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Cor pulmonale chronicum
About 70 y old patient with chronic dyspnoea, permanent atrial fibrillation (CHADS-Vasc-Scor 5), actually deterioration of clinical afflictions. A COPD is kown (stage III GOLD) In TTE and TEE we ccould see a distinct RV-hypertrophy with systolic and diastolic septal bounce (D-sign) as a sign for RV-volume overload and RV-pressure overload (PAPsystolic about 70 mmHg + CVP). In LAA you can see a distinct echocantrast (thrombus?). An another interesting finding is a PFO with right-to-left-shunt.
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About 70 y old patient with chronic dyspnoea, permanent atrial fibrillation (CHADS-Vasc-Scor 5), actually deterioration of clinical afflictions. A COPD is kown (stage III GOLD) In TTE and TEE we ccould see a distinct RV-hypertrophy with systolic and diastolic septal bounce (D-sign) as a sign for RV-volume overload and RV-pressure overload (PAPsystolic about 70 mmHg + CVP). In LAA you can see a distinct echocantrast (thrombus?). An another interesting finding is a PFO with right-to-left-shunt.
Runtime: 1m:20s
Aortic Regurg or something else
red flow in SAX of aortic valve, at 5, 6 and 7 o\'clock position.
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red flow in SAX of aortic valve, at 5, 6 and 7 o\'clock position.
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cardiogenic shock caused by STEMI
about 75 y old patient with dyspnoea and nausea 4 days ago, no chest pain; cardiovascular risk factors: arterial hypertension, diabetes mellitus type 2, hyperlipoproteinaemia. In ECG we could see distinct ST-elevation in I, aVL, V2-V6 as a picture for an anterolaterale infarction, the index-event is 4 days ago; in TTE I could see a dinstinct impairment of myocardial function with anteroapicale, lateral, septale and post./inf. akinesia; best-contraction in basal-septal, basal-lateral and basal-inf./post. segment. NO dynamic obstruction of LVOT caused by hyperdynamic basal segments (very important to see it!!! in that case NO catecholamines, volume and cardioselective beta-blockers, for example esmolol will remedy the situation). In LV-cavum you can see a ruptured tendon of mitral valve without severe mitral valve insufficiency.
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about 75 y old patient with dyspnoea and nausea 4 days ago, no chest pain; cardiovascular risk factors: arterial hypertension, diabetes mellitus type 2, hyperlipoproteinaemia. In ECG we could see distinct ST-elevation in I, aVL, V2-V6 as a picture for an anterolaterale infarction, the index-event is 4 days ago; in TTE I could see a dinstinct impairment of myocardial function with anteroapicale, lateral, septale and post./inf. akinesia; best-contraction in basal-septal, basal-lateral and basal-inf./post. segment. NO dynamic obstruction of LVOT caused by hyperdynamic basal segments (very important to see it!!! in that case NO catecholamines, volume and cardioselective beta-blockers, for example esmolol will remedy the situation). In LV-cavum you can see a ruptured tendon of mitral valve without severe mitral valve insufficiency.
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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.
Runtime: 0m:54s
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.
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Tachy-Cardiomyopathy
about 70 y old patient with tachycardia, dyspnoea and prolonged weakness. in ECG we could see a 2 to 1/ 3 to 1 atrial flutter. In TEE I could found a distinct decrease of myocardial function with pleural and pericardial effusion. Last TTE about 6 weeks ago in sinusrhythm told about a normal myocardial function, so that I assume a tachy-cadiomyopathy because of tachycardia caused by atrial flutter.
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about 70 y old patient with tachycardia, dyspnoea and prolonged weakness. in ECG we could see a 2 to 1/ 3 to 1 atrial flutter. In TEE I could found a distinct decrease of myocardial function with pleural and pericardial effusion. Last TTE about 6 weeks ago in sinusrhythm told about a normal myocardial function, so that I assume a tachy-cadiomyopathy because of tachycardia caused by atrial flutter.
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DCM
about 80 y old patient with prolonged dyspnoea. In TTE we could see a distinct lost of myocardial function with asynchrone myocardial wall motion (SPWMD about 150 ms, IVMD about 60 ms); high grade mitral insufficiency because of dialatation of mitral valve annulus (Carpentier I) and secondary pulmonary hypertension (PAPsystolic about 50-55 mmHg + CVP, RAP-approach on dilatated VCI without inspiratory collaps about 20 mmHg). actually there is no optimal medical therapy established. Some therapeutical options should be dicussed in future: CRT-D, mitral valve clipping.
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about 80 y old patient with prolonged dyspnoea. In TTE we could see a distinct lost of myocardial function with asynchrone myocardial wall motion (SPWMD about 150 ms, IVMD about 60 ms); high grade mitral insufficiency because of dialatation of mitral valve annulus (Carpentier I) and secondary pulmonary hypertension (PAPsystolic about 50-55 mmHg + CVP, RAP-approach on dilatated VCI without inspiratory collaps about 20 mmHg). actually there is no optimal medical therapy established. Some therapeutical options should be dicussed in future: CRT-D, mitral valve clipping.
