base of the mitral valve. Sometimes confused for mitral annular calcification, in this patient the density is a normally functioning mitral annuloplasty ring. LV function is normal.
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In this transthoracic parasternal long axis clip, there is an echodense structure at the base of the mitral valve. Sometimes confused for mitral annular calcification, in this patient the density is a normally functioning mitral annuloplasty ring. LV function is normal.
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Normal midventricular short axis
In this transthoracic parasternal short axis clip, the LV is seen in its midventricular view with normal LV function.
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In this transthoracic parasternal short axis clip, the LV is seen in its midventricular view with normal LV function.
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Normal aortic valve
In this transthoracic parasternal short axis clip, a normal tricuspid aortic valve is clearly seen in the center of the image.
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In this transthoracic parasternal short axis clip, a normal tricuspid aortic valve is clearly seen in the center of the image.
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4 to 1 flutter
This patient is in atrial flutter at about 4:1 conduction, with flutter waves seen on the ECG tracing. Because of the limited conduction, the mitral and tricuspid valves opening several times for each ventricular contraction, which is clearly seen in this apical 4 chamber clip.
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This patient is in atrial flutter at about 4:1 conduction, with flutter waves seen on the ECG tracing. Because of the limited conduction, the mitral and tricuspid valves opening several times for each ventricular contraction, which is clearly seen in this apical 4 chamber clip.
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HNOCM
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?
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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?
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severe pulmonary embolism
young pregnant woman (38 WOP) with dyspnoea, tachycardia was admitted from another hospital to our icu. We found the echocardiographic picture of an cute cor pulmonale with signs of decompensation. actually no catecholamines was needed. We started anticoagulation with UFH (PTT > 60 sec) and decided to do the sectio with cardiac-surgery-standby. No lysis because of possibility of ablatio of placenta.
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young pregnant woman (38 WOP) with dyspnoea, tachycardia was admitted from another hospital to our icu. We found the echocardiographic picture of an cute cor pulmonale with signs of decompensation. actually no catecholamines was needed. We started anticoagulation with UFH (PTT > 60 sec) and decided to do the sectio with cardiac-surgery-standby. No lysis because of possibility of ablatio of placenta.
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RV failure in context of severe COPD
about 85 y old patient with known severe COPD; intermittent paroxysmal AF is also known, condition after DDD-pacemaker-implantation in another hospital because of BTS and chronotropic incompetence. Actually the patient was admitted to our icu after severe hypoxaemia and therefor resulting sudden cardiac arrest with cardiopulmonary resusciation. In TEE we found a distinct RV-failure and RV-hypertrphy. The left ventricle had an ejection fraction about 50%, we found a notable LV-hypertrophy and diastolic impairment (deceleration-time about 500 msec, E/A 0,7, E/E´about 10-12 mmHg. Tei-index > 0,5, E`< A`). The pw-flow in mitral-valve-position showed a distinct reduction of LV-influx (distinct decrease of E-wave) with serious deterioration of haemodynamic during phases of paroxysmal AF in comparison with sinus rhythm. Volume, inotropics, amiodarone and - after 4 days - sildenafil: we could find a mild improvement of the right ventricle and actually a stabile haemodynamic situation.
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about 85 y old patient with known severe COPD; intermittent paroxysmal AF is also known, condition after DDD-pacemaker-implantation in another hospital because of BTS and chronotropic incompetence. Actually the patient was admitted to our icu after severe hypoxaemia and therefor resulting sudden cardiac arrest with cardiopulmonary resusciation. In TEE we found a distinct RV-failure and RV-hypertrphy. The left ventricle had an ejection fraction about 50%, we found a notable LV-hypertrophy and diastolic impairment (deceleration-time about 500 msec, E/A 0,7, E/E´about 10-12 mmHg. Tei-index > 0,5, E`< A`). The pw-flow in mitral-valve-position showed a distinct reduction of LV-influx (distinct decrease of E-wave) with serious deterioration of haemodynamic during phases of paroxysmal AF in comparison with sinus rhythm. Volume, inotropics, amiodarone and - after 4 days - sildenafil: we could find a mild improvement of the right ventricle and actually a stabile haemodynamic situation.
