Watch Videos
Videos: 1 - 20 of 510
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. Echocardiographic results: 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. In comparison: the PA-cath-results: 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.
Runtime: 0m:34s
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. Echocardiographic results: 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. In comparison: the PA-cath-results: 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.
Runtime: 0m:34s
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.
Runtime: 0m:45s
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.
Runtime: 0m:45s
bicuspid aortic valve ,aneurysm,dissection,coarctation
previously I have posted some elementary images from this case.Now I upload the complete clip including:bicuspid aortic valve (with mild eccentric aortic regurgitatio),aneurysm of the ascending aorta,type A dissection,atrial septal aneurysm and coarctation of the aorta.
Runtime: 1m:51s
previously I have posted some elementary images from this case.Now I upload the complete clip including:bicuspid aortic valve (with mild eccentric aortic regurgitatio),aneurysm of the ascending aorta,type A dissection,atrial septal aneurysm and coarctation of the aorta.
Runtime: 1m:51s
Mild LV-wall disturbance detected by speckle-pattern
About 45 y old patient with the typical clinical afflictions of acute coronary syndrom. in TTE I couldn´t see a LV-wall-motion-disorder. In Speckle-tracking/-pattern study I found a mild LV-wall-motion-disturbance. Troponin was positive. In coronary study we found a high-grade stenosis of RIVA compatible with the results of speckle-pattern-study. What do you think? Does anybody have any experiences with that kind of stuff? Is it a suitable kind of study?
Runtime: 0m:14s
About 45 y old patient with the typical clinical afflictions of acute coronary syndrom. in TTE I couldn´t see a LV-wall-motion-disorder. In Speckle-tracking/-pattern study I found a mild LV-wall-motion-disturbance. Troponin was positive. In coronary study we found a high-grade stenosis of RIVA compatible with the results of speckle-pattern-study. What do you think? Does anybody have any experiences with that kind of stuff? Is it a suitable kind of study?
Runtime: 0m:14s
Massive RV and RA dilation
In this apical TTE clip, the right ventricle and atrium (seen on the left side of the image) are massively enlarged.
Runtime: 0m:3s
In this apical TTE clip, the right ventricle and atrium (seen on the left side of the image) are massively enlarged.
Runtime: 0m:3s
septic shock caused by huge vegetation of tricuspid valve
young patient with septic shock. intravenous drug consumption is known. in TTE we found a huge endocarditic vegetation on tricuspid valve. in TEE we could verified this, no vegetations on mitral, aortic or pulmonary valve. beside we could see multiple small pulmonary abscesses caused by bacterial embolizations.
Runtime: 0m:24s
young patient with septic shock. intravenous drug consumption is known. in TTE we found a huge endocarditic vegetation on tricuspid valve. in TEE we could verified this, no vegetations on mitral, aortic or pulmonary valve. beside we could see multiple small pulmonary abscesses caused by bacterial embolizations.
Runtime: 0m:24s
cardiogenic shock caused by thrombembolic occlusion of left main stem
about 75 y old patient with STEMI and about 45 minutes cpr. the patient was admitted from our ER after cardiac catheter to our ICU. In cardiac catheter we found a thrombotic occlusion of left main stem, no plaques and no stenosis. in clinical history a permanent atrial fibrillation with condition after several thrombembolic strokes is known. in TEE we found a distinct cardiac wall movement disorder of left ventricle and a small parietal residual of thrombus in LAA. we think that a thrombembolic cardiac infarction caused by thrombus in LAA is the most plausible reason of this finding.
Runtime: 0m:19s
about 75 y old patient with STEMI and about 45 minutes cpr. the patient was admitted from our ER after cardiac catheter to our ICU. In cardiac catheter we found a thrombotic occlusion of left main stem, no plaques and no stenosis. in clinical history a permanent atrial fibrillation with condition after several thrombembolic strokes is known. in TEE we found a distinct cardiac wall movement disorder of left ventricle and a small parietal residual of thrombus in LAA. we think that a thrombembolic cardiac infarction caused by thrombus in LAA is the most plausible reason of this finding.