Runtime: 0m:34s
ischemic cardiomyopathy
about 65 y old patient with dyspnoe; a coronary disease is known, condition after surgical myocardial revascularisation in the 80´s. In TTE you can see a distinct decrease of myocardial funktion with septo-apical akinesia. In cardia catheter there is no chance for improve the coronary state. optimal medical therapy is established. We will implantate an AICD, no LBBB, so no indication for CRT-D to improve the clinical afflictions. Do you have some experiences with cardiac contractility modulation? Do you think that patient could have any benefit with this therapeutical option?
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about 65 y old patient with dyspnoe; a coronary disease is known, condition after surgical myocardial revascularisation in the 80´s. In TTE you can see a distinct decrease of myocardial funktion with septo-apical akinesia. In cardia catheter there is no chance for improve the coronary state. optimal medical therapy is established. We will implantate an AICD, no LBBB, so no indication for CRT-D to improve the clinical afflictions. Do you have some experiences with cardiac contractility modulation? Do you think that patient could have any benefit with this therapeutical option?
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acute pulmonary embolism
about 90 y old patient mit cyanosis, dyspnoea, tachycardia. In TTE we could see a distinct RV-dysfunction with high elevated pulmonary hypertension (PAPsystolic about 90 mmHg, RAP-approach in respect to dilatated VCI with no inspiratory collaps about 20 mmHg > RVSP about 100-110 mmHg). systolic and also diastolic septal shift as a sign of RV-pressure and volume-overload; you can also see the variation of transtricupidal flow dependend on in-and exspiration (inspiratory increase of transtricuspial flow > 45%). In my opinion there is a acute pulmonary embolism with the underlaying disease of chronic cor pulmonale (RV-Hypertrophie!). With ultrasound we found a thrombosis in lower legs. No CT-scan because of GFR of about 20 ml/min! Lysis wasn´t needed till up to now. We started anticoagulation with UFH (aPTT 60-80 sec). In my opinion you can see the classical McConnel sign (Hyperkinetic RV-Apex with hypo-akinetic lateral RV-wall). Any comments?
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about 90 y old patient mit cyanosis, dyspnoea, tachycardia. In TTE we could see a distinct RV-dysfunction with high elevated pulmonary hypertension (PAPsystolic about 90 mmHg, RAP-approach in respect to dilatated VCI with no inspiratory collaps about 20 mmHg > RVSP about 100-110 mmHg). systolic and also diastolic septal shift as a sign of RV-pressure and volume-overload; you can also see the variation of transtricupidal flow dependend on in-and exspiration (inspiratory increase of transtricuspial flow > 45%). In my opinion there is a acute pulmonary embolism with the underlaying disease of chronic cor pulmonale (RV-Hypertrophie!). With ultrasound we found a thrombosis in lower legs. No CT-scan because of GFR of about 20 ml/min! Lysis wasn´t needed till up to now. We started anticoagulation with UFH (aPTT 60-80 sec). In my opinion you can see the classical McConnel sign (Hyperkinetic RV-Apex with hypo-akinetic lateral RV-wall). Any comments?
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RVHD
Severe AR, Severe MS, Moderate AS, Right coronary cusp shows nodular shadow. Is it Perforated / Fenestrated aortic cusp?
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Severe AR, Severe MS, Moderate AS, Right coronary cusp shows nodular shadow. Is it Perforated / Fenestrated aortic cusp?
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Mitral stenosis
70 yo, male, po patient right femoropopliteal bypass because acute arterial occlusion (AAO). Vascular surgeon says the origin of AAO is thrombotic...but...TTE shows mild to moderate Mitral stenosis: look to anterior mitral valve doming, aliasing in mitral inflow, moderately enlarged LA...and no thrombi in LA (but is not TEE)...in contralateral lower limb triphasic spectral doppler waveform ...What do you think? thrombotic or cardioembolic? (he have implanted a DDDR permanent pacemaker a cup of years ago)
Runtime: 1m:46s
70 yo, male, po patient right femoropopliteal bypass because acute arterial occlusion (AAO). Vascular surgeon says the origin of AAO is thrombotic...but...TTE shows mild to moderate Mitral stenosis: look to anterior mitral valve doming, aliasing in mitral inflow, moderately enlarged LA...and no thrombi in LA (but is not TEE)...in contralateral lower limb triphasic spectral doppler waveform ...What do you think? thrombotic or cardioembolic? (he have implanted a DDDR permanent pacemaker a cup of years ago)
Runtime: 1m:46s
left atrial myxoma
left atrial myxoma attached to the interatrial septum( associated with moderate mitral regurgitation and mild aortic regurgitation). surgery:Dr A.Dabbagh.
Runtime: 0m:54s
left atrial myxoma attached to the interatrial septum( associated with moderate mitral regurgitation and mild aortic regurgitation). surgery:Dr A.Dabbagh.