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LV False tendon
An example of a false tendon in this apical 4 chamber TTE clip. See this image from Circulation for an autopsy specimen from another patient. /nhttp://circep.ahajournals.org/content/3/4/302/F1.expansion.html/nCirc Arr and EP Aug 2010 vol 3 no 4 p 302-304.
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An example of a false tendon in this apical 4 chamber TTE clip. See this image from Circulation for an autopsy specimen from another patient. /nhttp://circep.ahajournals.org/content/3/4/302/F1.expansion.html/nCirc Arr and EP Aug 2010 vol 3 no 4 p 302-304.
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RV Collapse?
In this TTE clip, the RV doesn\'t look quite right. There is an effusion, but does the RV collapse during diastole? Review of the accompanying M-mode suggested that the relaxation was not normal, but there was no true RV diastolic collapse. No other indications of hemodynamic compromise were seen.
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In this TTE clip, the RV doesn\'t look quite right. There is an effusion, but does the RV collapse during diastole? Review of the accompanying M-mode suggested that the relaxation was not normal, but there was no true RV diastolic collapse. No other indications of hemodynamic compromise were seen.
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Eccentric MR
In this TEE clip, MR is readily seen, but this jet is quite eccentric. The flow convergence permits easy estimation of severity using PISA.
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In this TEE clip, MR is readily seen, but this jet is quite eccentric. The flow convergence permits easy estimation of severity using PISA.
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Pericardial effusion with fibrous strands
pericardial effusion with clear fibrin strands - Typical of TB pericardial effusion(59-46% cases in Sub-Saharan Africa). Patient was asymptomatic i.e no respiratory distress, chest pain etc. RA diastolic collapse noted, however No significant respiratory variation could be detected in MV/TV flows. Spontaneous echo contrast was noted in A4CH views.
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pericardial effusion with clear fibrin strands - Typical of TB pericardial effusion(59-46% cases in Sub-Saharan Africa). Patient was asymptomatic i.e no respiratory distress, chest pain etc. RA diastolic collapse noted, however No significant respiratory variation could be detected in MV/TV flows. Spontaneous echo contrast was noted in A4CH views.
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Gigantic Left Atrium
Rheumatic Mitral stenosis with SEVERELY++ dilated LA and Moderate-Severe Mitral Regurgitation. Peak velocity over MV of 2.3m/s and a mean gradient of 6.6mmHg. LA measured 8.8cm in PLAX and had an A4CH area of 161cm².
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Rheumatic Mitral stenosis with SEVERELY++ dilated LA and Moderate-Severe Mitral Regurgitation. Peak velocity over MV of 2.3m/s and a mean gradient of 6.6mmHg. LA measured 8.8cm in PLAX and had an A4CH area of 161cm².
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RV pressure overload and septal bounce
In this parasternal short axis transthoracic clip, you can see the D shape of the LV common in patients with RV pressure overload. The IV septum also bounces in this particular patient with a history of sternotomy for aortic valve replacement.
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In this parasternal short axis transthoracic clip, you can see the D shape of the LV common in patients with RV pressure overload. The IV septum also bounces in this particular patient with a history of sternotomy for aortic valve replacement.
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severe endocarditis of aortic-valve-prosthesis and suspicion of partial-avulsion of prosthesis
about 75 y old patient, admitted from another hospital to our ICU with new heart murmur and septic constellation. In clinical history there is a condition after aortic-valve-replacement (in the late 1990´s). In TTE we could see a distinct aortic insufficiency (verifiable in subclavian artery); for that reason we performed a TEE: it looks like a partial-avulsion of this prosthesis high suspicious for endocarditis of prosthesis. Do you confirm with this diagnosis?
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about 75 y old patient, admitted from another hospital to our ICU with new heart murmur and septic constellation. In clinical history there is a condition after aortic-valve-replacement (in the late 1990´s). In TTE we could see a distinct aortic insufficiency (verifiable in subclavian artery); for that reason we performed a TEE: it looks like a partial-avulsion of this prosthesis high suspicious for endocarditis of prosthesis. Do you confirm with this diagnosis?
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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!
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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!
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Transapical mitral valve replacement
Transapical mitral valve replacement with aortic bioprothesis. in patient with severe LV disfunction. Permanent native valve.
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Transapical mitral valve replacement with aortic bioprothesis. in patient with severe LV disfunction. Permanent native valve.
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