Runtime: 0m:19s
Lambl's excresence?
In this zoom view of the aortic valve in parasternal long axis TTE, a small filamentous structure is visible on the ventricular side of the valve. Would you characterize this as a Lambl's excresence or would you even comment on it in a report?
Runtime: 0m:3s
In this zoom view of the aortic valve in parasternal long axis TTE, a small filamentous structure is visible on the ventricular side of the valve. Would you characterize this as a Lambl's excresence or would you even comment on it in a report?
Runtime: 0m:3s
Apical Thrombus with and without contrast
In this side-by-side pair of transthoracic apical clips, a thrombus is clearly visualized in the LV apex. The left image is without contrast and the right image is with echo contrast.
Runtime: 0m:4s
In this side-by-side pair of transthoracic apical clips, a thrombus is clearly visualized in the LV apex. The left image is without contrast and the right image is with echo contrast.
Runtime: 0m:4s
DCM
about 50 y old patient with dyspnoea and new diagnosed atrial fibrillation. In TTE we found a distinct decrease of myocardial function. In cardiac catheter there is no coronary disease. Approach to cardiac output by echocardiography: about 3,2 - 3,5 l/min.
Runtime: 0m:22s
about 50 y old patient with dyspnoea and new diagnosed atrial fibrillation. In TTE we found a distinct decrease of myocardial function. In cardiac catheter there is no coronary disease. Approach to cardiac output by echocardiography: about 3,2 - 3,5 l/min.
Runtime: 0m:22s
What on earth is this LV apical mass? 1 of 2
A man in his 40\s presents with an new onset heart failure, severe HTN (SBP ~240) and this mass in his LV. What could it be? Is it thrombus?
Runtime: 0m:3s
A man in his 40\s presents with an new onset heart failure, severe HTN (SBP ~240) and this mass in his LV. What could it be? Is it thrombus?
Runtime: 0m:3s
common atrium
common atrium : absence of the interatrial septum with common atrioventricular valve and 2 av orifices.apical view.
Runtime: 0m:11s
common atrium : absence of the interatrial septum with common atrioventricular valve and 2 av orifices.apical view.
Runtime: 0m:11s
thrombus of left atrial auricle
about 85 y old patient with atrial fibrillation. in TEE we found a thrombus in LAA.
Runtime: 0m:4s
about 85 y old patient with atrial fibrillation. in TEE we found a thrombus in LAA.
Runtime: 0m:4s
Tachy-Cardiomyopathy
About 50 y old patient with atrial fibrillation (HR about 150-170/min); the patient told clinical afflictions in the course of time of 3 weeks. In TTE we found a distinct LV-motion disorder and decrease of LV-EF. After exclusion of thrombus in LAA by TEE we did the elektrical cardioversion. After 1 week we saw a distinct improvement of LV-function.
Runtime: 0m:17s
About 50 y old patient with atrial fibrillation (HR about 150-170/min); the patient told clinical afflictions in the course of time of 3 weeks. In TTE we found a distinct LV-motion disorder and decrease of LV-EF. After exclusion of thrombus in LAA by TEE we did the elektrical cardioversion. After 1 week we saw a distinct improvement of LV-function.
Runtime: 0m:17s
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?
Runtime: 0m:38s
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?
Runtime: 0m:38s
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.
Runtime: 0m:2s
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.
Runtime: 0m:2s
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.
Runtime: 0m:2s
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.
Runtime: 0m:2s
LV False tendon 2
Another example of a LV false tendon in this apical 3 chamber clip.
Runtime: 0m:2s
Another example of a LV false tendon in this apical 3 chamber clip.
Runtime: 0m:2s
pericardial effusion with fibrinous strands
pericardial effusion with fibrinous strands,apical view.etiology:tuberculosis.
Runtime: 0m:18s
pericardial effusion with fibrinous strands,apical view.etiology:tuberculosis.
Runtime: 0m:18s
Copyright (c) 2006-2013 Cardiac Echoes and TEEs | EchoJournal. All rights reserved.