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Shock...and
Hello friends. Young girl in immediate postpartum period (normal delivery) in cold shock. Look the small and \"pseudo\" collapsed cardiac chambers and pericardial effusion, that, in pseuco A4C appears moderate...but...IVC is very small... Note what happens when fluid status became normal...chambers filled and pericardial effusion is minimal.
Runtime: 2m:7s
Hello friends. Young girl in immediate postpartum period (normal delivery) in cold shock. Look the small and \"pseudo\" collapsed cardiac chambers and pericardial effusion, that, in pseuco A4C appears moderate...but...IVC is very small... Note what happens when fluid status became normal...chambers filled and pericardial effusion is minimal.
Runtime: 2m:7s
pulmonary embolism
about 80 y old patient with acute dyspnoea, hypertension and tachycardia; immobile for years. underlaying diseases: arterial hypertension, diabetes mellitus 2, \"high grade\" adiposity. NO known pulmonary disease (no clinical signs of bronchospasm). In TTE (sorry for that bad quality) I could see a distinct pressure overload of RV with systolic shift of septum into LV. A classical McConnel-sign wasn´t seen. But in lower legs no thrombosis (maximum adipositas!). In my opinion that echocardipographic picture with the acute clinical afflictions is compatible with a pulmonary embolism. no ct of lung (kreatinine 3,0 mg/dl); I started UFH (aPTT 60-80 sec.). no catecholamines needed.
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about 80 y old patient with acute dyspnoea, hypertension and tachycardia; immobile for years. underlaying diseases: arterial hypertension, diabetes mellitus 2, \"high grade\" adiposity. NO known pulmonary disease (no clinical signs of bronchospasm). In TTE (sorry for that bad quality) I could see a distinct pressure overload of RV with systolic shift of septum into LV. A classical McConnel-sign wasn´t seen. But in lower legs no thrombosis (maximum adipositas!). In my opinion that echocardipographic picture with the acute clinical afflictions is compatible with a pulmonary embolism. no ct of lung (kreatinine 3,0 mg/dl); I started UFH (aPTT 60-80 sec.). no catecholamines needed.
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malignant pericardial tamponade
about 60 y old patient, underlaying malignant disease is known for a few years. Actually the patient was admitted to our hospital with new tachycardia, silent heart beats, low amplitude in peripheral lead of ECG and dyspnoea (Beck-sign of tamponade). in TTE we could see a distinct interstitial syndrom of apical lung, pleural effusion and pericardial effusion with sign of tamponade (collaps of right atrium, right ventricle and left atrium). Remarkable is the circumstance that there is a collapse of VCI despite of tamponade.
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about 60 y old patient, underlaying malignant disease is known for a few years. Actually the patient was admitted to our hospital with new tachycardia, silent heart beats, low amplitude in peripheral lead of ECG and dyspnoea (Beck-sign of tamponade). in TTE we could see a distinct interstitial syndrom of apical lung, pleural effusion and pericardial effusion with sign of tamponade (collaps of right atrium, right ventricle and left atrium). Remarkable is the circumstance that there is a collapse of VCI despite of tamponade.
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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.
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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.
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aortic valve fibroelastoma
aortic valve fibroelastoma attached to the anterior cusp (in a case of TIA).
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aortic valve fibroelastoma attached to the anterior cusp (in a case of TIA).
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fixed calcified mitral valve prolaps
about 80 y old patient with distinct dyspnoea, recurrend lung oedema and tachykardia. In TTE we found a calcification of posterior cup of mitral valve with severe mitral valve insufficiency. In TEE we could demonstrate a mitral valve prolaps of posterior cup: it seems that there is a \"fixed\" prolaps of posterior cup caused by calcification. The apex of posterior cup shows the picture of flail leaflet. The mitral valve insufficiency is high grade with distinct regurgitation in the pulmonary veins. What do you think? Is this a typical picture of mitral valve prolaps?
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about 80 y old patient with distinct dyspnoea, recurrend lung oedema and tachykardia. In TTE we found a calcification of posterior cup of mitral valve with severe mitral valve insufficiency. In TEE we could demonstrate a mitral valve prolaps of posterior cup: it seems that there is a \"fixed\" prolaps of posterior cup caused by calcification. The apex of posterior cup shows the picture of flail leaflet. The mitral valve insufficiency is high grade with distinct regurgitation in the pulmonary veins. What do you think? Is this a typical picture of mitral valve prolaps?
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abnormal tricuspid chord in a case of turner syndrom
a 9 year old girl with turner syndrom, was referred for evaluation of the ascending aorta(to eliminate an aneurysm of the ascending aorta).the aortic dimensions were normals,there was a bicuspid aortic valve and, as incidental finding,there was an abnormal tricuspid chord inserted directly on the apical septum.
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a 9 year old girl with turner syndrom, was referred for evaluation of the ascending aorta(to eliminate an aneurysm of the ascending aorta).the aortic dimensions were normals,there was a bicuspid aortic valve and, as incidental finding,there was an abnormal tricuspid chord inserted directly on the apical septum.
Runtime: 1m:3s
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